1193 PDF

Prelims_2.
pdf
Chapter-01_Children are Unique.pdf
Chapter-02_Know What is Normal and What is Not.pdf
Chapter-03_Essentials of History-taking and Examination in a Neonate.pdf
Chapter-04_Outline of Pediatric History and Examination.pdf
Chapter-05_Nutrition.pdf
Chapter-06_Developmental Assessment.pdf
Chapter-07_Central Nervous System.pdf
Chapter-08_Cardiovascular System.pdf
Chapter-09_Respiratory System.pdf
Chapter-10_An Approach to Abdomen.pdf
Chapter-11_An Overview on Importance of Dermatology in Diagnosis.pdf
Chapter-12_Vaccination.pdf
Chapter-13_Blood-Peripheral Smear.pdf
Chapter-14_Staining Microbiological Specimens (Part-I).pdf
Chapter-15_Staining Microbiological Specimens (Part-II).pdf
Chapter-16_Culturing Microbiological Specimen.pdf
Chapter-17_Cerebrospinal Fluid Examination.pdf
Chapter-18_Urine Examination.pdf
Chapter-19_Liver Biopsy.pdf
Chapter-20_Bone Marrow Tests (Aspiration Biopsy Hematopoietic Stem Cell Transplantation).pdf

Chapter-21_Reading an Electrocardiogram.pdf
Chapter-22_CT Scans.pdf
Chapter-23_Chest X-ray (Classical Chest X-rays and Newborn Chest X-rays).pdf
Chapter-24_Abdominal X-rays.pdf
Chapter-25_Bone X-rays.pdf
Chapter-26_Skull X-rays Spine X-rays.pdf
Chapter-27_Equipment (For Airway Obstruction For Circulation For Poisoning For Supportive Car
Chapter-28_Emergency Drugs.pdf
Chapter-29_Calcium Gluconate.pdf
Chapter-30_Sodium Bicarbonate.pdf
Chapter-31_Phenytoin.pdf
Chapter-32_Aminophylline.pdf
Chapter-33_Adrenaline.pdf
Chapter-34_Furosemide.pdf
Chapter-35_Dopamine.pdf
Chapter-36_Oral Rehydration Solution.pdf
Chapter-37_Digoxin.pdf
Chapter-38_Steroids.pdf
Chapter-39_Antibiotics.pdf
Chapter-40_Vitamins and Minerals.pdf
Chapter-41_Asthma Therapy.pdf
Chapter-42_Drugs in Seizure Therapy.pdf
Chapter-43_Drug Treatment of Malaria.pdf
Chapter-44_Drug Treatment of Tuberculosis.pdf
Chapter-45_Oxygen.pdf
Chapter-46_Anemia.pdf
Chapter-47_Lymphadenopathy.pdf
Chapter-48_Muscle Disorders.pdf
Chapter-49_Bleeding Disorders.pdf
Chapter-50_Acute Rheumatic Fever.pdf
Chapter-51_Nephrology Cases.pdf
Chapter-52_Turners Syndrome.pdf
Chapter-53_Achondroplasia.pdf
Chapter-54_Mucopolysaccharidosis.pdf
Chapter-55_Neural Tube Defects.pdf
Chapter-56_Dental Caries.pdf
Chapter-57_Fever.pdf
Index_2.pdf
Pearls in Clinical
PEDIATRICS
Pearls in Clinical
PEDIATRICS
Pushpendra Magon MBBS DCH MD (Pediatrics)

Head
Department of Pediatrics
Patel Hospital
Behind Sky Lark Hotel, Jalandhar
Punjab, India
Foreword
A Radhakrishna
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD.

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2013, Jaypee Brothers Medical Publishers
All rights reserved. No part of this book may be reproduced in any form or by any means
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This book has been published in good faith that the contents provided by the author contained herein are original, and is intended for educational purposes only. While every effort is
made to ensure accuracy of information, the publisher and the author specifically disclaim
any damage, liability, or loss incurred, directly or indirectly, from the use or application of any
of the contents of this work. If not specifically stated, all figures and tables are courtesy of the
author. Where appropriate, the readers should consult with a specialist or contact the manufacturer of the drug or device.
Pearls in Clinical Pediatrics
First Edition: 2013
ISBN 978-93-5025-021-1
Printed at
To
The Almighty
and
My Parents
Foreword
Upon reading this text, I realized that it is a simple presentation of sophisticated
ideas. Physicians often do not understand the value that lies in providing a
palatable approach for systematic diagnosis and management.
Based on my experience with students, I already had no reason to question
the need for such a concept book. We scarcely acknowledge the role of
such most skillfully written books. I wish this book will have wide acceptance
on recognizing the need to break away from total dependency on symptomoriented medical care.
Dr Pushpendra Magon is a tireless crusader with natural love towards
patient care and is an energetic cheerleader for many clinicians providing
invaluable direction, whenever needed by his colleagues and students.
A Radhakrishna MD
Professor of Pediatrics
Sri Venkateswara Medical College, Hospital and Research Centre
Ariyur, Puducherry, India
Preface
The objective of this book is to present the subject matter of pediatrics from
the clinical point of view in as concise form as possible to help in the diagnosis
and treatment of ailments in children.
By means of the clinical approach, we are able to analyze the problems in
pediatrics that baffle clinicians. History-taking and examination form its
essence, of course, supported by investigations. Special care has been taken
regarding nutritional aspect, immunization and development of a child to enable
clinicians deal with the patient as a whole and not merely treat the acute disease
state. The expert knowledge about use of the basic instruments, bedside tests
and X-rays, frequently not given their due importance, are useful for practical
purposes. Care has been taken to include what is likely to be of value especially
in practical examinations, for example, for considerable proportion of students,
even the use of sphygmograph is not stressed.
It is intended, however, not to confine the scope of the book to a description
of the usefulness of bedside tests and examination alone but special emphasis
has been given to procedures as well, the knowledge of which comes handy in
diagnosis, prognosis, and treatment of disorders. Also, by including information
and discussions on common problem cases, which may clear diagnostic and
therapeutic dilemma. I hope the medical practitioners would take the fullest
possible advantage of this book.
Pushpendra Magon
Acknowledgments
I acknowledge Dr Soibam Pritam Singh and Ms Seema Magon, Master Srijan
Magon and Dr Ranju Raj for their valuable help in completing my endeavor
of writing this book. At the same time, I cannot refrain from expressing my
sense of obligation and gratitude to Dr Manorama Verma, Dr Jugesh Chatwal,
Dr Tejinder Singh, Dr Betty Chacko, and my parents who shaped my destiny.
I am thankful to administration of Vinayaka Missions Medical College,
Karaikal, Puducherry, India, for kindly allowing me to use the medvarsity and
X-ray records of some of the patients at this institution. I wish to express my
thanks to my colleagues, postgraduate students, and Professor Dr A
Radhakrishna for the generous disposal of their time in offering many hints,
directed towards compiling the scattered and fragmentary knowledge into a
concise book form.
Although I have taken help from many people, directly or indirectly and it
is impossible to acknowledge my indebtedness to all of them separately, so I
wish to express my deep sense of gratitude to all of them, collectively.
I am extremely pleased to add in this book a chapter on Developmental
Assessment written by Dr Rakesh Magon (MD, MRCP) and another chapter
on Neural Tube Defects written by Dr Shally Magon.
Contents
SECTION 1: CLINICAL PEDIATRICS
1. Children are Unique ............................................................................... 3
Unique Development and Growth Right from the Womb 3 Disease
Presentation, Diagnosis and Management are Unique 3 Agewise
they are Unique 4 Unique Parenting and Psychopathology 5
2. Know What is Normal and What is Not? ............................................. 7
Why to Identify What is Normal? 7
3. Essentials of History-taking and Examination in a Neonate ............ 10
Structure of the History 10 Structure of Examination 11
4. Outline of Pediatric History and Examination .................................. 14
Structure of Pediatric History 14 Structure of Examination 15
5. Nutrition ................................................................................................ 18
Nutrients 18 What is Rainbow Diet = VIBGYOR 19 Vitamins 20
Minerals 23 Structure of Nutritional History 23 Examination
(Head-to-Toe) 24 Protein Energy Malnutrition 25
Anthropometry 25 Weight 26 Height 27 Head
Circumference 27 Mid Upper Arm Circumference (MUAC) 27
Laboratory Tests 28 Treatment 28 Prevention of Malnutrition
on National Scale 30
6. Developmental Assessment .................................................................. 33
Developmental DelayFive Groups 33 Diagnosis of Cerebral
Palsy 34 History Process 36 Physical Examination 37
Investigation 37 Tools for Developmental Assessment 38
7. Central Nervous System ....................................................................... 39
Embryology 39 Anatomical and Physiological Aspects 41
Upper Motor Neurons 41 Lower Motor Neurons 42 Autonomic
Nervous System and the Bladder 42 The Bladder 42 Approach
to a CNS Case 44 History 44 Examination 44 Neurological
Examination of the Infant 56
8. Cardiovascular System ......................................................................... 58
An Overview of Cardiovascular System 58 Heart Embryology 58
Anatomy 60 Physiology 60 Pathology 61 Symptomatology 62
Pathophysiology 64 Cardiovascular History and Examination 69
Structure of History 69 Structure of Examination 70 Systemic
Examination 70 Approach to Cardiovascular Problems of a
Newborn Infant 73 Treatment 75
xiv Pearls in Clinical Pediatrics

9. Respiratory System .............................................................................. 78
Developmental Peculiarities 78 Anatomical Peculiarities of
Children 78 Unique Respiratory Physiology and Pathology 78
Overview of History and Examination 81 Examination 82
Suppurative Complications of Pneumonias 85 Bedside Tests 86
10. An Approach to Abdomen ................................................................... 87
Adopt an Ask, Look, Feel and Hear Approach 87
11. An Overview on Importance of Dermatology in Diagnosis .............. 92
SkinA Diagnostic Marker 92 Hair 96 Nails 96
12. Vaccination ............................................................................................ 98
Immunization 98 Types of Vaccine 98 Infectious Vaccines 98
Noninfectious Vaccines 99 Combination Vaccines 99 Vaccines
for Special Situations 99 Indian Academy of PediatricsSchedule
for Vaccination (2011) 100 BCG (Bacillus Calmette-Gurin) 101
Polio Vaccine 101 Hepatitis B Virus (HBV) Vaccine 102 New
Hepatitis B Vaccine 102 DPT Vaccine (DTWP and DTAP) 102
Measles and MMR Vaccine 103 HIB Vaccine 103 Optional
Vaccines 104 Rotavirus Vaccine 104 Pneumococcal
Vaccines 106 Varicella Vaccine 107 A Killed Hepatitis A
Vaccine 108 Live Attenuated Hepatitis A Vaccine 108
Adolescent Vaccination 109 Cold Chain 110 Proper Storage of
Vaccines 110
SECTION 2: AN OVERVIEW OF BEDSIDE TESTING

13. BloodPeripheral Smear .................................................................. 117
Indications 117 Common Stains 117 Systematic Approach 118
Red Blood Cells (RBCs) 118 Reticulocytes 119 White Blood Cells
(WBCs) 120 Platelets 120
14. Staining Microbiological Specimens (Part-I) ................................... 121
Gram Staining 121 Potassium Hydroxide Preparation 122
15. Staining Microbiological Specimens (Part-II) .................................. 123
ZN Staining (Mnemonic-CSAM) 123
16. Culturing Microbiological Specimen ................................................ 124
Culture Media 124 Classical Media 124 Cultures 125
Blood Culture 125 Urine Culture 125 Stool Culture 126
17. Cerebrospinal Fluid Examination ..................................................... 127
Lumbar Puncture (LP) 127 Technique 127 Indications 127
Diagnostic Indications 128 Therapeutic Indications 129
Anesthetic Indications 129 CSF Interpretation 129
Early Clues 130 Complications 130
18. Urine Examination ............................................................................. 132
Urine 132 Aim of Urine Examination 132
Contents xv
Collection of Urine Sample 132 Naked Eye Characteristics 133
Microbiological Tests 133 Chemical Tests 134 Tests of
Glomerular Function 137 Tests of Renal Tubular Function 137
SECTION 3: PROCEDURES
19. Liver Biopsy ........................................................................................ 141
Indications 141 Equipment and Procedure 141 Contraindications 142 Complications of Percutaneous Liver Biopsy 142
20. Bone Marrow Tests (Aspiration, Biopsy, Hematopoietic
Stem Cell Transplantation) ................................................................ 144
Bone Marrow Tests 144 Indications 144 Equipment and
Procedure 144 Complications 145 Stem Cell Transplantation 146
Types of Stem Cells 146 Source of Stem Cells 146 Uses of
Stem Cells 147 Types of Transplant 148 Complications 148
21. Reading an Electrocardiogram ......................................................... 150
How Impulse Travels 150 Heart Rates (2 Methods) 150
Waves 150 Intervals 153 Assessment of Hypertrophy 153
Rhythms 154
SECTION 4: PEDIATRIC IMAGING

22. CT Scans ............................................................................................ 161
CT Fundamentals 161 Skull Fractures 162 Herpes Simplex
Virus Encephalitis 162 Tubercular Meningitis 163 Brain
Edema 164 Intracranial Hemorrhages in Children 165 Acute
Epidural Hematoma 165 Subdural Hemorrhage 165 Subarachnoid
Hemorrhage 165 Intracerebral Hematomas 166 Summary 167
Hydrocephalus 167
23. Chest X-ray (Classical Chest X-rays and Newborn
Chest X-rays) ....................................................................................... 168
First Observe the Following Points 168 Read the X-ray in
this Order 169 Cardiomegaly on Chest X-ray 171 Classical
X-rays 173 Tension Pneumothorax (Infant) 173 Emphysema 174
Foreign Body Aspiration 174 Croup 174 Chest X-rays of a
Newborn 175 Normal Chest Film of a Newborn 175 Neonatal
Pneumonia 175 Meconium Aspiration Syndrome 176 Hyaline
Membrane Disease 176 Transient Tachypnea of the Newborn
(TTN) 177 Diaphragmatic Hernia 177 Pneumothorax
(Newborn) 178 Congenital Lobar Emphysema 179
24. Abdominal X-rays .............................................................................. 180
Calcifications 180 Sites of Calcification 180 Types of
Calculi 181 Bone and Soft Tissues 181 Gas 182 Air Fluid
Levels 182 Anorectal Malformations 183
xvi Pearls in Clinical Pediatrics

25. Bone X-rays ......................................................................................... 185
Bone Age: Uses (Mnemonic ABCD) 185 Other Uses of X-ray of
Bones 186 Bone Age Assessment 186 Radiographic
Examination for Bone Age Estimation 186 Wrist X-ray 187
Elbow X-ray 188 X-ray Long Bones 188
26. Skull X-rays/Spine X-rays ................................................................. 190
Skull X-rays 190 Indications 190 Views 190 Note the
Following Points on Skull X-rays (Ten Points) 191 Spine
X-rays 195 Note the Following Points on Spine X-rays 195
SECTION 5: EQUIPMENT
27. Equipment (For Airway Obstruction/For Circulation/For Poisoning/
For Supportive Care of Newborns) ................................................... 201
Instruments for Airway Obstruction 201 Oropharyngeal
Airway 201 The Suction Trap (Dee-Lee Suction) 202
Suction Bulb 203 Suction Catheter 203 Suction Apparatus 203
Instruments for Ventilation 203 Resuscitation Bag 203
Instruments for Circulation 207 Instruments for Supportive Care
of Newborns 207 NG (Nasogastric) Tubes 207 Indications or
Uses of NG Tubes 208 Incubators 209 Radiant Warmers 210
Conventional Phototherapy 210 Oxygen Supply Devices 211
SECTION 6: MEDICATIONS
28. Emergency Drugs ............................................................................... 215
Drugs for Emergencies in Infants 215 Neonatal Resuscitation 215
Supraventricular Tachycardia 215 Documented Metabolic
Acidosis 216 Neonatal Seizures 216 Drugs for Emergencies in
Older Children 217 Cardiac Arrest 217 Anaphylaxis 217
Shock Despite Volume Resuscitation 217 Volume Overload 217
Diabetic Ketoacidosis 218 Tet Spells 218 Hypertensive
Crisis 218 Raised Intracranial Tension 218 Convulsions
219 Poisonings 219
29. Calcium Gluconate ............................................................................. 221
Calcium 221 Calcium Gluconate 221 Indications 221
Contraindications 222
30. Sodium Bicarbonate ........................................................................... 224
Sodium Bicarbonate 224 Indications 224 Inj. Sodium
Bicarbonate 225
31. Phenytoin ............................................................................................. 227
Phenytoin 227 Indications and Dosage 227 Adverse Effects 228
32. Aminophylline ..................................................................................... 229
Indications and Dosage 229 Mechanism of Action 229
Contents xvii
33. Adrenaline ........................................................................................... 231
Adrenaline 231 Indications and Dosage 231
34. Furosemide .......................................................................................... 234
Diuretics 234 FurosemideA Loop Diuretic 234 Indications
and Dosage 234 SpironolactoneA Potassium Sparing Diuretic 235
35. Dopamine ............................................................................................. 237
Actions 237 Drug Effects 238 Dosage 238
36. Oral Rehydration Solution ................................................................ 240
Oral Rehydration Solution (ORS) Therapy 240 History 240
Principle of ORS 241 Standard WHO ORS 241 Reduced
Osmolarity ORS 242 Killer ORS 242 Guidelines 243 Failure
of Oral Replacement Therapy 243
37. Digoxin ................................................................................................. 246
Indications and Dosage 246 Digoxin Toxicity 246
38. Steroids ................................................................................................. 248
Indications 248 Glucocorticoids 250 Types 250
Mineralocorticoids 250
39. Antibiotics ............................................................................................ 253
Common Antibiotics and Antibiotic Groups 254
40. Vitamins and Minerals ....................................................................... 258
Agewise Indications 258
41. Asthma Therapy ................................................................................. 260
Steps to Assess the Disease 260 Drugs for Prevention and
Management 260
42. Drugs in Seizure Therapy .................................................................. 265
Types of Seizures 265 Drug Treatment of Epilepsy 265
43. Drug Treatment of Malaria ............................................................... 269
Steps of Treatment 269 Drug Treatment 269 National Vector
Borne Disease Control Program: Suggestions 269 Second Line of
Treatment 270 Third Line of Treatment 271 Resistance 271
Chemoprophylaxis (Prevention by Suppression) 271
Reserve Drugs in Treatment 272
44. Drug Treatment of Tuberculosis ........................................................ 273
Consensus Statement of IAP Working Group 273
45. Oxygen ................................................................................................. 277
Sources of Oxygen 277 Oxygen Administration 278
Uses of Oxygen 278
SECTION 7: PROBLEM-BASED LEARNING

46. Anemia ................................................................................................. 281
Pallor (Problem-based Learning) 281 Case Presentation 281
xviii Pearls in Clinical Pediatrics
47.
48.
49.
50.
51.
Discussion 281 Iron Deficiency Anemia 282 Approach to a

Case of Microcytic Hypochromic Anemia 284
Lymphadenopathy .............................................................................. 288
Lymph Node Enlargement (Problem-based Learning) 288 Case
Presentation 288 Approach to a Case of Lymphadenopathy 289
Muscle Disorders ................................................................................ 291
Muscle Weakness (Problem-based Learning) 291
Case Presentation 291 Discussion 291 Highlight 294
Bleeding Disorders .............................................................................. 296
Petechial Rash (Problem-based Learning) 296
Case Presentation 296 Discussion 296 Approach to a Case of
Bleeding Disorders 297 Pathophysiology 297 Differentiate
Between Bleeding or Clotting Disorders 298
Acute Rheumatic Fever ...................................................................... 300
Joint Pains with Fever (Problem-based Learning) 300
Case Presentation 300 Discussion 300
Nephrology Cases ............................................................................... 304
Edema and Oliguria 304 Case 1 Presentation 304
Discussion 304 Case 2 Presentation 307 Discussion 308
SECTION 8: SPOTTERS
52. Turners Syndrome ............................................................................. 317
Spotter 317
53. Achondroplasia ................................................................................... 320
Spotter 320 Cardinal Features 320
54. Mucopolysaccharidosis ...................................................................... 323
Spotter 323 Clinical Features 323 Types 324 Treatment 326
55. Neural Tube Defects ............................................................................ 327
Spotter 327 Introduction 327 Types of Spinal Defects 328
56. Dental Caries ....................................................................................... 332
Spotter 332 Case Presentation 332 Discussion 332
SECTION 9: MISCELLANEOUS
57. Fever .................................................................................................... 337
Approach to a Case of Fever 337 Pyrexia of Unknown Origin
A Diagnostic Dilemma 338
Index ..................................................................................................... 341
Abbreviations
Abbreviation Interpretation
Abbreviation Interpretation
ABG
ACTH
ADH
AFB
AFP
A /G
AI/AR
ALL
AML
ANA
ANS
ARF
AS
ASD
AV
A-V
BBB
BMR
BP
BT Shunt
BUN
BW
C&S
CAD
CBC
CF
CHD
CHF
CMV
CN
CNS
CoA
COPD
CXR
D5W
DCM
DI
DIC
CP
CPK
CPR
Cr
CRP
CSF
CT
CVP
Arterial Blood Gas

Adrenocorticotropic Hormone
Antidiuretic Hormone
Acid-fast Bacilli
Alpha-fetoprotein
Albumin/Globulin Ratio
Aortic Insufficiency
Acute Lymphocytic Leukemia
Acute Myelogenous Leukemia
Antinuclear Antibody
Autonomic Nervous System
Acute Renal Failure
Aortic Stenosis
Atrial Septal Defect
Atrioventricular
Arteriovenous
Bundle Branch Block
Basal Metabolic Rate
Blood Pressure
Blalock-Taussig Shunt
Blood Urea Nitrogen
Body Weight
Culture and Sensitivity
Coronary Artery Disease
Complete Blood Count
Cystic Fibrosis
Congenital Heart Disease
Congestive Heart Failure
Cytomegalovirus
Cranial Nerves
Central Nervous System
Coarctation of the Aorta
Chronic Obstructive
Pulmonary Disease
Cerebral Palsy
Creatine Phosphokinase
Cardiopulmonary Resuscitation
Creatinine
C-reactive Protein
Cerebrospinal Fluid
Computerized Tomography
Central Venous Pressure
DKA
DM
DPT
DTR
ECG
EMG
ECMO
ENT
ESR
ET
FFP
FRC
FUO
GFR
GI
GU
HAV
HCG
HCM
HCT
HDL
HB
HIV
HLA
HLHS
H/O
HPF
HR
HSV
HTN
I&D
Chest X-ray
5% Dextrose in Water
Dilated Cardiomyopathy
Diabetes Insipidus
Disseminated Intravascular
Coagulopathy
Diabetic Ketoacidosis
Diabetes Mellitus
Diphtheria, Pertussis, Tetanus
Deep Tendon Reflexes
Electrocardiogram
Electromyogram
Extracorporeal Membrane
Oxygenation
Ears, Nose, and Throat
Erythrocyte Sedimentation
Rate
Endotracheal
Fresh Frozen Plasma
Functional Residual Capacity
Fever of Unknown Origin
Glomerular Filtration Rate
Gastrointestinal
Genitourinary
Hepatitis A Virus
Human Chorionic
Gonadotropin
Hypertrophic Cardiomyopathy
Hematocrit
High Density Lipoprotein
Hemoglobin
Human Immunodeficiency Virus
Histocompatibility Locus
Antigen
Hypoplastic Left Heart
Syndrome
History of
High Power Field
Heart Rate
Herpes Simplex Virus
Hypertension
Incision and Drainage
xx Pearls in Clinical Pediatrics

IG
IM
IT
ITP
IV
IVP
KUB
LAD
LDH
LE
LMP
LP
LV
LVH
MAP
MCH
MCHC
MCV
ML
MMR
MRI
MRSA
MS
MVP
NCV
NG
NPO
NSAID
OM
OPV
PA
PAC
PaO2
PAP
PAT
PDA
PEEP
PFT
pg
PKU
PMI
PMN
PND
PO
PPD
PR
PRBC
PRN
Immunoglobulin
Intramuscular
Intrathecal
Idiopathic Thrombocytopenic
Purpura
Intravenous
Intravenous Pyelogram
Kidneys, Ureters, Bladder
Left Axis Deviation
Lactate Dehydrogenase
Lupus Erythematosus
Last Menstrual Period
Lumbar Puncture
Left Ventricle
Left Ventricular Hypertrophy
Mean Arterial Pressure
Mean Cell Hemoglobin
Mean Cell Hemoglobin
Concentration
Mean Cell Volume
Milliliter
Measles, Mumps, Rubella
Magnetic Resonance Imaging
Methicillin Resistant Staph
Aureus
Mitral Stenosis
Mitral Valve Prolapse
Nerve Conduction Velocity
Nasogastric
Nothing by Mouth
Nonsteroidal Antiinflammatory
Drug
Otitis Media
Oral Polio Vaccine
Posteroanterior, Pulmonary
Atresia
Premature Atrial Contraction
Alveolar Oxygen
Pulmonary Artery Pressure
Paroxysymal Atrial
Tachycardia
Patent Ductus Arteriosus
Positive End Expiratory
Pressure
Pulmonary Function Tests
Picogram
Phenylketonuria
Point of Maximal Impulse
Polymorphonuclear Leukocyte
Paroxysmal Nocturnal Dyspnea
By Mouth
Purified Protein Derivative
By Rectum
Packed Red Blood Cells
As Needed
PS
PT
PTH
PTT
PVC
Q
QID
RA
RAD
RAE
RAP
RBBB
RBC
RDA
RDW
RIA
RNA
R/O
RTA
RVH
Rx
SA
SBE
S1
S2
S3
S4
SEM
SGA
SGGT
SGOT
SGPT
SIADH
SLE
S/C
STAT
TA
TAPVC
TB
TBG
TD
TGA
TGV
TIBC
Pulmonic Stenosis
Prothrombin Time
Parathyroid Hormone
Partial Thromboplastin Time
Premature Ventricular
Contraction
Every
Four Times
Rheumatoid Arthritis or Right
Atrium
Right Axis Deviation
Right Atrial Enlargement
Right Atrial Pressure
Right Bundle Branch Block
Red Blood Cell
Recommended Daily
Allowance
Red Cell Distribution Width
Radioimmunoassay
Ribonucleic Acid
Rule Out
Renal Tubular Acidosis
Right Ventricular Hypertrophy
Treatment
Sinoatrial
Subacute Bacterial Endocarditis
First Heart Sound
Second Heart Sound
Third Heart Sound
Fourth Heart Sound
Systolic Ejection Murmur
Small for Gestational Age
Serum Gamma Glutamyl
Transpeptidase
Serum Glutamic Oxaloacetic
Transaminase
Serum Glutamic- Pyruvic
Transaminase
Syndrome of Inappropriate
Antidiuretic Hormone
Systemic Lupus Erythematosus
Subcutaneous
Immediately
Tricuspid Atresia, Truncus
Arteriosis
Total Anomalous Pulmonary
Venous Connection
Tuberculosis
Total Binding Globulin
Tetanus-diphtheria Toxoid
Transposition of the Great
Arteries (same as TGV)
Transposition of the Great
Vessels (same as TGA)
Total Iron Binding Capacity
Abbreviations xxi
TIG
TOF
TOPV
TPN
TSH
TT
TU
URI
UTI
VCUG
Tetanus Immune Globulin

Tetralogy of Fallot
Trivalent Oral Polio Vaccine
Total Parenteral Nutrition
Thyroid Stimulating Hormone
Thrombin Time
Tuberculin Units
Upper Respiratory Infection
Urinary Tract Infection
Voiding Cystourethrogram
V/Q
VSD
VT
vWD
VZV
WBC
WPW
ZDV
Zn
Ventilation - Perfusion
Ventricular Septal Defect
Ventricular Tachycardia
von Willebrand's Disease
Varicella Zoster Virus
White Blood Cell or Count
Wolff-Parkinson-White
Zidovudine
Zinc
xxii Pearls in Clinical Pediatrics
Chart - 1: Growth Chart for Boys
Charts xxiii
Chart - 2: Intrauterine Growth
1
Clinical Pediatrics
1
Children are Unique
UNIQUE DEVELOPMENT AND GROWTH RIGHT
FROM THE WOMB
MicrochimerismA unique phenomenon of the womb: In the womb, blood

cells move between a mother and fetus and fetus to the mother during
pregnancy. Hence, some nonself cells, belonging to mother may persist in
baby in low levels and vice versa (microchimerism). These cells have been
demonstrated for many years after birth, with increased frequency compared
to normal adults, in children with diseased population, like juvenile
dermatomyositis, juvenile idiopathic inflammatory myositis, demonstrating
persistence of maternal microchimerism.
ProgrammingA unique phenomenon of the womb: It occurs during critical
period of brain growth, i.e. intrauterine and extrauterine (during first two
years). The popular view is that children have an advantage in learning a
second language, as childs brain is more flexible to minimum linguistic
input, during the critical period of brain growth.
Seed is sown in the womb: Sometimes prenatal or birth complications may
be the seed of neurological problems
e.g. Cerebral palsy: It may have its roots in prenatal or natal period.
DISEASE PRESENTATION, DIAGNOSIS AND MANAGEMENT

ARE UNIQUE
Their disease risk factors are different: Children are not compressed adults
Risk factors like, congenital heart disease and sickle cell disease are
common causes of stroke in children, while atherosclerosis is rare in
children
Immunologically, Acute Poststreptococcal Nephritic Syndrome is more
common in children compared to adults.
Disease presentation is different:
Examples:
Juvenile onset systemic lupus erythematosis (SLE) has more frequent
neurological and renal manifestations than adult-onset SLE but
immunological markers are similar in both groups
4 Pearls in Clinical Pediatrics
Also signs of meningitis are not seen in infants like kernigs, brudzinsky,
etc. Hence, high index of suspicion is needed
Childhood tuberculosis versus adult tuberculosis: Primary tuberculosis
is the commonest form encountered in children as compared to
reactivation TB in adults. There is a history of exposure to an adult
patient with TB, as childhood TB is usually noninfectious
Not gaining normal health after measles, pertussis, intrathoracic
lymphadenopathy and localized CNS disease occurs with greater
frequency in children.
Disease diagnosis presents special problems: Example- Tuberculosis:
Tests may be influenced by factors such as prior BCG vaccination
The lab diagnosis and the rates of drug-resistance to any drug is limited
because of paucibacillary nature of illness. Sputum is generally not
available for examination in children
Gastric aspirate is used as an alternative to sputum for identification of
acid-fast bacilli
Chest radiography often shows hilar or mediastinal lymphadenopathy.
Regions of cavitation and fibrosis are not apparent on chest radiography,
as healing occurs with calcification in children.
Children are often victims of circumstances: Children are dependent on
others, hence they are more likely to get victimized by abuse
Treatment is also unique:
Example: Tuberculosis
It is difficult to demonstrate AFB due to much lower bacillary load.
Hence, drug-resistance among children with TB is less compared to
adults and hence success is greater in children.
AGEWISE THEY ARE UNIQUE

Infants
They are totally dependent on others for their needs (hence extremely
vulnerable). The most dependent infant is a vulnerable neonate who is
exposed right from birth to gram-negative organisms in maternal vaginal
tract. Atypical organisms like Chlamydia, Mycoplasma are common (in
first 3 months). Later, viral (RSV) bronchiolitis is common (in second half
of infancy). Luckily, infants <6 months are somewhat protected by maternal
antibodies and breast milk.
Peculiarities of infants also include anatomical limitation and
immunological predisposition to particular organisms at particular age,
e.g. infants have small diameter of airways. Hence, they have more chance
of bronchospasm and pooling of secretions. Secondly, distance (Upper
respiratory tract to lower respiratory tract) is shorter allowing organisms
to rapidly move down. Also, the short eustachian tubes in infant predisposes
to otitis media.
Children are Unique 5

Toddler (1-3 years)
Toddlers want to maintain autonomy. They are explorers and hence need
supervision. Gross and fine motor skills develop during this period
Certain infections like Haemophilus influenzae and pneumococci are
common between 6 months and 2 years, causing community acquired
pneumonia.
They are structurally immature and vulnerable, e.g. enamel of a childs
tooth is structurally thinner than an adult tooth. Hence, decay can get into
the nerve of a tooth faster, especially in bottle fed toddlers.
Preschooler (3-6 years)
They have high imagination. They use senses for creative purpose and
learn right from wrong (but we need to curb excessive imagination)
Nephrotic syndrome is common in this age group.
School Goer (6-12 years)
They focus on achievement. Feelings of inferiority may occur due to high

expectations (need to be cautious)
Elimination disorders like Enuresis and Encopresis (wetting/soiling self)
beyond usual age of 5 years, are unique to these children and cause loss of
self-esteem if not managed well. Rheumatic fever is also common in this
age
Change of season (when virus mutates) and passive smoking has major
impact on these children.
Adolescent
Their aim is identity preservation. They are self conscious about appearance
of body changes and career decisions are in focus (they need space)
Societal pressures for thinness may lead to eating disorders like anorexia
and bulimia in teens/young girls.
UNIQUE PARENTING AND PSYCHOPATHOLOGY
Problems in children are unique and at times parenting style may be the
cause or the effect of a particular behavior
In behavioral disorders like attention deficit hyperactivity disorder (ADHD),
oppositional defiant disorder (ODD) and conduct disorder (CD), parenting
style like criticism and poor monitoring may be the cause or the effect
On the other hand, overprotective parental style may lead to mood and
anxiety disorders like fears or phobias, e.g. school phobia and separation
anxiety which may further lead to a more protective approach, creating a
viscious cycle.

BIBLIOGRAPHY
1. Comstock GW, Livesay VT, Woolpert SF. The prognosis of a positive tuberculin
reaction in childhood and adolescence. Am J Epidemiol 1974;99:131-8.
2. Donald PR. Childhood tuberculosis: Out of control? Curr Opin Pulm Med 2002;
8:178-82.
3. Enarson DA. The International Union Against Tuberculosis and Lung Disease Model
National Tuberculosis Programmes. Tuberc Lung Dis 1995;76:95-9.
4. Halil Y, Nuri PO, Sedat U, Sabrye D, Tuncer K. Sar-coidois child vs adult. Indian
Journal of Pediatrics 2006;73(2):143-5.
5. Kabra SK, Lodha R, Seth V. Tuberculosis in children, what has changed in last 20
years. Indian J Pediatr 2002;69(Suppl):S5-10.
6. Microchimerism in children with rheumatic disorders. What does it mean? Current
Rheumatology Reports Current Medicine Group LLC 1523-3774 (Print) 1534- 6307
(Online volume 5, Number 6/December, 200310.1007/s11926-003-0057-x458-62.
7. Miller FM, Seale RME. Tuberculosis in children, Bostan, Little Brown and Co; 1963.
8. Munoz FM, Starke JR. Tuberculosis in children. In: Tuberculosis: A comprehensive
international approach, 2nd edn. New York: Marcell Dekker Inc 2000;553-95.
9. Raviglione MC, Snider DE Jr, Kochi A. Global epidemiology of tuberculosis.
Morbidity and mortality of a worldwide epidemic. JAMA 1995;273:220-6.
10. Udani PM. BCG vaccination in India and tuberculosis in children: Newer facets.
Indian J Pediatr 1994;61:451-62.
Know What is
Normal and What is Not?
WHY TO IDENTIFY WHAT IS NORMAL?

When we know what is normal, then only we find out what is abnormal:
To identify variants of normal: One will not be able to recognize abnormal,

until it becomes comfortable to identify variants of normal, during
examination
Examples:
Retractile testes are thought to represent a normal variant of descended
testes
Hymenal anatomy has many normal variants, including clefts, cysts,
crescents, ridges and hymenal tags.
To allay parental anxiety

Examples:
White blood-tinged discharge and mastitis due to withdrawal of maternal

hormones after birth
Mongolian spots, epstein pearls on palate, milia, harlequin color change
and erythema toxicum are the common variants noted, which may
cause anxiety to parents.
Some normal variants may be hazardous as well, e.g. Anisocoria (unequal
pupil size), may be a normal variant, but at times may imply brain herniation
or coning
To avoid unnecessary treatment: Certain physiologic versus pathologic
states, need to be known to avoid unnecessary treatment Examples:
Physiological loose, frequent stools in a breast fed newborn are due to
increased gastrocolic reflex
Physiologic versus pathologic jaundice. Physiologic jaundice is caused
by increased bilirubin load due to various physiological factors.
Pedia Pearl: Erythema toxicum is rarely seen in preterms (scrapings show eosinophils).

Physiological factors responsible for physiological jaundice:
1. High red blood cell volume in newborns with shorter lifespan of
red blood cells.
2. Poor uptake, conjugation and excretion of bilirubin due to immature
liver in newborn.
3. Increased enterohepatic bilirubin reabsorption due to sterile gut of
newborn.
Unconjugated hyperbilirubinemia (usually not greater than 15 mg/dl)
that begins at 30 weeks and peaks by the fourth. day (ususally not greater
than 15 mg/dl) of life in full term newborns and then steadily declining by
1 week of age is physiological. It does not need treatment.
Pathological jaundice on the other hand either appears within the first 24
hours after birth or is characterized by a rapidly rising bilirubin level (>5
mg/dl per day), or is greater than 15 mg/dl at any age or is prolonged (>15
days in a full-term infant). Lastly, elevated direct bilirubin (more than 20%
of total serum bilirubin) is conjugated hyperbilirubinemia and is always
pathological. A typical example is Biliary Atresia.
Physiological processes may need intervention at times:
Example:
Physiological anemia of infancy due to increased demands, needs iron
supplements.
Knowledge of normalcy is crucial for diagnosis: Examples:
Cardiac remodelling can be a physiological or pathological. The heart
responds to increased demands by raising the stroke volume and heart
rate. Acute volume overload leads to increased stretching. The FrankStarling mechanism increases the contractile force, when the ventricle
wall is stretched. This cardiac hypertrophy is physiological
remodelling occuring as a response to exercise training, and
manifesting as homogeneous hypertrophy and improved cardiac
function However, pathological hypertrophy is inhomogeneous and
has disproportionate fibrosis, associated with cardiac dysfunction (e.g.
dilated cardiomyopathy).
Heart murmurs may also be either physiological or pathological. The
intensity, phase, shape, timing, length; pitch, quality, location, radiation,
the effect of maneuvers and age of onset differentiate them. Murmurs
that completely go away on standing up or sitting down are most likely
benign, while high pitched and/or diastolic murmurs or the ones with
a click, are likely to be pathological. Strangely, bicuspid pulmonary
valve presents a click but is physiological.
Few Innocentmurmurs are given below:
Pedia Pearl: Consistently pigmented stools and bile stained fluid on duodenal
intubation rules out biliary atresia.
Know What is Normal and What is Not? 9
Central venous hum is heard in toddlers as a continuous and soft,

plateau shaped murmur, below the clavicle, like patent ductus
arteriosus but unlike PDA it is innocent as it disappears by
maneuvers (on compression) and is almost, always on the right side
Stills murmur is a soft, low pitched, musical systolic, diamond-shaped
murmur in the left lower sternal border. This is commonly heard starting
at age 3 to 4 years and becomes louder during increased cardiac output
such as with fever, anemia or anxiety. Stills murmur decreases in intensity
with standing and during Valsalvas maneuver, while a similar murmur of
hypertrophic obstructive cardiomyopathy increases in intensity with
standing and during Valsalvas maneuver. Here, echocardiograms are usually
normal as opposed to cardiomyopathy.
For correct interpretation of reports:
Example:
Leukocytosis may be pathological or physiological but leukopenia is
always considered pathological.
POINTS TO REMEMBER
1. Loose golden yellow stools in newborn although frequent are not
pathological, and should not be treated.
2. Mild jaundice in a term baby with onset after 30 hours of life and before
completion of 72 hours is physiological. No treatment is warranted.
3. Murmurs in the immediate newborn period, soon after birth are mostly
functional, and caution should be exercised before announcing to the parents
that their child has a heart disease.
Essentials of
History-taking and
Examination in a Neonate
STRUCTURE OF THE HISTORY
Antenatal history (Aim: To find out risk factors): Enquire about:

1. Maternal age.
2. Number of previous pregnancies including abortions, stillbirths.
3. Duration of second stage of labor.
4. Investigations done during pregnancy like maternal ABO blood type,
TORCH titers.
5. Twin status.
6. Feeding intentions.
7. Background of sepsis (urinary tract infection during pregnancy). (Refer
Chapter 4).
Natal history (Aim: Perinatal asphyxia has to be ruled out):
Rough Apgar score is established by the knowledge of level of
consciousness, i.e. whether irritable, drowsy, lethargic or, flaccid at birth.
Level of resuscitation given (need for oxygen, intubation and assisted
ventilation)
History of instrumental delivery
Evidence of fracture of long bone, clavicle or skull.
Postnatal history (Aim: To establish future prognosis):
Find out:
Feeding practices followed
Respiratory distress or apnea soon after birth
Meconium aspiration, indicated by meconium below vocal cords and
history of meconium staining of liquor
History of jaundice and need for photo-therapy and/or transfusion
History of poor sucking or persistent vomiting, jitteriness, bleeding from
any site, history of low urine output or hematuria, etc. indicating sepsis.
Birth weight (SGA, AGA, LGA).*
Pedia Pearl: Birth asphyxia is the most common cause of seizure on the first day.
*
SGA small for gestational age weigh < 10th percentile

LGAlarge for gestational age weigh > 90th percentile
AGAappropriate for gestational age
Essentials of History-taking and Examination in a Neonate 11

STRUCTURE OF EXAMINATION
Head-to-toe Examination: Each part of the body gives a clue to the illness
Example:
Bulging anterior fontanelle gives clues to conditions like raised ICT
and a persistently open posterior fontanelle suggests a condition like
hypothyroidism
Look out for presence of congenital malformations, deformations or
disruptions: Example:
While eliciting Ortolani sign for congenital dislocated hip; an audible
click is heard when the hip goes into the socket (noted in infancy). If
the sign is elicited, the dislocation should be corrected at that time to
avoid hip dysfunction later
Look for evidence of asphyxia:
Apgar scoring, based on color, heart rate, respiration, reflex response to
nose catheter and muscle tone is done at 1, 3 and 5 minutes after birth
Apgar score = SUM of points for all five parameters. Minimum score:
0 and maximum score: 10 Interpretation: Score 1 to 3 = severe asphyxia;
score 4 to 6 = moderate asphyxia.
Assess nutrition:
It is based on:
Birth weight, fullness of face, prominence of ribs with intercostal
spaces, skin and subcutaneous tissue over thigh and the shape of
buttocks.
Assess gestational age:
It is based on
Dubowitz et al assessment or New Ballard score. Dubowitz et al
assessment has 10 neurological signs viz posture, square window,
ankle dorsiflexion, arm recoil, leg recoil, popliteal angle, heel to ear,
scarf sign, head lag, ventral suspension, edema (preterms are more
hypotonic and flexible).
The 12 external signs are: Skin texture, skin color, skin opacity, lanugo,
plantar creases nipple formation, breast size, ear form, ear firmness,
genitals female/male
Dubowitz has a minimum score of 0 and maximum score of 72
(neurological signs 35 + external signs 37) Formula for Gestational age
= (0.2642 (total score)) +24.595
New Ballard score assesses gestation by Neuromuscular maturity
(6) factors and Physical maturity (7) parameters. It has a min. score
of 13 and max score of 54.
Pedia Pearls:
Intrauterine TORCH infection may present like sepsis.
Severe cyanosis, retractions, grunting, silent chest and tachypnea >80/min indicate
severe respiratory distress.
Assess development: Follow-up high-risk infants who are at risk of

significant developmental abnormalities like those with:
Dysmorphic features, such as cleft palate, tracheoesophageal fistula
Low Apgar score
Premature/IUGR state
NICU hospitalization (for oxygen and/or nasogastric tube feeding,
jaundice, congenital infection, necrotizing enterocolitis, etc.).
Assess situation whether urgent or emergent (i.e. critical) or can wait
(because newborns deteriorate quickly, if action is not taken on time)
Example:
Heart diseases like HLHS (hypoplastic left heart syndrome) which is
ductal dependent for systemic blood flow and D-TGA which is ductal
dependent for pulmonary blood flow, need urgent PGE1 to keep the
ductus arteriosus open
In a neonate with critical CHD presenting with congestive cardiac
failure, stabilization of vital signs is a priority. Take vital signs like
HR/pulse, BP and respiratory rate for quick assessment. ABCs, judicious
oxygen and umbilical lines become a priority, rather than doing detailed
examination at that moment. Side by side, however, taking a quick
prenatal history, reviewing the ultrasounds, fetal echocardiographs and
examining for dysmorphisms, e.g. Trisomies 18, 21, Turners
syndrome and Williams syndrome is to be carried out. Confirmation of
diagnosis with CXR, EKG, ABGs, sepsis work up and echocardiogram, etc. is necessary.
Know that these hys are common in babies, to anticipate and correct
them urgently. They are:
- Hypoxia
- Hypothermia
- Hypocalcemia
- Hypoglycemia
- Hypomagnesemia
- Hyperglycemia.
Blood glucose is done using test strips in newborns (especially high risk,
like preterm infants). Blood glucose value of 40 mg/dl is the level for the
institution of therapy. If untreated, it may result in brain damage.
Portable blood glucose monitoring helpfully to decide on emergency
management.
Pedia Pearls:
Neonatal seizure with best prognosis is hypocalcemic seizure.
Warm and pink feet indicate thermal comfort, cold feel and warm abdomen indicate
cold stress. Entire body cold indicates hypothermia.
Essentials of History-taking and Examination in a Neonate 13

Caution: In case of polycythemia, there is less plasma and increased number
of erythrocytes. This may impede diffusion of glucose from plasma into the
test pad giving an impression of hypoglycemia.
Checking oxygen saturation has now become part of examination in a sick
neonate, e.g. checking pre-and postductal oxygen saturations in case of
differential cyanosis (preductal saturations higher than postductal
saturations). Upper limb pink and lower limb blue indicate left heart
abnormalities (such as aortic arch hypoplasia, critical aortic stenosis,
interrupted aortic arch) while reverse differential cyanosis (that is upper
limb blue and lower limb pink) indicates conditions like (Transposition of
Great Arteries (TGA) with Coarctation of Aorta (CoA).
Detailed systemic examination helps to know the lesion for further specific
management
BIBLIOGRAPHY
1. Apgar V. A proposal for a new method of evaluation of the newborn infant. Anesth
Analg 1953; 32:260.
2. Ballard JL, Khoury JC, et al. New Ballard score expanded to include extremely
premature infants. J Pediatr 1991;119:417-23.
3. Berkow R, Fletcher AJ, et al. The Merck Manual of Diagnosis and Therapy 1992;
16:1978-9.
4. Deter RL, Harrist RB. Chapter 35: Assessment of normal fetal growth. (Figure 35.9
page 378). In: Chervenak FA Isaacson GC Campbell S. Ultrasound in Obstetrics and
Gynecology. Little Brown and Company 1993;361-85.
5. Dubowitz LMS, Dubowitz V, Goldberg C. Clinical assessment of gestational age in
the newborn infant. J Pediatr 1970;77:1-10.
6. Durand M, Ramanathan R. Pulse oximetry for continuous oxygen monitoring in sick
newborn infants. J Pediatr 1986;109(6):1052-6.
7. Fanconi S. Reliability of pulse oximetry in hypoxic infants. J Pediatr 1988;
112(3):424-7.
8. Hay WW Jr, Brockway JM, Eyzaguirre M. Neonatal pulse oximetry: Accuracy and
reliability. Pediatrics 1989; 83(5):717-22.
9. Jennis MS, Peabody JL. Pulse oximetry: An alternative method for the assessment of
oxygenation in newborn infants. Pediatrics 1987;79(4):524-8.
10. Nelson WE, Behrman RE, et al. (Eds). Nelson Textbook of Pediatrics (15th edn).
WB Saunders Company. Chapter 79. The newborn infant pages 1996;433-40. Table
79.2 page 438.
11. Singh M. Examination of the baby, Care of the Newborn (6th edn). Sagar Publication,
New Delhi 2004;117-30.
Outline of Pediatric
History and Examination
STRUCTURE OF PEDIATRIC HISTORY
Chief complaint: Why was the medical attention sought?

History of present illness: Mention about the reliability of the informant.
Give chronological account of the illness and relevant negative history to
rule out various differential diagnosis
Past medical history: Previous hospital admissions, medications, past and
present known allergies and any significant history related to the case
Immunization status: Enumerate clearly (do not say up to date)
Birth history:
Antenatal history: Inquire regarding bleeding, hypertension, fevers,
rupture of membranes, stages of labor, fetal distress, type of delivery
(normal vaginal, cesarean section, use of forceps, breech delivery,
etc.)
Natal/postnatal history: Ask for gestational age at delivery, birth weight,
Apgar score if known, otherwise ask for color and activity of baby at
birth, first cry, breathing problems (use of oxygen) jaundice, birth
injuries, intensive care and length of hospital stay, feeding practiced
(Breast or bottle fed, types of formula, frequency and amount, reasons
for bottle feeding) and when the complementary foods (solids) were
introduced.
Developmental history: Ask history regarding developmental milestones,
sibling comparison, school problems and behavior (temper tantrums, pica)
Dietary history: Explained later in chapter on nutrition
Systemic history: This includes general history (like recent weight loss),
CNS, cardiac, respiratory, gastrointestinal, genitourinary, musculoskeletal,
skin, lymph and pubertal history
Family history: Ask for cardiovascular problems, bleeding, allergy, asthma,
tuberculosis and epilepsy in the family. Also ask about consanguinity, ethnic
background, etc.
Social history: Living situation and conditions especially toilets and crowding
(both inside and outside the house), composition of family and occupation
of parents (per capita income) should be enquired.
Outline of Pediatric History and Examination 15

Make rapport with the child. Let him be on parents lap if needed. Examine
least distressing area first and the more distressing areas later.
Vital Signs
Measure oral temperature (Axillary below six years)

Take heart rate (Femoral pulse in infant and radial pulse in an older child)
Observe respiratory rate (For a full minute)
Take blood pressure (With appropriate size cuff).
Anthropometry
Plot on appropriate growth curve the following parameters:
Take weight, mention expected normal and calculate deficit or excess if
any, and interpret accordingly
Take height/length, mention expected normal and calculate deficit or excess
if any, and interpret
Take greatest occipital frontal circumference, mention expected normal
and calculate deficit or excess if any, with interpretation
Take mid arm circumference only in the 1 to 5 years age group (age independent
in this age group).
General Physical Examination
Assess cooperativeness and look at any striking features from head-to-toe:
CNS (consciousness, mental state)
Face (toxic look, dysmorphic, cyanosis)
Lymph nodes (location, mobility, consistency)
Nutritional status (wasting, obesity)
Skin (turgor for hydration, rashes, petechiae, desquamation, pigmentation
and jaundice).
Head-to-Toe Examination
Head (Fig. 4.1)
Observe size and shape. Feel
the sutures and fontanelles (in
the sitting position), for size,
timing of closure and whether
depressed, bulging or at level.
Assess scalp and hair for
texture/pluckability/color and
alopecia.
Fig. 4.1: Metopic craniosynostosis
Pedia Pearl: Fused sutures may be seen in craniosynostosis which may present
as a ridge and/or asymmetrical head.

Eyes
Look at the pupils, conjunctiva, sclera, cornea, red reflex and assess visual
fields.
Ears/Nose
Look at the tympanic membranes and assess hearing. Observe the nasal mucosa
and septum.
Oral Cavity
Look at the lips for color, mucosal congestion, moistness or dryness. Observe
the tongue for color, papillae, position and tremor and look at the teeth and
gums for their number and for presence of caries, gingivitis, etc. Look at the
palate for intactness of arch and the tonsils for size and color and exudates.
Observe the posterior pharyngeal wall for hyperemia, lymphoid hyperplasia
or bulge. Test gag reflex for assessment of lower cranial nerves.
Neck
Look at the thyroid, tracheal position and masses for cysts, nodes, sinus,
discharge and tenderness and look for presence or absence of nuchal rigidity.
Chest
Inspect the chest wall for shape, use of accessory muscles and retractions.
Count the respiratory rate for one minute. Assess the type of breathing
abdominal/thoracic or periodic (pause <20 seconds is normal in infants).
Percussion is helpful in marking cardiac borders and upper border of liver.
Auscultate for equality of breath sounds (especially in both axillas) and hear
the adventitious sounds-rates, rhonchi (wheeze) and friction rubs, if any.
Abdomen
Inspect for shape (protuberant/scaphoid), visible peristalsis and umbilicus
(healthy/discharging/red). Palpate for liver/spleen/kidneys (which may be
palpable in a normal newborn). Feel for doughiness, guarding and elicit rebound
tenderness, if any. Elicit fluid thrill, shifting dullness or puddle sign, depending
on amount of fluid. Auscultate for bowel sounds.
Musculoskeletal
First of all assess posture. Then assess other aspects. Assess hips for dysplasia
and spine for kyphosis, scoliosis, neural tube defects and dimples. Assess
motion, stability, swelling and tenderness of joints. Now, look at the gait, bow
legs, knock knees, etc.
Outline of Pediatric History and Examination 17

External Genitalia
In boys: Gently look for hernias, hydroceles, cryptorchidism/retractile

testis (a retractile testicle can easily be brought down by hand into the
scrotum). During childhood, cremaster muscle is overactive causing
spontaneous appearance and disappearance of testis in the scrotum
(to control the temperature of the testicle). Most testes come down
permanently sometime before or during puberty. Sometimes, the testicle
is not movable due to Short spermatic cord. One should consider
undescended, or ascending testicle in such cases.
In girls: Especially look for signs of abuse, trauma, etc. Also, do Tanner
staging in both boys and girls during adolescence, for sexual maturity
rating.
Systemic Examination
Detailed systemic examination has been discussed separately in the next few
chapters.
POINTS TO REMEMBER
Rules of pediatric history:
1. Knowledge of differential diagnosis is a must. Rule out those differential
diagnosis one by one, from your history
2. Mother even though illiterate may be a good judge of childs condition. Do
not take her statements lightly
3. At times leading questions help, e.g. Asking the parentsdoes any body
have tuberculosis in the family may elicit a negative response owing to
social stigma, while asking it in another way as to who in the family is
suffering shows that doctor is almost sure about the condition. Relatives
then come out with the correct response in most cases.
5
Nutrition
NUTRIENTS
Different nutrients are classified into seven groups, viz (cereals, pulses, poultry,
meat/fish, fat/oils, vegetables/fruits and milk products). These groups are
discussed below under following headings:
Cereals
Rice contains Riboflavin, Iron, Complex carbohydrate, Energy (RICE)
and proteins. Whole grains (such as brown rice) contain good amounts
of insoluble fiber. It contains starch that reaches the bowel undigested
and encourages the growth of beneficial bacteria. Rice has low fat and
is also gluten free, so suitable for celiacs
Protein content = 8/100 gm of uncooked rice
All cereals and pulses have 350 kcal/100 gm of uncooked material
Wheat is a grain (seed). Whole wheat grain contain dietary fiber,
vitamins, minerals, basic amino acids (including arginine
and lysine), antioxidant phytochemicals, including phytates, phenolic
compounds, bioactive compounds (lignans, phytosterols) and
antinutrients including phytic acid and tannins. The top layer is the
germ husk (fiber), then there is a layer of bran. Next layer is the starchy
endosperm.
Pulses
Each 100 gm of pulse has a high protein content of 20 gm and has 350
kcal along with fiber, iron, B vitamins and calcium
Soybean has 40 gm protein and 350 kcal. It is a good source of iron
and calcium.
Eggs
Egg is a nutrient dense reference protein, i.e. one inexpensive egg
provides 6 gm of protein and only 60 calories along with choline, folic
acid, iron, zinc, vitamin E, vitamin A and riboflavin
Eggs have highest quality protein with all essential amino acids (efficacy
of protein for growth is 93.7).
Nutrition 19
Meat and fish are good source of first class proteins and essential fatty
acids
Fat/Oils and Sugar/Jaggery: 1 spoon sugar or jaggery = 20 calories while 1
spoon oil = 45 calories
Vegetables and fruits
Examples:
The drumsticks
The drumsticks pods are antibacterial and a wonderful cleanser, rich
in iron, vitamin C, beta carotene, copper and iodine
The fresh leaves contain twice as many calories and they are also rich
in iron, manganese, zinc, copper, vitamin B, vitamin C and calcium.
The leaves are edible as salad greens and also have potential anticancer
effects
It is even used as poultice for sores and headaches
The root juice has an antibiotic and counter-irritant effect
Drumstick seed powder is an efficient and cheap water purifying agent
that sediments most of the impurities in turbid water.
Carrot
It is a natural cleanser of teeth and an anthelmintic (effective against
the roundworms)
It has good amount of fiber and thus has carminative and antidiarrheal
properties as well
It also has some diuretic and galactogague action (i.e. promoting the
secretion of milk). Thus, it is an effective overall tonic of immune
system and antianemic as well
Carotene contains natural sugar and also beta-carotene which is a
vitamin A precursor.
Milk: It is a complete planned food by nature. However, goats milk lacks
in folic acid.
WHAT IS RAINBOW DIET = VIBGYOR

vibgyor (vi = violet, b = blue, gyor = green, yellow orange, red foods)
Green leafy vegetablesspinach, drumstick leaves, amaranth
Yellow vegetablescarrots, tomatoes, yellow pumpkin
Orangepapaya, amla, lemon mango. Red fruits apple.
GYOR are the various plant sources like the green leafy vegetables and the
yellow/orange vegetables, such as carrots which contain the provitamins such
as beta carotene/carotenoid. You would need all the colors to provide balance
of all nutrients.
Pedia Pearls:
Folic acid given to mothers prevents neural tube defects in offspring to a great extent.
Antacids diminish folic acid absorption and diminish iron levels as well (hence may
contribute to anemia if taken for too long).
VITAMINS
Vitamin A: Its main function is epithelialization. It is used for severe acne
and various skin and viral diseases like measles (Animal sources include
liver, fish, eggs, milk, and butter).
Visual pigment of Rod cells (for night vision) is rhodopsin which is
formed by vitamin A.
Vitamin A regulates gene expression and cell differentiation, influencing
certain proteins for development of white blood cells from stem cells
providing immunity against infectious diseases.
Vitamin A is even used to treat acute promyelocytic leukemia.
It helps in incorporation of iron into red blood cells preventing anemia
ensuring normal growth and development
Vitamin A given to mother, has a role in prevention of mother-to-child
transmission of HIV
Toxicity of vitamin A includes pseudotumor cerebri producing nausea,
headache, fatigue, loss of appetite, dizziness, dry skin, desquamation,
and cerebral edema. Also, symptoms of vitamin A toxicity in infants,
include bulging fontanels
Signs of chronic toxicity include dry itchy skin, desquamation, loss of
appetite, headache, cerebral edema, and bone and joint pain, liver damage,
and coma
Although beta carotene is safe in pregnancy, vitamin A as such is known
to cause serious birth defects.
Vitamin A exists in the form of retinol, retinal, retinoic acid and retinoids.
The maximal dietary tolerance of retinol is 1 times the Recommended Dietary
Allowance (RDA).
RDA for infants:
400 mcg/day of RE = 1,500 (IU/day)
RDA for children:
600 mcg/day of RE = 2,000 IU/day
RDA for adolescents:
900 mcg/day of RE= 3,000 IU/day
Vitamin D: In response to serum hypocalcemia regulates the mobilization

of serum calcium by:
(1) Increased intestinal absorption of Calcium (Ca) and Phosphorus (2)
Mobilization of Ca from bone (3) Increased reabsorption of Ca from the distal
renal tubules.
Vitamin D is found in two precursor forms: 7-dehydrocholesterol
(provitamin D3) in the skin, and ergosterol in plants. It is synthesized
Pedia Pearls:
1 retinol equivalent (RE) = 1 mcg of retinol = 6 mcg of -carotene.

One mcg of retinol = 3.33 IU of retinol.
Nutrition 21
Fig. 5.1: Knock knees
Fig. 5.2: Bow legs
(For color version of Figures 5.1 and 5.2, see Plate 1)
endogenously from its precursor in the skin, and found in dietary sources
such as deep seafish, plants, and grains as well.
Deficiency state produces rickets (Figs 5.1 and 5.2). Few signs of rickets are:
The first sign of rickets is craniotabes
Frontal bossing (D/D-Thalassemia, Congenital Syphilis, Pyknodysostosis,
Ehler-Danlos and Achondroplasia)
Short stature
Delayed dentition
If there is no eruption of teeth by 12 months, one should suspect:
Constitutional delay, protein-energy malnutrition, hypothyroidism and hypopituitarism, as well.
Vitamin E: It is an antioxidant and an important vitamin for nervous system
and red blood cells
In fat malabsorption, posterior column/dorsal root ganglion-related
signs, including absent tendon reflexes, ataxia, loss of position and
vibration sense, loss of pain sensations and ophthalmoplegia may occur
Anemia has been reported in premature babies due to deficiency of
vitamin E
Sources include: Vegetables, grains, nuts, dairy, fish, and meats.
Vitamin K deficiency may produce hemorrhagic disease of the newborn
Vitamin K is derived from vegetables and synthesized by intestinal
bacterial flora in the lower ileum and colon
Absorption of vitamin K in the small intestine is dependent on bile salts
Vitamin K is needed for the formation of factors II, VII, IX, and X
Vitamin K deficiency naturally occurs in fat malabsorption syndromes
(being a fat soluble vitamin) like the biliary tract disease, short gut
syndrome and advanced liver disease.

Vitamin B1: This regulates our ATP levels
Deficiency is caused by eating refined foods, such as polished rice,
white flour, and white sugar. Some of the deficiency states:
o Dry beriberi (polyneuropathy with toedrop/footdrop/wristdrop)
o Wet beriberi (cardiovascular manifestations including peripheral
vasodilation and high output cardiac failure)
o Wernicke-Korsakoff syndrome (encephalopathy with ataxia and
psychosis, including retrograde amnesia, confabulation).
Vitamin B2 (riboflavin is a redox vitamin)
It is derived from meat, diary or vegetable sources. It is used in oxidationreduction reactions, (as part of mitochondrial enzymes)
The clinical deficiency syndrome consists of cheilosis (fissures in the
lips), glossitis, and corneal ulcerations.
Niacin: It is a component of NAD and NADP coenzyme for
dehydrogenation reactions
It is endogenously made up from tryptophan and exogenously derived
from grains, legumes, seed oils and meats
Deficiency state called pellagra consists of dermatitis, diarrhea and
dementia. Isoniazid and 6-mercaptopurine toxicity may produce a
pellagra like state.
Vitamin B6 or pyridoxine (the ases vitamin)
It is lost by food processing. It is a vital cofactor in transaminases,
carboxylases and deaminase reactions
Deficiency syndrome is similar to that seen in riboflavin or niacin
deficiency like seborrheic dermatitis, cheilosis, glossitis, peripheral
neuropathy and sometimes seizures.
Vitamin B12 and Folate (nucleic acid vitamins)
They are an essential cofactor in nucleic acid synthesis and maturation
Giving folate reverses the megaloblastic anemia, but it does not reverse
the neuropathic consequences of B12 deficiency. Either or both folate
and B12 deficiency produce a megaloblastic picture
In addition, patients with B12 deficiency may exhibit posterior column
defects, such as paresthesias, sensory deficits, loss deep tendon reflexes,
as well as confusion and memory deficits
Vitamin B12 is derived from meats, milk and egg
Folates sources are whole wheat flour, beans, nuts, liver and green
leafy vegetables. It is heat labile and easily destroyed by cooking or
processing raw foods.
Vitamin C: Facilitates the hydroxylation of procollagen

It is involved in the activation of prolyl and lysyl hydroxylases from inactive
precursors. Ascorbic acid, is found in milk, liver, fish, fruits, and vegetables.
Populations at particular risk for vitamin C deficiency are those on poor
Nutrition 23
or erratic diets (the classic example is of malnourished sailors without
fresh vegetables), dialysis patients, or infants on processed milk only.
Vitamin C deficiency state produces:
Scurvy
Hemorrhagic disease (skin, mucosal, gum hyperplasia sub-periosteal
and joint bleeds)
Impaired wound healing, and anemia
Gum hyperplasia which may also be seen due to poor oral hygiene,
Phenytoin and Hurlers syndrome.
MINERALS
Calcium is present in Millets (like ragi, bajra) and milk

Iron is present in jaggery, tamarind, beetroot, green leafy vegetables
Iodine is present in iodized salt and in sea weeds.
STRUCTURE OF NUTRITIONAL HISTORY
Dietary history is more important in mal-nutrition (obesity or undernutrition)

For obese children ask for hours of television watching and snack
frequency, junk foods, bottle feeds and meals away from home. Only
giving milk diet without proper supplements produces a sugar baby
who is chubby but anemic
For undernourished children ask parents whether the child has any
feeding/swallowing difficulties, pica, any dental problems or any
gastrointestinal disturbances like diarrheas. Ask the type of food and
number of meals provided. If younger than 2 years, ask if he breastfeeds
or bottle feeds and at what age the complementary feeds were started.
A typical history includes:
Source of food
Knowledge of local foods
Meals and snacks taken per day
Feeding skills employed.
Estimation of serving size helps to calculate the daily protien and calorie
intake.
Calculate the amount of proteins and calories in each food consumed:
Total calories/expected calories and calorie deficit are to be calculated
Similarily, total/expected protiens and protiens deficit are to be calculated
Correlation with the childs nutritional status naturally follows.
For Cooked Food
Rule of 2 (cooked solids) Each Idli, chapatti, dosa contains 2 gm protein.
Also rice one serving of approximately 25 gm uncooked material contains
2 gm protein
Rule of 6 (cooked semisolids) like eggs contain 6 gm protein

Rule of 4 (Cooked liquids) Dals contain 4 gm protien/serving. Cows milk
(cup of 125 ml) also has 4 gm of protein.
For Uncooked Food
Cereals and pulses (rice, wheat and dal) contain 350 kcal in 100 gm of
uncooked material
EXAMINATION (HEAD-TO-TOE)
Hair Examination
Corkscrew or coiled hair are seen in vitamin C and vitamin A deficiency,

while they are easily pluckable in protein deficiency
Flag sign is seen in kwashiorkor
Hair are sparse and thin in protein, zinc and biotin deficiency.
Examination of Eyes
Photophobia, blurring and conjunctival redness are seen in vitamin B2

and vitamin A deficiencies
Night blindness is seen in vitamin A deficiency.
Examination of Neck
Goiter is a reliable sign of iodine deficiency in hilly areas, far from the sea.
Examination of Mouth
Sore mouth and tongue are seen in vitamin B12, vitamin C, niacin, folic
acid and iron deficiency
Leukoplakia is seen in vitamins A, B12, B-complex, folic acid and niacin
deficiency
Angular stomatitis, cheilosis and fissured tongue are seen in B2, B6, and
niacin deficiency
Bleeding and spongy gums are seen in vitamin C, vitamin A, vitamin K,
folic acid and niacin deficiency.
Glossitis is seen in riboflavin, niacin, folic acid and B12 deficiency.
Examination of Skin
Bruising and purpura are seen in vitamin K, vitamin C and folic acid
deficiency
Pigmentation/desquamation are seen in niacin deficiency and PEM (protein
energy malnu-trition)
Flaking dermatitis is seen in PEM, vitamin B2, vitamin A, zinc and niacin
deficiency
Follicular hyperkeratosis is seen in vitamin B and vitamin C deficiency
Pallor is seen in Folate, iron and B12 deficiency.
Nutrition 25
Examination of Nails
Transverse lines are seen in protein deficiency.

Spooning is rare in children with iron deficiency (koilonychia).
Examination of Joints and Bones

This helps to detect signs of:
Vitamin D deficiency (Rickets)
Vitamin C deficiency (Scurvy)
Look for rachitic rosary, Harrisons groove and bone tenderness, etc.
Also look out for limitation of movements in joints in condition where joint
destruction has set in due to tuberculous arthritis.
Examination of Abdomen
Protruding abdomen is seen in:
Hypotonic states like rickets
Hepatomegaly (due to fatty infiltration) as seen in kwashiorkor
Splenomegaly in condition like kala-azar
Gaseous distention in states like helminthiasis
Ascitic fluid in condition like tuberculosis of abdomen.
PROTEIN ENERGY MALNUTRITION

Classic states of malnutrition:
1. Marasmus is a classic description of visceral protein albumin being
maintained at the expense of the somatic protein compartment (Muscle).
Consequence: Generalized muscular wasting and the loss of subcutaneous
fat.
2. Kwashiorkor in contrast, is a deficiency of the visceral protein compartment,
resulting from acute protein deficiency in excess of caloric deficiency.
Consequence: Edematous state.
ANTHROPOMETRY
Anthropometry is the measurement of body height, weight and proportions to
evaluate and monitor the physical growth over a period of time. Variables like
Ht, Wt, MAC, HC, skin fold thickness reflect the nutritional status. Other
anthropometric measurements include mid-arm circumference, skinfold
thickness and head circumference.

WEIGHT
Equipment: Use a regularly calibrated
electronic or balanced-beam scale. Weigh
in light clothes (no shoes) and read to the
nearest 100 gm.
Weighing a Sick/Struggling or a
Small Child
Fig. 5.3: Infant weighing scale (Electronic)
First, the mother is weighed with the child and then she is weighed without the
child. So, the difference between the two measures is the childs weight. A variety
of weighing scales are used from simple spring scales (most common scale) to
hospital beam balances and electronic scales. Electronic scales (Fig. 5.3) are most
accurate scales for newborns. However, for community work, a light weight,
portable, stainless steel scale is used. It consists of a spring, hook, and handle, as
well as a diaper-like sling to hold the baby for weighing.
Weighing a Bigger Child
Measuring technique:
The child may require to be distracted to put on the scales and weighed
properly
The childs weight must be clearly plotted on a chart with a well-marked
dot and not a cross
The growth curve formed by joining these should leave the dots clearly
visible on the charts (printed with weight for age and height for age percent
or percentile lines)
Now, the date/time of measurement made and the name of the person
who made the measurement must be written.
Calculation: Measurements of growth need to be adjusted for prematurity, if
the child is born before 37 weeks gestation. The adjustment should continue
to be made until the child is two years old. After 2 years, a child behaves like
other counterparts (due to catch up growth).
For example, for a child who was born 26 weeks ago at 28 weeks gestation.
The measurement should be plotted at 14 weeks (age adjusted for gestation),
i.e. 26 (40 28) = 14. Naturally, a child born at or after 40 completed weeks,
gestation does not need any adjustments to be made and measurements should
be plotted from the expected date of delivery.
Calculate expected weight by formula (2 age in years + 8) for children
between 2 years and 6 years. Find the deficit to grade the nutrition. If edema
is present, add k to the grade.
Interpretation: Marasmic children generally fall as low as 60 percent of expected
weight, while children with kwashiorkor (and concurrent edema) tend to fall
between 60 to 80 percent of expected weight marasmus and kwashiorkor are
two ends of a spectrum of protein-energy malnutrition.
Nutrition 27
HEIGHT
Technique
The subject stands erect and bare footed on a stadiometer with a movable
head piece. The head piece is leveled with skull vault and height is recorded to
the nearest 0.5 cm.
Expected height = (Age in years 6) + 77.
Equipment: For length, use Infantometer (Measuring board) Children under 2
years of age are measured lying down on an Infantometer, i.e. for recumbent
length measurement. It is portable, lightweight, durable and capable of
measuring the recumbent length up to maximum of 100 cm. This board is
made up of smooth-finish wood with fixed head end and all parts glued and
screwed with the sliding footpiece.
HEAD CIRCUMFERENCE*
Equipment: A tape, which is neither stretchable nor rigid is used (to measure
the largest head circum-ference possible).
Precautions: Measure newborn babys head after 36 hours to allow effects of
moulding and edema from birth to settle.
For older children untie the hair or turban and then record serial measurements,
rather than a single measurement to allow for a more accurate assessment.
Technique: Place the measuring tape around frontal forehead at glabella and the
other end at occiput. Take largest of three measurements and then find the average.
Interpretation:
In normal term, newborns head circumference is 33 to 35 cm
Fast rate of growth could suggest hydrocephalus while slow rate may
mean craniosynostosis
A small head circumference with a low birth weight may be due to IUGR,
while a small head with a normal weight could indicate brain pathology
Rickets is one of the nutritional deficiency states producing a large head.
However, microcephaly is more likely in malnutrition
A separate head circumference chart is used for children with
achondroplasia.
Mid Upper Arm Circumference (MUAC)
Technique
This is the circumference of the left upper arm, measured at the mid-point
between the tip of the shoulder and the tip of the elbow (olecranon process
and the acromium). It is recommended for use in children between one and
five years of age as total of arm muscle and subcutaneous fat remains constant
in this age group.
* One should try to measure the head at the point where the circumference is greatest.

Equipment
MUAC tape: This arm circumference insertion tape measures mid-upper

arm circumference of children up to 25 cm
Shakirs tape: This is color-coded in red/yellow/ green, non-tear, stretchresistant plasticized paper. Bangle test uses MUAC as screening for preschool nutrition for estimating prevalence of undernutrition at a population
level (radius of bangle = 2 cm).
Interpretation
Level of undernutrition
Definite undernutrition
MUAC (cm)
< 12.5
LABORATORY TESTS
To Identify the Presence of Nutritional Deficiencies
Early changes before clinical findings are evident occur in:
Hemoglobin concentration (Hb)
Mean corpuscular volume (MCV)
Mean corpuscular hemoglobin (MCH)
Peripheral smear
Alkaline phosphatase estimation may detect early changes in rickets before
the appearance of overt signs.
In malnourished children, stool examination is useful for the presence of ova
and/or intestinal parasites (being one of the occult infestation).
To Monitor Recovery
Tests like potassium and phosphorus levels and albumin concentration are
used to monitor recovery, during refeeding of malnourished children.
TREATMENT
To break the cycle of undernutrition, there are certain proven interventions
called BEST.
B- Breastfeeding promotion. Appropriate infant and young child feeding need
E-Energy rich foods
S-Supplementation with vitamin A/zinc
T-Take affordable, acceptable, accessible, attractives, appropriate food for
appropriate management of severe acute malnutrition.
Breastfeeding promotion is self explanatory. Let us discuss energy rich
foods and infant and young child feeding.
Pedia Pearl: Causes of large head include Megalencephaly (Hydrocephalus, Tay-Sachs
disease), Subdural hematoma, Intracranial SOL, Arachnoid Cyst and Skeletal disorders
like Hurlers syndrome.
Nutrition 29
Energy Rich Foods
Many whole energy rich foods like ghee, butter, jaggery or sugar add to the
energy density of food.
Sprouting-Amylase Rich Foods (ARFs)
Pulses could be sprouted to increase their nutritional value. Germinated cereals
(sprouts) are rich in alpha-amylase that breaks down carbohydrates and reduces
food viscosity which improves acceptability and increases intake by
3 to 4 times. They are called amylase rich foods. Long chain carbohydrates
are broken down by amylases into short chain dextrins.
ARF: Whole-wheat grain is steeped in three times volume of water. It is covered
and left for twelve hours. Next, germinate grains by wrapping in wet cloth, in
a cool and dark place, for 48 hours and sprinkle with water every eight hours.
Then sun dry and occasionally stir for 8 hours, and finally roast them. Grind
the grains in grinder. The shelf- life is 30 days for amylase rich foods (ARFs).
Roast 25 gm wheat flour in 5 gm of oil until brown. Add jaggery water to
sweeten the halwa slowly and stir well. Now, add two fingers pinches of
ARF powder (prepared earlier) to enrich the food and stir well to get a
nutritious energy dense ARF meal.
Infant and Young Child Feeding
This includes age specific diet and specific interventions.
Age Specific Diet
Birth to 6 months: Early start of breastfeeding within half an hour, then

exclusive and unrestric-ted on demand breastfeeding
6-7 months: Breastfeeding + mashed cereals, vegetables and fruits, e.g.
mashed ripe banana, apple, papaya, etc. Give porridge made from milk,
sugar, and cereal (rice, wheat, or sooji). Give overcooked rice and mashed
vegetables like potato. Add oil/ghee/butter and sugar/jaggery while cooking
7-8 months: Add pulses (moong, tur), sprouted beans, dark green leafy
vegetables (mashed and mixed with cereal)
9-12 months: Breastfeeding + soft family diet Non-vegetarian foods may
be added.
12-15 months: Child should be eating family food (breastfeeding + the
adults diet). He may eat by him/herself
15-24 months: Regular family food + breastfeeding
A combination of both cereals and pulses provides mutual supplementation
(cereals are deficient in lysine and rich in methionine while pulses have the
opposite quality). Three parts cereal (rice) + one part pulse (moong dal)
are cooked with oil or ghee to provide all the essential amino acids
Adding sugar/oil makes the food energy dense.
Specific interventions:
In sick and the preterm: Total parenteral nutrition (TPN), is given to
such babies, who are unable to tolerate orally. Proteins produce better
nitrogen balance. Thus, parenteral amino acid intake is gradually
increased from 1.5 g/kg/d to 3.5 g/kg/d. Carbohydrate calories
improve growth. Hence, dextrose is given at 6 to 10 g/kg/d. Fats
(intralipids) are given from 1 g/kg/d increased to 3 g/kg/d as a
continuous infusion, but shielded from light with paper wrapped around
tubings. Minerals and vitamins are supplemented as well. Overall total
parenteral nutrition decreases hospital stay in sick and tiny babies
and decreases sepsis (First reported in 1971 for supporting breathing
of preterm neonates Cochrane Systematic Review, 2002)
Intervention in malnutrition: Give protein 2 gm/kg of the expected
weight and calories based on Holiday and Segar formula.
For example, calculate the calories required for child (25 kg) as
follows:
100 kcal/kg/day 10 kg = 1000 kcal/day (for first 10 kg)
50 kcal/kg/day 10 kg = 500 kcal/day (for second 10 kg)
20 kcal/kg/day 5 kg = 100 kcal/day
Hence, For 25 kg, 1600 kcal/day is required.
PREVENTION OF MALNUTRITION ON NATIONAL SCALE
Major nutrition supplementation programs in India are:
Integrated Child Development Services (ICDS) Scheme: Aims to give
preschool education to 3-6 year-old. Here, pregnant and lactating mothers
recieve supplementary nutrition; health check-ups; immunization; referral
services and treatment of minor illnesses.
Mid-day Meal (MDM) programs: The objective is to increase the enrolment
and attendance of children in primary school leading to learning and improving
their nutritional status by providing cooked meals of locally available foods.
Beneficiaries are the primary school-going children especially those belonging
to the backward classes, scheduled castes and scheduled tribe families.
Special Nutrition Program (SNP): This aims to provide supplementary
nutrition and services like the supply of vitamin A solution, iron and folic
acid tablets to the preschool children pregnant and lactating mothers.
Wheat-based Nutrition Program (WNP): This benefits preschool and
nursing/expectant mothers in areas with high infant mortality such as urban
slums and backward rural areas.
The Global Alliance for Improved Nutrition (GAIN): With grants from the
Bill and Melinda Gates Foundation, it provides loans, grants and technical
advice to help develop and distribute low-cost, easy-to-use nutritious foods.
Balwadi Nutrition Programs (BNPs): Aim is to supply about one-third of
the calorie and half of the protein requirements of preschool children.
National Nutritional Anemia Prophylaxis Program (NNAPP): Beneficiaries
are children of the 1 to5 age group and pregnant and nursing mothers,
Nutrition 31
female acceptors of terminal methods of family planning and IUDs. Iron

and folic acid tablets are supplied in this program.
National Program for Prevention of Blindness: Here, vitamin A is given,
first dose at 9 months and then 6 monthly till 3rd birthday. The program is
extended to 5 years if child is malnourished or has suffered from measles.
National Goiter Control (NGC) Program: Aim is to supply iodized salt to
the entire country.
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Developmental
Assessment
DEVELOPMENTAL DELAYFIVE GROUPS

1. Global Developmental Delay
Ask for development of various domains: Assess whether more than one
developmental area is lagging in a child behind normal for age, at which 75
percent children achieve a particular milestone.
Ask for age: Label as mental retardation if the intelligence quotient (IQ) and
adaptive behavior are below par even beyond 5 years of age, e.g. fragile X syndrome
and inborn errors of metabolism (IEMs).
Examples: Recessive disorders like metabolic encephalopathy, organic acidemias
and acidurias metabolic acidosis and hyperammonemia. In the presence of
mental retardation and development delay suspect Phenylketonuria and
congenital hypothyroidism, as well.
Ask for family history of consanguinity and neonatal deaths precipitated with
protein rich foods. Ask about developmental history of siblings.
Ask about behavior: For example, autism is suggested by stereotypies, selfinjurious, repetitive behavior and impaired communication skills.
2. Dysmorphisms
Evaluate for features of a particular syndrome;
Coarse facial features seen in metabolic disorders
Expressionless face seen in congenital myotonic dystrophy
Abnormal shaped ears found in Treacher-Collins syndrome
Grooved earlobes in Beckwith-Wiedemann syndrome.
Categorize the Features as Deformation, Disruption, Dysplasia, or
Malformation
Deformations are caused by mechanical forces, e.g. breech deformation
sequence producing clubfoot
Disruptions have normal structures with some cell death, e.g. amniotic
band sequence
Malformation is a disturbance in developmental process, e.g. cleft lip.
Note: In low set ears more than 2/3rd of ear is below the horizontal line
drawn from the corner of the eye to the occiput.

3. Motor Delay
Gross motor assessment: Motor disorders, like cerebral palsy produce a wide
spectrum of motor problems caused by a nonprogressive static lesion (while
the manifestations progress overtime) in the developing brain, during prenatal/
perinatal, or the postnatal period (up to the first 2 years).
ASSESS gait, asymmetries, bulk, strength, tone, stretch reflexes, plantar
responses and the pattern of movements (should be categorized as normal,
abnormal or atypical).
SPOT dyskinesiasby assessing Gowers sign, walking forwards,
sideways, on stairs, and manual dexterity like throwing and kicking a ball.
ASSESS fine motor skillsthrough the use of blocks in the infant and in
older child, copying various shapes or drawing a figure, e.g. good enough
draw a man test.
DIAGNOSIS OF CEREBRAL PALSY
POSTER Criteria by Levene
P = Posture; A child with spastic CP may have dislocation of the hip (due
to adductor and abductor muscle tone imbalance) plantar flexion of
the feet and Scoliosis
O = Oropharyngeal dysfunction; Presents as drooling, etc.
S = Squint; Due to poor muscle strength
T = Tone of muscle; Observe head control, scissoring of the lower
extremities
E = Evaluation of developmental reflexes
R = Reflexes (Deep tendon) should be assessed for hyperreflexia.
Children with CP may have persistent primitive reflexes such as the Moro
reflex and delayed emergence of parachute reflex as signs of delayed
maturation/CNS injury. Early detection of developmental disorder like cerebral
palsy is difficult due to lack of diagnostic techniques and infrastructure (in
most centers), to identify high- risk pregnancies (like breech position, maternal
TORCH infection, complicated labor or delivery) and to manage high-risk
infants (premature, asphyxiated, IUGR, septicemic and jaundiced babies)
who are likely to suffer brain damage (cerebral palsy). This detection is vitally
important for the better outcome.
Cerebral palsy (CP)* is a symptom complex rather than a specific disease.
Most often it is prenatal in origin. A postnatal type (Choreoathetoid) occurs
*Presentation vs Site of lesion in CP:
Spastic diplegiaPeriventricular leukomalacia;
Spastic quadriplegiaCerebral malformations;
Spastic hemiplegiaCerebral injury to MCA territory;
Dyskinetic CPBasal ganglia (Kernicterus);
Hypotonic CPCerebellar lesions.
Developmental Assessment 35
due to the bilirubin deposition in the
extrapyramidal area. Under stress it
worsens and manifests frankly.
According to the Center for Disease
Control:
1. A child over two months with
cerebral palsy-might scissor or
have abnormal muscle tone, either
hypotonia (relaxed) or hypertonia
(rigid) or have unusual posture
(Fig. 6.1).
2. A child over six months with
cerebral palsy might have hand
preference and fisting or favoring
one of the body when the child
Fig. 6.1: Squint in a child with cerebral palsy
moves.
(For color version, see Plate 1)
3. A child over 10 months with
cerebral palsy might have commando crawl.
Associated problems in cerebral palsy:
Visual, hearing and speech problems
Seizures, mental retardation
Feeding difficulties causing aspiration
Spasticity (may lead to contractures).
Prognosis: A good chance of ambulation exists, if the child is able to sit
independently by 24 months.
Treatment: Aim is to make child independent (mobility wise) by following
methods:
Family is involved
Play-based therapy
Use of a pictures/computer
Long-term cast/immobilization is avoided.
4. Language Delay
Assess voices from birth by the recognition of parents voices and response
to adult speech:
Normally, they achieve vowel-like sounds (cooing) at one month
Definitive vowel sounds are heard at 4 months of age
Babbling starts at 5 months
Sequential production of a consonant and vowels starts by ten months,
(e.g. ba-ba)
Longer sequences of consonants and vowels (jargon) are heard later.

Steps to Assess
First assess the comprehension which precedes language expression

Then assess for expression or articulation difficulties (e.g. speech disorders)
and language skills by asking to identify pictures, body parts, colors, shapes
Story-telling vocabulary content and grammar should also be checked
Next examine oral cavity: Look at the tongue, assess dental development
and perform articulation tests. Palate is critical for speech.
Disorders of language include autism or specific language impairment
Language acquisition delay occurs in Downs syndrome
Disorders of primary speech occur in macroglossia, hemifacial
microsomia, cleft palate, laryngeal edema or structural disorders of the
larynx, neuromotor incoordination in muscular dystrophies and cerebral
palsy.
5. Neuroregression
Neuroregression is defined as, "a previously healthy child begins to deteriorate
losing already attained skills with progressive loss of speech, hearing, vision
and muscle strength for more than three months".
Neurodegeneration can involve both the gray and white matter. Injury to
gray matter is irreversible The gray matter disease will have seizures as the
common presentation White matter, (myelinated axons) disease is dominated
by motor difficulties. Etiology of neuroregression could be genetic
(neurometabolic) or non-genetic (infections like HIV encephalitis, heavy metal
poisoning or brain injuries). Some examples are Alexander disease, Canavan
disease, adrenoleukodystrophy, metachromatic leukodystrophy, mitochondrial
disorders and Retts syndrome.
Here, the child has initial normal development followed by gradual loss of
milestones, e.g. a progressive loss of milestones with blindness seizures,
exaggerated startle and cherry red spot in retina is characteristic of TaySachs disease. CT scan often shows white matter demylination.
HISTORY PROCESS
Ask open-ended questions:
Antenatal events like vaginal leaking, bleeding, gestational diabetes, fever
with rash, maternal drugs, stages of labor, duration, mode of presentation,
and delivery, meconium staining of liquor. Indication for forceps/ventouse/
cesarean section has to be inquired
Pedia Pearls: (Language problems)
Dyslexia is difficulty in expressing self in writing with spelling mistakes and letter
reversal. However, social adjustment is normal.
Language delay is seen also in Autism associated with abnormal social relationships,
stereotypes, echolalia, etc.
Developmental Assessment 37
Natal history regarding birth weight, activity, pulse, grimace, appearance,

respiration (APGAR) scores and feeding difficulties, etc.
In postnatal period, history of parental neglect, abuse and timing of
acquiring the skills should be sought, i.e. developmental milestones.
PHYSICAL EXAMINATION
General physical and neurologic examination should be thorough.
Inspect
Look for dysmorphic features and neurocutaneous markers Palpate for
enlargement of the liver or spleen, e.g. storage disorder. The spine is to be
examined carefully for any defect. Examine cranial nerves as well.
Helpful Clues
Skin pigmentation, transverse palmar simian crease, syndactyly, clinodactyly
and fundoscopic changes (like cherry red spot) give indication of various
syndromes like Downs and Tay-Sachs diseases.
Take Measurements
Occipital frontal head circumference for macrocephaly or microcephaly

Height and weight for percentiles. Obesity with short stature should prompt
consideration of Laurence Moon Bardet Beidel syndrome, etc.
Disproportionate short stature should suggest consideration of a skeletal
dysplasia (e.g. achondroplasia).
INVESTIGATION
Neuroimaging is useful in cerebral palsy for brain malformations and for

early closure of sutures (Fig. 6.2)
Fluorescent in situ hybridization
(FISH) probe for karyotyping is
useful for dysmorphisms like
Downs
Metabolic screening is necessary
especially if there is positive
family history, parents consanguineous marriage or for
metabolic disorders presenting as
neuroregression or global
developmental delay. This is done
by obtaining a urine organic acid
screen, ferric chloride test, serum
Fig. 6.2: Craniosynostosis (There are no
amino acids, serum lactate
sutures seen as they are fused prematurely
ammonia levels, arterial blood gas
producing a small head)
and thyroid function studies
Nerve conduction studies are useful in the peripheral neuromuscular or white

matter diseases
EEG is useful if history of seizures is present
Hearing screening: Otoacoustic emissions (OAEs) serve as the primary
screening technique and the auditory evoked response (BERA) is done
later in children with family history of hearing impairment or language/
development delay; long neonatal intensive care, ototoxic drug ingestion
(like quinine, aspirin furosemide) hyperbilirubinemia, dysmorphisms and
in utero TORCH infections, etc.
TOOLS FOR DEVELOPMENTAL ASSESSMENT

Examples
1. Denver development screening test
2. Making a tower of cubes.
POINTS TO REMEMBER
Rules of developmental assessment:
1. When the parent is worried, it means child needs attention
2. Consider focal lesion in brain if seizures are associated
3. Developmental delay or regression could be due to a tumor in brain
4. No babbling by 12 months or single words by 16 months indicates a red
flag sign
5. In motor delay, myopathies and muscular dystrophy should be ruled out.
BIBLIOGRAPHY
1. Blackman JA. Cerebral Palsy. In: Wolraich ML (Ed). Disorders of Development and
Learning: A Practical Guide to Assessment and Management, St. Louis: Mosby 1996;
2:186-212.
2. Kuban KCK, Leviton A. Cerebral Palsy. New Engl J Med 1994;330(3):188-95.
3. Miller F, Bachrach SJ. Cerebral Palsy: A Complete Guide for Caregiving 1998,
Baltimore: John Hopkins University Press.
4. Motor development in canadian infants of Asian and European Ethnic Origins Journal
of early Intervention 2009;31(3):199-214.
5. Swaiman KF, Russman BS. Cerebral Palsy. In: Swaiman KF, Ashwal S (Eds). Pediatric
Neurology: Principles and Practice, St. Louis: Mosby 1999;3:312-24.
6. Taft LT. Cerebral palsy. Pediatr Rev 1995;16(11):411-8.
7. Williams PD, Williams ARJ. Denver developmental screening test norms: A crosscultural comparison. Pediatr Psychol 1987;12(1):39-59.
Central
Nervous System
EMBRYOLOGY
Gastrulation (Fig. 7.1)
First, the inner cell mass of embryo, differentiates into a layer of primitive
ectoderm (called the epiblast) on the germ disk over an underlying endoderm
(from the yolk sac)
Later, this epiblast forms the primitive mesoderm by invagination
The mesoderm in central region forms the notochord. This mesoderm
condenses on both sides of notochord into somites
Each somite has three parts, viz sclerotome, myotome and dermatome
(medial to lateral)
The sclerotome later surrounds the notochord to form the vertebral body
parts from either side. Failure of fusion of these expansion leads to neural
tube defects.
Neurulation (Fig. 7.2)
The notochord stimulates the overlying ectoderm to thicken into the neural
plate
The neural plate develops a neural groove which deepens until the neural
fold forms an enclosed neural tube
The roof of the developing neural tube is zipped from middle, away from
each other, toward the two ends of the embryo leaving neuropores at each
end (closure of pores completes the neural tube)
Fig. 7.1: Gastrulation

Neural Crest (NC)
Fig. 7.2: Neurulation
If the upper neuropore fails to close, an anencephalic baby is the outcome

The cluster of cells remaining in midline, after fusion of the neural folds
known as neural crest cells, migrate throughout the body of embryo making:
The peripheral nerves
Nerve roots
Ganglion cells of the peripheral nervous system.
Upper part of neural tube forms three dilatations (forebrain, midbrain and
hindbrain). Their walls become the nervous tissue and neuroglia and their
cavities become the ventricles
The lower part of the tube forms spinal cord. Here, also the wall becomes
nervous tissue and neuroglia, while the cavity forms the central canal.
Nerve Cell Migration

Cells move permanently from the inner zone adjoining the ventricles outwards
up to six cell layers. Each layer moves away from center and climbs on top of
previous layer by inside-out sequence. For this purpose, the glial cells act as
primitive nerve cell guide by providing a passage. If cells do not go on top of
previous layer due to some reason, then the next layer of cells behind it
accumulates. Such problems are called nerve migration disorders.
Central Nervous System 41
ANATOMICAL AND PHYSIOLOGICAL ASPECTS
Upper motor neurons

Lower motor neurons
Autonomic nervous system and the bladder
Sympathetic chain
Parasympathetic nervous system
Bladder.
UPPER MOTOR NEURONS

Corticospinal and Corticobulbar Tracts
Corticospinal (pyramidal) fibers are cortical neurons originating from the

pyramidal-shaped cell bodies of primary motor cortex (area four) of the precentral
gyrus and the adjacent paracentral lobule which join the lower motor neurons
within the ventral horns of the spinal cord
Corticobulbar tracts are cortical neurons originating from the pyramidal
shaped cell bodies of primary motor cortex (area four) of the precentral
gyrus and the the adjacent paracentral lobule which join the lower motor
neurons (cranial nerves) originating from brainstem motor nuclei.
Pyramidal System Projects into Corona Radiata

These are pyramidal system projection fibers converging from all parts of the
cerebral cortex into the internal capsule via the subcortical white matter.
Subcortical white matter also has commissural fibers and association fibers
(all three at right angles to each other).
Next Highway is the Internal Capsule
Anterior limb of internal capsule (IC) is of little clinical significance. The

genu contains corticobulbar fibers
Posterior limb has the thalamus medially and the basal ganglia laterally. It contains
corticobulbar fibers, corticospinal fibers, and the thalamocortical fibers. The
optic radiations and auditory radiations are also in the posterior limb.
Next Via Cerebral Peduncle Neurons

Pass Through Following Structures
Brainstem: They enter as fascicles in the center of basilar pons. Cranial

nerves originate from brainstem motor nuclei of corticobulbar tracts
Medulla: Next, they come to the the medulla as the pyramidal shaped tracts
(named after these pyramids in the medulla)
Pyramidal decussation occurs at the junction of the medulla and spinal
cord at the level of the foramen magnum
Finally, they enter the lateral funiculus of the spinal cord forming the lateral
corticospinal tract. Few fibers do not decussate called ventral (anterior)
corticospinal tract.

LOWER MOTOR NEURONS
Lower motor neurons leave the cord via the ventral roots and end as motor
endplates on skeletal muscle (The final common path neurons).
AUTONOMIC NERVOUS SYSTEM AND THE BLADDER
Sympathetic Chain (T1-L2)
It has short preganglionic and long postganglionic fibers
It activates body via postganglionic transmitter called norepinephrine
(except sweat glands which are activated via acetylcholine).
This Flight or Flight transmitter increases heart rate, causes sweating, dilates
pupil and diverts blood from skin and GI tract to skeletal muscles, thereby
inhibiting GI movement and closing the sphincters.
Parasympathetic Craniosacral Outflow (CN III, VII, IX, X and S2-4)
It has long preganglionic and short postganglionic fibers.
It is for rest and local responses via postganglionic transmitter called
acetylcholine. It enhances digestion and GI peristalsis, slows heart rate,
constricts pupil, empties bladder, relaxes sphincters and causes genital erection.
Pathologies of Autonomic Nervous System
Referred pain: Pain from heart involves segments T1-4 while that from
gallbladder involves segments T6-8. The segments involved from stomach
are T7-8
Horners syndrome: This occurs due to damage to the descending sympathetic
fibers from the hypothalamus or the superior cervical ganglia and presents
as miosis(pupillary constriction) anhidrosis (lack of sweating), ptosis
(drooping of the eyelid) and enophthalmos (eye appears to sink into the
orbit).
THE BLADDER
The Filling Phase
Bladder has a normal capacity of 250 to 400 cc. As volume increases, sensory
receptors transmit fullness to the sacral cord reflex center (S2, S3, and S4).
Sensory messages are sent from the spinal cord to the cerebral cortex through
the spinothalamic tract and posterior columns. Inhibitory centers in the frontal
lobe can override the micturition reflex by voluntarily contracting the external
sphincter. However, as bladder pressure increases and approaches the level of
urethral pressure, the detrusor muscle begins rhythmic contractions.
The Emptying Phase
This begins when message of fullness is processed in the frontal lobe and
motor messages are sent to the sacral reflex center. Then the parasympathetic

fibers and somatic fibers stimulate detrusor muscle contraction and sphincter
relaxation, causing bladder emptying.
Bladder dysfunction may be:
Filling dysfunction, which includes bladder over contraction (urge
incontinence) and urethral under contraction (stress incontinence)
Emptying dysfunction, which involves bladder undercontraction or urethral
over contraction causing overflow.
Neurogenic Bladder
This is incontinence due to upper motor neuron (UMN) or lower motor neuron
(LMN) lesion.
Upper Motor Neuron (UMN) Lesions
Spastic Bladder: UMN lesion occurs due to traumatic brain injury, tumors,
etc. in brain above pons.
This UMN bladder called spastic bladder or reflex bladder causes
failure of inhibitory fibers to suppress involuntary detrusor muscle
contractions, resulting in strong uncontrolled voiding contractions (Urge
incontinence).
Automatic Reflex Neurogenic Bladder: UMN lesion due to cord lesions
above T12-L1 cord level but below pons produce automatic reflex
neurogenic bladder (due to trauma, tumors, infection, infarction).
Loss of control from higher brain centers results in the spinal reflex arc
to take over control of micturition, which results in decreased bladder
capacity with high urine residuals due to lack of inhibition. Also, it
may be complicated by detrusor sphincter dyssynergia, causing high
bladder pressure.
Lower Motor Neuron (LMN) Lesions

There is disruption at the sacral spinal reflex arc at S2-S4 producing a flaccid
bladder or atonic bladder.
It may be of three types:
1. Sensory paralytic bladders: Here, afferents to spine are disrupted. So
fullness of bladder is not conveyed to spine resulting in increased bladder
capacity and overflow incontinence.
2. Motor paralytic type: Here, efferents to bladder are disrupted. So, despite
knowing that bladder is full, cannot cause contraction of bladder resulting
in increased bladder capacity and overflow incontinence.
3. Combined sensory and motor paralysis: It occurs when both motor and
sensory fibers are disrupted. Here, no message is taken to/away from
spine resulting in increased bladder capacity and overflow incontinence.
This independent autonomous reflex bladder causes micturition via vesical
plexus.
APPROACH TO A CNS CASE

HISTORY
Temporal profile: Note the onset of symptoms in chronological order to

know whether the problem is static, progressing, or improving
Birth history: It should be obtained by focusing on prenatal, perinatal, and
postnatal events
Immunization history: E.g. whether the child has received Hib (H influenza
B) and meningococcal vaccination, especially in infants and splenectomised
children
History of present illness: Note any history of alteration of sensorium,
trauma, dog bite, vaccination (recent)
Past medical history: It should include immunization status, accidents,
chronic medical problems, and medications (including anticonvulsants)
Good developmental screening assessment with milestones (such as the
Denver II)
Family history: It can also be useful since some diseases are transmitted
genetically.
EXAMINATION
Summary of CNS Examination
General physical examination

Global assessment of higher functions.
Cranial nerves (I-XII): Sense of smell (I), visual fields and acuity (II),
eye movements (III, IV, VI) and pupils (III, sympathetic and
parasympathetic), sensory function of face (V), strength of facial (VII),
shoulder girdle muscles (XI), hearing (VII, VIII), taste (VII, IX, X),
pharyngeal movement and reflex (IX), tongue movements (XII)
Reflexes: In general brisk, reflexes suggest an abnormality of the UMN or
pyramidal tract, while decreased reflexes suggest abnormality in the anterior
horn, LMN, peripheral nerve or motor endplate
Sensory system for the sensations of fine touch, pain and temperature.
Vibration, position sense, extinction and Rombergs test to examine
proprioception
Motor system: Assess, muscle strength, often graded on the scale 1 to 5.
Ask about tenderness/gelling, etc. Look for posture, i.e. decerebrate,
decorticate and hemiparetic. Perform, assessment of gait, Look for
abnormal movementsseizure, fasciculations, resting and tremors. Feel
the muscle bulk tone and signs of spasticity/rigidity. Elicit reflexes
Signs of meningeal irritation
Cerebellar testing: Dysmetria, finger-to-nose test, ankle-over-tibia test,
dysdiadochokinesis Rapid pronation-supination, ataxia nystagmus,
intension tremor and staccato speech
Autonomic nervous system testing.

General appearance: Dysmorphology and body odor are present in some

inborn errors of meta-bolism.
Skin and hair examination:
Ash leaf spots, Caf au lait spots, angiomas, axillary freckling, adenoma
sebaceum or shagreen patches in neurocutaneous disorders (see Figs
11.1A and B)
Friable kinky hair may signify Menkys kinky hair disease that is
associated with mental retardation and optic atrophy.
Disparities of thumbnail sizes and their convexity may signify a growth
disturbance, which may be a sign of hemiparesis
Examine the midline of the back and neck for sacral dimples, tufts of hair,
or other signs of spinal dysraphism
Specifically examine the skull
Inspection: Inspect for microcephaly, macrocephaly and craniosynostosis,
flattening or prominence of the occiput (Downs and Dandy-Walker
syndrome respectively)
Palpation: Ridging of the cranial sutures is a sign of craniosynostosis.
On palpation of the anterior fontanelle, bulging shows increased
intracranial pressure. Do anthropometry, specifically the head
circumference. If it is significantly smaller than the chest circumference,
then there might be microcephaly. A nice rule of thumb for head
circumference is the 3 and 9 rule. A newborn has a head circumference of
35 cm, at 3-month has a circumference of 40 cm, at 9-month has a
circumference of 45 cm. A 3-year-old has a circumference of 50 cm
and a 9-year-old has a circumference of 55 cm.
Percussion: Skull showing areas of tenderness may signify osteomyelitis.
Macewens (cracked pot) sign is positive when the sutures are separated
due to increased intracranial pressure
Auscultation: Use the bell of the stethoscope for bruits in anemia,
thyrotoxicosis and meningitis. Bradycardia and hypertension are seen
in raised (Intracranial Tension (ICT).
Pedia Pearl: In every child with large head, transillumination test should be done to rule out
the possibility of hydranencephaly where there is an abnormal transillumination whereas in
hydrocephalus there is no abnormal transillumination.

Higher Functions/Mental Status Exam
Assess States of Consciousness
Consciousness awareness of self-surroundings and appearance of alertness

Confusion reduced awareness, misinterpretation of surroundings
Delirium irritability, agitation, fearful disorientation
Coma-absence of alertness and cognition (thought process)
Encephalopathy-altered consciousness.
Also assess comfort level, mood, cooperation, memory, comprehension
and speech. Next step is to assess the cranial nerves.
Cranial Nerves
The corticobulbar tract axons of the upper motor neurons that synapse on lower
motor neurons of the cranial nerves (similar to the corticospinal fibers) end in the
brainstem motor nuclei or (BULB) of cranial nerves instead of the anterior horn
of spinal cord, e.g. nuclei V, VII, IX, X, XI and XII. The corticobulbar and
corticospinal axons are placed side by side in the internal capsule and cerebral
peduncle but they gradually leave the corticospinal tract to enter different nuclei
in the pons and medulla. All the lower motor neurons of the brainstem receive
corticobulbar input from both sides, except facial and hypoglossal nerve.
Therefore, lesion involving the left side of brain causes weakness of the right
facial muscles below the forehead only, due to decussation of these fibers.
CN I Olfactory (Special Sensory-fibers for Smell)
Route: From olfactory mucosa, the nerve enters the cribiform plate and
forms the olfactory bulb containing olfactory nuclei beneath the frontal
lobe. Olfactory tracts from the bulb divide into three branches, viz lateral,
intermediate and medial.
Test: Check patency of each nostril. Use volatile, pleasant substance (eyes
closed) under each nostril separately.
CN II Optic (Special Sensory-fibers for Sight)
Route: The optic nerve begins in the retina from the rods and cones as secondary
sensory neurons and enters brain through the optic canal. Then, temporal
fibers cross in the optic chiasm. The optic tract from the chiasm ends in the
lateral geniculate body where optic nerve nuclei lie. Here, tertiary neurons
arise (optic radiation) and go to the occipital visual cortex.
Test: Visual acuity tested with a Snellen eye chart. Visual fields for each eye
tested by checking when a patient can detect examiners hand coming in
their field of view. A prechiasmatic lesion results in ipsilateral blind eye while
lesions in and around the chiasma result in hemianopsia (field of vision testing
is done by confrontation method).
Testing one of the brainstem reflex, the pupillary light reflex tests for both CN
II and CN III. Light shown on one eye should cause constriction of both eyes,
as the sensory limb afferent of the reflex is CN II and the motor limb efferent
is CN III.

CN III Oculomotor Nerve (Motor Somatic and Visceral Motor)
Route: It starts from the oculomotor nuclei in the midbrain, enters
interpeduncular cistern, passes between cerebral and cerebellar arteries into
the cavernous sinus and leaves the skull through the superior orbital fissure.
Then, the somatic motor fibers go to levator palpebrae superioris, superior,
medial, inferior rectus and inferior oblique. Visceral motor parasympathetic
fibers go to sphincter pupillae via the ciliary ganglion.
Test: Check extraocular movements, pupillary size, symmetry and pupillary
reflex. Check constriction of ipsilateral pupil (direct reflex) and contralateral
pupil (contralateral reflex). If light reaction is abnormal, then test pupillary
accommodation. Pupils normally converge and constrict when brought at close
focus from distance. Pupillary abnormalities may be a result of either or both
optic or oculomotor lesions.
In oculomotor lesion, the affected pupil is fixed and dilated and may be
associated with ptosis and lateral deviation (due to unopposed action of CN
VI). In Horners sympathetic chain syndrome, the affected pupil is reactive
and small and also may be associated with ptosis.
Argyll-Robertson pupil: Small pupils that are not reactive to light but can
accommodate, i.e. constrict with near vision. It is seen in central nervous
system syphilis.
CN IV Trochlear Nerve (Somatic Motor Only)
Route: There is a center for vertical gaze located in the midbrain. This center
connects directly with the oculomotor and trochlear nuclei.The trochlear nerve
from trochlear nuclei in the midbrain exits brainstem and curves around
(crosses) upon exiting the brainstem. Then, it passes between cerebral and
cerebellar arteries. It enters the cavernous sinus and leaves the brain through
the superior orbital fissure where it supplies the superior oblique muscle
(for intorsion, depression and abduction of eye). Lesion affecting the gaze
center of the midbrain can cause loss of upward gaze but does not affect the
horizontal gaze (Sun set sign).
Test: A CN IV lesion will present as extorsion of the ipsilateral eye and worsening
of diplopia when looking downwards, e.g. going down the stairs.
CN V The Trigeminal Nerve (Sensory and Motor Supply to Face)
Route: Arises from the motor trigeminal nuclei in the pons, travels through the
Meckels cave in the middle cranial fossa, where it enters trigeminal ganglion.
From trigeminal ganglion three branches arise:
1. An ophthalmic branch leaves skull via superior orbital fissure
2. A maxillary branch leaves skull via the foramen rotundum
3. A mandibular branch leaves skull via foramen ovale.
Sensory nuclei are spread in areas from the midbrain to the cervical cord
(for facial sensation).

Test: Use a cotton wisp/safety pin and hot/cold objects to test facial sensation
to light touch,pain and temperature. Observe for deviation of jaw or asymmetry
in muscle contraction by asking child to clench teeth, while palpating the
temporal and masseter muscles. Another brainstem reflex is the corneal reflex
which tests for both CN V and CN VII (the sensory limb of the reflex is CN V
and the motor limb is CN VII).
CN VI Abducens (Motor)
Route: From abducens nuclei in the caudal pons, it passes through the cavernous
sinus and exits the skull through the superior orbital fissure. Then, it innervates
the lateral rectus. It has long intracranial course and hence affected quite often.
Test: Look for the presence of convergent squint.
Also look for Horizontal Eye Movements
There are cortical areas for control of eye movements. One of these is called
the frontal eye field (fef). (This fef controls horizontal gaze to the opposite
side). Fef cortical cells send axons through the internal capsule and cerebral
peduncle, decussate and terminate in an area of the pons. They are called
pontine reticular formation (prf), (prf or horizontal gaze center) which connects
with the abducens nucleus, thus exciting the motor neurons of cranial nerve
VI. This abducens nucleus has the interneurons whose axons ascend in the
opposite medial longitudinal fasciculus to the oculomotor nucleus to cause
concurrent stimulation of medial rectus muscle of the opposite side. Thus, a
right prf lesion impairs ability to voluntarily look to the right.
CN VII Facial Nerve (Motor and Special Sensory)
Route: The facial nerve from the facial nuclei in the pons and medulla travels
via the pontomedullary junction, joins along with CN VIII and enters via the
cerebellopontine angle cistern into the internal auditory canal.
Now, here it enters the facial canal in the temporal bone to reach the
geniculate ganglion (taste bodies) and branches into the greater petrosal nerve
and the chorda tympani nerve.
It leaves the cranium through the stylomastoid foramen and innervates the
muscles of facial expression.
Test: First observe the patients face at rest, and look for nasolabial fold,
flattening or drooping of the corner of the mouth. Next ask to raise eyebrows,
wrinkle forehead, show teeth, puff out cheeks and close eyes tightly.
A peripheral LMN lesion of CN VII will affect the upper and lower face
while a central lesion will only affect the lower face as seventh nerve has only
unilateral representation in brain for lower face.
CN VIII Vestibulocochlear Nerve (Special Sensory)
Route: Fibers that make up CN VIII travel from the spiral and vestibular
ganglions in the inner ear to the inner auditory canal. It then exits the internal
auditory canal with CN VII where it parallels the cerebellopontine angle cistern

until reaching the brainstem at the pontomedullary junction. Vestibulocochlear
nuclei are located in the pons and medulla.
Test: Assess hearing. This can be done by simply whispering to the patient.
Weber tuning fork test: A 512 Hz tuning fork placed on the forehead or on
incisors, will lateralize to the affected side in conductive hearing loss and will
lateralize to the unaffected side in sensorineural hearing loss.
Rinne tuning fork test: Place (512 Hz) tuning fork first on mastoid process,
then bring it in front of ear, without touching. It is done to demonstrate that if
the bone conduction is greater than air conduction, it suggests conductive
hearing loss.
CN 1X Glossopharyngeal Nerve (Somatic, Visceral and Special Sensory)
Route: It arises from the glossopharyngeal nuclei in the medulla and travels
with CN X and CN XI. It exits the skull through the jugular foramen to supply
stylopharyngeus and parotid. Somatic sensory fibers from posterior 1/3 tongue,
middle ear and visceral sensory from carotid body/sinus and special sensory
for taste from (posterior 1/3 tongue) are also present in CN IX.
Test: Tested along with cranial nerve X.
CN X Vagus (Sensory Somatic Motor) and Visceral Motor
Route: The vagus nerve from vagal nuclei in the medulla joins with CN IX and
CN XI and exits through the jugular foramen into the carotid sheath between
the internal jugular vein and internal carotid artery giving off a number of
branches including sensory branches to the ear, epiglottis, aortic body, somatic
motor branches to the soft palate, pharynx and larynx for speech/swallowing
and the visceral motor to cardiac, esophageal and pulmonary neural plexuses
responsible for bradycardia, peristalsis or vomting (pro/retro) and
bronchoconstriction, respectively.
Test: The cranial nerves IX and X are tested by looking for elevation of palate
by gag reflex (another brainstem reflex) or by saying ah. The uvula deviates
towards the affected side.
CN XI Accessory Nerve (Motor) Spinal and Cranial
Route: The accessory nerves spinal portion of nerves (C1-C5) enter the skull
through the foramen magnum and join with fibers from the glossopharyngeal
nuclei in medulla and then exit the skull jointly via jugular foramen.
Test: Observe for atrophy or fasciculation in the trapezius muscles and shoulder
drooping/displacement of the scapula. Next instruct to turn head and shrug
shoulders against resistance. Contralateral CN XI lesion causes weakness in
turning head in one direction, while ipsilateral CN XI lesion causes weakness
in shoulder shrug.
CN XII The Hypoglossal Nerve (Motor)
Route: The hypoglossal nerve nuclei are in the medulla. It exits at the ventrolateral
sulcus and leaves the skull through the hypoglossal canal. It passes between

the internal carotid artery and the internal jugular vein and supplies the tongue.
Hypoglossal nucleus (XII) lesion involving the left side of brain causes
weakness of the right genioglossus muscle Hence on protruding the tongue,
the normal left genioglossus muscle pushes the tongue to the right (flat muscles
push).
Test: First observe the tongue (while inside the mouth) for fasciculations, which
may indicate peripheral damage to nerve. On protruding the tongue it will
deviate toward the side of weakness (normal muscles push the tongue to the
weaker side).
Sensory Evaluation
Rule: Test sensations before motor system assessment (always):
Sensations can be assessed in an older child by pinprick, light touch, position
and vibration sense. Object discrimination, which tests for higher cortical
functions, can be done using coins, paper clips, or rubber bands. Assess
following points:
Light touch: Hypoesthesia, hyperesthesia, paresthesia, or anesthesia
Assess level of pain and temperature appreciation. Hand-and-glove
distribution of sensory loss occurs in peripheral neuropathies
Sensory extinction or sensory inattention: In parietal lobe lesions, if you put
a pinprick on both sides of the body of a patient simultaneously, the patient
will not perceive the prick on the affected side of the lesion. If the pins are
placed sequentially, then the patient still retains normal sensation on both
sides
Cortical sensations like stereognosis are lost, if sensory cortex is damaged,
being unable to identify objects with eyes closed
Loss of proprioception: Seen in posterior columns lesions resulting in unsteady
gait when eyes are closed but normal gait when eyes are open
Rombergs test: Patient cannot maintain balance with legs tight together,
with eyes closed.
Motor System Evaluation
Motor SystemGrading of Strength
Grade 0 No muscle contraction
Grade 1 Flicker or trace of contraction
Grade 2 Active movement without gravity
Grade 3 Active movement against gravity
Grade 4 Active movement against gravity and resistance
Grade 5 Normal strength
Strength for the upper extremities can be assessed by pronator sign.
Have the child raise his/her arms and note the position of the arms. Weakness
of the arm is seen by hyperpronation and elbow flexion. Strength of the flexors
of the knee can be tested by the Barr sign, which is performed by keeping
the child both knees at right angles while lying prone.

APPROACH: (Ask, Look, Feel and Move)
ASK:
About tender areas, gelling for inflammations.
LOOK:
a. Look at the posture
Whether decenbrate, decorticate, hemiparetic (externally rotated) or normal
b. Look at the skin
Caf au lait spots in neurofibromatosis.
Raynaud phenomenon pallor or blueness of fingers, toes, or nose brought
about by exposure to cold and less commonly by other stresses.
c. Look for signs
Gowers signchild climbs on own self, e.g. in Duchennes muscular dystrophy
Foersters signchild slips from mothers grip
d. Look at the gait
Festinating/shuffling gait, e.g. in Parkinsonism.
e. Look for Ataxia*
Romberg test: The Rombergs test is often mistaken to be a test for cerebellar
function, but it is actually a test of proprioception (dorsal columns). It is
for differentiation between peripheral and cerebellar ataxia. Increase in
clumsiness in movements and in width and uncertainty of gait when patients
eyes are closed indicate peripheral ataxia. No change indicates cerebellar
type. (Simple test for coordination: Both the feet are planted firmly together;
if the body sways, lack of coordination is indicated)
Fournier test is for determining ataxic gait. Ataxia is noted with the patient
moving about abruptly in walking, starting and stopping
Stairs sign is seen in locomotor ataxia: Difficulty in or failure to, descend
down stairs (but it may be confused with superior oblique muscle palsy as
here downward and outward gaze is impaired).
f. Look for tremors: Oscillating movements caused by involuntary contractions
of muscle groups.
g. Look for Fasciculations: Twitchings in the resting muscles are seen.
h. Look for tetany: It is seen in case of involuntary muscle spasms due to tetanus,
hypocalcemia, hypomagnesemia, hyperventilation and demonstrate Trousseaus
phenomenon. Inflate a blood-pressure cuff to systolic pressure and maintain for 1
to 2 minutes. Induction of carpopedal spasm indicates latent tetany.
Feel
Tap for chvostek sign for determining low serum calcium leading to tetany.
Tapping of cheek over facial nerve anterior to ear causes the facial muscles
*Recurrent respiratory infection and chronic conjunctivitis with ataxia suggest ataxia telangiectasia.

to twitch or go into spasm. (Shutting of eyes). In meningitis, tapping lightly on
any bone of the extremities causes patient to wince suddenly.
Feel the muscle bulk and tone* by passive movements, i.e. cogwheel
phenomenon is suggestive of rigidity and claspknife phenomenon indicates
spasticity.
Move
Move passively to assess tone and also actively for motor power. For muscular
weakness do the Trendelenburg test in poliomyelitis, rheumatoid arthritis and
congenital dislocations. With the patient standing, weight is removed from one
extremity. If gluteal fold drops on that side, it signifies muscular weakness of
the opposite weight-bearing hip and weakness of the abductor of the weightbearing hip. (Also called as the Trendelenburg sign).
For hemiplegia: Passive flexion of the hand and wrist of the affected side
shows no normal flexion at the elbow.
Morquio sign: In epidemic poliomyelitis, the supine patient resists, attempts to
raise trunk to a sitting position, until the legs are passively flexed.
Huntington sign: Patient is supine, with legs hanging over the examining table,
and is asked to cough; if coughing produces flexion of the thigh and extension
of the leg in the paralyzed limb, a lesion of the pyramidal tract is indicated.
Elicit Reflexes
Deep tendon reflexes: Evaluation needed for testing intactness of spinal cord to
muscle pathway.
Biceps reflex (C5-6): Elbow flexion
Triceps reflex (C6-8): Forearm extension
Brachioradialis reflex (C5-6): Tap distal radius flexion and partial
supination of the forearm
Patellar reflex (L2-4): Contraction of quadri-ceps (strongest muscles in
body) and extension of leg
Suprapatellar reflex: Above the knee; same response
Achilles reflex (S1-2): Causes plantarflexion of foot.
Enhancement of Reflexes
Use Jendrassik maneuver to enhance a deep tendon reflex. Here, when the
patient hooks hands together with flexed fingers and pulls apart as hard as
possible, then the reflex is tested.
Reflex Grading
Grade 0: Complete absence

Grade 1: Diminished
Hypotonia in infancy (Floppy infant) is seen in Down syndrome, Ehlers-Danlos syndrome,

Prader-Willi syndrome, Spinal Muscular Atrophy, etc.
Grade 2: Normal reflex

Grade 3: Hyperactive reflex
Grade 4: Clonus present (remember to test for this).
Babinskis Reflex
Babinskis sign: A positive Babinskis sign is seen when there is dorsiflexion
(extension) of the great toe and fanning of the toes. This response can be
normally seen in children up to 2 years of age or sometimes after a seizure.
Clonus can also be tested by maintaining dorsiflexion of the foot. Sustained
clonus signifies a lesion in the pyramidal tract (or cortical origin).
How to elicit?
Babinskis sign: Stroke lateral aspect of bottom of the foot fanning
(eversion) of big toe is seen
Chaddocks reflex: When the external malleolar skin area is irritated, extension
of the great toe occurs in cases of organic disease of the corticospinal
reflex paths
Oppenheims sign: Scratch inner side of leg extension of toes is a sign
of cerebral irritation, UMN lesion and pyramidal tract lesions
Gordons sign: Squeeze the calf muscles and note the response of the great
toe. Fanning or extension is considered abnormal
Hoffmans sign: Flexion of the terminal phalanx of the thumb and of the
second and third phalanges of one or more of the fingers occurs when the
volar surface of the terminal phalanx of the fingers is flicked. It is significant
for pyramidal tract disease when it is unilateral. If it is bilateral than the
meaning is uncertain
Hirschbergs sign: Internal rotation and adduction of foot on rubbing inner
lateral side indicates pyramidal tract disease
Pseudo-Babinskis sign: In poliomyelitis, the Babinski reflex is modified,
so only the big toe is extended, because all foot muscles except dorsiflexors
of the big toe are paralyzed.
Superficial Reflexes
Superficial reflexes: The absence of superficial reflexes often results from
upper motor lesions, e.g. cremasteric reflex. Stroke inner thigh to look for
elevation of testes. Also check abdominal reflexes.
Primitive Reflexes
Presence of primitive reflexes is often a sign of frontal lobe lesions in
developmentally delayed children. Persistence of primitive reflexes beyond a
particular age indicate cerebral palsy.
Sucking reflex: Gently tap or rub the upper lip elicit a reflexive sucking
or puckering response
Grasp reflex: Stroke the patients palm, causing him to grasp your fingers.
A positive test occurs when the patient does not let go of your fingers
Palmomental sign: Rub the thenar eminence elicit reflexive contraction

of the muscles of the chin
Moros reflex: For testing normal early neurologic development or the failure
to progress neurologically; the infant is placed on a table, then the table is
forcibly struck from either side, causing the embrace.
Signs of Meningeal Irritation
Kernigs sign for meningitis: In dorsal decu-bitus, the patient can easily
and completely extend the leg. In sitting or lying down with thigh flexed
upon the abdomen the leg cannot be completely extended
Brudzinskis sign: Flexion of the neck forward results in flexion of the hip
and knee. Also when passive flexion of the lower limb on one side is made,
a similar movement will be seen in the opposite limb
Guilland sign for meningeal irritation: When the contralateral quadriceps
muscle group is pinched, there is a brisk flexion at the hip and knee joint.
Cerebellar Function Assessment

Observing how a child reaches for and manipulates toys, look at the following
points.
Dysmetria: Inability to properly gauge the distance between two points. Test
with finger-to-nose movements, the patient attempts to put a finger on his
nose and then to the examiners finger, back and forth rapidly. Any
incoordination indicates test to be positive
Intention tremors and titubation: Body tremors when standing, walking or
doing any work
Dysdiadochokinesia: Inability to do rapid alternating movements
Scanning speech: Prolonged separation of syllables, often seen with
cerebellar dysfunction.
Gait disturbances: In central cerebellar lesions conventional cerebellar signs
may be normal but an unsteady wide based gait, may be seen.
For Testing Intactness of Brainstem Function
Dolls eyes sign: It is the normal coordinated eye motion seen while passively
turning the head of an unconscious patient, so as to test the intactness of
brainstem function.
Assessment of Autonomic Nervous System
The autonomic nervous system includes the somatic afferent pathway (from
brain and spinal cord), plus the efferents via sympathetic fibers
(norepinephrine mediated) and the parasympathetic fibers (acetylcholine
mediated) to all organs
Usually, in dysautonomias first sympathetic is affected and later
parasympathetic, while in diabetic patients parasympathetic autonomic
neuropathy may be earlier
Monitor blood pressure: All dysautonomias usually have orthostatic

hypotension within the first 30 seconds of standing (presenting as dizziness
or syncope). In autonomic neuropathy there is a marked reduction in the
standing blood pressure but unaccompanied by the usual compensatory
increase in heart rates
For example: Systolic blood decreases by 20 mm Hg but heart rate
increases less than 10 beats/min on standing.
Monitor heart rates: Mechanically monitor the heart rate or do ECG.
Note the effect of respiration and valsalva on heart rate. The difference
between maximum heart rate during inspiration and the least heart rate
during expiration of less than 10 beats/minute is abnormal. Similarly,
note difference in bradycardia (post valsalva) versus tachycardia (during
the valsalva)
Monitor the pupils: The pupil has both sympa-thetic dilator and
parasympathetic constrictor autonomic nerve supply. In Adies pupil, there
is parasympathetic denervation, whereas in Horners syndrome there is
sympathetic denervation (leading to miosis)
Monitor bowel and bladder in seizures: Autonomic bladder dysfunction
presents as nocturia, retention, dribbling, etc. Autonomic bowel dysfunction
presents with nocturnal diarrhea, fecal incontinence/encopresis
Monitor sleep chages: Look for sleep apnea, parasomnia sleep walking,
teeth grinding, excessive somnolence, restless legs syndrome and nocturnal
myoclonus
Reflex hammer and tuning fork are necessary for the evaluation of
peripheral neuropathy, which is often present in patients who have
autonomic neuropathy.
Developmental Assessment
Assess developmental age in various domainsFine motor, gross motor, language
and psychosocial as discussed in the Chapter 6.
Developmental delay may be grouped under following headings
a. Syndromic, e.g. Downs syndrome
b. Motor delay, e.g. Cerebral palsy
c. Global delay, e.g. Mito chondrial disorders and IEMs
d. Language delay
e. Neuroregression.
NEUROLOGICAL EXAMINATION OF THE INFANT

Assess the following things (additionally) in case of infants:
Assess posture and muscle tone by:
Resting posture: Frog like posture in Scurvy
Passive tone: The scarf sign
Active tone (Pull-to-sit): Infant of up to three months is slowly pulled
to a sitting position. If hypotonia is present, then the head lags backward;
later, when erect position is assumed, the head drops forward while if
hypertonia is present, the head is maintained backwards
Vertical suspension: The infant is suspended by holding the chest with
both hands and lifting the patient in an upright position, with the legs
dangling. If scissoring or hyperextension of the legs is seen, then
spasticity is present and cerebral palsy may be present
Horizontal suspension (Landau reflex): To perform this reflex, the infant,
while prone, (keeping examiners hand under the trunk) is gently lifted
upwards. Normally, the spine extends a little so that the eyes are looking
just below the horizontal. If the body collapses into rag doll, then hypotonia
is present.
Primitive reflexes. Primitive reflexes are usually present from the time of
birth and represents spinal reflexes. Later higher cortical functions suppress
them
The sucking reflex: It involves afferent fibers of CN V and IX, and
efferent fibers of CN VII, IX, and XII
Moro reflex (embrace reflex): This is done by having the head
hyperextended, falling back about three centimeters in relation to the
trunk. A normal response is seen when the infant opens his hands,
extends and abducts the arms, and then brings them together, followed
by a cry. It is present in all newborns and disappears before the age
of six months. It is a vestibular reflex
Tonic neck response (Fencers stance): This reflex can be elicited when
the head is turned to the side, while the rest of the body lies flat on the
table. A normal response is extension of the arm and leg on the side that
head is turned to, and flexion of the arm and leg on the opposite side
(fencing stance). It usually disappears in about six to seven months
of age
Palmar and plantar grasp reflexes: They are performed by applying
gentle pressure to the palm or sole. An abnormal response occurs when
this response is absent (before two-to-three months of age) or persists
after this time, or is asymmetrical
Parachute response: The infant is suspended horizontally with the face
down, and is brought quickly down toward the floor, making sure that
the infant is firmly held. A normal response is seen when the arms are
extended and the hands open up. This usually appears at 9 to 10 months
of age and persists for life

Reflex placing and stepping responses: Reflex placing is seen when the
dorsum of the foot is placed against the edge of the examination table.
Reflex stepping is seen when the sole of the foot is placed on the table,
and the infant appears to be walking. This reflex disappears at about
four to five months of age.
BIBLIOGRAPHY
1. Bates B. Nervous system. In: A Guide to Physical Examination and History Taking.
8th edn. Philadelphia, PA: Lippincott, Williams and Wilkins, 2004.
2. Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 4th edn.
Philadelphia, PA: Lippincott, Williams and Wilkins, 2004.
3. Carpenter MB, Sutin J. Human Neuroanatomy. 8th edn. Baltimore, MD: Lippincott,
Williams and Wilkins, 1983.
4. De Jong RN. The neurologic examination: Incorporating the fundamentals of
neuroanatomy and neurophysiology. 4th edn. Hagerstown, MD: Harper and Row,
1979.
5. DeMyer WE. Technique of the neurological exami-nation. 5th edn. New York, NY:
McGraw-Hill Professional, 2003.
6. Dias MS, McLone DG. Normal and abnormal early development of the nervous system,
in McLone DG (Ed.): Pediatric Neurosurgery: Surgery of the Developing Nervous
System. Philadelphia, WB Saunders 2001;31-71.
7. Dias MS, Schoenwolf GC. Molecular biology of early neural development, in McLone
DG (Ed): Pediatric Neurosurgery: Surgery of the Developing Nervous System.
Philadelphia, WB Saunders 2001;73-86.
8. Henry Gray (18211865). Anatomy of the Human Body, 1918.
9. Herlevich NE. Reflecting on old Olympus towering tops. Journal of Ophthalmic
Nursing and Technology 1990;9(6):245-6.
10. Hoeman S. Rehabilitation Nursing. St Louis: Mosby 2002; 383-444.
11. Kunimoto K. The development and reduction of the tail and of the caudal end of the
spinal cord. Contrib Embryol 1918;8:161-98.
12. Moore KL. The Developing Human: Clinically oriented embryology. Philadelphia,
WB Saunders Co, 1982.
13. Norman MG, McGillivray BC, Kalousek DK, Hill A, Poskitt KJ. Embryology of the
central nervous system, in Norman MG, McGillivary BC, Kalousek DK, Hill A, Poskitt
KJ (Eds): Congenital Malformations of the Brain: Pathological, Embryological, Clinical,
Radio-logical, and Genetic Aspects. New York, Oxford University Press 1995;9-51.
14. ORahilly R, Mller F. Developmental Stages in Human Embryos. Washington,
Carnegie Institution of Washington, 1987.
15. Parent A, Carpenter MB. Carpenters Human Neuroanatomy. 9th edn. Philadelphia,
PA: Lippincott, Williams and Wilkins, 1998.
16. Saladin, Kenneth S. Human anatomy (Second Edition). McGraw-Hill Higher Education,
2008.
17. Van Allen MW. A guide to the performance and interpretation of the neurologic
examination. In: Van Allens Pictorial Manual of Neurologic Tests. 3rd edn. St Louis,
MO: Mosby-Year Book Medical, 1988.
Pedia Pearls:
In a newborn with arm weakness, look for weak handgrip, because in Erbs palsy the
handgrip should be normal.
In a preterm with bulging AF with sunsetting sign, suspect intraventricular hemorrhage.
8
Cardiovascular System
AN OVERVIEW OF CARDIOVASCULAR SYSTEM
HEART EMBRYOLOGY
Cardiogenic Region (Fig. 8.1)
The cardiovascular system originates from the mesodermal germ layer.
The cardiogenic region is located at the cranial part of the embryonic disk
in an inverted U shape.
Fig. 8.1: Cardiogenic region
Cardiovascular System 59
Formation of Heart Tube
(Fig. 8.2)
Initially, a paired heart tube is formed
in this region. The two limbs of the
Ufuse into a single tube.
As the embryo flexes through
180 (cranial flexion) the arterial pole
of this tube comes to lie cranially.
The heart tube has five parts,
craniocaudallytruncus, bulbus
cordis, primitive ventricle, primitive
atria and sinus venosus
Looping of Heart Tube
Fig. 8.2: Formation of heart tube
The primitive heart tube loops to the

right, making a U shaped bend between bulbus cordis and primitive ventricle.
Due to looping the atria moves behind bulbus and ventricle and sinus venosus
moves behind the atria. The sinus venosus later gets absorbed into the right
side of atria.
Septation
The opening of the Atrioventricular canal fuses by forming the endocardial
cushions in the center, creating the mitral and tricuspid openings on it sides.
Atrial Septation
The septum primum starts from the roof and reaches the endocardial
cushions but leaves an opening called foramen primum. This gets obliterated
by extension from the endocardial cushions
The septum primum divides the atria into right and left side
The septum primum breaks in upper portion and an ostium secundum is
formed
This is overlapped by another septum secundum from atrial roof on
rightside of septum primum
The gap between two septums allows blood flow from right to left across
this ostum secundum (now called foramen ovale).
This gap closes after birth due to increase in left atrial pressures. Most of
the atrial septal defects occur in this region.
Pedia Pearl: The spiral septum is formed from neural crest cells

Ventricular Septation
The interventricular septum has a thick muscular part and a thin membranous
part which is formed from:
The endocardial cushions of the AV canal
The spiral septum descending from the truncus.
Actually, the truncus is divided into two parts with the formation of spiral
septum into a pulmonary trunk anteriorly and aorta posteriorly.
ANATOMY
Heart Borders and Relations
The heart is positioned, downwards, forwards, and to the left:
Anteriorly, it has the pleurae and lungs and posteriorly, are the atrias in
relation with the posterior mediastinum
The anterior aspect is almost made of right atria and ventricle
Right border of the heart is formed by the right atria and the left border
and the apex by the left ventricle
The upper border is formed by the right atria, the conus pulmonalis and
the tip of the left atrial appendix
Pericardium, myocardium, and the endocardium are the three layers with
the nerve supply from the vagus and the sympathetic system.
PHYSIOLOGY
Fetal Circulation
Shunts are necessary for survival:
Placenta is the oxygenator. It sends blood via ductus venosus (bypasses
liver) to the right atria
Then through foramen ovale (R to L atrial level shunt) blood goes to aorta
via left ventricle
Some blood from the Superior Vena Cava (SVC) comes to the right atria,
then enters right ventricle but cannot go to lungs due to high pressures in
pulmonary circulation. Hence, it goes via ductus arteriosus (R to L arterial
level shunt) to the descending aorta.
Transitional Circulation
With first few breaths, lungs expand and placenta is cut off.
Foramen ovale functionally closes and the ductus arteriosus usually closes
within first one to two days due to correction of hypoxia (the lungs can
expand) after birth
Timing of Shunt Closure
Functional closure of ductus arteriosus (10-15 hours); Anatomical closure of
ductus arteriosus (14-21 days); Functional closure of foramen ovale
(Immediately); Anatomical closure of foramen orale (3rd month).
Neonatal Circulation
Right ventricle (RV) pumps blood to pulmonary circulation and left ventricle
(LV) pumps to the systemic circulation
Pulmonary resistance (PVR) is high initially after birth
By six weeks, pulmonary resistance drops and LV becomes dominant
causing increased flow to the lungs
Hence in Acyanotic CHD, the left to right shunts may not be apparent
up to 6 weeks of age, due to high pulmonary resistance.
PATHOLOGY
Congenital Heart Diseases (CHD)
Acyanotic CHD: Left (L) Right (R) shunts, e.g. VSD, PDA, ASD and
atrioventricular canal
Cyanotic CHD:
RL shunts with pulmonary blood flow (PBF), e.g. Truncus
arteriosus, TAPVC and TGV. Pulmonary congestion worsens as
neonatal PVR lowers. So, saturation can be good if there is high
pulmonary blood flow and the child may look pink
RL shunts with PBF, e.g. ToF often presents with cyanosis and
oligemic lung fields. Here, closure of PDA may worsen cyanosis
Obstructive lesions may be ductal dependent, e.g. critical PS/AS. Critical
COA/HLHS. They present with shock at two to three days of age
when PDA closes, with or without cyanosis. They need PGE1 for
treatment to keep PDA open for blood flow to the abdomen and lower
extremities
Obstructive lesions (Nonductal dependent) are not cyanotic like mildmoderate AS, mildmoderate CoA and mild-moderate PS. They usually
present in older child with murmur, exercise intolerance or
hypertension.
Pedia Pearl: Obstructive lesions have no cyanosis and do not have frequent chest
infection. However, they have a heaving apex.
Syndromic associations
Charge
Conotruncal (ToF, truncus)
Down syndrome
Defective endocardial cushion, i.e. AV
canal and VSD
Edwards
VSD, PDA
Fetal alcohol
Fallots, LR shunts
Turner
Turns the aorta (COA, AS)
Hereditary diseases
Marfans (AD)
MVP, MR, AI
Noonan (AD)
HCM, PS
Williams (AD)
Supravalvar AS
Tuberous sclerosis Rhabdomyoma
DMD (X-linked)
DCM
Acquired Heart Diseases
Amongst aquired heart diseases, the commonest causes are:

Kawasaki
Rheumatic fever
Congestive cardiac failure (CCF)
Age at the time of CCF
0-3 daysAtresias
4-7 daysHypoplasia of left heart
7-28 daysCoarctation of aorta, complex heart disease.
> 28 daysDefects (VSD, PDA).
SYMPTOMATOLOGY
Central Cyanosis
Cardiac cyanosis is always central. It may also caused by an increase in the
percentage of deoxygenated hemoglobin due to a CNS distur-bance, or lung
disease. However, in severe anemia, the level of hemoglobin which could be
desaturated is too low to cause any significant bluish dis-coloration of the
blood (min 5 gm% of Hb needed).
For diagnosis of cardiac cyanosis look out for the following:
i. A prolonged capillary refill time indicates poor cardiac output in a congenital
heart disease.
ii. Syndromic features, such as in Turners and/or presence of murmur
may be a clue to diagnosis.
iii. Femoral and brachial arterial pulses should be felt simultaneously to
assess their strength and timing. In coarctation of the aorta, the femoral
Pedia Pearls: Cyanosis at birth TGA, TA, PA, Cyanosis after 6-8 weeks TOF ,
Cyanosis on crying reversal of shunt in large VSD.
pulsation is weaker and delayed in timing when compared to the brachial
arterial pulse. In right to left shunt, crying and activity worsens the
shunt.
iv. In heart failureA triad of cyanosis, tachy-cardia and hepatomegaly
usually coexist. Intractable wheezing (unlike asthma) may also exist in
such patients.
v. Sometimes differential cyanosis is seen due to RL shunt through the
PDA, while a right ventricular heave suggests RV pressure overload.
Chest Pain
Chest pain is rarely due to cardiac reasons in children:
Typical chest pain (retrosternal and radiating to left shoulder) due to coronary
artery disease/myocardial infarction may occur in Williams syndrome, or
Kawasakis disease
If the pain is localized and increases on breathing, it indicates a pleuropercardial
pain
Skin diseases (such as Varicella zoster, or herpes zoster) produce lancinating
pain from costal margin to the back
Psychogenic chest pain: Relieved by exercise
Pain in Chronic Bronchitis: Relieved by bronchodilators
Costochondritis is a musculoskeletal pain
Spinal root pain: Starts at back and comes to the front.
Dyspnea
Respiratory distress could be due to pulmonary or cardiac causes. To
differentiate these two, note the following points:
i. Easy fatigability and failure to thrive occurs due to cardiac problems,
more commonly. Ask for relief on putting to shoulder and worsening
on feeding or straining at stools in such cases, suggesting heart failure.
ii. Inadequate sleep and decreased urine output are often seen in heart
failure.
iii. Recurrrent respiratory infections are common in L-R shunts and also
in asthma but features of allergy and relief with bronchodilators in
asthma, clinch the diagnosis.
Syncope
This occurs usually due to fall in cardiac out put due to arrhythmia or
obstruction to blood flow history of syncope may thus predict presence of
heart disease.
Wheeze
If intractable, wheeze may point to Congestive Heart Failure (CHF) due to
any cause.

Hemoptysis
This may be seen in cardiovascular diseases causing pulmonary hypertension
or respiratory problems like bronchiectasis.
Failure to Thrive
This may be seen due to:
Acidosis, Basal Metabolic Rate (BMR), CHF, Difficulty in feeding,
Endocarditis, Fever and Hypoxia.
PATHOPHYSIOLOGY
Pulse
Assess rate, rhythm, palpability. Next the character is assessed
Sinus arrhythmia: Normal quickening of speed in inspiration and slowing
in expiration
Collapsing pulse (water hammer): It is a thready but strong, bounding
pulse
Anacrotic pulse is a slow rising pulse
Pulsus alternans (alternating pulse of big and small peaks) has a strong
then a weak pulse. Arterial pulse waveform showing alternating strong
and weak beats is an important manifestation of decreased myocardial
contractility or sign of LVF (carries a poor prognosis)
Pulsus bigeminus has groups of two heartbeats close together followed
by a longer pause. The second pulse is weaker than the first. Pulsus
bigeminus is caused by premature ventricular contractions after every
other beat. Seen in Hypertrophic obstructive cardiomyopathy, or it may
be innocent and a temporary phenomenon
Pulsus bisferiens (pulse with two peaks with a valley between) is a pulse
characterized by two strong systolic peaks separated by a midsystolic dip,
most commonly occurring in pure aortic regurgitation and in aortic
regurgitation with stenosis
Pulsus paradoxus is actually an abnormal inspiratory dip in arterial blood
pressure, seen in cardiac tamponade and caused by a decreased pulmonary
venous return, e.g. (constrictive pericarditis, pericardial effusion, and
severe asthma). A dip of > 10 is significant.
Inequality of Pulses
Pulsus differensInequality of the pulse observable at corresponding sites on
either side of the body.
For example:
Radial pulse: Aorta is the culprit in aortic arch aneurysm, a few cases of
coarctation of the aorta and supravalvular aortic stenosis (rarely), Takayasus
disease and occlusion of subclavian artery by external pressure. If the
radial pulses appear asymmetrical, the pressure should be measured in
both arms because a difference between the two may indicate aortic
dissection
Femoral pulses: Radiofemoral delay is seen in coarctation of aorta.
Heart Sounds
The first sound, heard at the apex along with the ventricular contraction is
longer and lower in pitch (due to the mitral and tricuspid valves). The second
sound is sharper and shorter (due to the closure of the aortic and pulmonary
valves) and is best heard over the base of the heart.
Auscultate Clockwise
First auscultate over the mitral area, then tricuspid, then aortic and then
pulmonary area. Lastly, auscultate veins at root of neck (venous hum)
Diminished intensity or absence of the heart sound may be an an indication
that hearts action is feeble. But loudness is relative
Whether first sound is loud or second is soft, is the question often difficult
to answer.
The First Sound

In hypertrophy of the left ventricle, the first sound at apex is long, sustained
and low in pitch. In dilatation (left ventricular) it is shortened, sharp, clear and
high in pitch. The first sound may be short and diminished indicating a weak
heart. In pure mitral stenosis, the first sound is short, sharp, and clear, like
the second sound. In tricuspid area an increase in the loudness indicates increase
in pressure within the pulmonary circuit, but if beyond a certain point, tricuspid
regurgitation starts causing a diminution in the intensity of the first sound.
Triple sounds audible due to duplication of the first sound are termed as the
gallop rhythm.
The Second Sound
It is a sound in aortic or pulmonary area which may be increased in intensity
due to valve closure with an unusual force. For example, increased blood
pressure in the pulmonary circulation and/or hypertrophy of the right
ventricle or loud aortic sound in high blood pressure. A split occurring at
semilunar valves indicates closure that is sooner on one side of the heart
than on the other.

Abnormal Sounds
Pericardial friction rub in pericarditis is not abolished in contrast to pleural
effusion rub, where the rub disappears with effusion and is affected by
respiratory movements.
Ejection click = Aortic Stenosis (AS) or PS

Mid-systolic click = (Mitral Valve Prolapse (MVP)
Loud S2 = Pulmonary Hypertension (HTN)
Single S2 = one semilunar valve (truncus), anterior aorta (TGA), pulmonary
HTN
Fixed, split S2 = ASD, Pulmonay Stenosis (PS)
Gallop (S3)may be due to cardiac dysfunction/ volume overload
Muffled heart sounds and/or a rub = pericardial effusion tamponade.
Murmurs or Bruits
They could be organic or functional. Look for the following points:
The Point of Maximum Intensity and Timing
Each murmur from different valve has separate point of maximum intensity.
The Point of Maximum Intensity at the Mitral and Tricuspid Area
Murmurs systolic in time in these areas denote regurgitation, since these valves
should be closed during the systole of the ventricles. AV valve presystolic, or
diastolic murmurs indicate obstruction caused by the onward flow of blood
through a narrowed orifice. A feature of diastolic murmurs is that they become
softer as they proceed while presystolic murmurs becoming louder as they
proceed.
The Point of Maximum Intensity at the Aortic and Pulmonary Areas
Diastolic murmurs in these areas indicate incompetence or regurgitation
backwards from the arteries into the ventricles. Most commonly the sound is
conveyed better in the direction of a moving current. A pulmonary systolic
murmur is usually audible outwards in the second left interspace, and upwards
towards the left clavicle. A pulmonary diastolic murmur may be audible over
a considerable area, its direction of selective propagation being downwards
along the left border of the sternum.
Character of Murmurs
They are rough in stenosis, soft, blowing in incompetence and musical in
functional or friable valve. The loudness of murmurs has no direct relation
with severity of the lesion. Mitral and tricuspid obstructive murmurs may
become faint when the patient lies down, whereas in regurgitant murmurs
opposite may happen.
Points to Remember
Ejection systolic murmur = turbulence across a semilunar valve
Holosystolic murmur = turbulence begins with systole (VSD, MR)
Continuous murmur = pressure difference is constant in systole and
diastole (PDA, BT shunt)
Thrill suggests that the murmur is organic.
Rub is commonly heard as a leathery sound in pericarditis.
Apex Beat
Character/type
Force:
Apex beat is a distinctly palpable, area of pulsation whose extent and position
is lowest and farthest to the left. Prominent apex is seen in thin children, in
retraction of the left lung, cardiac hypertrophy and diminished if lung or
fat or fluid covers it, e.g. emphysema, obesity, or effusion
The force of the apex is more in thin or on exertion or mental excitement,
and in hypertrophy
In cardiac hypertrophy, the apex beat is heaving slower and longer.
Apex beat is diffuse, weak and often difficult to locate if the apex beat lies
behind a rib or if it is due to weak cardiac function, e.g. in anemia, pyrexia,
acute myocarditis and in cardiac dilatation
In cardiac dilatation, it is of hyperdynamic type.
Location:
Sometimes, the lung or ascites may push it or it may rotate on its own
(in dextrocardia) while diseases of the heart like dilatation or hypertrophy
or both or pericardial effusion may displace it
In the dilatation and hypertrophy of the right heart, the apex beat is displaced
outwards to the left
In dilatation and hypertrophy of the left ventricle, the apex beat is displaced
chiefly downwards and only slightly outwards
In pericardial effusion, the apex beat may be displaced upwards
Enlarged right ventricle displaces the left ventricle backwards, so if the
apex beat is formed by the right ventricle the out-thrust is diastolic in time.
Pulsations: Easily seen in thin chest.
Systolic pulsations:
It tells the lesion according to area, e.g. the pulsation that is mostly to
the right of the sternum indicates ascending aorta involvement
If the pulsation is in the epigastrium the cause may be due to
cardiomegaly or pulsation of the liver in tricuspid regurgitation, etc.
If pulsation is felt in the aortic area then aortic incompetence should be
suspected
Pulsation in the pulmonary area (second left intercostal space) is usually
due to the pulmonary artery
Pulsation at the root of the neck is due to aneurysm of large thyroidea

ima artery.
Pulsation, diastolic in time are the right ventri-cle pulsations in the 3rd,
4th, and 5th intercostal spaces, near the sternum on the left side
Systolic recession. Here, systolic apical impulse is being replaced by an
indrawing, during cardiac systole due to an enlarged right ventricle,
displacing the left ventricle backwards, so that the apex is formed by the
right, instead of the left ventricle
Venous pulsation of the jugular veins may be due to stasis in the right atria
from any cause, such as tricuspid regurgitation or compression of the
superior vena cava
Arterial pulsations seen in hyperdynamic circulation. Capillary pulsation
is seen in aortic regurgitation, pyrexia and anemia (alternative flushing and
pallor with each systole). However, the skin (normally pale) some time
looks red due to pressure or friction.
Blood Pressure
The sphygmomanometer or mercurial manometer
has an armlet, containing an airbag, which is fixed round the upper arm and
indicates the amount of blood pressure within the airbag.
Korotkoffs ausculatory method: The bell of a stethoscope is placed over
the brachial artery 1 to 2 cm below the armlet encircling 60 percent of the
upper arm circumference. The pressure within the airbag is then steadily
raised until it is 10 to 12 mm above the point at which the pulse is no longer
palpable and it is then gradually reduced. A reading is made at the point of
reappearance of the pulse while the disappearance of the sound represents the
diastolic pressure.
Caution: Use cuff size of around 2/3nd the length of upper arm and 60% of
its circumference.
POINTS TO REMEMBER
1. Volume overload produces dilatation of the heart (downwards and outwards)
and the apex is hyperdynamic in nature
2. Pressure overload produces hypertrophy of the heart (outwards) and the
apex is heaving in nature (i.e. sustained lift)
3. Tapping APEX is felt in mitral stenosis.
CARDIOVASCULAR HISTORY AND EXAMINATION

STRUCTURE OF HISTORY
Take history of various symptoms in present illness and based on
symptomatology assess:
Cause
Severity
Future risk.
The various cardiac symptoms are:
Chest pain: Anginal pain is continuous pressing pain (not sharp or
interrupted) on front of the chest, upper abdomen, radiating to neck, jaw,
left arm or left shoulder
Breathlessness: Enquire about duration, on exertion, at rest, associated
cough (orthopnea, paroxysmal nocturnal dyspnea), accompanied by
wheezing/sweating
Rule out CCF by history of swelling, suck rest suck cycle, repeated
respiratory tract infections and relief on putting to shoulder.
Palpitations (precordial activity)
Associated symptoms: Pain, dyspnea, or syncope
Short episodes suggest paroxysmal tachycardia
Longer duration suggests atrial origin.
Failure to thrive: Look for oliguria, edema
Abdominal discomfort: Look for liver enlargement
Syncope of cardiac origin: May closely resemble vasovagal attacks, or
caused by aortic stenosis/regurgitation (or even pulmonary stenosis) and
dysrhythmias
Cyanosis: Ask whether it is increased on crying or improves on squatting.
History of Complications (4F)
Feeding problems (CCF)

Focal deficits, seizures (Brain abscess, infarct)
Frothy pink sputum (Pulmonary edema)
Fever (infective endocarditis).
Ask Past Medical History

Any history of rheumatic fever or heart problems as a child including history
of hypertension, stroke and syncope are vital.
Ask Family History
Ask about consanguinity, hypertension, ischemic heart disease, stroke, diabetes,
hyperlipidemia, congenital heart disease and early deaths in the family.
Ask Maternal Risk Factors
Ask about fever, irradiation, drugs, diabetes, hypertension and similar problems
in siblings.

Look for syndromic features, such as Down syndrome which may suggest
heart disease
Assess nutrition: look whether obese or wasted
Assess severity of illness: Look for difficulty in talking, sick look, etc.
Eyes look for pallor or polycythemia, jaundice, Cyanosis (best seen on
inner lining of eyelids or inner surface of lips) and roth spots.
Chest:
Precordial bulge indicates heart disease
Emphysematous chest may signify obstructive airway disease.
Hands:
Clubbing of digits and cyanosis indicate hypoxia
Visible capillary pulsations in nailbed (Quinckes sign is often seen in
aortic regurgitation)
Finger clubbing and splinter hemorrhages (in infective endocarditis)
Sweaty palms and tremors (in thyrotoxicosis)
Chorea (in rheumatic fever)
Lax joints are seen (in Marfans syndrome).
Neck: Veins are engorged or not.
Back and lower limbs:
Look for edema and whether it pits above medial malleolus
Also look for edema of sacral area, genitalia and back of the thighs
Look for edema in serous sacs, e.g. pleural effusion, pericardial effusion,
or ascites
Look out for arthritis as well.
SYSTEMIC EXAMINATION
Inspection and Palpation
Assess Pulse Rate, Rhythm and Strength
Examples:
Differential pulses (weak in Lower limbs) = COA
Bounding pulse = Run-off lesions (LR PDA shunt, AI, BT shunt)
Weak pulse = Cardiogenic shock or COA
Pulsus alternans - altering pulse strength LV mechanical dysfunction.
Check Blood Pressure
Usually poor cardiac output results in low systolic and high diastolic blood
pressure, hence a narrow pulse pressure. On the other hand, a low diastolic
Pedia Pearls (Causes of clubbing)
C = cyanotic heart disease; L = Lung abscess; U = Ulcerutive colitis; BB = Bronchiectasis;
I = Idiopathic; N = Neoplastic; G = Gauchers disease.
BP, such as with PDA or aortic regurgitation will cause a wide pulse
pressure.
Pulsus paradoxus is an exaggerated SBP drop with inspiration, tamponade
or bad asthma.
Jugular Venous Pressure
Beyond infancy, one may check the level of the jugular venous pressure.
Chest Wall Shape
Find out position of trachea in the suprasternal notch to look for displacement
of upper mediastinum. Check for respiratory rate and the symmetry of chest
wall movement and the degree of chest expansion (on both sides). Look for
inequality of expansion and displacement of lower mediastinum by finding the
position of apex beat. Apical impulse gives several clues (hyperdynamic apex
in volume overload and heaving apex in pressure overload). Precordial bulge
indicates that the ventricle hypertrophy started before eight years of age.
A palpable thrill over the precordium or suprasternal notch indicates a significant
murmur. The RV impulse (left lower sternal border) and LV (apical) impulse
may indicate hypertrophy of the respective chambers.
Palpation
Palpate the trachea to detect any deviation,
If the apex beat is displaced towards the axilla along with trachea, think of
mediastinal shift (not cardiomegaly)
Palpate with the flat hand or pulp of two fingers for the maximum apex
impulse in the rib spaces relative to midclavicular line. Look for any thrill,
pulsations [suprasternal (in AS and PDA), over liver (in Tricuspid Atresia)].
Percussion
Percuss to find any areas of dullness, if any mass, consolidation, collapse or
pleural effusion is suspected.
Percussion is not very useful in children, but to find the extent of heart using
the wrist and finger, the percussing finger should strike the pleximeter at a right
angle and go from resonant to less resonant area parallel with the border to be
percussed. Also corresponding areas on both sides should be compared.
Auscultation of the Heart
Auscultate for heart sounds:
Aortic area (2nd right intercostal space): Compare S1 and S2 (normally S1
is soft)
Pulmonary area (2nd left intercostal space): Listen for split, intensity and
variability with respiration
Tricuspid area (lower left sternal border): Listen for intensity of S1
Apex: Listen for S1, S2, S3 and S4. Pericardial rub and diastolic rumble are
better heard.
Auscultate for presence of murmurs:
Holosystolic murmurs: This indicate shunting of blood throughout systole
from higher to lower pressure, e.g. VSD
Midsystolic murmur (flow murmur): This indicates the high volume of
blood flowing through normal valves
Continuous murmur: Here the pressure difference persists between two
structures during systole and diastole, e.g. in PDA
Ejection systolic murmur: Indicate increase in blood flow turbulence as
systole progresses due to an increasing amount of blood flow through a
restricted orifice, e.g. PS
Early diastolic murmur: Indicate regurgitant blood flows from aorta or
pulmonary artery into the ventricles (e.g. aortic and pulmonary
regurgitation)
Late diastolic murmur: For example, Austin flint murmur in aortic
regurgitation (regurgitant blood flow causes vibration of left ventricular
free wall).
Abdomen
Palpation of abdomen is important as well. Hepatomegaly may be seen in CHF
due to elevated central venous pressure due to L-R shunt and also pushed
down in several respiratory conditions. Hence, liver span measurement is
more important to differentiate enlarged liver from a pushed down liver.
Clues: Hepatomegaly and splenomegaly (congestive cardiac failure), or spleen
alone (infective endocarditis) are useful cluses.
Cenral Nervous System (CNS)
Look for focal deficits and involuntary movements.
Respiratory System (RS)
Look for crepitations and rhonchi in CCF, etc.
APPROACH TO CARDIOVASCULAR PROBLEMS
OF A NEWBORN INFANT
Check Mother
Maternal serum alpha-fetoprotein, a marker for fetal aneuploidy or knowledge
of pre-existing maternal medical conditions such as diabetes may provide a
clue. Maternal medications should also be noted. Ultrasound may reveal
congenital heart, lung, or CNS anomalies but major anomalies frequently escape
prenatal detection. Maternal serologies (TORCH) and cultures often identify
newborns at risk for perinatal group B streptococcal pneumonia or intrauterine
toxoplasmosis infection.
Check Baby/Infant
Do Apgar scoring
Look for cyanosis:
A minimum of 5 g/dl or more of desaturated hemoglobin is necessary.
Look in an infants mouth to get a true assessment of oxygenation.
The polycythemic infant with a normal oxygen saturation may appear
cyanotic from peripheral sludging of desaturated red cells
Look for respiratory distress with or without cyanosis: Neonatal
respiratory disorders pre-senting with cyanosis includes respiratory
distress syndrome, meconium aspiration syndrome, neonatal pneumonia
and pneu-mothorax. Dyspnea, retractions and grunting, apnea and
asymmetry of breath sounds may suggest focal lung disorders. However,
a cyanotic cardiac disease may also produce respiratory distress if
pulmonary circulatory overload is present, e.g. TGV (Fig. 8.3)
Cyanosis associated with cardiac problems: Heart murmurs are common
in neonates during perinatal transition. The systolic murmurs of a patent
ductus arteriosus and tricuspid regurgitation are heard in normal
Fig. 8.3: Egg on side appearance

Transposition of Great Vessels (TGV)
Pedia Pearl: Apart from central, respiratory and cardiac causes of cyanosis,
methemoglobinemia due to any reason may produce cyanosis, as well.
neonates. Many cyanotic congenital heart malformations are not

accompanied by murmurs. Weak pulses denote systemic hypoperfusion
as in low volume states. Weak femoral pulses suggestcoarctation of
aorta. Bounding pulses suggest a widened pulse pressure. The severity
of the pulmonic stenosis is the most important factor in determining
the degree of cyanosis.
Cyanosis with dysmorphic features: May provide diagnostic information.
For example, Downs syndrome (trisomy 21), trisomy 18, trisomy
13 and Turners (XO) syndrome are associated with specific cardiac
malformations
Look for central nervous system dysfunction caused by hypoxic ischemic
injury, seizures, intracranial hemorrhage, infection, or metabolic
derangement such as hypoglycemia which may also lead to cyanosis.
Check Lab Investigations
Polycythemia may exaggerate or falsely mimic cyanosis, while anemia

may mask it (See iron levels)
The white count, differential, and platelet count provide clues to disorders
associated with inflammation and coagulopathy, such as sepsis
Blood glucose should be monitored, as hypoglycemia may be an
accompanying factor or the inciting cause of cyanosis. Check Serum
calcium, also
Echocardiography is useful in the majority of common congenital
heart lesions
Arterial blood gases and pulse oximeter probes give information on
ventilation and acid base
An anteroposterior chest X-ray will identify pneumonia, pneumothorax,
intrathoracic bowel and the cardiac silhouette. Egg on side in transposition
of the great vessels, snowman heart in total anomalous pulmonary
venous return and in tetralogy of Fallot (boot-shaped heart) give clues to
cardiac pathology
ECG to check for rate, rhythm, axis and hypertrophy of chambers
TORCH titers to rule out intrauterine infections.
Bedside Tests
The hyperoxy test is a rapid bedside screen for cyanotic diseases that do
not respond to supplemental oxygen. The patient is placed in a high
concentration oxygen hood (FiO2 at or near 100% for 10 minutes) and the
PaO2 or oxygen saturation by pulse oximetry is compared to the value in
room air. A significant increase in oxygen saturation or paO2 suggests
pulmonary pathology, whereas an insignificant change in oxygenation
Ventricular Septal Defect (VSD), Patent ductus Arteriosus (PDA), Pulmonary Artery
Hypertension (PAH).
suggests the fixed right-to-left shunting of a structural cyanotic congenital

heart disease, Persistent Pulmonary Hypertension (PPHN) or very severe
pulmonary disease.
Fundoscopy: Evidence of chororetinitis on fundus examination may indicate
TORCH infection.
TREATMENT
Medical
Prevention and treatment of anemia, chest infections, infective endocarditis,
cyanotic spells in TOF and control of congestive cardiac failure.
Surgical
Diagnosis
VSD (Large) with CCF
VSD with PAH*
VSD with AR /endocarditis
VSD* (Small)
PDA* (Large)
PDA (Moderate)
PDA (Small)
Coarctation of aorta (CoA)
With LV dysfunction
Hypertension/normal LV
No hypertension
TOF* (Stable) total correction
TGA* (< 1month age)
TGA (> 1 month age)
TGA with VSD
Timing of closure
Immediate
3 to 6 months
As early as possible
2 to 4 years.
3 to 6 months
6 to 12 months
12 to 18 months
Immediate
After 6 months
1 to 2 years
1 to 2 years
Immediate
3 to 6 months
By 3 months
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29. Onuzo OC. How effectively can clinical examination pick up congenital heart disease at
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9
Respiratory System
INTRODUCTION
In children, respiratory system has some peculiarities. They are:
DEVELOPMENTAL PECULIARITIES
Five stages of development include embryonic period (4th week of

gestation), pseudoglandular period (6th week), canalicular period (16-28
weeks), saccular period and alveolar period (28 weeks onwards).
The maxillary and ethmoid sinuses form during the third and fourth
gestational month, but at birth, are still very small.
The frontal sinuses develop by one to two years of age and assume their
final position above the orbital ridge by the fifth or sixth year. However,
the frontal sinuses are not completely developed until late adolescence.
Significancewhile treating bacterial sinusitis this knowledge comes handy.

ANATOMICAL PECULIARITIES OF CHILDREN
Remember that there is children have small diameter of airways, hence more
chance of bronchospasm and pooling of secretions. Secondly, the distance
(upper respiratory tract to lower respiratory tract) is shorter allowing organizms
to rapidly move down, causing pneumonias. Also, short eustachian tubes
predispose to otitis media. Luckily, infants < 6 months are protected by maternal
antibodies and breast milk. Somehow, between 3 and 6 months and > 5 years,
there is an increase in atypical infections.
UNIQUE RESPIRATORY PHYSIOLOGY AND PATHOLOGY
In children, upper respiratory tract infection (URI) is most common infection
and several URIs progress to acute bacterial sinusitis or acute pneumonias.
Respiratory System 79
Risk factors for development of sinusitis:
Passive cigarette smoke exposure
allergic rhinitis
viral infections
cystic fibrosis
foreign body.
They are most prevalent in children which cause nasal obstructions or
impaired mucociliary motility, thereby hampering drainage of frontal, ethmoid,
and maxillary sinuses through the ostiomeatal complex, located between the
middle and inferior turbinates.
Specific pathogens:
Bacteria like Streptococcus, Haemophilus influenzae and Moraxella
catarrhalis are common in infancy
Viruses (adenovirus parainfluenza, influenza, and rhinovirus, etc.) are
frequent due to activities, also like swimming.
Complications are more common and serious. They include:
Orbital cellulitis, orbital abscess and subperiosteal abscess.
Frontal osteomyelitis (Potts puffy tumor) epidural abscess, subdural
empyema, cavernous sinus thrombosis and meningitis are also seen.
Diagnostic and therapeutic delay is common and this is because:
Sinus tenderness is unreliable
X-ray findings of sinusitis are unreliable as neither opacification,
(mucosal thickening of 4 mm) nor an air-fluid level can differentiate
between viral/bacterial or acute/chronic disease.
Surgery is also difficult (less working space).
Peculiarities of Infection in Children
Most often tonsillar soreness, pharyngeal infection and bronchopneumonias

are seen in children However, lobar pneumonias are less frequent.
Croup syndromes are unique to children. They include epiglottitis, laryngitis,
LTB* and tracheitis, characterized by hoarseness, barkingcough,
inspiratory stridor and respiratory distress.
Organisms are also unique for each presentation. Examples are:
BronchiolitisRespiratory syncycitial virus
URIGroup A, -hemolytic Streptococcus
Hospital acquired LRIStaphylococcus and Pseudomonas
Community acquired LRI:
i. Chlamydia T and Mycoplasma (1-3 months >5 years)
ii. Haemophilus influenzae and pneumococci (6 months to 2 years).
As the presentations are unique, the management has to be individualized
for each case.
*
LTB - Laryngotracheobronchitis

Peculiarities of Respiratory Rate, Depth and Patterns
Normal Respiration
Rate: <60 in neonates <50 in infancy and < 40 in bigger children.
Depth: Depth of each respiration, varies with age.
Pattern: Abdominothoracic in young children. Sometimes deep breaths/sighs
may punctuate the normal breathing pattern.
Tachypnea (Fast Regular Breathing)
Tachypnea occuring in response to fear, fever, or exercise is more common
in children (Also it may be seen with respiratory insufficiency, pneumonias,
alkalosis, pleurisy, and lesions in the pons).
Bradypnea (Slow Regular Breathing)
Often, it is seen in drug-induced depression of the respiratory center, e.g.
diazepam, increased intracranial pressure and diabetic coma.
Hyperventilation (Fast Regular Deep Breathing)
Mechanism: Hyperventilation blows off carbon dioxide, causing a
decreased level in the blood leading to respiratory alkalosis.
It normally occurs with extreme exertion, fear, or anxiety.
Often it is seen in hysterical teenagers, diabetic ketoacidosis (called
Kussmauls respirations), hepatic coma, salicylate overdose, lesions of
the midbrain and alteration in blood gases.
Hypoventilation
This is seen in overdose of narcotics or anesthetics. Also may be seen with
prolonged bed rest or conscious splinting of the chest, if pain is present with
respiration.
Cheyne-Stokes respiration (regular waxing and waning) It is seen in CCF,
renal failure, meningitis, drug overdose and raised intracranial pressure:
Rate is difficult to determine due to variation of respiratory pattern. There
is cyclical pattern with respirations gradually waxing and waning in a
regular manner. There are alternating periods of breathing and apnea.
Depth: The periods of breathing show increased depth as respirations
continue, gradually decreasing again in depth before the apneic phase
(crescendo-decresendo). It can be seen normally in infants during their
sleep.
Biots respiration: (irregular waxing and waning):
Rate varies with the respiratory pattern. It is similar to Cheyne-Stokes
respiration, except that the pattern is irregular but the depth is similar.
This is seen in head trauma, brain abscess, heat stroke, spinal meningitis
and encephalitis.
Chronic obstructive respiration (irregular and increasingly shallow, rapid
breathing).
Depth is usually normal but it becomes very shallow during the periods
of air trapping. As the person attempts to get rid of air trapped in the
lungs, an increasingly shallow and rapid respiration ensues.
OVERVIEW OF HISTORY AND EXAMINATION
History
Complaints like dyspnea, wheezing and cough are usual presenting features
which may be constant or paroxysmal, progressive or static on time scale
with or without symptom free periods, which even affect day-to-day life:
Enquire into these, along with aggravating or relieving factors, e.g. dyspnea
on exertion. Find out on how much exertion.
Example: Whether dyspnea is even at rest and whether precipitated by cold
air, pollution, etc. or by lying flat and whether relieved by seeking fresh air, or
by sitting up.
Dyspnea: Dyspnea may be caused by disease of other systems, e.g.
Neuromuscular disease, severe anemia or even hysteria can cause dyspnea.
Congestive heart failure may cause typical dyspnea at night. Although
paroxysmal nocturnal coughing can be from heart failure but a nocturnal
cough could also be due to postnasal drip or gastroesophageal reflux or asthma.
Hence, it is very important to differentiate them.
Cough: Regarding cough, if productive (i.e. above 6 years) ask color of the
sputum. Green or yellow colour may suggest infection and blood-tinged sputum
may point to hemoptysis.
Wheeze: Remember only moderate asthma wheezes, others do not. Also, all
those who wheeze are not asthmatic. Response to beta-agonist inhaler is a
good clinical guide.
Stridor: Inspiratory stridor suggests laryngeal obstruction while expiratory
stridor suggests tracheobronchial obstruction. Biphasic stridor suggests
subglottic or glottic anomaly.
Review of Previous Diagnosis, Drug Treatment
and Family History
This helps to avoid unnecessary investigations because past history gives the
clue to the etiology, e.g. history of childhood asthma. Genetic component in
asthma and cystic fibrosis and infectious etiology in tuberculosis makes family
history vital-treatment with ACE inhibitors may cause cough. History of
anorexia, significant weight loss, passive smoking and allergies in family should
be enquired.
Pedia Pearls:
Acute Respiratory Infection program (ARI) is based on respiratory rate. A respiratory
rate of > 60/min below 2 months, > 50 min between 2 months to 1 year and >40/min
after 1 year indicates pneumonia.
Chest indrawing groaning, grunting and cyanosis are signs of severe pneumonia.

EXAMINATION
Inspection
Body Habitus, Nutritional State and Look give a Clue
Cushingoid appearance (suggests corticosteroid induced)

Anxious look (suggest hypoxia, salbutamol side effect)
Bloated (suggest edema)
Centrally, cyanosed (suggest 5 gm of deoxygenated hemoglobin per 100
ml of blood),
Pursed lips (suggest COPD as pursing raises the pressure in the airways
reducing their premature closure)
Halitosis (suggest sinusitis or mouth breathing due to adenoids).
Weight loss, and clubbing (suggest chronic hypoxemia)
Tremor (beta-agonist induced)
Fast respiratory rate and dyspnea (suggest acute hypoxemia) and scars
(suggest recent chest tube insertion, etc.).
Look at the Chest

Assess general shape of the thorax, its expansion and the pattern of respiration.
Hunch child forward slightly and cross the arms over the chest to examine
back of the chest for spinal deformities (scoliosis, kyphosis Lordosis). Privacy
is important (especially in adolescents).
Shape: In a normal infant, the thorax is barrel shaped chest with horizontal
ribs and slight kyphosis and prominent sternal angle. Pathological shapes
include pectus excavatum and pigeon chest (Fig. 9.1) when increase in AP
diameter may suggest Chronic obstructive airway disease (COPD) etc. a
parasternal heave may point to right ventricular hypertrophy.
Expansion: Asymmetrical or less expansion may be due to pneumothorax,
collapse, consolidation or effusion.
Type of breathing: Diaphragmatic/thoracic and striking abnormal patterns
of respiration like Cheyne-Stokes respiration, Biots breathing, sighing and
Kussmauls respiration, etc. should be noted.
Recessions: Subcostal recessions are seen in mild respiratory distress while
suprasternal recessions indicate severe respiratory distress.
Fig. 9.1: Pectus carinatum or pigeon chest

Palpation
Use the index finger to feel the trachea in the suprasternal notch. Use the palm
to feel the apex beat of the heart. They will be displaced if the mediastinum is
displaced or distorted. Atelectasis pulls the trachea while thyroid enlargement,
lymph nodes, pleural effusion, emphysema, and tension pneumothorax push
the mediastinum.
An important landmark is the angle of Louis, as the second interspace lies
immediately below it. Also assess thoracic expansion and spine by palpation.
Assessment of Tactile Fremitus
Fremitus is palpable vibration of the thoracic wall. produced by asking the
child to repeat one, two, three or ninety-nine while palpating the
corresponding areas on the each side of thorax, using the palmer bases of the
fingers, or the hypothenar eminence with the palms facing upwards. Fremitus
is increased in conditions that decrease the distance, for example, in
consolidation and decreased or absent over areas of effusion, collapse or
pleural thickening (where distance is increased).
Percussion
Percussion tones vary with air, liquid, or solid media.
Always percuss from the upper to lower chest, avoiding scapular and
bony areas.
The clavicle is percussed directly, then chest and area of cardiac dullness
(obliterated by excess air, e.g. a pneumothorax).
Dullness elsewhere may suggest collapse or consolidation but in effusion
dullness rises up into the axilla laterally (stony dullness).
Diaphragmatic Excursion
This is assessed if the breathing is shallow or painful. Ask the child to inhale
deeply and hold the breath.
Percuss down the scapular line on one side, starting at the end of the
scapula, until the lower edge of the lung is identified. Sound will change from
resonance to dullness. This point is the edge of the diaphragm at full inhalation.
Now instruct to take a deep breath, exhale completely, and hold the breath at
the end. Proceed to percuss upward from the marked point at the scapular
line. Mark the point where dullness of the diaphragm changes to the resonance
of the lung. This point is the level of the diaphragm at full expiration. Repeat
the procedure on the opposite side.
Pedia Pearl: Pectus carinatum or pigeon chest is seen in Rickets, Emphysema,
Mucopolysacchridosis IV and Marfans.

The diaphragmatic excursion is the distance between the upper and lower
marks (in centimeters) for each side of thorax. The diaphragm is usually
slightly higher on the right side, because of the liver.
Auscultation
a. Listen to the heart: Exclude a cardiac disease as the cause of the respiratory
symptoms. Vice-a-versa, lung disease may cause pulmonary hypertension
and a loud second heart sound (pulmonary component).
b. Listen to the respirations (at least one complete): Ask the child to breathe
through mouth. Side by side compare the findings heard at every point,
with the corresponding points on the opposite side of thorax. For vocal
fremitus, at various levels, ask the child to whisper ninety-nine each
time and note how well the sound is transmitted. Avoid, the stethoscopes
movement over the chest, because its movement over the hairs produces
sounds.
Next step is to evaluate breath sounds.
Normal Breath Sounds (Inspiratory Phase > Expiratory Phase)
They are called vesicular breath sound and heard over normal lung
parenchyma. The inspiratory phase is heard better than the expiratory phase
and ratio is 3:1. In children vesicular breath sounds are harsher compared to
adults.
Bronchial Breathing (Inspiratory Phase = Expiratory Phase)
with Gap in Between
Bronchial breathing is harsh in nature and unlike normal vesicular breath
sounds, there is a gap between the inspiratory and expiratory phase and
inspiratory and expiratory phases are of equal duration. Bronchial breath sounds
are normally heard over apex of the right lung and near the sternal borders
anteriorly and interscapular region posteriorly.
The sounds of bronchial breathing are generated by turbulent airflow in
large airways. The sounds of underlying bronchus are normally not heard
because they are attenuated by air filled alveoli and lung parenchyma.
Consolidation or fibrosis permits the sound of airflow in the bronchi to be
conducted more effectively to the chest.
Similarily, in Whispering pectoriloquy whispers can be heard with a
stethoscope over an area of lung consolidation Whispering pectoriloquy is
elicited as for vocal fremitus but here the patient is asked to whisper.
Bronchovesicular Breath Sounds (Expiration is Prolonged)
These are heard commonly in bronchopneumonias in children. They are similar
to vesicular breath sounds in that there is no gap between inspiration and
expiration, but the expiration is prolonged.
Absent Breath Sounds
It occurs in severe bronchitis, foreign body, bronchial obstruction, or in case
of very shallow breathing.
Adventitious Sounds
They are abnormal sounds superimposed on breath sounds.
Rhonchi: These are musical sounds produced by the movement of air
through narrowed passages in the tracheobronchial tree, heard on inspiration
and/or expiration due to turbulent airflow, but predominantly heard in
expiration because bronchi are shortened and narrowed during this
respiratory phase. Purely inspiratory rhonchi suggest that obstruction is
outside the thoracic cavity like a foreign body or disease of the larynx or
vocal cords. In severe asthma, there is too much of obstruction to allow
any air passage. Hence, there may be no wheeze.
Crackles: These are bubbling sounds produced by air passing through
fluid filled bronchioles, and/or alveoli, thus opening them. They suggest
consolidation if they do not clear on coughing while in case of mucus
plugs crackles may disappear on coughing. Fine crackles are found in
inspiration while coarse crackles are heard in both inspiration and expiration.
Basal rales are a classical feature of pulmonary congestion with left
ventricular failure (rales = crackles = crepts).
A pleural friction rub: This is a loud, dry, creaking or grating sound indicative
of pleural irritation produced by the rubbing together of inflamed and
roughened pleural surfaces during respiration (e.g. in pleurisy) best heard
during the later part of inspiration and the beginning of expiration. Because
thoracic expansion is greatest in the lower anterolateral thorax, pleural
friction rubs are most often heard there.
SUPPURATIVE COMPLICATIONS OF PNEUMONIAS
Pneumonia in a child less than 6 months, who is toxic and has respiratory
distress is a matter of concern. The most common cause of empyema is
pneumonia (Parapneumonic effusion due to gram +ve, ve or anaerobes).
In necrotizing pneumonia there is lack of perfusion (on Contrast High
Resolution CT) Hence, antibiotics do not reach the site. Surgery
thoracotomy, lobe/segment resection is the option.
Bronchiectasis is irreversible dilated and damaged bronchi associated with
chronic suppuration.
Lung abscess is a cavitary lesion having firm fibrous capsule which results
from a serious suppurative infection of the pulmonary parenchyma. On
X-ray air crescent sign is seen as a characteristic finding.

BEDSIDE TESTS
SPO2 (Saturation of Oxygen) and Blood Pressure (BP)
Monitoring
Pulsus paradoxus*. SPO2 measurement could tell the degree of hypoxia.
Hyperoxy Test
Giving 100 percent oxygen improves a respiratory case much significantly as
opposed to cyanotic heart diseases.
Cold Agglutinin Test
A bedside cold agglutinins test may help confirm the clinical suspicion of
mycoplasmal infection. This test is performed by placing a small amount of
blood in a specimen tube containing an anticoagulant and inserting this into a
cup filled with ice water. After a few minutes in the cold water the tube is held
up to the light, tilted slightly, and slowly rotated. Small clumps of red blood cells
coating the tube are indicative of a positive test result (Positive only in about one
half of the cases of mycoplasmal infection) which produced cold agglutinins.
BIBLIOGRAPHY
1. Cardoso WV, Lu J. Regulation of early lung morphogenesis: Questions, facts and
controversies. Development 2006;133(9):1611-24.
2. Chamberlain's. Symptoms and Signs in Clinical Medicine. An Introduction to Medical
Diagnosis by E. Noble Chamberlain, Colin Ogilvie, Christopher C. Evans. Hodder
Arnold, 1997.
3. Cherry JD, Newman A. Chapter 17-Sinusitis. In: Feign RD, Cherry JD (Eds). Textbook
of Pediatric Infectious Diseases, Philadelphia: WB Saunders Co 1998;4:183-90.
4. Chinoy MR. Lung growth and development. Front Biosci 2003;8:392-415.
5. Hall MJ, Xie A, Rutherford R, et al. Cycle length of periodic breathing in patients with
and without heart failure. Am J Respir Crit Care Med 1996;154:376-81.
6. Introduction to the Symptoms and Signs of Clinical Medicine. A Hands-on Guide to
Developing Core Skills. Gray D Toghill P. Hodder Arnold, 2000.
7. Kenna M. Part XVII, Section II-Upper Respiratory Tract. In: Behrman RE, Kliegman
RM, Jenson HB\ (Eds). Nelson Textbook of Pediatrics. Philadelphia: WB Saunders
Co 2000;16:11258-64.
8. Khoo MC, Gottschalk A, Pack AI. Sleep-induced periodic breathing and apnea: a
theoretical study. Journal of applied physiology 1991;70(5):2014-24.
9. Kumar P, Clark M. Clinical Medicine. Sixth edition. Elsevier Saunders 2005;733.
10. Nash D, Wald E. Sinusitis. Pediatr Rev 2001;22(4):111-6.
11. Pre- and postnatal lung development, maturation, and plasticity. Am J Physiol Lung
Cell Mol Physiol special edition, 2002.
Pulses paradoxus is the fall in blood pressure on inspiration in excess of 10 mm of Hg.
10
An Approach to Abdomen
ADOPT AN ASK, LOOK, FEEL AND HEAR APPROACH
ASK (HISTORY TAKING)
Important Points to Note in Child with Abdominal Symptoms
Referred pain: Pain may be in abdomen, however, the disease could be

elsewhere, e.g. tonsillitis, otitis media and meningitis. Sometimes the pain
may be elsewhere, but disease in the abdomen, e.g. biliary pain radiates to
the tip of the scapula and a diaphragmatic pain due to a perforation often
radiates to the supraclavicular region.
Mimicry: Frequency and urgency though common in UTIs, even an
inflammatory process such as an inflamed appendix lying against the bladder
can cause the patient to have frequency and urgency.
Origin of pain: In a patient with abdominal symptoms, ask whether driving
over rough road caused more pain with each impact, suggesting parietal
peritoneal involvement.
Age group specific problems: In menstruating girls a good history of the
menstrual cycle is important because pelvic abnormalities, including twisted
ovarian cysts, pelvic inflammatory disease, or ectopic pregnancy may
occur in teenagers.
LOOK
Look at the Child
Appearance gives a clue to the illness:
Writhing in pain (colic) or lying still (peritonitis)
During palpation, look at the face for signs of discomfort. A child with
intestinal colic will be lying quietly and suddenly grimace.
Some patients with pancreatitis, may not want to lie flat.
Look for jaundice, (hepatic involvement), dehydration (diarrhea), weight
loss or wasting, angular stomatitis (malabsorption), thrush, perianal
excoriation (diarrhea).
Look for purpura (hypersplenism), spider naevi (liver disease), Kayser
Fleischer rings (Wilsons disease), etc.

Look at the Hands
Look for:
Clubbing: This is seen in conditions like ulcerative colitis, Crohns disease,
celiac disease, cystic fibrosis or other malabsorption syndromes.
Koilonychia: It is seen in iron deficiency anemia.
Palmar erythema and Asterixis (flapping tremor): are seen in liver failure,
renal failure and even respiratory failure.
Perfusion: Cold /clammy hands (poor perfusion).
Look at the Abdomen
Observe with knees bent: This relaxes abdominal muscles, so that the
hernias, peristalsis, pulsations, scars, striae, etc. are better seen. A mass
usually becomes prominent enough on straining or when the head is lifted
up from the bed (for anterior masses), while the Valsalvas maneuver is
done for lateral regions. In cases of intestinal obstruction, a loop of bowel
may become prominent at the time, the patient is complaining of pain.
Observe the site of any pain pointed by child. Site may be in Right/Left
Upper Quadrant, Right/Left Lower Quadrant, Upper/Lower quadrant,
Midline Epigastric, Periumbilical or Suprapubic region.
Observe the contour: Whether flat, scaphoid, or protuberant or any
asymmetry. Coughing jolts the parietal peritoneum. Hence, cough is an
excellent way to inspect the abdomen because it tests rebound tenderness
without actually placing a hand on the patient.
Observe the posture: The psoas muscle extends down from the posterior
abdominal wall. If there is an inflammatory process lying against psoas
muscle, e.g. acutely inflamed appendix, the child may lie with the hip
flexed.
Inspect prepubertal childs genitalia by external visualization and by gentle
labial traction downward and laterally to look at - skin over Labia majora
and minora and vagina and urethral meatus for discharge, bleeding, petechiae,
foreign bodies and vascularity. Note inflam-mation and signs of trauma
like tears, ecchymotic areas, bleeding and discharge. It should be done
after taking the child into confidence because even positioning may be
emotionally traumatic. Observe younger girls in the supine, frog leg position,
supine in the preadolescent population and supine lithotomy position for
cooperative adolescents. Assess pubic hair, inguinal nodes, tanner stage
and medial thigh for evidence of sexual assault, etc. Male genitalia are examined
fortesticular descent, retractile nature, signs of atrophy and Tanner staging.
Penis is examined for edema circumcision, size, lacerations, etc. Urethral
meatus is looked for scars discharge, bleeding and scrotum for rugosity,
for gestation assessment, erythema, ecchymoses and abrasions.
An Approach to Abdomen 89
FEEL (PALPATION)
Palpation in children is difficult as they are apprehensive and tense. Guarding
may be overcome by pressure and easily missed.
During abdominal examination, ideally the child should have an empty
bladder. In an acute abdomen, one needs not to perform a detailed examination,
initially.
Light palpation: Elicit
Tenderness (facial expression)
Guarding (Rigidity of the abdomen or movement of one side more than
the other can represent involuntary guarding).
Deep palpation is done for abdominal masses, etc. Reach deeper during each
relaxation phase of respiration:
Localized guarding represents peritonism.
Generalized board-like rigidity and absent bowel sounds may indicate
peritonitis.
Rebound tenderness on quickly releasing pressure after deep palpation
suggests peritoneal irritation.
Costovertebral tenderness checked in sitting position by striking with heel
of closed fist over the costovertebral angles for renal problems suggests
pyelonephritis or a distended renal capsule from acute obstruction.
In appendicitis, tenderness is felt in the right lower quadrant or even when
palpation is performed on the left is called Rovsings sign. In Murphys
sign pressing fingers over the gallbladder area, accentuates the pain.
Palpation of the Spleen
To detect splenomegaly, place the hand flat below the left costal margin in the
left anterior axillary line. Press inwards and upwards and ask the patient to
breathe in (distending the abdomen during inspiration) better still in right lateral
position. An enlarged spleen is felt against the fingertips. Even if you can just
feel the tip of the spleen, it is significant (twice the size of normal). Rarely it
may be due to spleen being pushed down as in emphysema.
Palpation of the Liver
Normally the edge of the liver presses or slides against fingers as the patient
exhales.
Ballottment for Enlarged Kidneys
For renal masses or loin tenderness use two hands. One hand is kept a round
the patients right loin, with other hand over the right upper quadrant and
pressed simultaneously during respiration.

For Masses Arising from the Pelvis
Perform a rectal examination in a boy and a rectal and pelvic examination in a
girl, if feasible. For masses arising from the pelvis such as an enlarged bladder
or an ovarian cyst, examine the abdomen as before, but starting above the
umbilicus and working down towards the pubis.
Hernial Orifices
Examination for hernial orifices is a must.
Perrectal Examination
Rectal examination is done to assess perianal skin, anal sphincter folds, anal
tone and presence or absence of stool in the rectal ampulla. Also per rectal
examination is important in sexual abuse in girls where per vaginal examination
is not possible.
FEEL AND HEAR (PERCUSSION)
Percussion is done to differentiate solid or cystic tumors, ascites (dull) or
gas (resonant) and also for liver span (hepatic dullness in the right
midclavicular line).
If fullness of flanks is seen check for:
Shifting dullness (peritoneal fluid)- dullness on percussion shifts, i.e. the
dull spot becomes resonant when the patient is rolled on the side from
supine position, due to shifting of peritoneal fluid (ascites).
Eliciting a fluid thrill is easy. It is done in case of massive amount of ascitic
fluid. With one hand on the patients flank, tap with a finger over the other
flank where impulse or fluid thrill may be felt, indicating a positive sign.
Keep the patients hand along their midline longitudinally to dampen
transmission by the abdominal wall during their test.
Puddle sign is elicited by keeping the child in knee-elbow position to check
for minimal fluid in the abdomen.
HEAR (AUSCULTATION)
Auscultation should be done first, since bowel sounds may change with
manipulation.
Listen for bowel sounds that are transmitted widely in the abdomen. Hence,
auscultation of more than one quadrant is not necessary.
Normal sound frequency is 6/minute.
Bowel sounds are absent in paralytic ileus or peritonitis.
Increased bowel sounds (borborygmus) are heard in diarrhea or intestinal
obstruction.
A quiet abdomen does not always mean that the patient has peritonitis.
Conversely, the presence of audible peristalsis does not exclude the
possibility of peritonitis (stomach peristaltic sounds are the loudest).
Sometimes heart murmur may be transmitted to the abdomen.
An Approach to Abdomen 91
POINTS TO REMEMBER
1. One of the most common cause of abdominal pain in children is worm
infestation
2. Intermittent colicky abdominal pain following diarrhea and associated with
sudden cessation of loose stools could be a sign of intussusception
3. Central abdominal pain is likely to be due to small intestinal pathology
while pain the flanks and peripheries of abdomen could be large intestinal
in origin
4. Tonsil tummy is the common referred pain in the abdomen due to
inflammation of tonsils
5. Crampy abdominal pain (tenesmus) often occurs in dysentery.
BIBLIOGRAPHY
1. A Guide to Physical Examination and History Taking, Sixth Edition by Barbara Bates,
published by Lippincott in 1995.
2. Clinical examination. Mosby, 2003.
3. Munro J. Macleods Clinical Examination Churchill Livingstone, 2000.
Pedia Pearl: Always examine the chest especially for pleural or pulmonary problems
when evaluating an abdominal complaint.
11
An Overview on
Importance of
Dermatology in Diagnosis
SKINA DIAGNOSTIC MARKER

What you see on the skin, can provide valuable clues of what is happening
inside. Especially neurocutaneous disorders, autoimmune diseases, nutritional
deficiencies, and vascular anomalies are often first picked up based on these
clues on the skin. Also, just running the fingers over the whole body may give
early clues to several illnesses. Findings like open fontanelle are a marker for
various conditions like craniotabes (seen in rickets).
The following disorders are often revealed by cutaneous examination.
Neurocutaneous Disorders (Phakomatosis)
Neurofibromatosis
Caf au lait macules (Figs 11.1A and B) are light brown, roundish macules
or patches. Caf au lait spots spare the face.
Axillary or inguinal freckling may also be seen.
Caf au lait spots are seen in tuberous sclerosis, McCune-Albright
syndrome, Ataxia telangiectasia, Gauchers disease and Fanconis anemia.
Caf au lait spots are considered significant if:
The presence of at least 6 Caf au lait macules 5 mm or more in
diameter in preadolescence or at least 15 mm after puberty suggests
Neurofibromatosis type I (autosomal dominant).
Any caf au lait spot in the center of the body.
Isolated caf au lait spot > 15 cm in size
Neurofibromas appear after 5 years of age as small, pink-violet nodules
that invaginate into the subcutaneous tissue when pressed.
Ataxia-Telangiectasia
Ataxia-telangiectasia is suspected in presence of ocular and cutaneous

patches of telangiectasia over eyelids, cubital and popliteal fossas and
neurologic symptoms (mainly ataxia abnormal eye movements and
Pedia Pearls:
Neurofibromatosis 1 is an autosomal dominant disorder (gene on chromosome 17).
Scoliosis is the most common orthopedic manifestation but is not a diagnostic criterion.
An Overview on Importance of Dermatology in Diagnosis 93
Fig. 11.1A: Caf au lait spots

Fig. 11.1B: Caf au lait spots with

axillary freckling
choreoathetosis) Progeric changes of hair and skin are a cardinal feature

of ataxia-telangiectasia.
Tuberous Sclerosis
The earliest manifestation of Tuberous sclerosis are:

Hypopigmented ash-leaf macules which may increase in number
with age.
Forehead plaques may be present even at birth.
Shagreen patches seen at lumbosacral region have an orange peel
consistency.
Periungual fibromas occur during adolescence.
Sturge-Weber Syndrome
Sturge-Weber has unilateral facial naevus while seizure occurs in the side
contralateral to the facial naevus.
Port-wine stain (PWS) is most often present at birth.
Unlike salmon patches which are a normal variant, PWS represents a
capillary malfor-mation that tends to persist unchanged during childhood
and darkens in adolescence.
It may suggest a systemic condition depending on location.
A facial PWS, can be associated with Sturge-Weber syndrome and
glaucoma.
Similarily, a dorsal midline PWS can be a marker for underlying neural
tube defect.
Malignancies Like Leukemias
Cutaneous leukemic infiltrates can be observed in children with standard

risk as well as in high risk acute lymphoblastic leukemia (ALL).
The most frequent location of skin lesions in children with ALL is
on the head.

Vascular Anomalies
Hemangioma in certain sites may be associated with an underlying abnormality
or systemic condition:
Hemangiomas in the beard distribution may be associated with lifethreatening or subglottic hemangiomas compromising the airway.
Facial hemangioma should be evaluated for PHACE (Posterior fossa
malformations, facial hemangioma, arterial anomalies, cardiac defects, and
eye abnormalities).
In case of midline lumbosacral region hemangioma, a neural tube anomaly,
such as tethered cord or spina bifida occulta should be ruled out.
Multiple hemangiomas can reflect other internal hemangiomas in various
organs. Evaluate for signs and symptoms of high-output cardiac failure
and anemia in such cases.
Nutritional Deficiencies
B12 deficiency: Hyperpigmentation of knuckles, mucocutaneous lesions

or unexplained and nonresolving skin lesions with multisystem involvement
can be a red flag sign for vitamin B12 deficiency.
Zinc deficiency: The first sign of deficiency is often a diffuse,
papulosquamous, scaly eruption with perioral, perirectal, and acral involvement, e.g. in acrodermatitis enteropathica.
Immunodeficiency Disorders
Primary Immunodeficiency
These children present with failure to thrive and chronic refractory systemic
manifestations, often with family history, recurrent furuncles, abscesses,
folliculitis and impetigo (markers of hyper IgE syndrome):
Eczematous dermatitis (marker of Wiskott-Aldrich syndrome), extensive
telangiectasia (a mucocutaneous marker of ataxia telangiectasia) and silver
hair unresponsive to therapy (a marker of Chediak-Higashi syndrome)
have bacterial infections common to them.
In Chromic granulomatous disease, the earliest lesions are usually the
staphylococcal infections of the skin and localized candidiasis.
Acquired Immunodeficiencies (AIDS in Particular)
They have high frequency of viral lesions such as molluscum contagiosum.

Also, oropharyngeal candidosis (OPC), oral hairy leukoplakia (OHL), are
good indicators of early immune dysfunction in HIV.
Acanthosis nigricans seen on the neck region is a marker that signals
elevated insulin levels and a risk of developing Type 2 Diabetes and high
blood pressure in the future.

Poisonings
Chronic iron toxicity presents as:
Sparsely distributed, coarse hair
Alopecia of the eyebrows
Dry, rough skin
Dry eyes
Cracked lips.
Skin Changes and the Corresponding Suspected Disease
Subcutaneous nodules ( circumscribed solid lesion 1 to 2cm are seen in

rheumatic fever
Secondary lesions due to scratching and trauma are seen in scabies
Keloid (hypertrophic scar) is seen after trauma or surgery
Perianal excoriation (loss of epidermis secondary to scratching) is seen in
diarrhea with acidic stools of lactose intolerance
Lipoatrophy is seen in HIV
Crusts (dried serum) are seen in chicken pox
Guttate lesions (drop-like lesions) are seen in psoriasis
Verrucous lesions (wart-like lesions) are seen in sexually transmitted diseases
Splinter hemorrhages are seen in Infective endocarditis
Prolonged capillary filling time (>3 seconds) is seen in shock.
Infectious Rashes
Eruptions on the skin either herald the onset of some disease or pinpoint a
sinister illness lurking in the body as for example HIV or are associated with
arthritis. Some key examples are highlighted:
Maculopapular Eruptions
Kawasaki disease: Periungual desquamation is typical of kawasaki disease.

Roseola infantum (6th disease): Fever occurs after rash in roseola infantum
and then rash disappears on onset of fever.
Erythema infectiosum (parvovirus B19 infection, or 5th disease) has a
slapped cheek appearance.
Scarlet fever due to Streptococcus: It can lead to rheumatic or nephritis,
both are possible.
Measles: Cough corrhyza conjunctivitis Kopliks spots and fever are first
seen followed by rash, when fever begins to subside.
Rubella rash is often associated with painful occipital lymphadenopathy.
Most of these have a prodrome. Most involve face first followed by other
parts except roseola infantum where trunk is first involved. Eruptions common

in the west have high fever, i.e. scarlet fever, kawasaki disease and roseola
infantum.
Vesicular Eruptions
Hand-Foot and Mouth disease involves palms and soles and oral cavity.
Chickenpox is highly infectious and occurs in crops centripetally and is
pruritic.
Prodrome is mild or not present in both of them.
Exanthems with Arthritis

They include:
Erythema infectiosum
Henoch-Schnlein purpura and
Kawasaki disease.
There is no specific treatment except for Kawasaki disease where IVIG is
treatment of choice.
HAIR
Coarse hair is seen in hypoythyroidism

Easy pluckable hair is seen in protein deficiency
Transverse depigmentation of hair is seen in copper deficiency
Alopecia is seen in anemia, heavy metal poisoning and hypopituitarism.
NAILS
Koilonychia (spoon nails that have lost their convexity) are a sign of
hypochromic anemia, especially iron-deficiency anemia
Pitted nails are seen in psoriasis
Beaus lines (deep grooved lines that run from side to side on the fingernail)
are seen in diabetes, psoriasis and malnutrition.
Clubbing is the bulbous digital deformity (Overcurvature of the nails with
enlargement of periungual soft tissue) caused due to hypoxia by elaboration
of VEGF or by the action of platelet clumps that get lodged in the distal
capillary beds. It is seen in acute condition like infective endocarditis apart
from causes mentioned in Chapter 8.
Pedia Pearls:
Koilonychia is extremely rare in children
Flag sign of kwashiorkor is not a cardinal sign. The alternate region of
depigmented and pigmented hair suggest alternate periods of poor and good
nutrition.

BIBLIOGRAPHY
1. Baker SJ, Ignatius M, Johnson S, Vaish SK. Hyperpigmentation of skin. A sign of
vitamin B12 deficiency. Br Med J 1963;1(5347):1713-5.
2. Barbagallo JS, Kolodzieh MS, Silverberg NB, et al. Neurocutaneous disorders.
Dermatol Clin 2002;20:547.
3. Buckley RH. The T-B and NK-cell system. In: Behrman RE, Kliegman RM,
Jenson HB. Nelson text book of pediatrics. USA: Saunders 2004;683-701.
4. Cutaneous markers of primary immunodeficiency diseases in children. Pediatr
Dermatol 2000;17(2):91-6.
5. Danl MV. Clinical immunodermatology. Philadelphia: Mosby 1996;147-66.
6. Dohil MA, Baugh WP, Eichenfield LF. Vascular and pigmented birthmarks. Pediatr
Clin North Am 2000;47:783.
7. Enjolras O, Riche MC, Merland JJ. Facial port-wine stains and Sturge-Weber
syndrome. Pediatrics 1985;76:48.
8. Flynn JA, Editors. Cutaneous Medicine. London: Hamilton 2001;263-72.
9. Frieden IJ, Eichenfield LF, Esterly NB, et al. Guidelines of care for hemangiomas of
infancy. American Academy of Dermatology Guidelines/ Outcomes Committee.
J Am Acad Dermatol 1997;37:631.
10. Goskowicz M, Eichenfield LF. Cutaneous findings of nutritional deficiencies in
children. Curr Opin Pediatr 1993;5:441.
11. Greenwald MJ, Paller AS. Ocular and dermatologic manifestations of neurocutaneous
syndromes. Dermatol Clin 1992;10:623.
12. Hong R, Clement LT, Gatti RA, Kirkpatrick CH. Disorders of the T cell system. In:
Stiehm RE, Editor. Immunologic disorders in infants and children, Philadelphia:
Saunders 1996;339-409.
13. Lim DH, Thong By, Ho Sy, Shek LP, Lou J, Leong KP, et al. Primary
immunodeficiency disease in Singapore-the last 11 years. Singapore Med J
2003;44(11):579-86.
14. Metry DW, Dowd CF, Barkovich AJ, et al. The many faces of PHACE syndrome.
J Pediatr 2001;139:117.
15. Orlow SJ, Isakoff MS, Blei F. Increased risk of symptomatic hemangiomas of the
airway in association with cutaneous hemangiomas in a "beard" distribution. J Pediatr
1997;131:643.
16. Paller AS. Cutaneous manifestations of immunological disorders in children. Adv
Dermatol 1991;6:199-216.
17. Paller AS. Immunodeficiency syndromes. In: Harper J, Oranje A, Prose N, Editors.
Textbook of pediatric dermatology. Oxford: Blackwell 2000;1678-709.
18. Paller AS. Primary immunodeficiencies. In: Bolognia J. Jorizzo J. Rapini R, Editors.
Dermatology. Spain: Mosby 2003;832-52.
19. Richard SE, Ochs HD, Winkelstein JA. Immunodeficiency disorders: General
consideration. In: Stiehm EE, Ochs HD, Winkelstein JA, Editors. Immunologic disorders
in infants and children. Philadelphia: Saunders 2004;289-356.
20. Sidbury R, Paller AS. Dermatologic clues to inherited disease. Pediatr Clin North Am
2000;47:825.
21. Sillevis Smitt JH, Wulffraat NM, Kuijpers TW. The skin in primary immunodeficiency
disorders. Eur J Dermatol 2005;15(6):425-32.
12
Vaccination
IMMUNIZATION
Active Immunization
Vaccination is the administration of all or part of microorganism to elicit an
antibody response (Live attenuated or killed virus, toxoid, conjugated
polysaccharide, recombinant subunit and bacterial antigen). Active
immunization with vaccines provokes a host response that potentially confers
durable immunity and protects against subsequent infection and disease,
following exposure to naturally occurring infection.
Passive Immunization
Here, preformed human or animal-derived protective antibodies are administered
to provide immediate but temporary protection. These hyperimmune
products given for protection from various diseases, produce effective
concentrations of neutralizing antibody. For example RSVIG*, hepatitis B
immune globulin, (HBIG), the varicella zoster immune globulin and rabies
immune globulin. Passive immunization against the virulent toxins associated
with infection are called antitoxins. A typical example of an antitoxin is the
diphtheria antitoxin.
TYPES OF VACCINE
INFECTIOUS VACCINES
They are attenuated live virus vaccines (measles, mumps, rubella, varicella)
which should not be administered to immunologically impaired host, due to
the potential risk of the expected subclinical infection, following immunization.
To produce an immune response, attenuated live virus vaccines should either
be administered simultaneously or separated by an interval of at least 1 month
(to prevent antibody cross reaction). It should be noted that attenuation retains
the antigenicity but viral pathogenicity is lost. They may be given orally as in
OPV or even intranasally as in influenza vaccine.
*
RSVIG = Respiratory Syncitial Virus Immunoglobulin

OPV = Oral Polio Vaccine
Vaccination 99
NONINFECTIOUS VACCINES
These are either killed virus, recombinant subunit, toxoid, or conjugated
polysaccharide bacterial antigens. They may be given to immunologically
impaired host However, there may be suboptimal response to these vaccines.
COMBINATION VACCINES
The new super vaccines simply combine multiple vaccines into a single
shot, thereby reducing the number of injections.
There are already a few of these combinations available:
H Influenza type B (HiB) and Hepatitis B vaccines
Diphtheria, Tetanus and acellular Pertussis (DTaP), Hepatitis B and HiB
used to require three shots
DTaP and HiB.
The side effects of combination vaccines are similar to the vaccines, given
separately.
VACCINES FOR SPECIAL SITUATIONS
Vaccines given in special situations include:
Rabies vaccination for pre-exposure (veterinarians) or postexposure
prophylaxis (after dog bite).
Pneumococcal vaccine for high-risk groups like postsplenectomy (being
a capsulated organism)
Meningococcal vaccine is for high-risk groups and during epidemics.
Japanese encephalitis vaccine is given during epidemics.
On steroid therapy (>2 weeks): Wait for 4 weeks after stopping steroids
before giving live vaccines.
Bleeding disorders: Use 23 G needle and give pressure for 5 minutes.
Primary immudeficiency: Avoid live vaccines.
Vaccines that can be given after discussion with parents
More than
6 weeks
Pneumococcal conjugate
3 primary doses at 6, 10, and 14 weeks,

followed by a booster at 1518 months
More than
6 weeks
Rotaviral vaccines
(2/3 doses (depending on brand) at 48

weeks interval
After 15
months
Varicella
Age less than 13 years: one dose

Age more than 13 years: 2 doses at 48
weeks interval
After 18
months
Hepatitis A
2 doses at 612 months interval

INDIAN ACADEMY OF PEDIATRICSSCHEDULE FOR
VACCINATION (2011)
Age
Vaccines
Birth
BCG
OPV zero
Hepatitis B-1
6 weeks
OPV-1 + IPV-1/OPV-1
Note
OPV alone if IPV cannot be given. We

should continue to use OPV till we achieve
polio eradication in India. IPV can be used
additionally for individual protection.
DTPw-1/DTPa-1
Hepatitis B-2
Hib-1
10 weeks
OPV-2 + IPV-2/OPV-2
DTPw-2/DTPa-2
Hib-2
OPV alone if IPV cannot be given
14 weeks
OPV-3 + IPV-3/OPV-3
DTPw-3/DTPa-3
Hepatitis B-3

Third dose of Hepatitis B can be given at 6
months of age
Hib-3
9 months
Measles
Under special circumstances (e.g.

epidemics), measles vaccine may be given
earlier than 9 months followed by MMR at
1215 months
15-18 months OPV-4 + IPV-B1/OPV-4

DTPw booster-1 or DTPa
booster-1
Hib booster
MMR-1
2 years
Typhoid
Revaccination every 34 years
5 years
OPV-5
DTPw booster-2 or
DTPa booster-2
MMR-2
10 years
Tdap
HPV
The second dose of MMR vaccine can be

given at any time 8 weeks after the first
dose
Only girls, three doses at 0, 12 and
6 months
Vaccination 101
BCG (BACILLUS CALMETTE-GURIN)
It is supplied as a lyophilized (freeze dried) preparation and reconstituted
with sterile normal saline. It should be used within 4 to 6 hours since it is
heat labile and contains no antibacterial substance.
It is given as an intradermal injection on convex aspect of the left shoulder
to raise a wheal of 5 mm after cleaning with saline (antiseptics may kill the
live bacteria)
BCG induces cell mediated immunity. It protects against disseminated forms
of tuberculosis Avoid BCG in symptomatic HIV infection
Sequence of events after BCG (0.05 ml for neonates-intradermal)
2 weeksNo skin reaction, 4 weeksSmall papule, 6 weeksBig
papule (4-8 mm), 8-12 weeksScar.
INH Resistant BCG is given for children on INH chemoprophylaxis.
Side Effects
Left axillary/cervical lymphadenopathy (spontaneous regression).
Abscess formation
POLIO VACCINE
Oral polio vaccine: (Sabin vaccine; OPV)
OPV vaccine is an attenuated live virus vaccine that uniquely protects against
any enteric infection following exposure to wild-type virus. This vaccine acts
by promoting gut immunity as the vaccine virus establishes an infection in the
gut. It also provides herd immunity to other children exposed to fecal shedding
of the vaccine strain.
Schedule-(2 drops/dose) is as follows:
OPV is given as birth dose called zero dose and then given along with DPT
and measles vaccine. Extra doses are given on National Immunization Days.
(As the Polio is about to be eradicated, soon the risk of paralytic poliomyelitis
due to the OPV would be more than the risk due to wild-type poliovirus).
Inactivated polio vaccine (IPV; Salk) is a trivalent killed virus vaccine
(formalin-inactivated) grown in monkey kidney cells or human diploid cells:
This vaccine protects against paralytic polio but it may not protect against
subclinical infection, due to lack of gut immunity in IPV.
Now-a-days, there is a new enhanced potency IPV (eIPV) that contains:
Poliovirus 1 = 40 D antigen units
Poliovirus 2 = 8 D antigen units
Poliovirus 3 = 32 D antigen units.
eIPV and IPV have no risk of vaccine-associated poliomyelitis. But IPV
is slower than OPV in outbreak control.
IPV is relatively heat stable.
Side effects: Fever and local reactions at the injection site (each dose is
0.5 ml IM).

HEPATITIS B VIRUS (HBV) VACCINE
A recombinant subunit vaccine of purified hepatitis B surface antigen is
synthesized by insertion of plasmid (encoding for the hepatitis B surface
antigen protein) into bakers yeast. Side effects include fever and local reactions
(each dose 0.5 ml IM).
Schedules
For older children 0, 1 and 6 months (IDEAL).
Birth 6 and 14 weeks
6,10 and 14 weeks (combination possible with DPT)
At least a 1 month interval is necessary between the first and second

vaccine doses and, a 5 months interval between the 2nd and 3rd dose.
If the mother is HBsAg +ve (and HBeAg+ve) the baby should also be given
Immune globulin within 12 hours of birth at a dose of 100 to 200 IU initially
followed by a booster of 32 to 48 IU/kg. after 2 months.
If immune globulin is not available then Hepatitis B vaccine is given at 0, 1,
2, and 9 months.
NEW HEPATITIS B VACCINE
It is the single dose controlled release vaccine

Another oral vaccine using transgenic plant like banana for incorporating
HBV genes is under development.
DPT VACCINE (DTWP AND DTAP)

Diphtheria (D;d)toxoid: This is a formalin inactivated nonpathogenic diphtheria
exotoxin, produced by Corynebacterium diphtheriae which stimulates an
immune response to neutralize the pathogenic exotoxin (cardiotoxin and
neurotoxin).
Tetanus (T) toxoid: This is a formalin inactivated toxoid against the
neuromuscular toxin tetanospasmin produced by Clostridium tetani, producing
toxin neutralizing antibodies Monovalent (TT), (DT or dT) (DTP/DTaP) are
available. Side effects are fever, local allergic reaction Guillain-Barr, syndrome
and brachial neuritis.
Pertussis: Whole-cell pertussis vaccine consists of inactivated Bordetella
pertussis bacteria. Recently vaccine has been developed, which has the purified
individual cell-free (acellular) antigen (DTaP). Allergic reactions occur
infrequently with the acellular pertussis (DTaP) vaccine.
Serious reactions of whole cell vaccine (DTwP):
1. High fever >40.5 degree centigrade
2. Prolonged crying.
3. Hypotonic-hyporesponsive episodes.
4. Seizures.
Vaccination 103
Schedule
3 doses 0.5 ml each of DTwP are given IM at 6, 10, 14 weeks

A booster 1 year after the last dose
Second booster is given at 5 years
(dT) is given above 7 years (the amount of d is 2 Lf units)
The triple vaccine (DTP) is given <7 years and has D=20-30Lf-units;
P=4 IU; and T=5-25Lf units.
DTaP is given intramuscularly as:

A primary 3 dose series at 2, 4, and 6 months of age in the west and
2-dose booster at 18 months and 4 to 6 years in India (only for booster
doses). Different types of acellular vaccines contain different pertusis
components and hence same type of vaccine should be used each time.
MEASLES AND MMR VACCINE
They are live attenuated viral vaccines, given as a s/c injection (0.5 ml/ dose)
to children at 9 and 15 months respectively. The second dose of the MMR
vaccine is given between 4 to 6 years, prior to school entry. Mumps component
of MMR contains live attenuated particles of > 5000 TCID50 per dose.
Inclusion of the vaccine in the national immunization schedule may
increases the risk of congenital rubella syndrome where the vaccine coverage
is likely to be around 50 percent, due to epidemiologic shift.
Mass scale immunization of adolescent girls with monovalent Rubella
RA 27/3 vaccine or MMR is beneficial. However, it is contraindicated in
pregnant women and within 3 months of conception.
Side effects of each component:
1. Measles: Fever and local reactions at the injection site, rashes and transient
thrombocytopenia may occur. Encephalitis has been suggested as an
extremely rare complication of measles immunization.
2. Mumps and Rubella: Orchitis and parotitis have been rarely reported from
mumps vaccine. Occasionally, transient arthralgia/arthritis and peripheral
neuritis may occur from rubella vaccine.
HIB VACCINE
Hemophilus influenzae type b (Hib) vaccine is a capsular polysaccharide (the
major virulence factor) conjugated with a carrier protein to enhance
immunogenicity. If it is given earlier than six weeks it produces suboptimal
antibody response. Conjugation primes the memory T cells and give good response
when the risk of disease is highest, i.e. below two years. Polysaccharide antigens
do not stimulate T Lymphocytes, thus the protection is shortlived.

Dosing Schedule (Each Dose 0.5 ml)
Infants receive four dose series of Hemophilus influenzae type b vaccine.

Three doses are given at interval of 1 month at 6, 10 and 14 weeks and
a booster dose is given between 15 to 18 months of age.
If the first dose of vaccine is given between 7 to 11 months of age, then
only three doses are required to complete the regimen (2 primary + 1
booster at 15 to 18 months of age).
If the first dose of vaccine is given between 12 to 14 months of age, then
only 2 doses are required to complete the regimen (no booster).
If the first dose of vaccine is not administered until the child is 15 months
of age, then only a single dose is required to complete the regimen.
Side Effects
Fever and local reactions at the injection site. Allergic reactions occur
infrequently.
OPTIONAL VACCINES
Rotavirus
Rotavirus is a common cause of seasonal diarrhea in infants and young children.
Rotaviral diarrhea is sometimes called winter diarrhea. It occurs between
three months and two years of age. It is not only transmitted by the fecal-oral
route but also by aerosol. Ingested virus particles (any of the Four G serotypes
of rotavirus Group A. 1, 2) infect the cells in the villi of the small intestine.
Copious acute watery diarrhea occurs after an incubation period requiring
rehydration, and often hospitalization. Also prior exposure to rotavirus provides
only incomplete protection from the virus and reinfection is possible.
ROTAVIRUS VACCINE
Two types of rotavirus vaccine are available:
Rotarix (G3P8) monovalent vaccine
It is a lyophilized preparation stable at room temperature. It is available
in single-dose vials
Diluent contains citrate-bicarbonate and sodium bicarbonate to neutralize
stomach acidity and protect the acid-labile rotaviruses from degradation.
Administration
This is done by oral route. One need not readminister the dose to infant that
regurgitates, spits out or vomits during administration of vaccine.
Rotarix (RV1) is administered in a 2-dose series, that can be started
when an infant is as young as six-weeks-old. The second dose can be
given as early as four weeks later and must be given before the baby is 8
months and 0 days (previous recommendation: 32 weeks). The maximum
age for dose 1 is 14 weeks and 6 days. Vaccination should not be initiated
Vaccination 105
for infants aged 15 weeks and 0 days or older because of safety reasons.
Vaccine virus is shed during the first weeks after administration of rotavirus
vaccine; handwashing after diaper changing is always recommended.
Rotateq pentavalent vaccine (RV5) is liquid virus mixed with buffer. It is
administered at 6, 10 and 14 weeks in India and at 2, 4 and 6 months in the
west.
Precautions: (1) Latex rubber is contained in the monovalent RV1 oral
applicator, so infants with a severe (anaphylactic) allergy to latex should not
receive monovalent rotarix RV1.
Efficacy
Most infants are protected by the third dose of the vaccine once they achieve
high serum IgA titers.
Advice: Proper handwashing techniques when changing diapers until 3 to 4
weeks after immunization till protective antibody levels are achieved.
Interactions
Coadministration of rotavirus vaccine with OPV may have slightly decreased
serum antibody response but this is not evident after the third dose of either
vaccine.
Rotavirus Vaccine (Rota) in Special Situations
Rota vaccine is administered to infants living in households with persons who
have or are suspected of having impaired immune status. For example:
1. Blood dyscrasias
2. High dose systemic corticosteroids
3. HIV/AIDS.
Precautions
Acute gastroenteritis (Moderate severe illness)

Pre-existing chronic GI disease (i.e. congenital malabsorption syndrome)
History of intussusception
Severe hypersensitivity to any component of vaccine
Experience of a serious allergic reaction to previous doses
Increased risk for intussusception was observed as a rare complication
following immunization with oral tetravalent rotavirus vaccine, now with
drawn from market.

Pneumococcus
Streptococcus pneumoniae causes bacteremia, cellulitis and meningitis, etc.
PNEUMOCOCCAL VACCINES
Previously a 23-valent polysaccharide pneumococcal (23PS) vaccine was used
but it did not induce immunologic memory in children younger than 2 years.
The vaccine did not significantly affect the nasopharyngeal carrier state, either.
The capsular polysaccharide is the virulence factor of S. pneumoniae and
spleen has the capacity to opsonize capsulated organisms to an extent. Hence,
children with asplenia, congenital and acquired immunodeficiency, spinal fluid
leak, sickling hemoglobinopathy, chronic pulmonary cardiac, hepatic, or renal
disease, should get this vaccine.
Now conjugate pneumococcal vaccines (7, 9, 11, 13 valent) have been developed
by conjugation, e.g. coupled to nontoxic diphtheria toxin and protein CRM1
It is given to infants (>2 months) and toddlers.
The hepta valent vaccine includes-Seven common serotypes,
responsible for most of the invasive pneumococcal diseases worldwide.
It is safe and effective in preventing invasive diseases caused by
Streptococcus pneumoniae (7 serotypes).
Simultaneous administration with other vaccines is not a problem.
Contraindications
1. Hypersensitivity to the diphtheria toxoid.
2. Thrombocytopenia or any coagulation disorder (being an intramuscular
injection).
Side effects: Fever, irritability, inflammation of injection site, drowsiness,
restlessness, anorexia, vomiting, diarrhea and rash.
Dosing
Given intramuscularly (IM) 0.5 ml on anterolateral aspect of the thigh in infants/
deltoid muscle/in toddlers and above usually in a series of three doses at two
month intervals followed by a fourth dose at 12 to 15 months of age.
Based on Age of Starting the Vaccination the Number of Doses Vary
2-6 months: 3 doses, 6 to 8 weeks apart and 1 booster dose at 12 to 15
months of age.
7-11 months: 2 doses, 6 to 8 weeks apart and 1 booster dose at 12 to 15
months of age.
12-23 months: 2 doses, 8 weeks apart.
> 24 months: 1 dose.
> 24 months and at high-risk: 2 doses. These children may also receive
23 valent type to expand the serotype coverage.
Note: Booster doses of PCV are to be given, at least 6 weeks after the final dose
of the primary series.
Vaccination 107
High-risk groups:
Splenic dysfunction (Sickle cell disease, asplenia)
Immune deficiencyCongenital or Aquired (human immunodeficiency)
Oral corticosteroids/immunosuppressive therapy/radiation in chronic
asthma and nephrotic syndrome
Cerebrospinal fluid rhinorrhea
Diabetes mellitus
Cyanotic congenital heart disease and cardiac failure.
Side Effects
Fever and local reactions at the injection site. Febrile seizures may occur.
Varicella
Chickenpox is caused by varicella zoster virus. It usually occurs among
children below 15 years and spreads mainly during spring season, through
personal contact (secondary attack rate 90%).
It manifests within 2 weeks or so with a rash which is seen in crops in
various stages of development as macules, papules, vesicles (a dew drop on
a rose petal appearance or glistening, water-drop vesicle on the palate) and
scabs simultaneously.
It may lead to viral pneumonia, bleeding, encephalitis and secondary bacterial
infection during the acute attack and herpes zoster later in the life. The disease
gives lifelong immunity.
VARICELLA VACCINE
It is an attenuated live virus vaccine (Oka strain), it is a monovalent vaccine.
Indications
Adolescent
Close contacts (within 3-5 days)
High socioeconomic status
No need to vaccinate if there is past history of chickenpox.
Varivax is administered (0.5 ml s/c) as:
A single subcutaneous injection for children from12 months through
12 years of age
A two dose regimen separated by an interval of at least 4 weeks for children
of 13 years age group and older
Varicella vaccine also protects against herpes zoster.

Side Effects
Fever and local reactions at the injection site generalized varicella-like rash or
mild breakthrough chickenpox due to wild-typevirus following exposure to
naturally occurring disease. Embryopathy may occur if given in first trimester.
A KILLED HEPATITIS A VACCINE
This is a killed virus vaccine (formalin-inactivated) of Hepatitis. A virus derived
from the virus strain propagated in the MRC-5 human diploid cells. The
adjuvant used here, is aluminium hydroxide.
Pediatric dose: 0.5 ml = 720 elisa units of virus antigens. The first dose is
given after 1 year of age and the booster dose 6 to 12 months later. The
deltoid muscle is the preferred site of administration for older children.
LIVE ATTENUATED HEPATITIS A VACCINE
This is indicated above 1 year (up to 15 years).
Dosage Schedule: 1 ml s/c, single dose
Routine childhood immunization with hepatitis A vaccine is recommended for:
Travelers to hepatitis A endemic areas
Persons who have chronic liver disease
Persons who have clotting factor disorders
HBV, HCV carriers
Drug addicts and homosexual.
Side Effect
Local reaction at the injection site drowsiness headache, fatigue, fever, anorexia,
nausea, vomiting, diarrhea and pharyngitis can occur.
Vaccine Efficacy
Universal immunization of toddlers has resulted in a significant decrease in the
rate of disease in western countries.
Contraindications
Patients with a known hypersensitivity to components of the vaccine or neomycin.
Vaccination 109
ADOLESCENT VACCINATION
Adolescents become more susceptible to certain diseases, as the immunity
wanes with age and they travel more often.
Recommended Vaccines for Adolescents
Rubella-RA 27/3 is given if MMR Measles, Mumps, Rubella has not been
given at 15 months or thereafter. Arthralgia, arthritis and idiopathic
thrombocytopenic purpura may occur.
Hepatitis-B WHO has recommended universal Hepatitis B vaccination.
For adolescents 0,1 and 6 months is a preferred schedule (no booster is
needed), if not vaccinated earlier.
Typhoid Vi polysaccharide vaccine. It is given at 10 and 16 years of age.
Dose of 0.5 ml (25 g) is given every 3 years, lifelong.
Hepatitis A. Two doses are given at 6 months interval (from 1 year
onwards). If exposed, give within 10 days to the contacts.
Chickenpox: Give to children >13 years since symtoms are more severe
in adults. Two doses are given. 4 to 8 weeks apart. After vaccination,
protection is only partial and child may develop a mild breakthrough disease.
Human Papilloma Virus Immunization HPV Vaccine A New Vaccine: Human
papilloma virus HPV has been linked to cancer of cervix and genital warts.
The quadrivalent HPV vaccine (Gardasil) is given in age group of 9 to
26 years to girls ideally, prior to the onset of sexual activity.
It protects against vulvar and vaginal cancers, as well.
Efficacy is good and seroconversion is excellent and better than the
naturally occurring infection.
It has purified recombinant virus-like particles of major capsid (L1)
protein of HPV.
Mainly four types can cause cervical cancers, genital wart and
precancerous lesions. Each 0.5 ml IM dose given in the deltoid region
contains these four types:
o 20 mcg of type 6
o 40 mcg of type 11
o 40 mcg of type 16
o 20 mcg of type 18.
Dosage Schedule
3 doses of Gardasil are given at 0, 2 and 6 months

3 doses of Cervarix are given at 0, 1 and 6 months.
Side Effects
Hematoma, allergic reactions, fever, headache and gastroenteritis. Avoid the
vaccine in pregnancy.
COLD CHAIN
PROPER STORAGE OF VACCINES
Most vaccines are inactivated at high temperatures (thermal damage) with
little physical evidence. Hence, to maintain the potency of a vaccine, refrigeration is a must right from the origin, i.e. from manufacturer to the consumer
by mechanism of cold chain.
Storage Units
Domestic refrigerators and ice-lined refrigerators with Dial

thermometers (Fig. 12.1) are meant for short-term storage.
Walk-in coolers are for vaccines storage in regional stores for long periods.
Deepfreezer with stem thermometer for vaccines that can be frozen. The
vaccines have a shelf-life of one to two years at proper temperature.
Vaccine carriers are used for carrying the vaccine to an outreach center.
These carriers maintain an ideal temperature (+2C to +8C) with the help
of fully frozen ice packs, contained in them.
Cold boxes are alternative vaccine storage equipment, in the event of short
duration of electricity cut.
To Freeze or not to Freeze

Vaccines that are not to be frozen:
1. The T series of vaccines namely inj DPT, DT, TT, Typhoid Vi and capsule.
2. B Series, i.e. Hepatitis B vaccines; H. influenzae type b; and BCG after
reconstitution.
3. Meningococcal and Pneumococcal (polyvalent) vaccine
4. Hepatitis A, IPV, Influenza virus, Japanese encephalitis and rabies vaccines.
Once frozen the aluminium salt (adjuvants) may get dry and act as irritants
(sterile abscess).
How to check whether frozen earlier or not?
Perform a shake test for tetanus vaccines. The insoluble clumps
form which do not dissolve even with vigorous shaking of the vial. Hence,
never allow direct contact of vaccine with ice. A shake test is done before the
use of either single or multidose vials of tetanus vaccines to make sure that
the solution is uniform.
Vaccines that could be frozen (15C) are:
Oral poliomyelitis
BCG (before reconstruction)
Measles/MMR
Varicella
Yellow fever.
Vaccination 111
Fig. 12.1: Ice lined refrigerator (cold chain)
Testing the potency of any vaccine (VVM):

The OPV is the most thermolabile vaccine. If the OPV is found to be potent,
the rest of vaccines are presumed to be equally potent. For this, a vaccine vial
monitor (VVM). Here the inner square is lighter than the outer square if the
vaccine is potent.
Where to Store?
The safe zone for vaccine storage for short-term (1 to 2 months) is +2C to
+8C. For long-term storage, 15C is preferred (only for live vaccines like
BCG, OPV and Measles/MMR, as live attenuated vaccines are more heatlabile).
Ideally, frozen vaccines should be stored in freezer unit, in the middle of
the compartment, away from the walls and not in the freezer door, due to
frequent temperature fluctuations. Do not refreeze vaccines once thawed.
Other vaccines should be stored in a refrigerator at +2C to +8C, with a
desired average temperature of +5C. The temperature near the floor and in
the refrigerator door is unstable, so it is unsuitable for vaccine storage. To

allow for cold air circulation the refrigeration unit should not be overcrowded
with vaccines.
Trays and containers should not be air-tight and should only store vaccine
of the same type. Never store eatables inside vaccine storage unit. Only the
diluents may be stored in the door. The cooled water bottles give a cold mass
effect in times of power failure. A thermometer that records all temperature
fluctuations should be used.
Storage precautions:
1. Monitor temperature twice daily.
2. Monitor expiry dates.
3. Similar sounding names should not be stored together, for example, DT
and Td.
4. Use only the specific diluent provided by the manufacturer for each type
of lyophilized vaccine.
5. Each vaccine should be clearly labelled.
6. Vaccines and diluents should be stored in original packs (administration
errors are less).
7. Avoid the exposure of the vaccines to light.
8. Diluent which has been frozen by mistake should not be used because of
the risk of damage to the vial that may cause contamination.
Stability of Vaccines before Reconstitution
at Room Temperature
6-8 hoursBCG
1 dayHaemophilus influenzae type B; Measles
2 daysHepatitis B
3 daysDPT (diphtheria, pertussis, tetanus)
4 daysInactivated poliomyelitis (IPV)
7 daysHepatitis A; Influenza virus; MMR (measles, mumps, rubella) and
Rabies.
IndefiniteTetanus toxoid.
Pedia Pearls:
Vaccination tips:
Use 26 gauge or 25 gauge needles.
Immediate breastfeeding after vaccination or sweet to older child can work like
magic, according to Dr Jacob John.
Vaccination 113
BIBLIOGRAPHY
1. American Academy of Pediatrics Committee on Infectious Disease Policy Statement:
Recommendations for the prevention of pneumococcal infections, including the use of
pneumococcal conjugate vaccine (Prevnar), pneumococcal polysaccharide vaccine,
and antibiotic prophylaxis. June, 2000.
2. Australian Government, Department of Health and Ageing. National vaccine storage
guidelines: Strive for 5 Australia 2005;3:3-23.
3. Beauchamp J, Mansoor O. Temperature and the storage of vaccines. New Zealand
Med J 1992;105:135.
4. Bishop RF. Development of candidate rotavirus vaccines. Vaccine 1993;11:247-9.
5. Black S, Shinefield H, Fireman B, et al. Efficacy, safety and immunogenicity of
heptavalent pneumococcal conjugate vaccine in children. Pediatrics Infect Dis J
2000;19:187-95.
6. Casto DT, Brunell PA. Safe handling of vaccines. Pediatrics 1991;87:108-12.
7. Centers for Disease Control and Prevention. Diph-theria, tetanus, and pertussis:
Recommendations for vaccine use and other preventative measures recommendations
of the Advisory Committee on Immunization Practices (ACIP). MMWR 1991;40(RR10):1-28.
8. Centers for Disease Control and Prevention. Global polio eradication initiative strategic
plan, 2004. MMWR 2004;53:107-8.
9. Centers for Disease Control and Prevention. Global progress toward certifying polio
eradication and laboratory containment of wild polioviruses-August 2002-August
2003. MMWR 2003;52:1158-60.
10. Centers for Disease Control and Prevention. Hepatitis B virus: A comprehensive
strategy for eliminating transmission in the United States through universal childhood
immunization: Recommendations of the Advisory Committee on Immunization
Practices (ACIP). MMWR 1991;40(RR-13):1-19.
11. Centers for Disease Control and Prevention. Intussus-ception among recipients of
rotavirus vaccine United States, 1998-1999. MMR 1999;48:577-81.
12. Centers for Disease Control and Prevention. Measles, mumps, and rubellavaccine
use and strategies for elimination of measles, rubella, and congenital rubella syndrome
and control of mumps: Recommendations of the Advisory Committee on Immunization
Practices (ACIP). MMWR 1998;47(RR-8):1-57.
13. Centers for Disease Control and Prevention. Preven-ting pneumococcal disease among
infants and young children: Recommendations of the Advisory Committee on
Immunization Practices (ACIP). MMWR 2000;49(RR-9):1-38.
14. Centers for Disease Control and Prevention. Prevention of hepatitis A through active
or passive immu-nization: Recommendations of the Advisory Committee on
Immunization Practices (ACIP). MMWR 1999;48(RR-12):1-37.
15. Centers for Disease Control and Prevention. Pre-vention of varicella: Recommendations
of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(RR11):1-25.
16. Centers for Disease Control and Prevention. Progress toward poliomyelitis eradication
Nigeria, January 2003 March 2004. MMWR 2004;53:343-6.
17. Centers for Disease Control and Prevention. Recommendations for use of Haemophilus
b conjugate vaccine and a combined diphtheria, tetanus, pertussis, and Haemophilus b
vaccine: Recommendations of the Advisory Committee on Immunization Practices
(ACIP). MMWR 1993;42(RR-13):1-21.

18. Centers for Disease Control and Prevention. Recommended childhood immunization
scheduleUnited States, 2002. MMWR 2002;51:31-3.
19. Committee on Infectious Diseases, American Academy of Pediatrics. Prevention
of rotavirus disease: Guidelines for use of rotavirus vaccine. Pediatrics 1998;
102:1489-91.
20. Dagan R, Muallem M, Melamed R, et al. Reduction of pneumococcal nasopharyngeal
carriage in early infancy after immunization with tetravalent pneumococcal vaccines
conjugated to either tetanus toxoid or diphtheria toxoid. Pediatr Infect Dis J
1997;16:1060-4.
21. Eskola J, Anttila M. Pneumococcal conjugate vaccines. Pediatr Infect Dis J 1999;18:54351.
22. Food and Drug Administration. Product approval information-licensing action, package
insert: RotaTeq (Rotavirus Vaccine, Live, Oral, Pentavalant), Merck. Rockville, MD:
US Department of Health and Human Services, Food and Drug Administration, Center
for Biologics Evaluation and Research; 2006.
23. Food and Drug Administration. RotaTeq clinical review. Rockville, MD: US Department
of Health and Human Services, Food and Drug Administration; 2006. Part 1 available
at http://www.fda.gov/cber/review/rotamer020306rp1.pdf. Part 2 available at http://
www.fda.gov/cber/review/rotamer020306rp2.pdf
24. Glass R, Kilgore P, Holman RC, et al. The epidemiology of rotavirus diarrhea in the
United States: Surveillance and estimates of disease burden. J Infect Dis 1996; 174
(Suppl 1): S5-11.
25. Grassby PF. Safe storage of vaccines: Problems and solutions. Pharm J 1993;251:323-7.
26. Hovi T. Inactivated poliovirus vaccine and the final stages of poliovirus eradication.
Vaccine 2001;18:2268-72.
27. John TJ. A developing country perspective on vaccine-associated paralytic
poliomyelitis. Bull World Health Organ 2004;82:53-7.
28. Lemon SM, Milstien JB. The thermostability of vaccines. Technologies for improving
the thermostability of the oral poliovirus vaccine. Internat J Tech Assess Health Care
1994;10:177-84.
29. Live attenuated human rotavirus vaccine, Rotarix. Bernstein DI - Semin Pediatr Infect
Dis 2006;17(4):188-94.
30. Offit P. Host factors associated with protection against rotavirus disease: The skies
are clearing. J Infect Dis 1996;174 (Suppl 1):S59-64.
31. Offit P. Host factors associated with protection against rotavirus disease: The skies
are clearing. J Infect Dis 1996;174(Suppl 1):S59-64. Ward R. Mechanisms of protection
against rotavirus in humans and mice. J Infect Dis 1996;174 (Suppl 1): S51-8.
32. Schmiedeskamp MR, Kockler DR. Human papillomavirus vaccines. Ann Harmacother
2006;40:1344-52.
2
An Overview of
Bedside Testing
13
Blood
Peripheral Smear
Peripheral smear is the king of blood tests.

INDICATIONS
To Establish a Diagnosis
The smear alone may establish a diagnosis as it tells the physiological

status of the bone marrow by assessing states like, anemia, leukopenia and
thrombocytopenia.
In hemolytic anemia, presence of Heinz body suggests the ultimate
diagnosis like oxidant damage to the red cell secondary to drugs.
In white cell disorders, diagnosis of disease may depend upon finding
abnormal cells.
The presence of Auer rods patients with acute myeloid leukemia.
Atypical lymphocytes in viral infections,
Hypersegmented neutrophils in megaloblastic anemia.
Lymphoblasts in acute lymphoblastic leukemia.
To Give Warning Signals

Peripheral smear may give warning signals of high prognostic value and give
early indication of patients at increased risk.
For example, presence of several nucleated RBCs (NRBCs) indicate that
the bone marrow is rapidly releasing red cells before full maturity, signaling
conditions like severe anemia and/or sepsis.
COMMON STAINS
They are Romanowsky variants based on acidic and basic dyes like methylene
blue and eosin, Wright stain and May-Grunwald-Giemsa stain.
SYSTEMATIC APPROACH
Cells are seen in high power (40x power) or oil immersion (1000x
magnification) for details.
Look at RBCs, WBCs and platelets, as discussed.
RED BLOOD CELLS (RBCS)

Number
Low counts occur in aplasia or nutritional anemia like iron deficiency while
high counts are seen in polycythemic states, most often secondary to hypoxia.
Color (Hypochromia or Normochromia)
In hypochromia, the normally pale center of the RBC is even more pale, (more
than ) suggesting reduced concentrations of hemoglobin within the cell, e.g.
iron deficiency, thalassemia and lead poisoning.
Size (Anisocytosis/Microcytosis)
In a fully developed iron deficiency, RDW is wide because we see small and
normal sized cells. If the Red Cell Distribution Width is more it means some
small and some large cells are present.
The mean corpuscular volume (MCV) tells about the mean red blood cell
size. Low MCV indicates microcytosis (small cells).
The major causes of microcytosis with normochromia are:
Iron deficiency in the initial stages due to: nutritional deprivation,
malabsorption, blood loss, and increased iron demand. Serum iron is
decreased, transferrin saturation and ferritin are decreased but total
iron binding capacity is increased
Anemia of chronic disease like malignancies or inflammatory conditions
may produce normocytic normochromic anemia or micro-cytic anemia
but iron stores and serum ferritin are usually normal.
Causes of microcytosis with hypochromia:
Iron deficiency
Thalassemia: There is the failure in globin chain synthesis (ineffective
erythropoiesis) with compensatory, extramedullary hematopoiesis in
liver, spleen and flat bones. Hepatosplenomegaly hemolytic facies
and crewcut picture on radiology of skull are due to extramedullary
hematopoiesis.
Sideroblastic anemias: They are characterized by ringed sideroblasts.
It occurs due to defective ineffective erythropoiesis.
Lead poisoning: This is a type of sideroblastic anemia. but globin
synthesis is also inhibited. The anemia is usually microcytic, with
basophilic stippling and ringed sideroblasts.
FEP is the amount of free protoporphyrin not incorporated into heme.
It helps to differentiate between iron deficiency and lead poisoning as it
is high in iron deficiency.
BloodPeripheral Smear 119

Shape
Poikilocytosis: Bone marrow rapidly releases these abnormal shaped red

cells due to the fast pace of RBC production.
Schistocytes: They are bizarre-shaped RBCs, resembling triangles or spirals
which are seen withburns, DIC, artificial heart valves and vascular spasm.
Sickle cells: These crescent-shaped RBCs, are associated with abnormal
hemoglobin formation (Hemoglobin S, SS, SC, SD or Sickle-thalassemia).
They present with hemolytic anemia.
Spherocytes (actually microspherocytes): Micro is smaller and sphero
means rounder than normal RBCs, e.g. hereditary spherocytosis.
Target cells: Smaller than normal RBCs, with a central concentration of
hemoglobin give them the appearance of a target. They are seen in iron
deficiency anemia, liver and splenic (reticuloendothelial) disorders, e.g.
thalassemia.
Macrocytes: They are seen in liver disease, B12 deficiency, etc.
Spherocytes: They are seen in: 1. Hereditary spherocytosis, 2. Hemolytic
transfusion reactions.
Elliptocytes (Oval cells) are seen in elliptocytosis.
Schistocytes (Fragmented red blood cells) are seen in DIC, TTP and HUS.
Dacryocytes (teardrop RBC) are seen in extramedullary hemopoiesis.
Acanthocytes (Spur cells) are seen in abetalipoproteinemia and liver/kidney
damage.
Contents
Parasites, e.g. malarial parasite

Howell-Jolly bodies after splenectomy
Heinz body (Aggregates of denatured Hemoglobin)due to oxidative stress
Basophilic stippling (aggregated ribosomes)seen in lead poisoning.
RETICULOCYTES
They are immature form of RBCs that have no nucleus, released in response to
strong stimulus, and seen in brilliant cresyl blue stain. Usually basophilic stippling
is seen in reticulocytes, in cases of clinically significant lead poisoning.
Otherwise, polychromasia is seen on usual staining. Reticulocytosis is most
commonly seen in: Thalassemia and in iron deficiency on treatment.
Increased reticulocyte count suggests that bone marrow is active, e.g. due
to fall in the RBC count which stimulates production of erythropoietin. It also
increases when the body is provided the substrate to manufacture RBCs like
Iron, B12 and Folic acid therapy.

WHITE BLOOD CELLS (WBCS)
Number
Leukopenia, e.g. in enteric fever and neonatal sepsis

Leukocytosis, e.g. in leukemias
Leukemoid reaction in infections or inflammation
Eosinophilia is seen in allergy, asthma and parasitic illnesses.
Contents
Auer rods in a blast form are seen in patients with acute myeloid leukemia
while we see atypical cells in viral infections, hypersegmented neutrophils in
megaloblastic anemia, lymphoblasts in acute lymphoblastic leukemia, giant
cytoplasmic granules in Chediak-Higashi syndrome and toxic granulations
in bacterial infections.
PLATELETS
Evidence of thrombocytopenia and giant platelets seen on peripheral smear,
may give clue to diagnose conditions like Idiopathic thrombocytopenic purpura
(ITP) and dengue hemorrhagic fever.
POINTS TO REMEMBER
1.
2.
3.
4.
5.
Spherocytes are hyperchromic

Basophilic stippling is due to altered ribosomes
Howell-Jolly bodies are nuclear fragments
In hemolytic anemia polychromasia suggest increased retic count
In liver disease the macrocytes are present but the hypersegmented
neutrophils may be lacking.
BIBLIOGRAPHY
1. Lee. Wintrobes Hematology, Lippincott 1999;23-25.
2. Ravel. Clinical Laboratory Medicine 1995;14-16.
14
Staining Microbiological
Specimens (Part-I)
GRAM STAINING
The Gram stain, named after Hans Christian Gram is used to identify grampositive and gram-negative organisms. Gram reactions help to guide therapy
as well.
Gram staining is the first step to determine the identity of bacteria and
differentiating them on the basis of their staining characteristics.
Gram-positive microbes have a cell wall which stains purple, while gramnegative bacteria have lipopolysaccharide endotoxin in their outer membrane
which stains pink. In gram-variable patterna mix of pink and purple cells
are seen. The genera Actinomyces, Corynebacterium, Mycobacterium and
Propionibacterium have cell walls particularly sensitive to breakage during
cell division, resulting in gram-negative staining of these gram-positive cells,
hence called gram variable.
Fixing
Collect the specimen and fix it. Put and air-dry the specimen on a clean glass
slide or pass the slide through a flame rapidly several times. Even 95 percent
methanol application to the slide for one minute chemically fixes the specimen.
Staining (Mnemonic-CGAS)
Flood the slide with crystal violet for one minute. Once this is taken up by
the bacterial cell wall rinse with water
Flood the slide with grams iodine solution for one minute to bind the dye
to the cell wall
Decolorize with 95 percent ethyl alcohol for up to 30 seconds or if quick
result is needed use acetone ethyl alcohol mixture for 10 seconds
Now counterstain the slide with safranin solution for one minute and rinse
off the excess safranin
Air-dry or carefully blot with filter paper
Finally do microscopic examination first in low-power and then with an

oil immersion lens for better identification of leukocytes, erythrocytes
and bacteria
Gram-positive cell wall (a thick peptidoglycan layer) resists
decolorization, thus appearing purple in color
The Gram-positive organisms retain the crystal violet dye
Gram-negative organisms also take up the dye but are then susceptible
to decolorization and on microscopic examination appear pink
Yeast cells are gram-positive and mycelia of fungus are gram variable.
POTASSIUM HYDROXIDE PREPARATION

The Potassium Hydroxide (KOH) Preparation
This is used for fungi who have polysaccharide containing cell wall
The KOH solution is an alkali that digests proteinaceous material, such as
host cellular material, while leaving the fungal cell wall intact. Thus, using
the KOH preparation can help, confirm the diagnosis.
Procedure
Take the specimen from the active edge of the lesion with scalpel over
skin, and cotton for vaginal swab and place on a glass slide (remember
cotton strands may resemble fungal hyphae)
Apply one to two drops of KOH solution (10%) and top up with the
cover slip
Wait for five (up to ten minutes) before proceeding with the
microscopic examination, as alkali digestion of proteinaceous debris
takes sometime.
Microscopic Examination
First try to look for the presence of fungal Pseudohyphae (budding

structures that remains fixed to the mother cells)
Fungi produce spores asexually, which may be identified by microscopic
examination as well, e.g. arthroconidia have square, rectangular or barrelshaped thick-walled cells.
BIBLIOGRAPHY
1. Larone DH. Medically Important Fungi: A Guide to Identification. 2nd edn. New
York: Elsevier 1987; 173-7.
2. Walsh RD, Cunha BA. Diagnostic significance of the sputum Gram stain in pneumonia.
Hosp Physician. October 1992; 37-44.
15
Staining Microbiological
Specimens (Part-II)
The Ziehl-Neelsen stain is also known as acid fast stain in used for bacteria
like mycobacteria. Kochs original method of staining tubercule bacilli was to
use an alkaline mixture of aniline dyes.
ZN STAINING (Mnemonic-CSAM)
Heat the smear to fix it.
Primary staining (5 minutes): Flood with enough Carbol Fuchsin to stain
the entire slide. Using bunsen burner, steam the slide slowly for
5 minutes by intermittently passing the flame under the slide as too much heat
can char the smear.
Mycobacterial cell wall has waxy mycolic acids. Heating allows dye entry
through this mycolic barrier. Rinse the slide with filtered water.
Decolorizing (5 minutes): Flood the slide with 20 percent Sulphuric Acid and
add Alcohol separately (2-3 minutes each) and allow to decolorize until the
slides are clear of stain. Rinse thoroughly with filtered water as tap water may
have AFB. The acidfast bacteria retains the red color as they are resistant to
elusion (washing out with solvent) due to mycolic acid wall, and therefore,
look pink or red. Non-acid fast bacteria will not be red in color as they get
decolorized. Counterstain creates a background.
Counterstaining (1 minute): Flood the slide with the counterstain and rinse the
slide thoroughly with water. If methylene blue is used, then the non-acid
fast organisms appear blue, and if malachite green is used, then the background
appears green.
Note
Five percent sulphuric acid is used for staining Mycobacterium leprae instead
of the 20 percent sulphuric acid used for Mycobacterium tuberculosis.
16
Culturing Microbiological
Specimen
CULTURE MEDIA
A culture is cultivation of microorganisms in the laboratory (in vitro). A pure
culture contains only a single species of microbe. Nutrient preparations on
which microorganisms feed, in a suitable atmosphere are called culture media.
Bacteria are classified as follows:
Non-fastidious like E.coli, etc. which multiply in any media or fastidious
like the Neisseriaceae which need special atmosphere for their growth
Obligate aerobes need O2
Microaerophilic need O2 at 5%
Faculative anaerobes live with or without O2
Strict anaerobes need complete absence of O2
Capnophilic need CO2.
Remember
Most human pathogens are faculative anaerobes.

Viruses need living cells for their growth.
CLASSICAL MEDIA
Types
Solid (agar) Media
They use solidifying agent (agar 2-3%) in Petri dish/tubes, etc. to grow bacterial
colonies (smallest bacterial unit visible), e.g. blood agar, chocolate agar.
Semisolid Media
They contain small amounts of agar to transport or to check motility of
organisms in Petri dish or tubes.
Liquid (broth) Media
This is used for biochemical tests, especially blood culture where turbidity
indicates growth, e.g. nutrient broth and Selenite F broth.
Culturing Microbiological Specimen 125

Enriched Culture Media
They are enriched with special nutrients, e.g. whole blood in blood agar, lysed
blood (heated to 80C) in Chocolate agar and serum in Loefflers medium.
Selective Culture Media
They contains substances that inhibit the growth of all microbes other than
the suspected bacteria:
Bile salts containing media inhibit the normal fecal flora and is selective
for Salmonella and Shigella.
TCBS media is selective for V. cholerae.
Lowenstien-Jenson (LJ) medium is selective for tuberculosis and has
malachite green as an inhibitor.
Differential Media
They have an indicator to differentiate the organisms:
MacConkey media contains neutral red to differentiate between lactose
fermenter and nonlactose fermenter.
Lactose fermentors (E. coli) produce acid, thereby low pH causing red color.
CULTURES
BLOOD CULTURE
Blood taking requires meticulous cleansing and disinfection of the skin before
blood culture. Blood quantity should be proper, e.g. 5 ml for infants,
and 1 ml for neonates (roughly-1 ml for each 10 ml of broth).
Number and timing of taking blood sample is important:
Bacteremia may be transient, continuous or intermittent as in sepsis,
meningitis, osteomyelitis and pyelonephritis.
Three samples are taken from different veins, 30 minutes apart in acute
endocarditis, preferably before starting the antimicrobial therapy.
Every sample is taken in one aerobic and one anaerobic vial, ideally.
URINE CULTURE
Urine culture is indicated in:
Cystitis (frequency, urgency and suprapubic pain).
Pyelonephritis (fever and flank pain; leukocytosis, pyuria, hematuria with
or without features of cystitis).
Steps
Ideally, take first morning void, clean-catch midstream urine (high

concentration of bacteria) or a suprapubic aspirated urine and transport
within 1 hour of collection.
Insert (1 l) sterile top of the loop into the sample.

This 1 l loopful sample is inoculated as streak and cross streaks on solid
media and then incubated for 24 hours at 35 to 37C in ambient air or CO2
incubator.
Growth of each colony is counted and multiplied by 1000 as the size of
inoculum is in microliter, but the report is per milliliter.
Do not culture urine from collection bag in catheterized patients. Use

sample for smears to report Gram morphology only after streaking, to
prevent contamination.
A pathogen is likely if:
>105 Colony Forming Units (CFUs) are seen per milliliter of urine
There is doubtful pathogenicity if:
103 to 105 Colony Forming Units CFU/ml are seen.
Normal Urogenital Flora
Report of coagulase-negative staphylococci is significant only if S.

saprophyticus is reported.
Lactobacillus species, viridans streptococci, nonhemolytic streptococci and
most diphtheroids are part of normal urogenital flora.
Sterile Pyuria
A sterile routine culture but with pus cells.
Prior antibiotic treatment, glomerulonephritis and mycobacterial infection
cause sterile pyuria.
STOOL CULTURE
Selective media like MacConkey agar and xylose lysine deoxycholate or
enrichment media are needed in stool culture to isolate potential pathogens
from normal flora. Stool is collected in a clean, non-sterile container and the
specimen processed within two hours. The specimen is inoculated into an
enrichment broth (e.g. selenite F broth for Salmonella species) and incubated
at 35C. Twelve hours later, the broth is subcultured onto selective media for
isolation e.g xylose lysine deoxycholate agar, which inhibits the commensals.
BIBLIOGRAPHY
1. Forbes BA, DF Sahm AS. Weissfeld, Eds. Infections of the Urinary Tract in Bailey
and Scotts Diagnostic Microbiology 2002;11:927-38.
2. Isada CM, et al Eds. Disease Syndromes and Organisms in Lexi-Comps. Infectious
Disease Handbook 2003;5:329-31.
17
Cerebrospinal
Fluid Examination
LUMBAR PUNCTURE (LP)

TECHNIQUE
The child is placed in lateral decubitus fetal position and the 25G bevelled
spinal needle with stylet, is inserted towards the umbilicus after povidoneiodine skin preparation (and optional 1% lignocaine to minimize pain) at
the level of the lumbar L3/L4 or L4/L5 till there is a give.
Next, stylet is removed and CSF is collected into 3 sterile tubes (approx. 8
drops each).
Brief pressure is applied to the puncture site and then occlusive dressing
is done.
Note: An imaginary line between the top of the iliac crests and spine is drawn
to mark the L3-4 interspace, because conus medullaris finishes near L3 at
birth, but at L1-2 in adults. The use of needles without a stylet has an associated
risk of spinal epidermoid tumors.
Caution
Withhold procedure in an unstable child who may have signs of raised
intracranial pressure, cardiovascular/respiratory compromise, recent seizures
(within 30 minutes), shock and local infection at LP site. Bleeding diathesis
may also preclude LP (lumbar puncture).
INDICATIONS
It is done for:
Diagnostic (analysis of CSF)
Therapeutic and
Anesthetic purposes
Pedia Pearl: Group B Streptococcus and E. coli are most common causes of neonatal
meningitis. Citrobacter is the most common cause of neonatal brain abscess.

DIAGNOSTIC INDICATIONS
To Identify the CNS Infections
CSF smears/cultures help to diagnose infections (bacterial, spirochetal,
mycobacterial, fungal, viral and protozoal) causing meningitis/encephalitis
and PUO.
Staining Characteristics
Gram stain is often positive if there is bacterial meningitis.

Budding yeasts are seen in Candida meningitis cases.
Acid fast staining is done if tuberculosis is suspected. A Cryptococcus is
seen on an India ink preparation.
Toxoplasmosis can be diagnosed with Wright or Giemsa stain.
To Differentiate the Infections
Cultures of cerebrospinal fluid are still the gold standard for confirming
the diagnosis of bacterial meningitis.
PCR can be done with small volumes of CSF and is especially useful in
the diagnosis of viral meningitis.
All encephalopathies have raised proteins and all itis involving CNS
have pleocytosis (a useful test to differentiate encephalitis from
encephalopathy).
As a general rule, CSF glucose is about two thirds of the serum glucose.
CSF-to-serum glucose ratio is:
Decreased much more in Bacterial compared to Fungal Tubercular
meningitis
Almost normal in viral meningitis.
Polymorphs (PMNs) predominate in Bacterial compared to Fungal or
Tubercular meningitis and viral meningitis where lymphocytes
predominate.
In bacterial meningitis, white cell counts are usually in thousands/cubic
mm while in viral meningitis/encephalitis they are in hundreds.
To Diagnose Inflammatory Diseases

Look for
Albuminocytological dissociation in Guillain-Barr syndrome

IgG oligoclonal bands in multiple sclerosis
Hypoglycorrhachia (low glucose level in CSF) in several inflammatory
conditions including chemical meningitis.
Pedia Pearls:
Culture of CSF becomes sterile within 24 hours of appropriate treatment.
CSF sugar normalizes by 3 days in most cases.
Cobweb coagulum in CSF is seen in tubercular meningitis.
Cerebrospinal Fluid Examination 129

In Subarachnoid Hemorrhage
CSF shows a bloody tap, but uniformly all three consecutive tubes used for
collecting the CSF are blood stained, whereas the 2nd and 3rd tubes become
clearer in traumatic LP. Proteins are falsely elevated in hemorrhage (1 mg per
dL of protein for every 1,000 RBCs per mm3).
Myelography
For diagnoses of some spinal pathologies.
THERAPEUTIC INDICATIONS
To Relieve Increased Intracranial Pressure
In pseudotumor cerebri, the raised ICT may be lowered by guarded LP, at
times.
To Inject Medications Intrathecally
Perform LP in:
Tetanus for injecting intrathecal tetanus globulin.
CNS leukemia for injecting corticosteroids, antibiotics, and
chemotherapeutic agents.
ANESTHETIC INDICATIONS
For Spinal Anesthesia and Epidural Anesthesia
Precautions
Ideally do LP prior to antibiotic administration. Do fundus examination before
the procedure to rule out papilledema and monitor pulse oximetry during the
procedure. CT Scans should be done if focal neurological signs are present,
although raised ICT can be missed on CT scan.
CSF INTERPRETATION
Careful Interpretation in Newborns
Newborn patients have up to 150 mg per dL protein. Normal CSF may contain
up to 5 WBCs per mm3 in adults and 20 WBCs per mm3 in newborns.
Reactionary Findings
White cells can be reactionary due to repeated lumbar punctures, medicines
or dyes, recent convulsion, or metastatic cells. However, the presence of
polymorphs is always an abnormal finding. In traumatic tap or central nervous
system bleed, the cells will be present in the ratio, same as that in the peripheral
blood (that is approximately 1:600) 1 WBC for 600 RBCs.
Dilution or Leakage
Low CSF protein levels may occur due to repeated lumbar puncture/chronic
leak and in acute water intoxication.

EARLY CLUES
Opening Pressure
It is measured with a manometer and naked eye examination gives valuable
clues. Normal opening pressure in lateral decubitus is 10 to 100 mm H2O up
to 8 years, 60 to 200 mm H2O after eight years of age, and up to 250 mm H2O
in obese patients. Straining increases and hyperventilation lowers the opening
pressure. Increased CSF pressure can indicate excess fluid in heart, brain or
meningeal/ spinal inflammation. Decreased CSF pressure is seen in complete
subarachnoid block, shock, hyper- osmolality and traumatic tap.
Color of CSF
Pink, orange or reddish color of CSF is a reliable predictor of hemorrhage and
xanthochromia may point to hyperbilirubinemia or high protein 150 mg per
dL. Cobweb indicates high levels of protein like in tuberculous meningitis or
spinal block secondary to exudation, due to increased permeability or
obstruction of CSF (Table 17.1).
COMPLICATIONS
Bleeding or CSF leak from the lumbar puncture (Postdural puncture

headache).
Traumatic tap. Rarely trauma causes weakness or loss of sensation.
Withdrawal of fluid in raised ICT pressures could result in cerebellar
tonsillar herniation.
Rarely respiratory arrest may occur if airway is compromised due to
positioning.
Table 17.1: Differences between CSF examination of tubercular
meningitis and bacterial meningitis
TBM (Tubercular meningitis)

Appearance
Cells
Protein
Sugar
Treatment
Clear with cobweb formation

Lymphocyte premominate
Very high
Low
Steroids 6 weeks
Bacterial meningitis
Purulent (turbid)
Polymorphs predominate
High
Very low
Steroid (only 1 dose in H-influenza
meningitis, before treatment)
Pedia Pearls:
Tubercular meningitis produces basal exudates (picked up on CT scan).
HSV encephalitis involves temporal lobe and has high concentration of protein in CSF.
Hypoglycorrhachia (Low CSF sugar) is also common in mumps meningoencephalitis.
Cerebrospinal Fluid Examination 131

BIBLIOGRAPHY
1. Ahmed A, Hickey SM, Ehrett S, Trujillo M, Brito F, Goto C, et al. Cerebrospinal
fluid values in the term neonate. Pediatr Infect Dis J 1996;15:298-303.
2. Arevalo CE, Barnes PF, Duda M, Leedom JM. Cerebrospinal fluid cell counts and
chemistries in bacterial meningitis. South Med J 1989;82:1122-7.
3. Conly JM, Ronald AR. Cerebrospinal fluid as a diagnostic body fluid. Am J Med
1983;75(1B):102-8.
4. Davis LE. Fungal infections of the central nervous system. Neurol Clin 1999;17:76181.
5. Dougherty JM, Roth RM. Cerebral spinal fluid. Emerg Med Clin North Am
1986;4:281-97.
6. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage.
N Engl J Med 2000;342:29-36.
7. Fishman RA. Cerebrospinal fluid in diseases of the nervous system. 2nd edn.
Philadelphia:Saunders, 1992. Khurana RK. Intracranial hypotension. Semin Neurol
1996;16(1):5-10.
8. Garcia-Monco JC. Central nervous system tuberculosis. Neurol Clin 1999;17:73759.
9. Greenlee JE. Approach to diagnosis of meningitis. Cerebrospinal fluid evaluation.
Infect Dis Clin North Am 1990;4:583-98.
10. Jeffery KJ, Read SJ, Peto TE, Mayon-White RT, Bangham CR. Diagnosis of viral
infections of the central nervous system: Clinical interpretation of PCR results. Lancet
1997;349:313-7.
11. Kaplan SL. Clinical presentations, diagnosis, and prognostic factors of bacterial
meningitis. Infect Dis Clin North Am 1999;13:579-94.
12. Leonard JM, Des Prez RM. Tuberculous meningitis. Infect Dis Clin North Am
1990;4:769-87.
13. Lyons MK, Meyer FB. Cerebrospinal fluid physiology and the management of
increased intracranial pressure. Mayo Clin Proc 1990;65:684-707.
14. Morgenlander JC. Lumbar puncture and CSF examination. Postgrad Med
1994;95(8):125-31.
15. Pruitt AA. Infections of the nervous system. Neurol Clin 1998;16:419-47.
16. Zunt JR, Marra CM. Cerebrospinal fluid testing for the diagnosis of central nervous
system infection. Neurol Clin 1999;17:675-89.
18
Urine Examination
URINE
Urine examination is considered as a liquid biopsy that reflects the status

of entire body and more so of the kidneys
Symptomatology of kidney diseases like-fever with flank pain, frequency,
urgency, squatting, day wetting, poor stream, prolonged voiding, soiling,
straining and even constipation, indicate the presence of some urinary
pathology.
AIM OF URINE EXAMINATION

To identify:
The type of renal anomaly
The site of infection
To distinguish between acute changes from an already established renal
disease
To prevent further damage by early detection and treatment of urinary
infection (UTI).
COLLECTION OF URINE SAMPLE
In Older Children
Collect fresh midstream urine specimen which means that the first part of
urine is not collected
Collect urine in the early morning (long bladder time, allows the bacteria
to multiply)
Next step is to transfer the urine to the laboratory for immediate culture
and microscopy.
In Infants and Small Children

The risk of getting contamination is high with:
Pads, Adhesive bags, Urinary catheters.
Even if growth is more than 105 CFU/ml urine, repeat sample may be
necessary (preferably perform the suprapubic aspiration).
Urine Examination 133

Suprapubic Puncture
The bladder is an intraabdominal organ during infancy. Hence, after the

baby has been fed or given a fluid bolus, the bladder gets full which is
confirmed on dullness by percussion or ultrasonography just above pubic
symphysis
Then with the child in supine position, a thin needle attached to a syringe
is inserted vertically in the midline, 1 to 2 cm above the symphysis pubis
Urine is usually obtained at a depth of approximately one inch.
Complications: Microscopic hematuria is common. Rarely, bowel penetration
may also occur, but it is unlikely to create havoc.
NAKED EYE CHARACTERISTICS
Urine Volume
Oliguria: < 400 ml/m2/24 hours: Seen in acute nephritis, sereve shock and urinary
tract obstruction.
Anuria: < 100 ml/m2/ 24 hours: Seen in acute renal failure.
Color
Hematuria: Microscopic hematuria is defined as more than 5RBCs/hpf on a
centrifuged urine specimen. Naked-eye hematuria is defined as more than 1
ml blood in one liter urine.
Hemoglobinuria: The color looks like strong tea or wine because of the
existence of free hemoglobin.
Pyuria or bacteriuria: Presence of more than 5 WBCs/hpf or bacteria with a
cloudy-look.
Bilirubinuria: Presence of direct bilirubin with a dark-yellow color.
Crystolluria: Presence of salts and/or crystals with a smoky/cloudy look.
MICROBIOLOGICAL TESTS
Urine Microscopy
Microscopy of uncentrifuged urine showing more than 10 leukocytes/L

in a boy and 50 in a girl is suggestive but not diagnostic of UTI
These leukocytes may be found even otherwise. Examples include febrile
state and inflammatory disease like glomerulonephritis
White cell casts in urinary sediment may suggest renal infection. However,
these casts are easily dissolved, in alkaline urine
Presence of hematuria or albuminuria is of no value in establishing a
diagnosis of UTI with certainity.
Pedia Pearl: Mild proteinuria and cola brown urine with RBC casts suggest glomerular
hematuria (i.e. AGN), while frank red urine with no casts suggests extraglomerular hematuria
wherein UTI, sickle cell, urolethiasis and drugs are more common causes.

Microscopic Urine Sediment Tests
Cells
The presence of:
Red blood cells (RBCs) may suggest autoimmune nephritis and/or
pylonephritis
White blood cells (WBCs) may suggest urinary tract infection/inflammation
as well.
Casts and Their Associated Conditions
Red blood cell casts (erythrocyte cast): In glomerulonephritis, vasculitis,

etc.
White blood cell casts (leukocyte cast): In interstitial nephritis,
pyelonephritis, etc.
Epithelial cell casts: In Acute tubular necrosis interstitial nephritis,
glomerulonephritis, etc.
Granular casts (coarse and fine granule): In renal parenchymal disease
(nonspecific)
Waxy, broad cast: In advanced renal failure
Hyaline cast: Normal finding in concentrated urine
Fatty casts: In heavy proteinuria.
Urine Culture
Sample collected for culture of urine should always be immediately

transported in an ice box or refrigerated until cultured, to prevent growth
of contaminating bacteria
The Colony forming units (CFUs) of more than 1lac suggest a definite
infection and less than 103 CFUs indicate that the sample is contaminated.
CHEMICAL TESTS
Urine pH
Specific Gravity
Protein
Glucose
Ketone bodies
Blood in urine
Bile salts
Bile pigments.
pH
Biochemical analysis of urine is useful, especially pH and nitrite test for

diagnosing UTI. Alkalinization of urine often helps in restricting further
growth of bacteria.

Specific Gravity (Density)
Low in:
Chronic renal failure
Diabetes insipdus.
High in:
Acute nephritis
Diabetes mellitus
Heart failure.
Urine Protein
Normally less than 20 to 80 mg/24 hours

Protein of (1 +) = 30 mg / dl
Protein of (2 +) = 100 mg /dl
Protein of (3 +) = 300 mg / dl
Protein of (4 +) = > 2 g / dl.
Quantitative 24 hours protein estimation
Normal: 4 m g/m2/hr or 50 to 100 mg/m2/d
Mild: < 500 mg/m2/d
Moderate: 500 to 1000 mg/m2/d.
Massive: >1000 mg/m2/d or 40 mg/m2/hr.
Tests for qualitative assessment
Principle: Heat and acid, coagulate the proteins.
Heat coagulation5 ml urine. Boil well. Add 1 ml acetic acid. A white
precipitate is formed
Sulfosalicylic acid-2 ml urine + 2 ml sulfosalicylic acid. Mix. A white
precipitate appears.
Urine Glucose
Principle: Copper ion reduction in Benedicts solution by reducing sugars.
Benedicts test: 1 ml urine + 5 ml Benedicts reagent. Mix and boil well. Look
for color change to green, orange or brick red.
Fehling test: 1 ml urine + 1 ml fehling (a) solution +1 ml fehling (b) solution.
Mix and boil well. Look for color change to green-orange or brick red.
Urine Ketone Bodies
Rotheras test (Nitroprusside test): 5 ml urine saturated with ammonium sulfate
+ 0.5 ml Na nitro-prusside. Mix well. + 2 ml conc. Ammonia. Mix.
A purple ring appears.

Blood in the Urine
Principle: Heme catalyses the oxidation of benzidine with H2O2.
Benzidine test: Mix 3 ml benzidine reagent +3 ml urine. Add 1 ml H2O2. Blue
color indicates blood.
Bile Salts in Urine
Principle: Bile salts lower the surface tension of urine.
Hays sulfur test: Take 5 ml urine in a small beaker. Sprinkle sulfur powder. If
the sulfur floats, then bile salts are absent but if sulfur powder sinks to the
bottom of the beaker, then bile salts are present.
Bile Pigments in Urine
In normal children:
Urobilinogen is formed in the intestines by action of bacteria on conjugated
bilirubin
Later, some of this urobilinogen formed is reabsorbed, taken up by the
hepatocytes (enterohepatic circulation) into the blood and then excreted
by the kidney
Urobilinogen is converted to the yellow pigmented urobilin apparent in
urine
Some of the urobilinogen remaining in the intestine (stercobilinogen) is
oxidized to brown stercobilin which gives the feces their characteristic
color.
In hemolysis:
Overburdening of the liver with bilirubin due to excessive RBC breakdown
increases the urobilinogen production in the intestines
Consequent reabsorption leads to increased urobilinogen in the urine.
In biliary obstruction:
Here due to the obstruction, low amount of conjugated bilirubin reaches
the intestine for conversion to urobilinogen
With less urobilinogen available for reabsorption and excretion, the amount
of urobilin found in the urine is low
High amounts of the soluble conjugated bilirubin enters the circulation
where it is excreted via the kidneys.
These mechanisms are responsible for the dark urine and pale stools observed
in biliary obstruction.
Absence of urine urobilinogen may result from complete obstructive
jaundice or treatment with broad-spectrum antibiotics, which destroy the
intestinal bacterial flora, required for deconjugation of conjugated bilirubun
to urobilinogen
Also, low urine urobilinogen levels may result from congenital deficiencies
of enzymes which conjugate bilirubin
In liver disease (such as hepatitis), the intrahepatic urobilinogen cycle is
inhibited. Thus increasing urobilinogen levels.

Bile Pigments in Urine
UrobilinogenErhlichs test
Principle: Erhlichs reagent in conc HCI reacts with urobilinogen to form a
pink colored aldehyde complex in chloroform.
BilirubinFouchets test
Principle: It is based upon the idea of oxidising a bilirubin-barium precipitate
spread on a filter-paper. A green or blue color indicates bilirubin.
TESTS OF GLOMERULAR FUNCTION
The creatinine clearance rate inceases with age. The creatinine clearance
(Ccr) = UV/P
Ccr = urinary creatinine volume of urine in 24 hours/plasma creatinine
Normal is equal to 80 to 120 ml/min/1.73 m2
GFR is determined by the creatinine clearance.
TESTS OF RENAL TUBULAR FUNCTION
Urine specific gravity (3 hours urine) test reflects the tubular concentration
function.
A hydrometer (urinometer) and a suitable container can be used to
determine specific gravity. An indirect colorimetric method for estimating
specific gravity is available on reagent strips (urine dipsticks). This
method uses a pad that contains a complex, pre-treated electrolyte that
undergoes a pH change based on the ionic concentration of the urine. Loss
of concentrating ability is often of the earliest signs of kidney disease,
clinically evidenced as nocturia (voiding at night) and polyuria (increased
urine output)
High SG is > 1.025
Low SG is < 1.003
Urinary electrolytes, reflect the state of salt and water balance. One should
remember that:
a. Nephrogenesis is completed by only 36 weeks of gestation.
b. Maturation continues in infancy.
Pedia Pearls:
An infant can concentrate urine up to 700 to 800 mosm/kg while an older child can
concentrate up to 1400 mosm/kg
GFR (Glomerular Filteration Rate) at term = 15 to 20 ml/min/1.73 m2; GFR in
preterms = 10 to 15 ml/min/1.73 m2
Adult values are attained by 3rd year of life.

BIBLIOGRAPHY
1. Abuelo GJ. Proteinuria: Diagnostic principles and procedures. Annals of Internal
Medicine 1983;98:186-91.
2. Hermmsen MC, Blogdgett EM. Prospective evaluation of routine admission urinalysis.
American journal of Diseases of Children 1981;135:126-30.
3. Intgesell M. Practicality of screening urinalysis in asymptomatic children in a primary
care setting. Pediatrics 1978;62:103-5.
4. Is routine urinalysis worthwhile? Lancet 1988;1(8588):747.
5. Kroenke K, et al. The admission urinalysis: Impact on patient care. Journal of General
Internal Medicine 1986;1:238-42.
6. Madan E, et al. Urine screening as an alternative to urine culture. Annals of Clinical
Laboratory Science 1988;18(2):116-9.
7. Mant D, Fowler G. Urine analysis for glucose and protein: Are the requirements of
the new contract sensible? British Medical Journal 1990;300(6731):1053-5.
8. Mortier E, et al. Assessment of urine analysis for the diagnosis of tuberculosis. British
Medical Journal 1996;312(7022):27-8.
9. Pardo V, et al. Benign primary hematuria. Clinico-pathologic study of 65 patients.
American Journal of Medicine 1979;67:817-22.
10. Ruttimann S, Clemencon D. Usefulness of routine urine analysis in medical outpatients.
Journal of Medical Screening 1994;1(2):84-7.
11. Schumann GB, Greenberg NF. Usefulness of micro-scopic urinalysis as a screening
procedure. American Journal of Clinical Pathology 1979;71:452-6.
3
Procedures
19
Liver Biopsy
A liver biopsy is a procedure, in which tissue samples are removed with a
needle biopsy or open biopsy.
INDICATIONS
To Assess Liver Damage Based on
Extent of liver enlargement: Whether diffuse (Parenchymal) or focal

enlargement
Degree of inflammation and fibrosis of liver: Stage the degree of fibrosis
and grade of inflammatory activity, e.g. by grading of cirrhosis.
To Diagnose
Cholestatic liver disease

Inborn errors of metabolism
Cause for abnormal unexplained LFT.
To Evaluate Response to Therapy
Status after liver transplantation

Evaluate for any rejection.
EQUIPMENT AND PROCEDURE

Needles may be divided into three broad categories:
Suction needles (Jamshidi, Klatskin and Menghini)
Cutting needles (Tru-cut and Vim-Silverman)
Spring-loaded cutting needles.
Each needle type has proposed advantages and disadvantages. Suction
needles yield desirable sample size but may fragment cirrhotic livers. Cutting
needles do not fragment liver tissue but may deliver inadequate tissue samples.

Procedure: An intravenous (IV) line may be started. The skin is cleansed with
an antiseptic solution. The patient is placed supine on a flat surface and the
right arm is kept behind the head.
Ultrasound/CT scan is done to locate the site of procedure, usually along
right midaxillary line, corresponding to the area of maximum dullness.
After local anesthesia, a biopsy needle is introduced close to the upper
aspect of the lower rib (to avoid the intercostal nerve and vessels) while patient
holds the breath. A series of resistance levels are encountered, the last being
that of the liver edge. Pressure is applied to the site, followed by an adhesive
bandage after the procedure. Vital signs are frequently monitored.
CONTRAINDICATIONS
Bleeding tendency: Increased prothrombin time, international normalized ratio
(INR) greater than 1.6 and thrombocytopenia (platelet count of less than 60,000/
cubic mm) predispose to bleeding.
Local problems like ascites, suspected hemangioma and suspected hydatid
cyst infection.
COMPLICATIONS OF PERCUTANEOUS LIVER BIOPSY
Vasovagal episode or anesthetic reaction

Excessive blood loss: Hemobilia presents as biliary colic, gastrointestinal
bleeding and jaundice. Intraperitoneal hemorrhage up to 24 hours,
postprocedure tachycardia, hypotension. and abdominal pain
Excessive bile loss: (Biliary peritonitis) Severe abdominal pain and
vasovagal hypotension herald its occurrence
Excessive air loss: Air leaks like pneumothorax and subcutaneous
emphysema
Infection: Peritonitis.
BIBLIOGRAPHY
1. Bravo AA, Sheth SG, Chopra S. Liver biopsy. N Engl J Med 2001;344(7):495-500.
2. Conn HO. Intrahepatic hematoma after liver Biopsy. Gastroenterology
1974;67(2):375-9.
3. Counihan TC, Islam S, Swanson RS. Acute cholecystitis resulting from hemobilia
after tru-cut biopsy: A case report and brief review of the literature. Am Surg
1996;62(9):757-8.
4. Garcia-Tsao G, Boyer JL. Outpatient liver biopsy: How safe is it? Ann Intern Med
1993;118(2):150-3.
5. Gilmore IT, Burroughs A, Murray-Lyon IM, et al. Indications, methods, and outcomes
of percutaneous liver biopsy in England and Wales: An audit by the British Society of
Gastroenterology and the Royal College of Physicians of London. Gut 1995;36(3):43741.
6. Hederstrom E, Forsberg L, Floren CH. Liver biopsy complications monitored by
ultrasound. J Hepatol 1989;8(1):94-8.
Liver Biopsy 143

7. Janes CH, Lindor KD. Outcome of patients hospitalized for complications after
outpatient liver biopsy. Ann Intern Med 1993;118(2):96-8.
8. Mahal AS, Knauer MC, Gregory PB. Bleeding after liver biopsy. Western J Med
1981;134:11-4.
9. McGill DB, Rakela J, Zinsmeister AR. A 21-year experience with major hemorrhage
after percutaneous liver biopsy. Gastroenterology 1990;99(5):1396- 400.
10. Piccinino F, Sagnelli E, Pasquale G. Complications following percutaneous liver biopsy.
A multicentre retrospective study on 68, 276 biopsies. J Hepatol 1986;2(2):165-73.
11. Reddy KR, Jeffers LJ. Evaluation of the liver B: Liver biopsy and laparoscopy. In:
Schiffs Diseases of the Liver. Philadelphia, Pa. Lippincott-Raven Publishers
1999;8:245-66.
12. Reddy KR, Schiff ER. Complications of Liver Biopsy. In: Taylor MB, (Ed)
Gastrointestinal Emergencies. 2nd edn. Baltimore, Md:. Williams and Wilkins, 1996.
13. Reichert CM, Weisenthal LM, Klein HG. Delayed hemorrhage after percutaneous
liver biopsy. J Clin Gastroenterol 1983;5(3):263-6.
14. Sandbolm P. Hemobilia. In: Diseases of the Liver. Philadelphia, Pa:. JB Lippincott
Co 1993;7:1489-97.
15. Schiano TD, Azeem S, Bodian CA, et al. Importance of specimen size in accurate
needle liver biopsy evaluation of patients with chronic hepatitis C. Clin Gastroenterol
Hepatol 2005;3(9):930-5.
20
Bone Marrow Tests

(Aspiration, Biopsy, Hematopoietic
Stem Cell Transplantation)
BONE MARROW TESTS
INDICATIONS
To Diagnose and Stage the Hematologic Disease
Aplastic anemia, thrombotic thrombocytopenic purpura, etc. are often diagnosed
by bone marrow.
To Assess the Overall Bone Marrow Cellularity
Cellularity approximates 100 percent at birth and declines with age (replaced by
myeloid/erythroid cells).
To Diagnose Various Storage/Infiltrative Disorders
Examples includeAcute Lymphoblastic leukemia, myelodysplastic syndrome
and lymphomas.
For Therapeutic Follow-up
For example, post-chemotherapy.
For Stem Cell Transplantation
Examples includeLeukemias and hodgkins.
EQUIPMENT AND PROCEDURE
There are two main types of bone marrow test needles a bone marrow
aspiration and a thicker bone marrow trephine biopsy needle. It removes a 1
or 2 cm core of bone marrow.
Bone Marrow Aspiration Needle
The needle is quite thin and is inserted into the bone (iliac crest), after some
sedation and a syringe is then used to withdraw the fluid, in the bone marrow.
Bone Marrow Tests 145

Bone Marrow Trephine Biopsy Needle
Biopsy is the removal of soft tissue from iliac crest using biopsy needle
The trephine biopsy needle is a thick needle made of autoclavable, strong
stainless steel material with polished sharp cutting edge
It has a hollow cannula with a handle having an interlocking device and a
trocar (bevel stylet) being removably insertable into said hollow cannula
Another interlocking device fits with the interlocking device in the cannula
handle, holding the handles securely together during procedure (as the pin
engages the notch easily being neither too loose nor too tight, allowing stable
manipulation and removal of the trocar without displacing the outer cannula).
Procedure
The needle is inserted by placing accurately at the right place and penetrating
quickly by rotating the needle into the bone or by turning the needle back
and forth while pushing it through the outer hard layer of the bone further
into the marrow to get some core of marrow out in one piece
Once the soft bone is reached, the trocar is removed and the cannula is
carefully withdrawn so as to retain the solid marrow material.
Types of Samples
Bone Marrow Aspirate
After taking aspirate particles they are placed on slide and spread with
another slide (pulled apart) or the particles are placed between slide and
cover slip and pulled apart
Microscopy reflects marrow morphology with or without cytochemical
staining
Buffy coat smears may be made to reveal better morphology.
Bone Marrow Biopsy

Biopsy core is fixed, decalcified, processed, embedded in paraffin or plastic,
sectioned and then stained with Hematoxin/Eosin or PAS stain, etc.
Biopsy Imprints (Touch smear)
Here, slide is only gently touched to biopsy core. Hence, it shows poor
morphology.
Note: Malignancies which may have patchy marrow involvement (e.g.
lymphoma, metastatic disease) may require specimens from multiple sites.
COMPLICATIONS
Excessive bleeding: Hematoma may occur but retroperitoneal hemorrhage

is unlikely
Infection: Wound infection and osteomyelitis.
Damage to needle, bone or nerve: Needle breakage, fracture and rarely
neuropathy.
STEM CELL TRANSPLANTATION

TYPES OF STEM CELLS
Remember: Stem cells on division can produce the original cell and a daughter
cell unlike other cells that just produce two daughter cells. Types include:
Totipotent: Undifferentiated cells that are formed during the first few
divisions, e.g. cell in morula stage are totipotent, i.e. they can become any
cell in the body
Pluripotent: Slightly more differentiated cells that are formed when
totipotent stem cells undergo the first few divisions, e.g. cells at a blastocyst
stage. Totipotent and pluripotent cells can form entirely new organism
Multipotent: These cells are limited to mostly cells of the blood, heart,
muscle and nerves, which repair damaged tissue. Adult stem cells are
multipotent stem cells
Further, specialization produces oligopotent and unipotent cells which
on division cannot produce the original cell and a daughter cell.
A signal that instructs cells to grow into one organ and not another in
a particular enviornment is not known, e.g. bone marrow stem cells
migrate to bone marrow to make blood cells and may migrate to another
environment and make cartilage. This is termed as Plasticity of Hematopoietic Stem Cells.
SOURCE OF STEM CELLS
Bone Marrow
By repeated aspirations of the posterior iliac crests.
Peripheral Blood
Stem cells in the bone marrow can be mobilized into the peripheral blood by
granulocyte colony stimulating factor (GCSF) by priming process (boosting
the number of hematopoietic stem cells) and then collected via anticoagulated
leukocyto phoresis machine which separates stem cells. These harvested stem
cells have a CD34 molecule a cell surface marker on the hematopoietic cells
that helps in counting stem cells because as such stem cells are invisible. A
total of 2.5 106 cells/kg are needed in a transplant.
Cord Blood
Blood from umbilical cord and placenta can easily be collected (has relatively
immature donor T cells and is rich in hematopoietic stem cells). It has decreased
risk of adverse effects, (e.g. GVHD) and increased tolerance to HLA-mismatch
as the cells are immunologically nave.

Embryonic stem cells and embryonic germ cells: These are other sources.
Ethically it is an issue, to take an embryo at morula or blastocyst stage in vivo
and harvest the cells, in the process destroying a potential life.
Prerequisite
Prerequisite of a transplant is immunosuppression, as an immunocompetent
body may destroy the foreign stem cells.
How the Stem Cells Act
Engraftment
When the stem cells are injected, they undergo active division and travel to
the bone marrow, where they begin to produce and replenish new white
blood cells, red blood cells, and platelets within a month, in a process known
as engraftment and also yield the original self-renewing cells.
Apoptosis
This is the process of programmed cell death that leads cells to self-destruct
excess stem cells injected. Hence, more the number, better the engraft-ment.
Graft Versus Tumor (GVT) Effect
After an allogeneic transplant, the graft identifies any residual tumor left
(postchemotherapy and/or postradiation therapy) as foreign, and attacks it.
USES OF STEM CELLS
Regeneration:
Spine injury: Local stem cell injection hastens recovery
In myocardial damage as in cardiomyopathy it renews cardiac muscle
Neurodegenerative disorders of brain also may be helped by stem cells.
Hematopoietic stem cell transplantation: (Old name bone marrow transplant
is not used now because the source need not to be bone marrow). Stem
cell transplant is useful
In high-risk ALL leukemia
Hodgkins disease
Neuroblastoma
Congenital immuno-deficiency disorders.
After chemotherapy and radiation therapy: High-dose therapy affects live
cancer cells and even destroys the patientsbone marrow. So, there is a
need for stem cell transplantation.

TYPES OF TRANSPLANT
Autologous Transplants
Children receive their own stem cells, hence immunosuppression is not required,
e.g. as a rescue therapy after high-dose myeloablative therapy.
Syngeneic Transplants
Children receive stem cells from their identical twins.
Allogeneic Transplants
Children receive stem cells from their brother, sister, or parent. An unrelated
donor also may be used. Human leukocyte antigens HLAs) matching is needed.
HLAs are expressed on the surface of WBCs on the short arm of chromosome
6. Conditioning regimens are required (killing all residual cancer cells by
chemotherapy and immunosuppression for engraftment success).
COMPLICATIONS
Early effects: Mucositis (mouth sores, diarrhea)

Graft versus host disease (allogeneic trans-plantation): Immune response
of donor T lymphocytes against host cells
Hemorrhagic cystitis: Cyclophosphamide can cause dysuria and hematuria
Veno-occlusive disease: Total-body irradiation (TBI) and drugs such as
oral busulfan and cyclophosphamide may lead to this syndrome due to
damage to the sinusoidal endothelium, which results in sinusoidal obstruction
Neutropenia: Use of steroids, and immuno-deficiency can lead to Aspergillus
cytomega-lovirus or bacterial infections
Ocular effects: Posterior subcapsular cataract
Endocrine effects: In children, growth and development are impaired; these
children may require growth hormone supplements. Hypo-thyroidism, both
overt and subclinical, is also common in these patients
Pulmonary effects: Chest infections due to immunosuppression
Musculoskeletal effects: Osteopenia, osteoporosis and avascular necrosis
Neurocognitive and neuropsychological effects: These are common after
cranial radiation
Immune effects: Host immunity is suppressed. Immune reconstitution is
most efficient in children and young adults because they have an active
thymus. Most killed vaccines are considered safe but use of live virus
vaccines is generally contraindicated, until at least 18 months
posttransplantation.

BIBLIOGRAPHY
1. Bailey LC, Lange BJ, Rheingold SR, Bunin NJ. Bone marrow relapse in paediatric
acute lymphoblastic leukaemia. Lancet Oncol 2008; 9(9):873-83.
2. Copelan EA. Hematopoietic stem-cell transplantation. N Engl J Med 2006;
354(17):1813-26.
3. Couriel D, Caldera H, Champlin R, Komanduri K. Acute graft-versus-host disease:
Pathophysiology, clinical manifestations, and management cancer 2004; 101(9):193646.
4. Cutler C, Antin JH. Peripheral blood stem cells for allogeneic transplantation: A
review. Stem Cells 2001; 19(2):108-17.
5. Fish JD, Grupp SA. Stem cell transplantation for neuroblastoma. Bone Marrow
Transplant 2008; 41(2):159-65.
6. Koh LP. Unrelated umbilical cord blood transplantation in children and adults. Ann
Acad Med Singapore 2004; 33(5):559-69.
7. Miano M, Faraci M, Dini G, Bordigoni P. Early complications following haematopoietic
SCT in children. Bone Marrow Transplant 2008; 41 Suppl 2:S39-42.
8. Nguyen K, Devidas M, Cheng SC, et al. Factors influencing survival after relapse from
acute lymphoblastic leukemia: A Childrens Oncology Group study. Leukemia Sep
25, 2008.
9. Satwani P, Sather H, Ozkaynak F, et al. Allogeneic bone marrow transplantation in
first remission for children with ultra-high risk features of acute lymphoblastic leukemia:
A childrens oncology group study report. Biol Blood Marrow Transplant 2007;
13(2):218-27.
21
Reading an Electrocardiogram
INTRODUCTION
Reading ECGs is an art but one should correlate the ECG together with other
parameters like pulse, capillary refill, blood pressure and heart sounds to make
effective conclusions. EKG paper is a grid where time is measured along the
horizontal axis. Each small square is 1 mm in length and represents 0.04
seconds. Voltage is measured along the vertical axis. (10 mm is equal to 1mV
voltage).
HOW IMPULSE TRAVELS
The normal direction of impulse is (SA Node AV Node Bundle of His
Right and Left Bundle branches Purkinje Fibers).
HEART RATES (2 METHODS)
1. Count the number of R waves in 6 seconds and multiply the number by
10.
2. 300 is divided by the number of large squares between two R waves,
e.g. R-R interval of two large squares denote that the heart rate is 150.
Newborn to 3 years: SA node beats at 100/min, AV node at 50/min and Purkinje
(ventricles) at 35/min approximately.
Three years to teenage: SA node beats at 55120/min, AV node (junction) at
3565/min and Purkinje (ventricles) at 25-45/min respectively.
WAVES
P Waves
Note whether P waves are present or not: The normal P wave is less than
2.5 mm in amplitude and negative portion is less one small square in amplitude
and duration.
Look at the rhythm: Sinus or not, i.e. whether one P wave is seen for every
QRS complex. If not, consider heart block as a possibility.
Reading an Electrocardiogram 151

QRS Complex
This indicates ventricular depolarization (contraction). The amplitude is
reduced in myocarditis and pericardial effusion, as the ejection fraction falls.
Absent QRS complex, indicates asystole or ventricular fibrillation.
Relation of P wave to QRS complex tells about heart blocks. In third degree
AV block or complete AV block due to digitalis toxicity or an acute infection,
the atrial rate is usually normal, the ventricular rate is usually less than normal
and P wave is not followed by QRS complexes.
Width of QRS complex: QRS may become wide in some heart blocks when
another pacemaker distal to the block takes charge in order to activate the
ventricles.
In premature ventricular contractions, the impulse originates below the
branching of the Bundle of His. Hence, there is early contraction
It may occur in bigeminy, trigeminy or quadrigemini followed by a
compensatory pause
Here, the QRS is wide (> 0.12 seconds); and the morphology is bizarre
with the ST segment and the T wave opposite in polarity to QRS.
Treatment modalities include pacing and atropine.
Note: Do not suppress this ventricular rhythm as it protects from standstill.
QRS amplitude: If less than 5 mm in lead I, II or III suspect pericardial effusion.
QRS Axis (Fig. 21.1)
Usually, if the axis is abnormal, AVF is predominantly negative.
Calculation of QRS Axis
For example: L1 and AVF are at right angles. If L1 is to the right and AVF is
towards the bottom then find the net deflection of QRS by subtracting the
number of little squares below the baseline in lead 1 from the number above
the baseline and plot horizontally towards the lead. Repeat the same for lead
AVF and plot vertically. If the sum is negative then plot the number of squares
by extending the line towards the opposite side away from the lead. Join the
dots at right angles to find the axis.
R and S Waves
The right ventricle is directed to the right and is reflected by the height of the
R wave on right chest lead, i.e.V1 and the depth of the S wave on left chest
lead, i.e. V6. The opposite is true for the left ventricle (assessed by the sum of
S in V1 and R in V6).
Pedia Pearl: Left axis deviation in first couple of monthssuspect endocardial cushion
defects or myocardial disease in later age (rarely L.V.H.)
8-16 yr old child
Fig. 21.1: If net deflection in lead 1 is 5 mm and deflection in

AVF is 4 mm then the axis is as above
V2-V5 are the transitional leads and so the sum of R in V4 and S in V4

(normal maximum value 50 mm) is used to assess, whether there is biventricular hypertrophy.
ST Segment
This indicates early ventricular repolarization.
Helpful Normal Values
S in V6 = SV6S Sinks by 6 from 10 mm in (neonate) to 4 mm as adult.
R in V6 = RV6R Rises by double of 6 that is 12 from 11 mm (in neonate)
to 23 mm as adult.
S in V1 = SV1Sinks to a Valley by 1 month from 23 mm (neonate)
decreasing to 11 mm by 1 month and then rising again to 21 mm as adult.
R in V1 = RV1 26 mm (neonate) decreasing to 10 mm as adult.
SV1 + RV6 28 mm (neonate) decreasing to 21 mm by 1 month and increasing
to 41 mm as adult.
Normal values for the sum of the R and S waves are greater than 5 mm in the
limb leads and 8 mm in the ventricular leads.
T Wave
T wave indicates ventricular repolarization Morphology (Remember T becomes
upright at ten). The T waves are upright for the 1st week of life, then remain
inverted in V1-V3 until 10 yrs age (except in RVH).
T waves in myocarditis: T waves may become flattened or inverted and
amplitude of the QRS complexes are reduced.
Pedia Pearl: ST elevation in presence of wheeze/cough
Suspect ALCAPA (anomalous left coronary artery from pulmonary artery)

INTERVALS
PR and QRS Interval
PR is measured from the onset of the p wave to the onset of the QRS complex.
PR interval (duration)
0.10 sec in a neonate and 0.10- 0.12 secs in infancy
0.12 0.15 seconds in toddlers
0.16 0.18 seconds in school goers.
QRS interval increases with age (as HR falls)
0- 3 years HR is 100- 180/min QRS is 0.03 - 0.08
>6 years HR is 50 130/min QRS is 0.04 - 0.10
Corrected QT interval
QTc =
QT Interval
RR Interval
Normal values of QTc

N in males 440 ms
N in females 450 ms
Measurements are made in seconds (1 small square = 0.04s). The longest QT

interval is measured and the preceding RR interval. The normal value is <
0.44 seconds for this ratio.
ASSESSMENT OF HYPERTROPHY
a. Right atrial enlargement: Suspect when the amplitude of p is greater than
2.5 mm in lead II & VI
b. Left atrial enlargement: P wave duration > 10 ms above 1 year
c. Right ventricular hypertrophy (RVH): QR pattern in right chest leads is a
reliable sign of RVH and implies a markedly elevated RV pressure. T wave
changes are specific but not sensitive sign of RVH. Also R wave amplitude
in V1 greater than normal value and S wave amplitude in V6 greater than
normal value and Right Axis Deviation correlate well with RVH in children.
d. In left ventricular hypertrophy (LVH): Q waves are seen in leads II, III,
AVF, V5-6. T wave inversion seen in V5-6 are reflective of significant
LVH. R wave amplitude in V6 greater than normal value and S wave
amplitude in V1 greater than normal value is specific but not sensitive for
left ventricular hypertrophy.
e. Biventricular hypertrophy R + S in v3 + v4 > 70 mm
Pedia Pearl: Normal value (upto 98th percentile) RV dominance is normal in

first couple of months of life

RHYTHMS
They may be normal, fast or slow. Some may be dangerous like Vent Fibrillation,
Pulseless V-Tach and Asystole. Immediate CPR may be life saving. For analyzing
the rhythm we need a 12 second lead. Look at rhythm(regular or not). Irregularity
can be due to premature atrial or Premature Ventricular Contraction. Premature
beats are very common in normal children and teenagers (Fig. 21.2).
Recognition of abnormal heart rhythms: They occur due to parasympathetic
(vagal) or sympathetic stimulation and also due to drugs, lack of sleep and
even ectopic foci caused by ischemia.
First look at P wave and PR interval.
P wave indicates atrial depolarization. If P wave, is absent, the rhythm is atrial
fibrillation. In sinoatrial Block type I the P-P interval shortens until one P
wave is dropped.
PR interval indicates conduction time between atria to ventricles. In first degree
AV block due to digitalis toxicity, hyperkalemia, increased vagal tone acute
rheumatic fever and myocarditis the P-R interval may be prolonged. Next assess
heart rates.
Fast Rhythms
Tachycardia
A newborn has tachycardia if the resting rate is more than 160 beats. A teenager
is considered to have tachycardia if the resting heart rate is more than 90 beats
per minute. In Tachycardia see the child. A calm patient in a fast rhythm is much
dangerous than an irritated patient. We need to treat the patient, not the rhythm.
Sinus Tachycardia
It is the increase in the heart rate with fever, excitement and exercise or due to
anemia or thyroid excess. Atria and ventricular contractions are present and
Fig. 21.2: Normal and abnormal rhythms on ECG

the rate measures 100 to 160 beats/minute in older children. Regular P wave,
QRS complex and T waves are present.
Supraventricular Tachycardia (SVT)
The most common abnormal tachycardia in children is supraventricular
tachycardia (SVT), a time-limited illness. It includes paroxysmal atrial
tachycardia (PAT) and wandering pacemaker For many infants heart rate is
usually more than 220 beats a minute. SVT is treated with medications,
Valsalvas maneuver and/or sometimes cardioversion.
Ventricular Tachycardia (VT) (Fig. 21.3)
Ventricular tachycardia (VT) may result from serious heart disease. It requires
prompt medication and/or radiofrequency ablation which may control the
tachycardia. Atrial rhythm is not apparent (P wave is not visible). Ventricular
rhythm is usually regular but rapid (100-250 beats/minute).
(QRS complex is wide and bizarre). The T wave is present and always
pointing in the opposite direction of the QRS complex.
Ventricular Flutter
There is no evidence of atrial contraction (no visible P wave). The ventricular
rhythm may be regular or irregular (QRS complex is wide and not in a typical
pattern) and rate is 150 to 300 beats/minute. The T wave is absent.
Ventricular Fibrillation (Fig. 21.4)
Rapid and chaotic looks like an uneven line. No P wave, no QRS complex,
and no T wave.
Fig. 21.3: Ventricular tachycardia
Fig. 21.4: Ventricular fibrillation

Wolff-Parkinson White Syndrome (WPW)
Here an abnormal conduction pathway runs between atria and ventricles, so
the electrical signal may arrive at the ventricles sooner than normal, hence the
risk of sudden cardiac arrest.
Atrial Flutter
It has many atrial contractions for one ventricular contraction

Atrial rate is 250 to 350 beats/minute
Ventricular rate is usually between 60 and 100 beats per minute
Both atrial and ventricular patterns are regular but they dont match in
rate. It has a P wave (sawtooth or flutter waves), a QRS complex but T
wave is not seen (because it is obscured by the many P waves).
Atrial Fibrillation
Here both the atrial rhythm and the ventricular rhythm are irregular
Atrial pattern is a quivering line 400 beats/minute
Ventricular pattern is normal or faster than normal
There is no actual P wave but rather a fine wavy line. QRS complex is
present. The T wave is not evident.
Slow Rhythms
Bradycardia
A heart rate that is too slow is called bradycardia. A newborn usually wont
have a heart rate of less than 100 beats a minute. Look at the P wave for sinus
bradycardia waves.
Sinus Bradycardia
Both the atria and ventricles beat less than 60 times/min but in regular pattern.*
P wave, QRS complex, and T waves are present.
Sinus Arrhythmia
P wave, QRS complex, and T wave, are present but are slightly irregular.
Atrial and ventricular contractions are present and measure between 60 and
100 beats/minute.
Sick Sinus Syndrome
This is unusual in children but sometimes occurs after open-heart surgery. The
child looks tired, or may faint and may have tachycardia followed by bradycardia
and vice versa. Treat with an artificial pacemaker, medications or both.
* Sinus bradycardia has a heart rate of less than 60/mt in older children and 80/mt in an
infant. Sinus tachycardia has a heart rate of greater than 100/mt in older children and
160/mt in an infant.

Heart Blocks
They commonly occur following cardiac surgery: Here beats are regular but
rate is 40 to 60 beats per minute, if the focus is junctional and 20 to 40 beats
per minute if focus is ventricular.
Look at:
P waves:
They are upright and uniform but there are more P waves than QRS
complexes as all are not transmitted
There is no relationship between P waves and QRS complexes and P
waves occasionally are superimposed on QRS complexes.
QRS duration:
It is less than 0.12 seconds if focus is junctional but 0.12 seconds or more,
if focus is ventricular (remember that independence leads to laziness)
Heart block (congenital) may be present at or even before birth in
maternal SLE
Partial RBBB* may be a normal feature of the ECG but is associated
with RVH found in atrial septal defects. Here, the QRS duration is
normal but an rSR pattern is found in V1-V2.
Junctional Escape Rhythm
They are slow (because AV node is slow intrinsically) but regular (40-60
beats per minute)
P wave is inverted because impulse starts at AV node (not at SA node) and
may be seen either before, during, or after QRS complex as and when the
atria escapes from SA nodal influence
PR interval can be measured only if P wave precedes QRS complex but if
measurable will be less than 0.12 seconds
The QRS is also less than 0.12 seconds because the contraction is faster,
due to stimulation of AV node alone.
Idioventricular Rhythm
It is slow because of independent and lazy ventricular action but usually it is
regular at 20-40/min. However, there are no P waves (hence no PR interval)
and the QRS is wide and bizarre (0.12 seconds or greater).
Asystole (Ventricular Standstill)
Atrial pattern may be seen which is regular: P wave is often present but the
ventricular pattern is absent (QRS complex absent) and no T wave is visible.
* RBBB = Right bundle branch block

Pedia Pearl: rSR pattern indicates bundle branch block.

BIBLIOGRAPHY
1. Braunwald E (Ed.). Heart Disease: A Textbook of Cardiovascular Medicine, 5th
edn., Philadelphia, WB Saunders Co., 1997.
2. Davis AM, Gow RM, McCrindle BW, Hamilton RM. Clinical spectrum, therapeutic
management, and follow-up of ventricular tachycardia in infants and young
children. American Heart Journal 1996;131:186-91.
3. Hurt JW. Current Perspective: Naming of the Waves in the ECG, With a brief
account of their Genesis Circulation. 1998;98:1973-42.
4. Mark JB "Atlas of Cardiovascular Monitoring". New York:Churchill Livingstone,
1998.
5. Trippel DL, Parsons MK, Gillette PC. Infants with long-QT syndrome and 2:1
atrioventricular block. American Heart Journal 1995;130:1130-34.
6. Verrier, Richard L. Dynamic Tracking of ECG Heterogeneity to Estimate Risk of
Life-threatening Arrhythmias. CIMIT Forum. September 2007;25:13.
Pedia Pearls:
Q = Septal depolarization Q (width of) wave > 1 mm or in V1 is abnormal or deep
Q waves in V6 or lead III suggest LVH
Q waves are N in lead II, III, avF, V5, V6
In absence of Q waves suspect VSD
4
Pediatric Imaging
22
CT Scans
CT FUNDAMENTALS
Types of CT
Plain CT scans
Contrast enhanced CT scans.
Before the use of iodinated contrast the patient needs to be NPO at least 4
hours and should have no contraindication to it, i.e. allergy or renal insufficiency.
Attenuation
Attenuation is measured in Housefield units (Scale -1000 up to +1000)

Minus 1000 is air, i.e. Hypoattenuating (hypodense)
0 is water, i.e. Isoattenuating (isodense)
Plus 1000 is cortical bone, i.e. Hyperatten-uating (hyperdense).
Examples:
Grey matter is light grey (isodense)
CSF is black (ww density)
Bone calcification, contrast, metallic foreign bodies and acute
hemorrhage appears white. Weeks later hemorrhage become isodense
with brain tissue and months later, it becomes an area of low density
(black)
Areas of abnormal calcification (white) are too dense to represent blood
and show no surrounding edema.
Grey/White Matter Differentiation
Normal pattern may not be apparent because of cerebral anoxia causing

tissue edema
The fatty content of the myelin (white matter) is of lower density (darker)
than the overlying grey matter
Normally, the cerebrospinal fluid spaces (ventricles) are symmetrical and
it should be ensured that the midline remains central
An area of infarct is seen as low density within the vascular territory
involved
Chronic ischemic change leads to encephalomalacia.

SKULL FRACTURES
Linear Skull Fractures
These occur in infancy with a diastasis (separation) of more than 3 mm

It causes a dural tear at the time of fracture and consequent brain injury
beneath the fracture.
Growing Skull Fractures
Enlargement of the fracture to form a cranial defect secondary to the

rapid increase in the brain growth (seen in infancy) is called as a growing
skull fracture or leptomeningeal cyst or posttraumatic meningocele
This prevents healing of the fracture margins
Seizures (often intractable), hemiparesis and psychomotor retardation may
occur
Treatment includes the reconstruction of dura and overlying skull and
excision of excessive scalp tissue.
CT Findings
Scan done months after the injury may demonstrate:

Unilateral ventricular enlargement
Shift towards the skull defect.
HERPES SIMPLEX VIRUS

ENCEPHALITIS
Herpes Simplex Virus
HSV is a double-stranded DNA virus which can infect the skin, central
nervous system and viscera
Prolonged seizures, refractory to anticonvulsants and status epilepticus are
often seen
The virus may remain latent in neuronal ganglia and may subsequently be
reactivated.
Note: The mucocutaneous lesions are not essential in HSV encephalitis.
HSV Encephalitis (Fig. 22.1)
Acyclovir is the specific antiviral drug used

The prognosis relies heavily upon the expediency of acyclovir initiation
Dose is 10 mg/kg every 8 hours (for a total of 30 mg/kg per day) for 14
days
For HIV+ patients, foscarnet is drug of choice
The CSF of HSV meningitis has decreased glucose
Hemorrhagic CSF may be seen but these CSF findings are not
pathognomonic of HSV encephalitis.
CT Scans 163
Fig 22.1: Herpes encephalitis
CT Findings (Fig. 22.1)
Areas of low absorption

Mass effect
Contrast enhancement in the temporoparietal regions of the brain on CT
Location: Inferior and medial regions of the temporal lobe and the orbital
gyri of the frontal lobes
Differential diagnosis:
Bacterial cerebritis with abscess formation.
TUBERCULAR MENINGITIS
CT Findings
Hydrocephalus with periventricular ooze due to basal exudates

Infarcts/cerebritis/calcifications/cerebral edema
Tuberculoma (Fig. 22.2)
Fig 22.2: Edema around the lesion (Tuberculoma)

BRAIN EDEMA
It may be of several types as given below:
Vasogenic Edema
This is extracellular edema around a focus, e.g. brain tumor, abscess, infarct,
hemorrhage. Treatment is dexamethasone and hypertonic solutions like
mannitol.
Cytotoxic Edema
This is cellular edema caused by cell damage, e.g. Hypoxia/asphyxia, water
intoxication, meningitis, encephalitis and Reyes syndrome.
Interstitial Edema
This is due to increased water and sodium in periventricular white matter, e.g.
due to obstructive hydrocephalus. Treatment is surgical shunting and
acetazolamide.
Osmotic Cerebral Edema
Normally cerebrospinal fluid (CSF) and extracellular fluid (ECF) osmolality

of the brain is only slightly greater than that of plasma
With excessive water intake, syndrome of inappropriate antidiuretic
hormone secretion (SIADH), hemodialysis, or rapid reduction of blood
glucose, the brain osmolality greatly exceeds that of serum. Hence, water
will flow into the brain from weaker to the stronger solution causing edema.
CT Findings (Figs 22.3A and B)
In early brain edema, there is decrease in the size of the third ventricle and
the basal cisterns
In frank cerebral edema, there is loss of the sulci, small lateral ventricles
and the brain matter appears hypodense.
B
Figs 22.3A and B: Brain edema
CT Scans 165
INTRACRANIAL HEMORRHAGES IN CHILDREN

ACUTE EPIDURAL HEMATOMA
Epidural hematoma is typically seen in a young child with head trauma

Hemorrhage is a result of a tear through a meningeal artery
The treatment for most epidural hematomas is neurosurgical evacuation
as it deteriorates rapidly.
CT Findings
The dura is closely applied to the inner table anchored at the suture lines
(so it does not cross sutures), distinguishing it from a subdural hematoma
As the hematoma from the bleeding expands, the dura bulges inward,
giving it the biconvex or lens-shaped appearance
They may extend across a venous sinus crossing the midline.
SUBDURAL HEMORRHAGE (FIG. 22.4A)
Subdural hematoma may be caused from direct trauma, severe accelerationdeceleration trauma or shaking injury
Venous bleeding occurs from cortical bridging veins
The location is mostly interhemispheric in children
The bleeding is not constrained by a tight dura and the clot has room to
expand
It is seen in older age group
There may be loss of consciousness with some recovery but not complete
return to normalcy
Signs and symptoms of a subdural hematoma in an infant may be like
meningitis
Skull fracture is found in only about third of cases
Intensive medical therapy is needed to control the increased intracranial
pressure or it may even need surgery.
CT Findings
Subdurals are crescent shaped, while epidurals are biconvex

Subdural hematomas do not cross the midline
As the hematoma ages, it becomes isodense with respect to the gray matter
(7th-21st day) and then hypodense.
SUBARACHNOID HEMORRHAGE (FIG. 22.4B)
Subarachnoid hemorrhage is the most common location for bleeding after

an acute head injury. Others causes are aneurysm, vascular malformation,
tumor and meningitis
Generally seen in a younger age group. Newborn intracranial hemorrhages
associated with birth trauma are most commonly subarachnoid
Figs 22.4A and B: Cross section of brain and skull showing

(A) Subdural hemorrhage; (B) Subarachnoid hemorrhage
These babies develop seizures after 48 hours of life

The treatment of subarachnoid hemorrhage is often medical, rather than
surgical.
CT Findings
The underlying cerebral cortex is usually of normal density with

subarachnoid bleed and the dense falx should be examined closely for a
scalloped appearance, as blood may accumulate in the cortical sulci
Subarachnoid hemorrhage may have pronounced cerebral edema
With cerebral edema, the brain is hypodense and the normal falx may
appear to have increased density.
INTRACEREBRAL HEMATOMAS
They are uncommon in children

Intraventricular hemorrhage usually due to rotational forces is caused by
rupture of subependymal veins.
CT Scans 167
SUMMARY
Acute hemorrhage < 2 days: CT investigation of choice

Chronic hemorrhage > 2 days: MRI investigation of choice
Extradural hemorrhage: Biconvex hyperdense (Arterial)
Subdural hemorrhage: Concavo-convex (Venous)
Contrast CT scan can be identified by the falxcerebri (White).
HYDROCEPHALUS
If the ratio of ventricle to parenchyma is more than 1:3, then suspect

hydrocephalus
If the line joining the anterior horns of lateral ventricles is more than half
of the same line touching the boundary of the skull, then it is hydrocephalus
Normally, the 4th ventricle is slit like round and small. It is enlarged along
with other ventricles in hydrocephalus (communicating).
BIBLIOGRAPHY
1. Amin MM, et al. Ionic and nonionic contrast mediac: Current status and controversies.
Appli Radiol 1993;22:41-54.
2. Beckett WW, Ball WS. Craniocerebral trauma. In: Ball WS (Ed). Pediatric
Neuroradiology. Lippincott-Raven, Philadelphia 1997;454-55.
3. David J Brenner, et al. Estimated Risks of Radiation- Induced Fatal Cancer from
Pediatric CT. AJR 2001;176:289-96.
4. Lende RA, Erickson TC. Growing skull fractures of childhood. Journal of Neurosurgery
1961;18:479-87.
5. Luerssen TG, Eisenberg HM, Levin HS. Late compli-cations of head injury. In:
Cheek WR (Ed). Pediatric Neurosurgery. WB Saunders Company, Philadelphia
1994;297-98.
6. Luerssen TG. Skull fractures after closed head injury. In: Albright AL, Pollack IF,
Adelson PD (Eds). Principles and Practice of Pediatric Neurosurgery. Thieme, New
York 1999;821-23.
7. Raffel L, Litofsky NS. Skull fractures. In: Cheek WR (Ed). Pediatric Neurosurgery.
WB Saunders Company, Philadelphia 1994;258.
8. Tomita T. Growing skull fractures of childhood. In: Wilkins RH, Rengachary SS (Eds).
Neurosurgery. McGraw Hill, New York 1996;2757-61.
9. Tyler KL. Aseptic Meningitis, Viral Encephalitis, and Prion Diseases. In: Fauci AS,
Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo
DL (Eds). Harrisons Principles of Internal Medicine, 14th edn. USA, McGraw-Hill
1998;2440-45.
Pedia Pearls: 1 CXR approximates the same risk as one year watching TV . Head CT is
approximately 20 CXR CT abdomen and pelvis is equivalent of 200 CXR.
23
Chest X-ray
(Classical Chest X-rays
and Newborn Chest X-rays)
Use the analytical method to interpret X-rays:

1. Physiology first, pathology later.
2. Probability of two common conditions together is greater than probability
of one rare condition.
FIRST OBSERVE THE FOLLOWING POINTS
View
PA film is ideal. P=posterior and A=anterior
Remember: Heart is enlarged on an AP film.
Exposure
In under penetrated film one will not be able to see the thoracic vertebrae.
Verify Right and Left
Look for the gastric bubble and R written on X-ray film. R stands for
right.
Rotation
Look whether the thoracic spine is in the center of the sternum and between
the clavicles. It is essential to evaluate the CXR for the presence of any rotation
because a rotated chest film can both mimic and obscure a mediastinal shift.
Phase of Inspiration
10 posterior or 6 anterior ribs are visible in good inspiration.
Chest X-ray 169

READ THE X-RAY IN THIS ORDER
A = Airway
These are the trachea and mainstem bronchi.
Look whether the trachea is in midline.
B = Bones
Look at structures of the chest (bony cage)

Look at the bones and joints for fractures, rachitic lesions, cervical ribs,
etc. Also, the bony thorax may show increased space between the ribs on
one side, indicative of emphysema or pneumothorax
Rib notching (due to enlarged collaterals) is unusual before 10 years of
age and affects the fourth to eighth ribs. If the coarctation is proximal to
subclavian artery, the notching is on the right side.
C = Chest Tissues (Lung Parenchyma)

Look for:
Infiltrates
Increased vascularity (plethora)
Increased interstitial markings or emphysema
Air bronchograms
Collapsed lung
Silhouette signs
A mass (Thymus, Lymphoma, Teratoma)
Congenital heart disease.
Opacities: They may be seen in miliary mottling, eosinophilia, loefflers,
hemosiderosis and histiocytosis
Callcified spots are seen in TB, hemosiderosis and fungal balls.
Round spots are seen TB, abscess, fungal balls, etc.
Air: Air in the chest does not always mean that it is a pneumothorax. An
intrapulmonary pneumatocele, cystic malformations of the lung, diaphragmatic
hernia at birth and congenital lobar emphysema resemble pneumothorax. If
chest tube thoracostomy is done in these cases, it will result in (pneumothorax).
Also, a decubitus film can demonstrate failure of the emphysematous lobe to
deflate when placed down in contrast to pneumothorax.
Cyst: Cyst in chest radiographs is either air filled, fluid filled or air and fluid
filled. An air filled cyst is called a pneumatocele. Fluid filled cysts appear like
solid masses. The presence of air-fluid levels on erect or decubitus films imply
tracheobronchial communication and/or active infection:
In lung abscess, the cavity is thick walled with ragged outline
In Bronchiectasis, there are fluid filled cavities (Honeycomb)
Pedia Pearl: Pneumatoceles are seen in staphylococcal pneumonia, tubercular
pneumonia and klebsiella pneumonia.
Fig. 23.1: Hilar prominence
Hilar region: Look for size and shape of aorta, hilar nodes, prominence of
hilar blood vessels and elevation of vessels (hilar prominence) (Fig. 23.1).
Blood flow: Pulmonary edema shows a bat wing appearance and Kerley B
lines. In pulmonary venous congestion, the margins of heart are hazy due to
congestion centrally, while plethora due to arterial hypertension or increased
flow shows vascular markings extending up to outer periphery of lung. A typical
example of plethoric lung fields is transposition of great vessels (see Fig. 8.1).
Lung volumes: An elevated hemidiaphragm implies small chest volume
(volume loss in that hemithorax) due to atelectasis, hypoplasia, a diaphragmatic
hernia, weak muscles or stiff lungs, e.g. HMD.
Check costophrenic angles for fluid or pleural scarring.
C = Cardiac Outline
Assess:
CT ratio
Size, shape
Calcified valves
Signs of heart failure and fluid overload
A uniformly large heart has a globoid shape because all of the chambers
are dilated, e.g. cardiomyopathy. However, physicians who suspect heart
failure in a patient should not conclude that it is not there if a chest
radiograph is negative.
Margins of the Heart Seen on X-ray
The chest X-ray can determine the heart size:
Right borderSVC and right atrium
Superior borderRight and left auricles
Left borderAorta, pulmonary artery and left ventricle
Inferior borderis mostly, the right ventricle.
Chest X-ray 171

D = Diaphragm
Check level of diaphragm for evaluation of emphysema, air under diaphragm,
eventeration or diaphragmatic hernia.
Look for tenting, free air and abnormal elevation. A compressed
hemidiaphragm implies emphysema of an adjacent lobe or tension
pneumothorax. An elevated hemidiaphragm implies volume loss in that
hemithorax due to atelectasis, hypoplasia or a diaphragmatic hernia.
Look at the costophrenic and costocardiac margins. In lateral films, follow
the right hemidiaphragm all the way from the costovertebral angle to where
the diaphragm meets the sternum; the left hemidiaphragm will be partially
obscured by the heart.
Costophrenic angle is obliterated in hydro pneumothorax, pleural effusion
(lateral edge higher than medial edge).
Note: Errors in film reading may occur due to skin fold projected over the
lungs which may camouflage, causing errors.
E = Evaluate
Evaluate:
For placement of tubes used for treatment, like catheters, chest tubes, etc.
For mediastinal shift
For coiling of NG tube in oesophageal atresia.
CARDIOMEGALY ON CHEST X-RAY (FIG. 23.2)
Causes
CCF secondary to volume or pressure overload due to rheumatic/valvular

heart disease/anemia, left to right shunts and hypertension
Cardiomyopathy, e.g. in endocrinopathies
Pericardial effusion secondary to infectious or inflammatory conditions
like tuberculosis
Mediastinal mass.
Fig. 23.2: Cardiomegaly

Check the Following Points
1. The Cardiothoracic Ratio
In an upright, posterioranterior view of chest, the cardiothoracic ratio is a
reliable indicator of cardiomegaly. It is the transverse cardiac diameter
horizontally (on each side through the widest part of the cardiac silhouette
from a vertical line drawn in the central part of spine) divided by the chest
diameter (measured at the widest part between the inner surface of the ribs).
Ratios of up to 0.55 are normal in children and up to 0.65 in neonates.
2. The Hilar Vessels
In pericardial effusion fluid accumulation in the pericardium appears flask
shaped and obscures the hilar vessels whereas in CHF, the vessels become
congested and appear more prominent than normal.
Also, a radiolucent area on the lateral chest film between the anterior surface
of the heart and that of retrosternal mediastinal fat, of greater than 1 to 2 mm
is an indicator of pericardial effusion.
3. Global or Local Dilatation
A family history of early CHF and premature sudden death may indicate
cardiomyopathy.
Note: There is global dilatation and not isolated chamber enlargement in
cardiomyopathy and myocarditis. Mediastinal mass also mimics cardiomegaly.
4. Aorta
It is located between the heart and spinal column. Esophagus is located
immediately posterior to it:
A prominent ascending and a small descending aorta with a notch in
between form a classic 3 sign in coarctation
A nasogastric tube in situ while taking X-rays helps to define relations.
5. Pulmonary Artery
This is seen as a convexity in pulmonary arterial hypertension and left to

right shunts
Pulmonary bay is seen in Tetralogy of fallots, due to undeveloped
pulmonary artery (Boot shaped heart)
Emboli from the heart may lodge at the bifurcation of the artery, as a saddle
embolus.
Chest X-ray 173
CLASSICAL X-RAYS
TENSION PNEUMOTHORAX (INFANT) (FIG. 23.3)
Clinical Features
Tension pneumothorax is the progressive build-up of air within the pleural
space, usually due to a lung laceration which allows air to escape into the
pleural space but not to return. Positive pressure ventilation may exacerbate
this one-way-valve effect. Progressive build-up of pressure in the pleural
space pushes the mediastinum to the opposite hemithorax, and obstructs venous
return to the heart. This leads to circulatory instability and may result in
traumatic arrest.
The classic signs of a tension pneumothorax are deviation of the trachea
away from the side with the tension, a hyper-expanded chest, an increased
percussion note and a hyper-expanded chest that moves little with respiration.
The central venous pressure is usually raised, but will be normal or low in
hypovolaemic states. Classic signs. Remember infants with tension
pneumothorax have small chest and a mobile mediastinum, so despite free
air, compression is on both lungs resulting in faint breath sounds and decreased
chest movement bilaterally, rather than the differential findings. Features of
tension pneumothorax like persistent hypoxia (hypotension and/or bradycardia)
may also be seen in severe emphysema of one or more lobes of the lung.
If an infant has a true tension pneumothorax, staphylococcal pneumonia
should be highly suspected. It is most common in the first six months of life
and often has an extremely rapid onset with fever, tachypnea and grunting.
Chest X-ray Findings
In pneumothorax the lung marking are absent in hyperlucent area. Visualize
lung markings and the lung edge within the hyperlucent space. Remember
that lung markings may be very faint
because the blood vessels are spread out
in emphysema.
In pneumomediastinum: There is
evidence of subcutaneous emphysema
in the neck on the PA view. Vertical air
densities seen closer to the lungs in a
pneumomediastinum on the PA view
(double outline of the tracheal air
column) is again suggestive of
pneumomediastinum.
Fig. 23.3: Tension pneumothorax

EMPHYSEMA
Hyperexpanded lung may even herniate into the opposite chest with
compression of the hemidiaphragm and wide-spreading of ribs and shift
of the mediastinum to the opposite chest
No infiltrates or fluid are seen
If emphysema is present in the lung, suspicion of a foreign body should
be very high.
FOREIGN BODY ASPIRATION (FIG. 23.4)

Clinical Features
Sudden noisy and abnormal breathing after a
choking episode, mild inspiratory stridor cyanosis,
choking and dyspnea and decreased or absent breath
sounds on one side. They are often misdiagnosed
as croup, asthma, pneumonia or bronchitis because
features like coughing, wheezing, stridor,
tachypnea, retractions, rales, and fever are present
in all. It is often seen in toddlers.
Fig. 23.4: Foreign body

aspiration-left side
The expiratory view of a child with a foreign body on one side shows air
trapping with some hyperexpansion on that side. Normally in the expiratory
view, both lung volumes should normally be decreased
Unilateral expansion during expiration, indicates air trapping and a possible
foreign body on the other side
In bilateral air trapping, consider asthma but do not rule out a foreign
body. Another finding is that differential inflation of the affected lung is
most common abnormality seen in lateral decubitus view
Normal lung should appear smaller in the dependent position
Remember: Many children with retained airway foreign bodies have
nondiagnostic films.
CROUP
Clinical Features
They are fever, noisy breathing, a harsh croupy cough and inspiratory stridor
in viral croup and associated drooling in epiglottitis.
Viral croup have a mild degree of subglottic airway narrowing Steeple sign
The epiglottis is thumb-like in appearance (instead of triangular) in
epiglottitis.
Pedia Pearl: Reticulogranular densities are seen in meconium aspiration syndrome,
hyaline membrane disease pulmonary edema and congenital pneumonia.
Chest X-ray 175
CHEST X-RAYS OF A NEWBORN

NORMAL CHEST FILM OF A NEWBORN
On normal AP chest film, the dome of diaphragm is at the level of the sixth rib
anteriorly and the eighth rib posteriorly. The cardiothoracic ratio of newborns
is normal up to 0.65, beyond which it is termed cardiomegaly.
The thymic shadow is seen in anterosuperior mediastinum overlapping
the aorta and pulmonary arteries of newborns. Inferior border of the thymus
blends with the cardiac borders or may produce an acute angle called sail
sign (Fig. 23.5). Occasionally, this sail sign may be misinterpreted as right
upper lobe pneumonia because of rotation.
NEONATAL PNEUMONIA
Group B Streptococcus, gram-negative rods (usually E. coli) and Listeria
monocytogenes commonly cause newborn pneumonia. A term infant with
respiratory distress should be considered to have pneumonia until proven
otherwise. They may have either leukocytosis or leukopenia with band forms
of >20 percent of the total neutrophils suggestive of infection, as are
neutrophilic vacuoles and toxic granulation. Treatment with an aminoglycoside
and penicillin is the standard to treat the common organisms. Supportive care
may include mechanical ventilation, supplemental oxygen, inotropic agents
for hypotension and nitric oxide for infection asso-ciated pulmonary
hypertension.
Reticulogranular densities as seen in chest films of neonatal pneumonia

due to Streptococcus, Staphylococcus aureus and Escherichia coli
In most patients patchy, lung opacities and hyperaeration are seen (pleural
effusion may also be seen)
In some patients multilobar, consolidation occurs.
Fig. 23.5: Sail sign of thymus

MECONIUM ASPIRATION SYNDROME
This occurs more often in postmature (>42 weeks gestation) neonates as they
pass meconium into the amniotic fluid due to stress in utero and then inhale it
into the upper airways. The meconium may cause complete or partial occlusion
of airways with a ball valve effect causing collapse or hyperinflation, distal to
the occlusion, respectively. Thorough suctioning of the oropharynx with a
large bore catheter upon the delivery of the head is typically performed by the
obstetrician. Also intubate on and suction of the trachea of any infant with
meconium in the amniotic fluid, is recommended if the infant is depressed.
Mild cases show over aeration with small patchy opacification

Severe cases show over aeration with atelectasis. Pneumothorax and
pneumomediastinum may also occur because of vigorous resuscitation.
HYALINE MEMBRANE DISEASE (FIG. 23.6)

It occurs in premature infants and also infants of diabetic mothers due to
deficiency of pulmonary surfactant. They have progressively more severe
respiratory distress after birth with cyanosis, grunting, nasal flaring, intercostal
and subcostal retractions and tachypnea. As the alveolus is compressed the
pressure within the alveolus increases, the gas under this pressure is forced out
of the alveolus to an adjacent larger alveolus with a larger radius, ultimately
collapsing the smaller alveolus. Grunting is the infants attempt to maintain the
pressures by causing expiratory stop, using the closed glottis during exhalation
(to maintain alveolar distending pressure during exhalation). The surfactant
decreases alveolar surface tension. Hence, the treatment includes positive
pressure ventilation and artificial surfactant replacement and continuous positive
airway pressure (CPAP) therapy, as needed.
Fig. 23.6: Hyaline membrane disease showing ground

glass appearance with air bronchogram
Chest X-ray 177

Network of air-filled alveoli juxtaposed to atelectatic alveoli creates ground

glass appearance of the lung parenchyma and air bronchograms are seen,
extending peripherally
Later, white out lung may be seen.
TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)

In TTN symptoms occur soon after birth. The pathophysiological mechanism
is the delayed resorption of fetal lung fluid which eventually clears over the
next several hours to days.
Normally lung fluid is expelled through the bronchi squeezed during a vaginal
delivery and absorbed through lymphatics and capillaries but in cesarean section,
precipitous delivery and very small infants the squeeze may not occur. So
respiratory distress occurs due to fluid in alveoli. It usually subsides by three
days of age. Close observation and supplemental oxygen may be necessary.
In transient tachypnea of the newborn (TTN) radiographs reveal:
Hyperinflation (emphysematous lung) and mostly clear lung parenchyma,
except for perihilar linear densities, symmetric streaky opacities and fluid
in the fissures
At times pleural effusion and areas of consolidation are seen.
DIAPHRAGMATIC HERNIA (FIG. 23.7)
This occurs when visceral organs (stomach, bowel, even spleen or the liver)
go through the opening created by defective fusion of pleuroperitoneal canals
during embryogenesis and put pressure on lungs causing pulmonary hypoplasia.
Fig. 23.7: Left sided diaphragmatic hernia

Bochdalek (left posterolateral) hernia is more common while retrosternal
morgagni hernia is less common. It presents with severe respiratory distress
(immediately after birth) with a scaphoid abdomen. High frequency ventilation,
nitric oxide therapy and extracorporeal membrane oxygenation (ECMO)
therapy is used to treat the bilateral hypoplastic lungs. The hypoplastic lungs
develop excessive and abnormal musculature of the pulmonary vessels which
lead to pulmonary hypertension.
Abdomen is usually devoid of the bowel gas

Gas-filled loops of bowel are seen in the hemithorax
The mediastinum is displaced to the other side Pulmonary artery may be
prominent
Both diaphragm are pushed down.
PNEUMOTHORAX (NEWBORN) (FIG. 23.8)

It occurs when air leaks from inside of the lung to the space between the lung
and the chest wall. The lung then collapses. The dark side of the chest (right
side of the picture) is filled with air that is outside the lung tissue in the pleural
space.
First assess rotation. With rotation clavicles may be at different level and/or
the ribs on each side may have unequal lengths. (Rotation can obscure a
pneumothorax and mimic a mediastinal shift).
A skin fold can be mistaken for a pneumothorax. Complete collapse of the
lung towards the hila is surely a pneumothorax.
Also there is deep lateral costophrenic angle as air rises to this area in supine
X-rays.
Fig. 23.8: Right side pneumothorax showing collapse of lung towards hilum
Chest X-ray 179

Due to air in the pleural cavity, there is increased rib separation, diaphragmatic depression with contralateral deviation of mediastinal structures.
CONGENITAL LOBAR EMPHYSEMA
Here, there is hyperdistended and hyperlucent lung, on one side and shift of
the mediastinum (causing atelectasis) and herniation of the emphysematous
lung to the other side. Lung markings are visible in the hyperlucent areas.
SUMMARY
RDS: Prematurity CXR: Ground glass appearance, air bronchogram
TTN: Short labor, C-section delivery.... CXR: Fluid in the fissures, central/
perihilar congestion.
Meconium aspiration: Meconium in amniotic fluid CXR: Infiltrates
Pneumonia: Prolonged rupture of membranes, maternal GBS, prematurity.
CXR: Infiltrates or hazy lungs (may be identical to RDS)
Pneumothorax: Sudden deterioration, often while on positive pressure
ventilation CXR: Collapsed lung, free air in the hemithorax.
BIBLIOGRAPHY
1. Donnelly LF, Frush DP. Localized radiolucent chest lesions in neonates: Causes and
differentiation. AJR 1999;172:1651-8.
2. Frishman WH. Cardiomegaly on chest X-ray: Prognostic implications from a tenyear cohort study of elderly subjects: A report from the Bronx Longitudinal Aging
Study. Am Heart J 1992;124:1026-30.
3. Gibson AT, Steiner GM. Imaging of the neonatal chest. Clin Radiol 1997;52:172-86.
4. Hedlund GL, Griscom NT, Cleveland RH, Kirks DR. Respiratory system. In: Kirks
DR, Griscom NT, (Eds). Practical pediatric imaging: Diagnostic radiology of infants
and children. Philadelphia: Lippincott-Raven 1998;3:667-715.
5. Hedlund GL, Griscom NT, Cleveland RH, Kirks DR. Respiratory system. In: Kirks
DR,Griscom NT, (Eds). Practical pediatric imaging: Diagnostic radiology of infants
and children. Philadelphia: Lippincott-Raven 1998;3:690-3.
6. Leonidas JC, Berdon W. The neonatal chest. In: Silverman FN, Kuhn JP, (Eds). Caffey's
pediatric X-ray diagnosis: An integrated imaging approach. Mosby: St. Louis
1993;9:2002-7.
7. Mandell GA. Imaging evaluation of the neonate. In: Goodman LR, Putman CE, (Eds).
Critical care imaging. Philadelphia: WB Saunders 1992;3:416-8.
8. Mandell GA. Imaging evaluation of the neonate. In: Goodman LR, Putman CE, (Eds).
Critical care imaging. Philadelphia: WB Saunders 1992;3:443-4.
9. Swischuk LE. Respiratory system. In: Imaging of the newborn, infant, and young
child. Baltimore: Williams and Wilkins 1997;4:28-36.
24
Abdominal X-rays
INTRODUCTION
An erect abdominal X-ray is ideal for visualization of calcification, calculi
and air-fluid levels (in obstruction). Also, shades of black and white provide
valuable clues, e.g. black for gas, white for calcified structures, grey for soft
tissues, dark grey for fat and metallic foreign objects like, coins, etc. as bright
white. Also, look for fractures spine, etc.
CALCIFICATIONS
Calcium appears as a white radiopaque substance on X-ray (artefacts look
similar). Calcified mesenteric lymph nodes can be confused with small kidney
stones. Blood vessels (Chiefly the aortoiliac and splanchnic arteries pelvic
vein) may show clots. Phleboliths may be difficult to differentiate from small
ureteric stones.
SITES OF CALCIFICATION
Pancreatic Calcification
Located at region of T9-T12 vertebrae. Calcification of the pancreas is usually
found in chronic pancreatitis.
Biliary Calcification
Calculi are seen in the right upper quadrant of the radiograph.
Renal Calcification
Located between the T12-L2 vertebral region. Calcification may be seen as
staghorn calculus.
Pedia Pearls:
Fluid - Hazy appearance of the entire abdomen is seen in ascites
Gas - Mottled lucencies due to gas trapped in meconeum is seen in meconeum ileus.
Abdominal X-rays 181

Ureteric Calcification
Ureteral stonescalcification is seen along the line of the transverse processes
of the vertebral bodies across the sacroiliac joint to the level of the ischial
spine. They obstruct at some favored locations, which include the pelviureteric/
vesicoureteric junctions and brim of the pelvis. (IVP or computed tomography
may confirm their presence).
TYPES OF CALCULI
Renal Stones
Calcium stones: They form majority of renal stones.
Struvite stones: (magnesium ammonium phosphate). They occur due to chronic
UTIs (gram-negative bacteria). They sometimes fill the renal pelvis and calyces
to produce a staghorn calculi.
Uric acid stones: These are radiolucent, but if they complex with calcium
they become radiopaque. Cystine stones are less radiopaque.
The renal stones move and subsequently they may lodge at three sites:
The ureteropelvic junction, the point at which the ureter crosses the iliac vessels,
and the ureterovesical junction. Conservative approach is tried (6 weeks) to
let the stones pass out spontaneously.
Appendicular Stones
Appendicolith is an appendicular calculi.
Bladder Stones
Bladder stones are usually quite large and often, multiple. Tooth shape tumor
in the bladder area suggests a teratoma.
BONE AND SOFT TISSUES
Bone
In ankylosing spondylitis (bamboo spine), there is evidence of syndesmophyte
formation and calcification of the longitudinal spine ligaments.
Fractures: Abnormalities like vertebral, pelvic and rib fractures are self
explanatory. Generalized osteoporosis is seen as osteopenia.
Soft Tissues
Solid organs, such as the kidneys liver and spleen can be observed on Xrays
On observing organs a fatty rim (properitoneal fat lines) surrounds them.
In fact, the loss of these fat planes may indicate peritonitis
Look at the size and position of the liver and spleen

Kidneys are lateral to the midline in the region of T12
T12-L2 vertebrae outline the psoas muscle shadow(s)
Loss of the psoas muscle shadows may indicate intraperitoneal disease
while prominent psoas shadow may be seen after psoas bleed in hemophilia
Finally, try to identify the outline of the bladder, seen more clearly if full,
within the pelvis
The appearance of what looks like a soft tissue mass in the region of the
stomach is gastric fluid within the fundus.
GAS
Intraluminal Gas
On the erect X-ray, the gastric gas bubble seen in the left upper quadrant of the
film is a normal finding. This can make visibility of free air on this side
problematic. For this reason right side is favored to look for crescentic appearance
of free gas.
Gas is also normally seen within the large bowel, most notably the
transverse colon and rectum. Sometimes gas filled transverse colon looks like
free gas under the diaphragm. Large bowel should lie at the periphery of the
film with small bowel distributed centrally. Fecal matter in the bowel gives a
mottled appearance, representing a gas-liquid-solid mixture.
Within the Bowel Wall (Intramural Gas)
This is the gas within the bowel wall when gas has escaped from the lumen of
the gastrointestinal tract but remains within the bowel wall. It occurs in
necrotizing enterocolitis. Sometimes, there is a fatal migration of gas to the
portal vein in NEC.
Extraluminal Gas
Usually air under the right diaphragm is seen, indicating pneumoperitoneum
on erect view. It is a supine abdominal radiograph is the only film available,
the falciform ligament sign should be seen. Here, free air outlines the
falciform ligament which is identified as a thin straight line starting in the
right upper quadrant, and ending at or near the region of the umbilicus.
AIR FLUID LEVELS
They may be seen in following conditions:
Intussusception
Consider the diagnosis of intussusception in all cases of bloody diarrhea and
presenting with the clinical features of intermittent crampy abdominal pain,
Pedia Pearl: Intussusception - on barium swallow appears as coiled spring appearance
Abdominal X-rays 183

emesis and bleeding from the mucosa due bowel ischemia and infarction.
Currant jelly stools may occur resembling blood mixed with stool as in
dysentery. After 6 to 12 hours of symptoms, air fluid levels are seen due to
bowel obstruction. However, plain abdominal films may be normal and cannot
be used to rule out intussusception. Sometimes the target sign, the crescent
sign and the absent liver edge sign may be seen.
Worms in the GIT
A bag of worms may sometimes appear as an air fluid level on X-ray.
Subphrenic Abscess
It appears as air fluid level below the diaphragm.
ANORECTAL MALFORMATIONS
An invertogram is a lateral abdominal film done after 17 to 18 hours. of life.
The baby is positioned upside down so that the air ascends towards rectum.
A marker is kept at the anal dimple. If the distance from the marker is > 1.5
cm, it is suggestive of a high anomaly.
BIBLIOGRAPHY
1. Buonomo C, Taylor GA, Share JC, Kirks DR. Gastrointestinal tract. In: Kirks DR,
(Eds). Practical pediatric imaging: Diagnostic radiology of infants and children 3rd
edn. Philadelphia, Pa: Lippincott-Raven, 1998;890-3.
2. Cho KC, Baker SR. Extraluminal air diagnosis and significance. Radiol Clin North
Am 1994;32:829-3.
3. Ehel KD, Blickman H, Willich E, Richter E, (Eds). Differential diagnosis in pediatrics
radiology New York, NY: Thieme, 1999;289-90.
4. Eisenberg RL, Heineken P, Hedgcock MW, et al. Evaluation of plain abdominal
radiographs in the diagnosis of abdominal pain. Ann Intern Med 1982;97:257-61.
5. Hart D, Wall BF. Radiation exposure of the UK population from medical and dental
X-ray examinations. Didcot: National Radiological Protection Board, 2002.
6. Lee JB, Ahmad S, Gale CP. Detection of coins ingested by children using a handheld
metal detector: A systematic review. Emerg Med J 2005;22839-44.
7. Levine JA, Neitlich J, Verga M, et al. Ureteral calculi in patients with flank pain:
Correlation of plain radiography with unenhanced helical CT. Radiology
1997;204:27-31.
8. Levine MS, Scheiner JD, Rubesin SE, Laufer I, Herlinger H. Diagnosis of
pneumoperitoneum on supine abdominal radiographs. AJR Am J Roentgenol
1991;156:731-5.
9. Miller RE. Perforated viscus in infants: A new toentgen sign. Radiology
1960;74:65-7.
10. Mulligan ME. Classic radiologic signs an atlas and history New York, NY:Parthenon,
1996.
11. Pochaczevsky R, Bryk D. New roentgenographic signs of neonatal gastric perforation.
Radiology 1972;102:145-7.

12. Rice RP, Thompsib WM, Gedaudes RK. The diagnosis and significance of extraluminal
gas in the abdomen. Radiol clin North Am 1982;20:819-37.
13. Rothrock SG, Green SM, Hummel CB. Plain abdominal radiolography in the
detection of major disease in children: A prospective analysis. Ann Emerg Med
1992;21:1423-9.
14. Thompson WM, Kilani RK, Smith BB, et al. Accuracy of abdominal radiography
in acute small-bowel obstruction: A prospective analysis. Ann Emerg Med
1992;21:1423-9.
15. Turkyilmaz Z, Sonmez K, Konus O, et al. Ureteral calculi in patients with flank
pain: Correlation of plain radiography with unenhanced helical CT. Radiology
1997;204:27-31.
16. Weiner CI, Diaconis JN, Dennis JM. The Inverted V: A new sign of
pneumoperitoneum. Radiology 1973; Richardson WR. Diagnosing surgical
emergencies on the day of birth. Am J Dis Child 1961;102:134-50.
17. Mettler FA. Gastrointestinal system. In: Mentler FA. (Ed). Essential of Radiology.
2nd edn. Philadelphia, Pa: Saunders Elsevier; 2005.
25
Bone X-rays
INTRODUCTION
They may detect fractures, tumors, or degenerative conditions of the bone
and also used to assess bone age, etc.
BONE AGE: USES (MNEMONIC ABCD)
Adult height prediction

Basal blood hormone levels can be interpreted better at puberty. They
should be evaluated according to bone age rather than chronological age
because bone age is the actual biological age
Constitutional growth delay (delayed bone age) can be differentiated from
familial short stature (normal skeletal maturation) (Fig. 25.1)
Dwarfism with either advanced puberty or hypogonadism can be treated
better as bone X-ray can decide the right time to treat and predict the
response to therapy.
Fig. 25.1: Delayed bone age (bone age 2-3 years but chronological age 7 years)

OTHER USES OF X-RAY OF BONES
To pick catch-up growth: Transverse Harris growth lines of high radiodensity
are seen in an over-stimulated child, e.g. on initiation of thyroid replacement
therapy in a hypothyroid child.
To identify a disease state: For example
Look for wide and short bones in hypochondroplasia
Irregular metaphyses in Turners syndrome
Splaying and fraying at metaphysis, in rickets
Thin bones, multiple fractures in Osteogenesis Imperfecta
Normal bones, multiple fractures (commonly ribs) in Battered Baby
Syndrome
Bone in bone appearance of vertebra seen due to high density of bone in
Osteopetrosis.
BONE AGE ASSESSMENT
The appearance of the various ossification centers and their consequent fusion
usually occurs in well defined timed pattern. This process valuable in estimating
the skeletal maturity is called bone age. In normal health, there is no difference
between childs real age and the bone age because growth, puberty and related
endocrine changes follow a pattern reflecting physical maturity.
Two methods are in vogue:
a. Greulich-Pyle Atlas method (GP method) and
b. Tanner-Whitehouse 2 Individual method.
RADIOGRAPHIC EXAMINATION FOR BONE AGE ESTIMATION
The determination of bone age by radiographic examination of the

ossification centers is independent of the chronological age
The X-ray of knee is usually taken at birth to look for evidence of lower
femoral or upper tibial epiphysis, while in the first year; X-ray of the
shoulder may be more useful
Later, X-ray of the wrist is used to calculate the bone age
At puberty, X-ray of the elbows are useful.
The rough formula for calculating the bone age is: (number of carpal
bones +1) for boys before puberty and equal to the number of carpal bones in
case of girls.
Pedia Pearls:
Aplastic anemia occurs due to absent medullary cavity in osteopetrosis.
In scurvy, the knee joint X-ray shows pencil thin cortex, ground glass shaft,
calcified subperiosteal bleed, a white line of frenkel in the zone of preparatory
calcification with rarefaction below it.
Bone X-rays 187

WRIST X-RAY
Introduction
They are useful to diagnose growth disorders, endocrine disorders, pediatric
syndromes and for the prediction of final adult height. Each bone cartilage is
ossified from the primary center in the middle of the bone, which becomes
the diaphysis even before birth, e.g. carpal bones ossify entirely from this
primary center. Long bones are also ossified from a secondary center at the
end of bone which becomes the epiphysis. Most of the epiphyses are not
ossified at birth, e.g. distal femoral epiphysis starts to ossify in last trimester
and proximal epiphysis of the humerus, even later in last week. Hence, any
damage before birth causes shortening of the diaphysis while growth arrest
later affects epiphyseal maturation.
In the wrist, the ossification center appears in the usual sequence as follows:
Capitate (1), then hamate (2), triquetral (3), lunate (4), trapezium (5), trapezoid
(6), navicular or scaphoid (7) and pisiform (8). The distal epiphysis of the
radius ossifies before the triquetum and that of the ulna before the pisiform.
Rickets (Fig. 25.2)
X-ray of wrist is useful in rickets as it is a disease of growing end of bones:
Anteroposterior and lateral radiographs of the wrist of rickets demonstrate:
Cupping
Splaying
Fraying (Irregular moth eaten appearance) of the metaphyseal region
with epiphyseal widening.
In healing rickets, the zones of provisional calcification shows white line
of healing
Radiolucent transverse bands are seen at diaphysis after four weeks of
treatment with vitamin D.
Fig. 25.2: Wrist X-ray (cupping, fraying) in rickets

Where and When to Focus Our Attention
Focus on the carpal bones and radial epiphyses in Infancy

Epiphyses is visible in the phalanges of the hand (proximal then distal) in
Toddlers except distal phalanx of the thumb
Later at Prepuberty and Pubertal stage focus on width of the phalangeal
epiphyses and look for epiphyseal fusion towards the end stage of puberty
During postpuberty assess the degree of epiphyseal fusion of the radius
and ulna.
ELBOW X-RAY
There are six ossification centers around the elbow joint appearing in a specific
sequence at different ages and they all fuse to the adjacent bones at various
ages.
The order of appearance of individual ossification centers seen with elbows
in supination is capitellum, radial head, internal (medial) epicondyle, trochlea,
olecranon, external (lateral) epicondyle. In the same order, the rough ages for
appearance are 1-3-5-7-9-11 years, respectively. Knowing the sequence is
helpful in determining whether a small piece of bone about the elbow joint
represents a fractured fragment or an ossification center, because the
ossification centers always appear in this order specified above.
Example: If you see only three accessory bony fragments about an elbow
joint, these bony pieces should be in the areas of the capitellum, radial head
and the internal (medial) epicondyle. If one of the three bony fragments is in
the area where you would expect to see the external epicondyle, then that
piece actually represents an avulsion fracture of the distal, lateral humerus,
rather than a normal external epicondyle.
X-RAY LONG BONES
In congenital syphilis one can see:
Periostitis - reaction to granulation tissue
Metaphysitis- white callus
Osteitis-erosion of tibia
Osteomyelitis.
BIBLIOGRAPHY
1. Do TT. Clinical and radiographic evaluation of bowledge. Curr Opin Pediatr.
2001;13(1)42-6.
2. Green M. Pediatrics diagnosis. (Ed 6) Philadelphia WB Saunders, 1998, p. 276.
3. Greenfield GB. Radiology bone disease. (Ed 5) Philadelphia: Lippincott, 1990.
4. Greulich WW, Pyle SI. Radiographic atlas of skeletal development of hand and wrist.
Stanford, CA: Stanford University Press, 1959.
Bone X-rays 189

5. Hochberg Z. Endocrine control of skeletal maturation. Basel: Karger, 2002.
6. Kottamasu SR. Metabolic Bone Diseases. In: Kuhn JP, Slovis TL, Halle JO, (Eds).
Caffey's Pediatric Diagnosing Imaging. 10th edn. Philadelphia, Pa: Mosby;2004:
2242-53.
7. Poznanski AK. The Hand in Radiologic Diagnosis. (Ed 2) Philadelphia: WB Saunders,
1984.
8. Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. Hosp Med.
1998;59(5):399.
9. Rieth KG, et al. CT of cerebral abnormalities in precocious puberty. AJR
1987;148:1231-8.
10. Stephen Chapman, Richard Nakielny. Aids to Radiological Differential Diagnosis
(Eds). 4th edn, 2003.
11. Taybi H, Lackman RS. Radiology of syndromes, Metabolic Disorders, and Skeletal
Dysplasias. (Ed 4) St. Louis: Mosby-Year Book, Inc, 1996,p.1052.
12. Taybi H, Lackman RS. Radiology of syndromes, Metabolic Disorders, and Skeletal
Dysplasias. (Ed 4) St. Louis: Mosby-Year Book, Inc, 1996,p.1053.
13. Wagner CL, Greer FR. Prevention of rickets, osteomalacia and hyperparathyroidis.
Hosp Med. 1998;59(5):399.
14. Yasuda T [Rickets]. Clin Calcium. 2009;19(1):109-16.
26
Skull X-rays/Spine X-rays
SKULL X-RAYS
INDICATIONS
Following Trauma
After a head injury (mnemonic is SCALP)
S = Significant or due to unknown mechanism of the injury
C = Consciousness loss and/or memory loss
A = Age under 5 years
L = Laceration (full thickness), hematoma or palpable vault abnormality
which feels bony
P = Puked or vomited, recently
To Aid in Diagnosis
Chronic headache
Seizure disorder
Ear problems
Sinus disease
Intracranial SOL
Pituitary problems
Craniosynostosis
For tumors and raised ICT (Silver beaten appearance, Fig. 26.1)
For bone lesions
For soft tissue calcifications.
VIEWS (FIG. 26.2)

They include Waters view, AP view, a Townes view, and two lateral views.
However, each X-ray film taken must have justification as radiation is involved.
An X-ray is a negative image. Hence, dense bone looks whiter because it
blocks more beams (radiopaque). Passage through soft tissue is easier and
easiest through air hence produce radiolucent air shadows. Thin parietal
bone, on a lateral X-ray, records a darker gray image compared to the edge of
Skull X-rays/Spine X-rays 191
Fig. 26.1: Silver beaten appearance (sutural separation, lacunae, erosion of posterior
clinoid process can also be seen in raised intracranial tension)
Fig. 26.2: Skull X-ray lateral view (with labels)
the skull which is brighter. Increasing the volume lowers the density and
hence, the tissue within the skull will be darker gray than the normal tissue in
raised ICT.
NOTE THE FOLLOWING POINTS ON
SKULL X-RAYS (TEN POINTS)
1. Clarity
Sites closer to the film display greater clarity in the image compared to those
away. On the AP X-ray, fractures in the occipital bone, are clearer.
2. Size
Take head circumference especially in dysmorphic and retarded children.

Small Head
Microcephaly means that the occipitofrontal head circumference is more than
2 standard deviations (3 standard deviations by some authorities) below the
normal (mean) for age, sex, race, and gestation. Normally, microcephaly is
known to have a heterogeneous etiology with environmental and genetic causes.
Primary microcephaly (microcephaly vera) (genetic disease) is an autosomal
recessive trait with absence of associated malformations and of secondary
or environmental causes. Here, the brain weight may be less but the gyral
pattern is normal.
Rule out other causes of microcephaly like.
Craniosynostosis
Malformation syndromes (e.g. chromosome abnormalities like cri-duchat syndrome, trisomy 18 (Edwards syndrome), trisomy 13 (Patau
syndrome)
Secondary microcephaly is secondary to various causes
o Birth asphyxia
o Radiation
o Intrauterine infections such as with rubella, cytomegalovirus (CMV)
and toxoplasmosis
o Maternal PKU and medications.
Large Head
This is commonly seen in:
Skeletal disorders: Pyknodysostosis, Cleidocranial dysostosis, Hurlers
syndrome, Rickets, Achondroplasia and Hydrocephalus.
3. Shape
It is decided by timing of closure of various sutures of the calvarium.
Craniosynostosis often causes abnormal shape and needs to be corrected by
surgery, so that the brain can grow and develop.
4. Fontanelles
Skull radiographs in infants can have many normal lucencies due to tontaneller
and sutures. For example the anterior fontanelle is often visible. Metopic suture
extends from the anterior tip of the anterior fontanelle into the frontal bone.
5. Skull Sutures
Normally, the sutures are wavy and located in their anatomic locations
(coronal, sagittal, and lambdoidal)
In increased intracranial pressure progression of sutural diastasis or sutural
separation
Premature fusion called craniosynostosis is seen as:

Parasutural sclerosis
Bony ridging
Increased convolutional markings.
Asymmetric head
Specific sutures are not visible or are sclerosed earlier than expected.
Primary Craniosynostosis
In primary craniosynostosis, the problem is primarily in mesenchymal layer
ossification itself where skull bone sutures or multiple sutures fuse and get
ridged prematurely. If it occurs very early, while the brain is still increasing in
size, the intracranial pressure can increase, especially if multiple sutures are
involved, e.g. craniofacial abnormalities like Crouzon, Apert, Chotzen, Pfeiffer,
or Carpenter syndromes which may be evident at birth.
Examples of craniosynostosis and the suture which closes prematurely are given
below:
Scaphocephalysagittal suture (commonest)
Anterior plagiocephaly1 coronal suture
Brachycephalybilateral coronal suture fusion (mostly syndromic like in
Down)
Posterior plagiocephaly1 lambdoid suture (which resembles a
parallelogram)
Trigonocephalymetopic suture.
Secondary craniosynostosis is more common: Here, the problem is in the brain
and not in the bone. Here, there is an underlying hypoplasia of the cerebral
cortex rather than abnormal development of the overlying skull and there is no
major abnormality in cortical architecture. So, bony plates do not spread at
sutures. Intracranial pressure is usually normal. Hence, surgery is not needed
urgently and conservative approach is taken.
Systemic disorders also may cause craniosynostosis, e.g. rickets and
hypercalcemia renal osteodystrophy, hyperthyroidism sickle cell disease and
thalassemia.
6. Intrasutural Bones
Wormian bones are intrasutural bones and are a normal variant. Differential
diagnosis includes osteogenesis imperfecta, cleidocranial dysostosis,
hypophosphatasia and hypothyroidism.
7. Fractures
Skull X-ray may be done after trauma if CT scanning is not possible. A

normal skull X-ray may give a false sense of security in intracranial injury
Fractures are not wavy (usually linear, stellate, or depressed)
Many linear skull fractures require usually no intervention

Parietal skull fractures may be associated intracranial hemorrhage for which
CT scan is better as diagnostic tool
Plain X-ray skull radiographs are not reliable in ruling out a basilar skull
fracture
Follow-up radiograph, one month later may show a growing fracture
that results from a meningeal tear.
8. Skull Density
Focal/lytic density is suggestive of conditions like eosinophilic granuloma

and Langerhans cell histiocytosis (Fig. 26.3)
Calvarial vault crew-cut appearance is seen in a hematopoietic disorder like
thalassemia. Here, the vertical ossification produces hair-on-end appearance
Also, chronic therapy with phenytoin produces vault thickening
Osteopetrosis shows a marked increase in bone density (phantom skull)
Silver beaten appearance is seen in raised ICT.
9. Intracranial Calcification
Brain calcification: They are seen in tuberous sclerosis, sturge weber and
hypoparathyroidism.
Diffuse calcification is seen in toxoplasmosis
Periventricular calcification is seen in CMV
Calcification in sella turcica region in craniopharyngioma
Basal calcification is seen in tuberculosis.
10. Sella Turcica
Sella turcica is small in Down and Prader-Willi syndrome. It may be enlarged
and shallow in pituitary lesions and in raised ICT, the effacement of clinoid
process may be seen.
Various important types include the J shaped shallow pituitary fossa and
the flask-shaped variety. The normal variant includes the omega shaped
sella turcica.
Fig. 26.3: Focal/lytic density (Lacunar skull)
Pedia Pearl: Hair-on-end appearance thinning of bone cortices, wide diploic spaces
are also seen in sickle cell disease and hereditary spherocytosis.
SPINE X-RAYS
NOTE THE FOLLOWING POINTS ON SPINE X-RAYS
Effect of Age
Normal neonatal spine shows bone-within-bone picture. Fusion is
neurocentral and synchondroses occurs by 3 to 6 years. Ring apophyses
appear by 6 years and fusion occurs by 18 years.
Birth Trauma Causing Spinal Injury
Spine (on conventional imaging) often appears normal in injury. During delivery
by cephalic presentationupper cervical injury is common while during breech
presentation cervicothoracic injury is more likely. Severity ranges from
extradural hematoma to complete cord transection. However, X-rays cannot
pick these changes, easily.
Dysmorphisms
Mucopolysaccharidosis may show anterior beaking of vertebrae (see Fig.

54.2)
In Klippel-Feil or Sprengels deformity or winging of scapula, most
commonly fusion of cervical segments and associated genitourinary
anomalies are seen.
Infections
Osteomyelitis by Staphylococcus aureus and in sickle cell anemia due to
Salmonella, affects endplate vascular territories and cause progression to
discitis. Typical changes of osteomyelitis may be picked up on X-rays.
Developmental Defects
a. Split Notochord Syndrome
Extensive splitting of vertebral body, anterior and posterior defects are
associated with neurenteric fistulas.
b. Sacral Agenesis
The sacrum is formed by five vertebrae just above the coccyx. Sacral
agenesis occurs due to problems in third to seventh week of pregnancy
(especially insufficient amount of folic acid may play a part). Sacral agenesis
and maternal diabetes, orthopedic anomalies, skin defects and anorectal/
tracheoesophageal anomalies are commonly correlated. It may affect the
nerves to bowel and the anal sphincters leading to constipation and/or the
bladder and the bladder sphincters leading to, incontinence, urinary tract
infections (neuropathic bladder) and/or lower limbs muscles paralysis.
Many children have persistent dribbling of urine. Even kidney damage is

possible secondary to vesicoureteric reflux and infections of urinary tract.
Tethered cord is another complication. Prenatal diagnosis is possible in
these cases.
Types of Sacral Agenesis
Type 1 is defined as unilateral agenesis of the sacrum in part or in toto

Type 2 is bilateral sacral agenesis but partial with a stable articulation
between the ilia and the normal or hypoplastic first sacral vertebra
Type 3 is bilateral sacral agenesis but complete (associated with lumbar
agenesis of varying degrees with the ilia articulating with the distal lumbar
vertebra)
Type 4 is bilateral lumbar and sacral agenesis but total. Here the ilia only
interarticulate with each other.
Treatment: Needs multidisciplinary approach.
BIBLIOGRAPHY
1. A study of the utilisation of skull radiography in 9 accident-and-emergency units in
the UK. A national study by the Royal College of Radiologists. Lancet
1980;6;2(8206):1234-6.
2. Bartlett J, Kett-White R, Mendelow AD, et al. Recommendations from the Society of
British Neuro-logical Surgeons. Br J Neurosurg 1998;12(4):349-52.
3. Congenital Anatomical defects of the spine and Ribs. Sever JW, Boston Med Surg J
1992;186:799-821.
4. Early Management of Patients with a Head Injury, SIGN, 2000.
5. Early management of patients with a head injury. A National clinical guideline. Scotish
Intercollegiate Guideline - Network, 2000.
6. Erden E, Agildere M, Eryilmaz M, Ozdirin E. Intracranial calcification in children on
computed tomography. Turk J Pediatr. 1994 Apr-Jun;36(2):111-22.
7. Head injury. Triage assessment, investigation and early managment of head injury in
infants, children and adults. National Institute for clinical Excellence. Clinical Guideline
4 (June 2003).
8. Jackson AP, Eastwood H, Bell SM, Adu J, Toomes C, Carr IM, Roberts E, Hampshire
DJ, Crow YJ, Mighell AJ, Karbani G, Jafri H, Rashid Y, Mueller RF, Markham AF,
Woods CG. Identification of microcephalin, a protein implicated in determining the
size of the human brain. Am J Hum Genet 2002;7:1136-42.
9. Jackson AP, McHale DP, Campbell DA, Jafri H, Rashid Y, Mannan J, Karbani G,
Corry P, Levene ML, Mueller RF, Markham AF, Lench NJ, Woods CG. Primary
autosomal microcephaly (MCPH1) maps to chromosome 8p22-pter; Am J Hum
Genet 1998;63:541-6.
10. Johnson K, Williams SC, Balogun M, et al. Reducing unnecessary skull radiographs in
children: A multidisciplinary audit. Clin Radiol 2004;59(7):616- 20.
11. Kinsman SL, Johnston MV. Congenital anomalies of the central nervous system. In:
Kliegman RM, Behrman RE, Jenson HB, Stanton BF, (Eds). Nelson Textbook of
Pediatrics. 18th edn. Philadelphia, Pa: Saunders Elsevier, 2007;chap 592.
12. Radiology and neuroradiologic findings in the mucopolysaccharidoses Journal of
Pediatric Rehabilitation Medicine 2010;3, Number 2/109-118.
13. Ridgway EB. Skull deformities. Pediatr Clin North Am. 2004;51(2):359-87.

14. Roland Talanow. Multiple ossification within cranial sutures (WORMIAN bones).
PedRad [serial online] vol 2, no. 3.
15. Royal College of Radiologists. Making the best use of a department of clinical radiology.
Guidelines for doctors, 4th edn. London: RCR, 1998.
16. Samartzis DD, Herman J, Lubicky JP, Shen FH "Classification of congenitally fused
cervical patterns in Klippel-Feil patients: Epidermiology and role in the development
of cervical spine-related, 2006
17. Simon SD, Dodds RD. The use of skull X-rays in the accident and emergency
department. Ann R Coll Surg Engl 2003;85(2):120-2.
18. Stephens Chapman, Richard Nakiehty. Aids to Radiological Differential Diagnosis
Fourth edn. 2003.
19. Taylor AI. Patau's, Edwards' and Cri du chat syndromes: A tabulated summary of
current findings. Dev Med Child Neurol. 1967 Feb;9(1):78-86.
20. Teasdale GM, Murray G, Anderson E, et al. Risks of acute traumatic intracranial
haematoma in children and adults: Implications for managing head injuries. BMJ.
1990;300(6721):363-7. [abstract] Sacral agenesis contact group.
5
Equipment
27
Equipment
(For Airway Obstruction/
For Circulation/For Poisoning/For
Supportive Care of Newborns)
INSTRUMENTS FOR AIRWAY OBSTRUCTION

There are various levels of obstruction:
At the level of the pharynx obstruction may occur due to the tongue falling
backwards
Obstruction at the larynx may be due to burns, inflammation or anaphylaxis.
Obstruction below the larynx can arise from bronchospasm, pulmonary
edema, aspiration, pneumothorax, etc.
OROPHARYNGEAL AIRWAY (FIG. 27.1)
This is a curved plastic piece

introduced into the oral
cavity in the upside-down
position and then rotated
through 180 as it passes
below the hard palate and
into the oropharynx
It is used for suction and
preventing the tongue from
falling back and blocking the
Fig. 27.1: Oropharyngeal airway
airway.
It is possible to insert an oral
airway only when the patient is completely unconscious or does not have
a gag reflex (if the patient has a gagreflex they may vomit).
Select an airway with a length corresponding to the distance between the
corner of the patients mouth and the angle of the jaw.
It is lifesaving in patients with lock jaws, maxillofacial injuries.
Too large sizing can cause bleeding, and can close the glottis.
Small size is difficult to fix at the lips.
Indications for Oral Airway
Bilateral choanal atresia.

Pierre-Robin syndrome.

THE SUCTION TRAP (DEE-LEE SUCTION) (FIG. 27.2)
Mucus trap or filter is a small sterile, disposable single-use, plastic body,

fluid collection device for collecting liquid secretions from an infants airway,
during delivery.
It has a catheter connected to a transparent 20 ml graduated collection
canister called mucus or sputum trap which is further connected in series
to a flexible tubing terminating in a mouthpiece, connectable to a source of
suction (oral or mechanical).
Usually the doctor sucks on a tube to create a negative suction pressure.
There is ease of insertion and withdrawal, but can contaminate the doctor
with aerosol materials like HIV virus at all times during use and even with
direct secretions, if the canister tilts.
To overcome the danger of contamination, use a source of external suction
pump connectable to the mouth piece with pressure that is never more
than 100 mm Hg.
10 French, 8 French and 6.5 French sizes are available for suction.
Indications for Use

At birth, the first thing is to adequately suction the mouth and then the nose
prior to the baby taking its first breath. This can decrease or prevent the risk
of serious complications, e.g. aspiration of meconium or liquor.
Fig. 27.2: Dee-Lee suction trap (Mucus extractor)

Equipment 203
SUCTION BULB
This is safe, easy-to-use small, rubbery nasal aspirator that provides gentle
suction to remove excess mucus or secretions from a babys oral and nasal
cavity (mouth first then the nose). Before inserting the suction bulb is held in the
palm of hand. All the air is pushed out and then the thumb is slowly released.
This draws the fluid out of the nose or mouth.
Note: Efficacy of bulb and Dee-Lee suction in clearing the naso and oropharynx
of the neonate in the final outcome, is similar.
SUCTION CATHETER
It is a flexible straight catheter (without collection apparatus) connectable to a
source of external suction pump. It is provided with orifice or opening that
breaks the continuity of the tube system diverting suction pressure to ambient
air when such orificial vent is not sealed with a finger of an assistant and allows
transmission of undivided suction pressure to catheter end, upon sealing. Thus,
intermittent sealing of the vent creates intermittent suction. Suction catheter
must be wide enough to remove meconium/liquor effectively. The recommended
size for the catheter is 12 F and it should have a few side holes at the tip.
SUCTION APPARATUS
It is preferable to use a mechanical equipment to generate negative pressure
for suction. Negative pressure should not exceed 100 mm Hg (130 cm water).
INSTRUMENTS FOR VENTILATION

RESUSCITATION BAG (FIG. 27.3)
It is a self-inflatable silicone reusable, easyto- clean bag. It is a hand-held
device to mechanically ventilate a child, before a mechanical ventilator is
attached. The bag refills due to elastic re-coil of the bag after compression.
Fig. 27.3: Resuscitation facemask, bag and reservoir


Self-inflating Bag Parts
Inlets: Separate inlets for O2 and air.
Reservoir (for 100% oxygen): An attachment called reservoir fills passively
with oxygen while the patient is breathing out (This causes oxygen to
enter through both inlets, in the next compression. Hence, the amount of
oxygen delivered to the patient is nearly 100%).
When the bag is compressed, air/oxygen goes into the babys lungs
and when the bag is released, it self-inflates, drawing in ambient air
and/or supplemental oxygen supplied from a source and that which is
collected in the reservoir.
Valve assembly
Pressure release valve: The valve assembly is equipped with a pop-off
valve system that helps to prevent giving high pressure into the patients
lungs by venting the pressure when a pre-set pressure is reached.
This limits the chances of a pneumothorax.
One-way fish mouth valve: One-way fish mouth, directs the air oxgen
mixture (or 100% oxygen if reservoir is attached) to the child when
bag is compressed.
Patient outlet or expiratory valve directs the exhaled air out into the
open
Face mask: This is a hand-held, reusable, easy-to-clean device to be
attached to the bag with or without a cushioned contour and soft seal
It is round or anatomically shaped so as to form a proper seal around the
face
However, the face mask gives inadequate ventilation and gastric inflation
can occur
Masks of varying sizes for infants and children are available.
Dos of Ventilation
Airway Management is an Art
Head tilt/Chin lift is the best method of opening the airway, especially in an
unconscious patient
Ventilation should involve a minimum of two rescuers
The patients chest should rise by 1 inch with each inhalation
Compress once every 3 seconds for an infant or child to provide adequate
circulation.
Always decompress the stomach with NG tube to prevent aspiration.
Equipment 205
Bag and Mask Ventilation
Procedure
Follow a squeeze-one-two-squeeze sequence at 40 to 60 breaths/minute

Select the size one mask for a term healthy newborn and size zero for
a smaller newborn
Check the seal and squeeze the bag with the neck slightly extended.
Successful ventilation means a foggy mask and the rising of chest with
delivery of positive pressure with audible breath sounds in both axillas, on
auscultation. Hence, it requires both an airtight seal fit and patent airway.
Leak is the most common problem.
Indication of Bag and Mask Ventilation

Ventilate an apneic or gasping baby or even if babys breathing is spontaneous
but the heart rate is below 100/ min.
Contraindications
Diaphragmatic hernia
Thick meconium stained babies, (bag and mask ventilation may only be
done after tracheal suction)
Choanal atresia (Bilateral).
Bag and Tube Intubation/Ventilation

Equipment and Procedure
A laryngoscope (Fig. 27.4) is a rigid instrument used to examine the larynx
and to facilitate intubation of the trachea.
It is composed of two separate parts:
The handle, to hold the instrument
The blade, to view the larynx.
The straight miller blade is inserted deep into the oropharynx, past the
epiglottis providing sufficient lifting force, (without turning the wrists) in
parallel with the handle
The blade is slowly withdrawn, exposing a view of the larynx.
Endotracheal tube (Fig. 27.5) made of polyvinyl chloride of appropriate internal
diameter (depending upon babys weight) should be inserted:
Try to complete the procedure in 20 seconds. If it takes longer, stop the
procedure. Stabilize and try again. Be gentle while intubating and give free
flow of oxygen during intubating.
It has a radio-paque line and a Murphys eye hole at the beveled, distal
end.
Fig. 27.4: Laryngoscope

Fig. 27.5: Endotracheal tube (upper end of vocal

cord guide should be at level of vocal cords)
Types of Endotracheal Intubation

1. Oral endotracheal intubation is less traumatic than nasal route. It permits
use of a larger endotracheal tube.
2. Nasal endotracheal intubation is difficult.
Indications
When bag and mask ventilation is ineffective or when chest compression

is indicated
When prolonged positive pressure ventilation is required
Diaphragmatic hernia
For tracheal suction (e.g. meconium aspiration)
For medications through endotracheal route.
Relative Contraindications
Obstruction of the upper airways is due to foreign objects.

Cervical fractures.
Equipment 207
Before intubation confirm that the equipment is working properly. After
intubation, immediately check the symmetry of chest for expansion. Auscultate
breath sounds in axilla, bilaterally. Order for chest X-ray to confirm. Monitor
oxygen saturation (by pulse oximetry), heart rate and blood pressure. A visible
mist should appear in the T-piece or ventilator tubing.
On extubation: Give oxygen by face mask Note stridor, color and change in
mental alertness or behavior.
Complications of Intubation
Laryngospasm, bronchospasm, laryngeal edema, aspiration, fractured teeth,
hypoxemia, nosocomial infection displacement of tube and dysrhythmias can
occur. Hence, fixation of the endotracheal tube, suctioning and oral care to
remove secretions is vital.
INSTRUMENTS FOR CIRCULATION
IV Cannula
IV Fluids
IV Set
Drugs
Chest compression is done to improve circulation when HR is persistently

below 80/mm.
Thumb technique: The two thumbs are used to depress the sternum at the
rate: 120 per min with hands encircling the chest and fingers supporting the
back of the baby.
Two-finger technique: The tips of the middle and index or ring finger are
used to compress the lower third of sternum to depress it by to inch.
Other hand is used to support the infants back.
Chest compression: Ventilation ratio is 3:1.
INSTRUMENTS FOR SUPPORTIVE CARE OF

NEWBORNS
NG (NASOGASTRIC) TUBES
Insertion Technique
Measure the distance of tubing from bridge of nose to ear lobe and then to
the xiphisternum.
Insert through the nose or tell the patient to swallow.
Stop immediately and withdraw tube if patient coughs, becomes distressed,
or is cyanosed.
Although the tubes are simple to insert they are easily displaced. Hence,
the position of tubes should be checked before each feed by obtaining an
acidic tube aspirate of pH<5.5 on litmus paper or by auscultation (after

pushing some air) for bubbling sounds over epigastrium, X-rays confirm
the position.
Securing and monitoring the tube is necessary before the administration
of feed.
Check for prefeed aspirate before giving the next feed. If more than 20
percent of the feed is present, then feed may be withheld. However,
minimum aspirate of 3 to 4 ml is acceptable.
INDICATIONS OR USES OF NG TUBES

For Feeding Newborns
NG feeds are given to sick babies and preterms less than 32 weeks or low
birth weight babies less than 1800 gm.
Give EBM, formula feeds preferably by gavage feeding with gravity as a
bolus or as continuous feeds (flush with distilled water after use as it
blocks easily).
Babies < 30 weeks, need IV fluids.
Babies 30 to 32 weeks usually need nasogastric feeding.
Babies 32 to 34 weeks, may be given cup spoon/breast-feeding.
Babies > 34 weeks may be given breastfeeding. (Sucking and swallowing
reflexes are coordinated)
Offer extra spoon feeds after breastfeeding.
An energy of 50 kcal/kg/d is sufficient to prevent catabolism, but does not
support growth. Minimum energy requirement for growth is 120 kcal/kg/d.
For Stomach Wash
It should be performed if there was meconium staining, operative delivery or
poisoning.
For exchange transfusion.
For checking patency of nares and anal orifice.
For administration of medications
For NG on drainage.
To give rest to bowel, e.g. after surgery and for decompression during
mechanical ventilation .
Before X-rays.
Relative position of esophagusStomach trachea and heart diagnose
diaphragmatic hernia tracheoesophageal fistula (TEF), etc.
As a torniquet.
As a tube for venesection.
For rectal medication like diazepam in emergency.
For bowel wash.
Equipment 209
Complications of NG Feeding
Refeeding syndrome may occur in previously malnourished patients who

are fed with high carbohydrate diet due to an increase in oxygen
consumption and increased respiratory and cardiac workload which may
precipitate acute heart failure. High carbohydrate diet increases the
circulating insulin level which increases extracellular fluid (ECF) volume.
Thus, it may precipitate acute heart failure or cause ascites.
Nasopharyngeal discomfort, nasal erosions, esophageal ulceration, stricture,
and pharyngeal or rarely esophageal perforation.
Epistaxis is due to damage to the nasal mucosa.
Bacterial contamination of enteral feed can cause serious, infection,
bloating, cramps, etc.
INCUBATORS (FIG. 27.6)
Due to high surface area to volume ratio, babies lose heat faster than
adults. What is just uncomfortable for adults is comfortable for babies.
Hence, incubators are used for babies <1500 g. Remember, not to place
incubators near cold walls
Neonates cannot shiver. Heat can be lost by conduction, convection, evaporation
and radiation which are minimized in incubator. Increasing humidity inside
the incubator reduces the losses as well.
For babies:
The normal temperature is 37C
Cold stress begins at 36.5C
Moderate hypothermia starts at or below 36C
Severe hypothermia begins at or below 32C
Preterm babys skin is thin. The brown fat is less and vasomotor center is
underdeveloped.
Double walled incubators minimize loss by radiation.
Fig. 27.6: Neonatal incubator


RADIANT WARMERS (FIG. 27.7)
They are routinely being used to maintain temperature in bigger newborns.
CONVENTIONAL PHOTOTHERAPY (FIG. 27.8)
This is useful in pathological jaundice in neonates. Sources of bilirubin are:

a. Heme 1g Hb = 34 mg bilirubin.
b. Non-heme source 1 mg/kg of meconium.
Combination of fiberoptic, biliblanket and conventional phototherapy using
fluorescent light is better than conventional phototherapy.
Bilirubin is converted to soluble isomers at 420 to 500 nm. Special blue
lamps have this wavelength. Daylight and cool white lamps have much
higher wavelength and hence less useful.
Halogen lamps and blue gallium nitride LED are effective but costly.
Side Effects
Phototherapy may lead to:
Hot, dry, parched, or bronze skin.
Increased insensible water loss and diarrhea.
Bronze baby syndrome and hypocalcemia.
Fig. 27.7: Radiant warmer

Fig. 27.8: Phototherapy

Equipment 211
OXYGEN SUPPLY DEVICES
Low Flow Devices
Here the flow rate should never cross >3 to 4 L/min because it interferes with
patients ventilation.
Nasal cannula
Face mask
Nasal prongs.
Face masks are of two types:
Simple face mask
Anatomical face mask
They are used for providing free flow O2, CPAP or IPPV.
Side Effects
Bruising of face, leakage of air in the abdomen (distension).
Oxygen Hood
They are transparent head boxes made out of perspex plastic kept over babys
head and shoulders to give consistent concentration of O2 to the infant.
Excessive oxygen may be deleterious causing, free radical formation.
BIBLIOGRAPHY
1. Caring for the patient with a nasogastric tube; Nursing Standard 2005;20(3):59-65.
2. Critical Care Nursing Book by Patricia Gonce Morton- M.Gallo- Fontaine -Hudak
Page 524 to 526 Medical-Surgical Nursing Book by Suzanne C. Smeltzer-Brenda
Bare. Page 610 to 613.
3. Daniel Limmer, Michael F.OKeefe. 2005. Emergency Care 10th edn. Edward T.
Dickinson, Ed. Pearson, Prentice Hall. Upper Saddle River, New Jersey. Page 140.
Stoy, Walt. Mosby/JEMS. Emergency Care 2004;142-3.
4. Nasogastric and feeding tubes. The importance of proper placement; Postgrad Med
1996;99(5):165-8,174-6.
5. pH testing of feeding-tube aspirates to determine placement. Nutr Clin Pract
1994;9(5):185-90.
6
Medications
28
Emergency Drugs
DRUGS FOR EMERGENCIES IN INFANTS
NEONATAL RESUSCITATION
Naloxone
Indication: Used for respiratory depression induced by opioids.
Dosage: Give IV 0.1 mg/kg (IM absorption erratic)
Side effects: It is a partial agonist/antagonist, hence large doses may themselves
cause respiratory depression.
Prostaglandin E1
Indication: Used to keep the ductus open for ductal-dependent cardiac
malformations in the neonatal period.
Dosage: 0.05 to 0.10 mg/kg/min as an infusion in 5% dextrose.
Side effects: Apnea, desaturation, hyperthermia and seizures may occur. Be
prepared with ventilator.
SUPRAVENTRICULAR TACHYCARDIA
Adenosine
Dosage: Initial dose: 0.05 mg/kg as rapidly as possible followed by flushing
of the IV catheter.
If an atrioventricular block occurs or if there is no response within 30
seconds, increase the dose by 0.05 mg/kg followed by flushing the IV catheter.
If no response occurs increase to 0.15 mg/kg and so on. Maximum dose is 12
mg.
Side effects: Profound bradycardia. The antidote for profound bradycardia is
aminophylline 5 to 6 mg/kg over 5 minutes.

DOCUMENTED METABOLIC ACIDOSIS
Sodium Bicarbonate (8.4% Solution W/V)
Indication: Given in documented metabolic acidosis after effective ventilation
has been established.
Dosage: IV: 1 to 2 mEq/kg (1 ml provides 1 mEq of bicarbonate). The solution
is hyperosmotic. Hence, it is given in double dilution to the newborns.
Side effects: Cerebral edema may occur due to hypertonicity. Paradoxical
acidosis occurs, if given without establishing ventilation.
NEONATAL SEIZURES
Calcium
Indication: It has a role in ionized hypocalcemia and hyperkalemia (with or
without seizures).
Dosage: IV: 200 mg/kg of elemental calcium in calcium gluconate is given
slowly. The maintenance dose of calcium 100 mg/kg Q 6 hourly.
Side effects: Monitor HR, as bradycardia can occur. Also avoid extravasation
as calcinosis cutis or even necrosis of skin may occur.
Glucose
Indication: Hypoglycemia (blood sugar less than 40 mg%), with or without
seizures.
Dosage: Initial dose: IV: 250 to 500 mg/kg or 2.5 ml/kg of 10 percent Dextrose.
Maintenance dose: Constant infusion of 10 percent dextrose in water at a rate
of 3 ml/kg/h (4-8 mg/ kg/min). The rate should be titrated to appropriate
glucose values.
Note: Neonates should receive 10 to 12.5 percent glucose administered slowly.
Glucose levels should be determined before and after administration.
Side effects: If large volumes of dextrose are administered, check electrolytes
to prevent hyponatremia and hypokalemia.
Phenobarbital
Indication: It is a drug of choice for neonatal seizures.
Dosage:
IV: 20 mg/kg loading dose. Repeat the dose once, if necessary, for clinical
effect after 15 minutes.
Emergency Drugs 217
The maintenance dose is 5 mg/kg/day (divided doses).
Side effects: There is an increased incidence of apnea when combined with

other sedative agents. Monitor oxygen saturation and be prepared to provide
respiratory support.
DRUGS FOR EMERGENCIES IN OLDER CHILDREN

CARDIAC ARREST
Epinephrine
Indication: Cardiac arrest or profound bradycardia, asystole, ventricular
fibrillation, or pulseless electrical activity.
Dosage: (Initial dose)
IV or Intraosseous: 10 mcg/kg or 0.1 ml/kg of 1:10 000 dilution (0.01 ml/
kg of 1:1000 dilution).
Endotracheal: 100 mcg/kg 0.1 ml/kg of 1:1000 dilution (flush with saline).
ANAPHYLAXIS
Epinephrine
Dosage:
Subcutaneous (SC): 10 mcg/kg per dose (maximum 3 doses every 20
minutes).
Intravenous (IV): 10 mcg/kg per dose: 0.01 ml/kg of 1:1000 dilution or 0.1
ml/kg of a 1:10 000 dilution.
SHOCK DESPITE VOLUME RESUSCITATION
Epinephrine
Dosage:
Continuous IV infusion. Infuse at 0.1 mg/kg/min (by infusion pump,
preferably).
Prepare by adding 1 mg in 1000 ml normal saline.
VOLUME OVERLOAD
1. Fluid overload.
2. Congestive heart failure. Causes and manifestations of volume overload
3. Pulmonary edema.
Furosemide
Dosage: IV is : IV, IM: 1 - 2 mg/kg.
Side effects: Hypokalemia.

DIABETIC KETOACIDOSIS
Insulin, Regular
Give appropriate fluids along with insulin.
Dosage:
Subcutaneous (SC): 0.25 to 0.5 unit/kg per dose.
Intravenous (IV) at infusion rate of 0.05 to 0.1 unit/kg/h.
Neonatal dose: 0.05 unit/kg/h.
Side effects: Hypoglycemia and Hypokalemia.
TET SPELLS
Morphine Sulfate
Dosage: IV (slowly) or IM: 0.05 to 0.1 mg/ kg. Repeat dose for clinical effect.
HYPERTENSIVE CRISIS
Diazoxide
Dosage: IV: 1 to 3 mg/kg rapid IV push. Note: Alternative regimen: 3 to 5 mg/
kg IV over 30 minutes.
Side effects: Hypotension and/or hyperglycemia.
Nitroprusside Sodium
Dosage: IV: 0.5 to 10 mg/kg/min. Start at the lowest dosage and titrate for the
desired clinical effect. Prevent accidental bolus injection.
Note: Bottle, burette, or syringe pump but not the IV tubing should be covered
with protective foil to avoid breakdown by light.
Side effect: Profound hypotension. Also cyanide toxicity can result from large
doses and/or prolonged infusions. Patients should be closely monitored for
the development of metabolic acidosis. Patients with decreased renal function
may be at increased risk.
RAISED INTRACRANIAL TENSION
Dexamethasone
Indication: For elevated intracranial pressure.
Dosage:
Loading dose: IV: 1 to 2 mg/kg.
Maintenance dose: 1 mg/kg/24 h.
For croup IV, IM, PO the dose is less: 0.6 mg/kg.
Side effect: Steroid toxicity.
Emergency Drugs 219

Mannitol
Indication: Increased intracranial pressure.
Dosage: IV: 0.25 g/kg given over a 15 min infusion. A larger dose (0.5 g/kg
given over 15 minutes) may be appropriate in acute intracranial hypertension.
Side effects: Very rapid administration causes hypotension, hyperosmolarity,
and paradoxically elevated intracranial pressure, as it crosses blood brain barrier.
CONVULSIONS
Diazepam
Dosage for status epilepticus: 0.1- 0.3 mg/kg every 2 minutes (maximum 10
mg/dose) intravenously.
Rectal: 0.5 mg/kg up to 20 mg. Avoid IM injection.
Side effects: There is a chance of apnea when combined with phenobarbitone/
other sedatives. Respiratory depression may also occur.
Phenytoin
Indication: Status epilepticus.
Dosage: IV: 10 to 20 mg/kg as an initial dose. Maximum rate of administration,
50 mg/min or 1 mg/kg/min, whichever is less. It should be diluted in normal
saline to avoid precipitation.
The rate of administration is 0.1 ml of undiluted preparation per kg/min
with heart rate monitoring (for bradycardia).
POISONINGS
Charcoal (Activated as a Slurry)
Indication: Acute poisoning.
Dosage: 1 to 2 g/kg. Alcohols, alkalies, mineral acids, do not bond to activated
charcoal.
Atropine Sulfate
There is no role of atropine in neonatal bradycardia due to hypoxia. Give
oxygenation, ventilation and epinephrine, in such cases.
Indications
1. Symptomatic bradycardia
Dosage:
Intramuscular (IM): 0.02 to 0.04 mg/kg
Intratracheal (IT): 0.02 to 0.04 mg/kg. Dilute the dose in saline and
flush (1-5 ml) based on tube size.

Intravenous (IV): Minimum dose, 0.1 mg and Maximum dose, 0.5 mg
for child and1.0 mg for adolescent). This dose may be repeated once.
2. Anticholinesterase poisoning: Large doses of atropine IV: 0.05 mg/kg
are given repeatedly till atropinization.
Note: Details of some important emergency drugs are given in next few
chapters.
BIBLIOGRAPHY
1. American Academy of Pediatrics and American College of Emergency, Physicians,
Joint Task Force on Pediatric Life Support. APLS: The pediatric Emergency Medicine
Course. Elk Grove Village, IL: American Academy of Pediatrics, 1993.
2. American Academy of Pediatrics. Guidelines for monitoring and management of
pediatric patients during and after sedation for diagnostic and therapeutic procedures.
Pediatrics 1992;89:1110-5.
3. American Heart Association, Subcommittee on Pediatric Resuscitation. Pediatric
Advanced Life Support. Dallas, TX: American Heart Association, 1994.
4. KidSTAT Plus (CD-ROM). Elk Grove Village, IL: American Academy of Pediatrics,
1996.
Calcium Gluconate 221
29
Calcium Gluconate
CALCIUM
This is a mineral supplement. The normal serum calcium is 9 to 11 mg/dl. The
active form is ionized form of calcium which increases in an acidic environment
and decreases with protein binding. The True calcium = Total calcium + 0.8
(4.0 - Serum albumin).
CALCIUM GLUCONATE (FIG. 29.1)
It is the form of calcium most widely used in treatment of
hypocalcemia (Calcium gluconate 10 percent W/V contains
10 gm per 100 ml, i.e. 100 mg/ml).
Dosage
Neonates: 2 ml/kg elemental calcium stat, then 1 ml/kg 6th
hourly doses.
Prophylactic dose: For example, in preterms we give 100
mg/kg/dose elemental calcium twice a day.
For exchange transfusion: Use 0.45 mEq of elemental
calcium, i.e. 1 ml of 10 percent preparation is infused for
each 100 ml of stored citrated blood (low in calcium) to
prevent hypocalcemia.
Fig. 29.1: Calcium

gluconate
INDICATIONS
Hypocalcemia in preterm and IUGR babies: It presents as lethargy, poor

feeding and jitteriness and tetany or focal seizures in older children (on
exclusive top milk feeding).
Hypocalcemia secondary to citrated blood: Infusion or exchange
transfusion, as stored blood has less calcium.
Pedia Pearls:
On ECG hypocalcemia causes QT prolongation and hyperkalemia causes
t wave tenting.
In hypomagnesemia, the child may be refractory to calcium therapy.
Acute hyperkalemia: The cardiac toxicity of potassium is prevented by

calcium.
Supplementation in pubertal girls: Testosterone has a positive effects on
calcium protein kinetics in prepubertal boys.
CONTRAINDICATIONS
Do not give along with sodium bicarbonate, as it forms a precipitate. Avoid if
child has renal stones and/or hypophosphatemia (because Calcium
Phosphorus is a constant, so if phosphorus decreases, Calcium increases
automatically).
Side Effects (Cardiac Mainly)
Vasodilation may cause syncope and hypotension.

Extravasation causes tissue necrosis.
Cardiac arrest in systole or ventricular fibrillation or bradyarrhythmia.
If toxicity develops: Forced saline and furosemide diuresis is given.

BIBLIOGRAPHY
1. Abrams SA, Schanler RJ, Yergey AL, Viehra NE, Bronner F. Compartmental analysis of
calcium metabolism in very-low-birth-weight infants. Pediatr. Res. Marshall, W.J. (1995)
(Paperback), Clinical Chemistry 3rd edn. London: Mosby 1994;36:424-428.
2. Abrams SA. Pubertal changes in calcium kinetics in girls assessed using 42Ca. Pediatr.
Res. 1993;34:455-9.
3. Bronner F, Harris RS, Maletskos CJ, Benda CE. Studies in calcium metabolism. The
fate of intravenously injected radiocalcuim in human beings. J. Clin. Invest. 1956;42:898905.
4. Bronner F, Stein WD. Calcuim homeostasis-an old problem revisited,. J. Nutr. 1995.
5. Bronner F. (1987) Calcuim absorption. In: Physiology of the Gastrointestinal Tract,
2nd edn. (Johnson LR, Christensen J, Jacobson ED & Walsh MJ, eds), pp. 14191435. Raven, New York, NY.
6. Bronner F. Calcium and osteoporosis. Am J. Clin. Nutr. 1994;60:831-836.
7. Bronner F. Calcuim homeostasis, In: Disorders of Mineral Metabolism (Bronner F &
Cobum, JW Eds.), vol 2, 1982;43-97. Academic Press, New York, NY.
8. Bronner F. Dynamics and functions of calcium. In: Mineral Metabolism-An advanced
Treatise (Comar CL, & Bronner F, eds.), vol. 2A, Academic Press, New York, KY
1964;341-444.
9. Frost HM. Obesity and bone strength and "mass": a tutorial based on insights from a
new paradigm. Bone 1997;21:211-4.
10. Gertner JM. Disorders of calcium and phosphorus homeostasis. Pediatr clin North Am.
Dec 19 2007;356(6):1441-65.
11. Guise TA, Mundy GR. Clinical review 69: Evaluation of hypocalcemia in children and
adults J Clin Endocrinal Metab. May 1995;80(5):1473-8.
12. Leitch I, Aitken FC. The estimation of calcium requirement a re-examination. Nutr.
Abstr. Rev. 1959;29:393-411.
13. Medical Physiology; Guyton, Saunders and Co. 1976 pp. 1062.
Calcium Gluconate 223

14. Mimouni F, Tsang RC. Neonatal hypocalcemia to treat or not to treat? (A review). J Am
Coll Nutr. Oct 1994;13(5):408-15.
15. Mitchell HH. The dietary requirement of calcium and its significance. Actualities
Sciendifiques et Industrielles, no. 771 (Nutrition). Hermann & Cie, Paris, France 1939.
16. Moore LJ, Machlan LA, Lim MO, Yergey AL, Hansen JW. Dynamic of calcium
metabolism in infancy and childhood I. Methodology and qualification in the infant.
Pediatr. Res. 1985;19:329-34.
17. Sanchez GI, Venkataraman PS, Pryor RW, et al. Hypercalcitonemia and hypocalcemia in
acutely ill children: studies in serum calcium, blood ionized calcium and calcium-regulating
hormones. J Pediatr. Jun 1989;114(6): 952-6.
18. (The parathyroid Glands and Vitamin d) in: Walter F. PhD. Boron (2003). Medical
Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. pp. 1300.
30
Sodium Bicarbonate
SODIUM BICARBONATE
Sodium hydrogen carbonate is the chemical compound with the formula
NaHCO3.
INDICATIONS
Documented Metabolic Acidosis (pH < 7.15)
It dissociates into ionic Na+ and HCO3 which neutralizes hydrogen ion.
For example in:
Diarrheas
Life-threatening asthma
Diabetic Keto Acidosis (DKA), salicylate poisoning and renal tubular
acidosis
Birth asphyxia
Cyanotic spells.
For Alkalinization of Urine
In UTIs sodium bicarbonate is used to titrate to desired urinary pH in order to
inhibit bacterial growth and in hemoglobinuria, to prevent acid hematin from
blocking the tubules. Also used for forced-alkaline diuresis (alkali +
furosemide) for poisonings with acids like acetylsalycylic acid.
For Treatment of Hyperkalemia with or without Cardiac Arrest
Give sodium bicarbonate only after adequate alveolar ventilation and
effective cardiac compressions have been given, because in hypoxic state it
dissociates into Na+, H+ and CO2. This CO2 dissolves in blood to form
carbonic acid which worsens acidosis (called paradoxical acidosis).
Sodium Bicarbonate 225

INJ. SODIUM BICARBONATE (FIG. 30.1)
Sodium bicarbonate: (NaHCO3) 8.4%. This compound
provides 1 mEq of HCO3 for each ml of Sodium Bicarbonate
(NAHCO3).
Dose of Sodium Bicarbonate (in mEq)
If ABG Status is not Known
Give 2 mEq/kg diluted 1:1 with sterile water.
If ABG Status is Known
Give 0.3 weight (in kg) base deficit (in mEq/l).
Administer half the dose slowly over 6 hours, then
remaining 1/2 dose over the next 24 hours.
Adverse Reactions
Fig. 30.1: Sodium

bicarbonate
High tonicity of NaHCO3 may lead to cerebral hemorrhage and edema.

High salt content may lead to hypernatremia, CHF (aggravated), edema,
pulmonary edema and even seizures.
High alkali content may lead to tissue necrosis on extravasation.
Metabolic effects: Hypokalemia/hypocalcemia.
Drug Interactions: Mnemonic ABCD
Acids, bicarbonate, calcium, dopamine are incompatible with each other.
BIBLIOGRAPHY
1. Bell MJ, Ternberg JL, Feigin RD, Keating JP, Marshall R, Barton L, Brotherton T.
Neonatal necrotizing enterocolitis. Therapeutic decisions based upon clinical staging.
Annals of Surgery 1978;187:1-7.
2. Bland RD, Clarke TL, Harden LB. Rapid infusion of sodium bicarbonate and albumin
into high-risk premature infants soon after birth: a controlled, prospective trial.
American Journal of Obstetrics and Gynaecology 1976;124:263-7.
3. Finberg L. The relationship of intravenous infusions and intracranial hemorrhage - a
commentary. Journal of Pediatrics 1977;91:777-8.
4. Graf H, Leach W, Arieff AI. Evidence of detrimental effect of bicarbonate therapy in
hypoxic lactic acidosis. Science 1985;227:754-6.
5. Howell JH. Sodium bicarbonate in the perinatal setting revisited.Clinics of Perinatology
1987;14:807-16.
6. Kette F, Weil H, Gazmuri RJ. Buffer solutions may compromise cardiac resuscitation
by reducing coronary perfusion pressure, JAMA 1991;266:2121-6.
7. Lokesh L, Kumar P, Murki S, Narang A. A randomized controlled trial of sodium
bicarbonate in neonatal resuscitation - effect on immediate outcome. Resuscitation
2004;60:219-23.

8. Lou HC, Lassen NA, Friis-Hansen B. Decreased cerebral blood flow after
administration of sodium bicarbonate in the distressed newborn infant. Acta
Neurologica Scandinavica 1978;57:239-47.
9. Murki M, Kumar P, Lingappa L, Narang A. Effect of a single dose of sodium
bicarbonate given during neonatal resuscitation at birth on the acid-base status on
first day of life. Journal of Perinatology 2004;24:696-9.
10. Murki M, Kumar P, Lingappa L, Narang A. Effect of a single dose of sodium
bicarbonate given during neonatal resuscitation at birth on the acid-base status on
first day of life. Journal of Perinatology 2004;24:696-9.
11. Niermeyer S, Kattwinkel J, Van Reempts P, Nadkami V, Phillips B, Zideman D et al.
International Guidelines for Neonatal Resuscitation: An excerpt from the Guidelines
2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care:
International Consensus on Science. Contributors and Reviewers for the Neonatal
Resuscitation Guidelines.Pediatrics 2000;106:E29.
12. Ostrea EM Jr, Odell GB. The influence of bicarbonate administration on blood pH in
a "closed system": clinical implications. Journal of Pediatrics 1972;80:671-80.
13. Papile LA, Burstein J, Burstein R, Koffler H, Koops B. Relationship of intravenous
sodium bicarbonate infusions and cerebral intraventricular hemorrhage. Journal of
Pediatrics 1978;93:834-6.
14. Resuscitation Council (UK). Resuscitation at birth. Newborn Life Support Manual
2001.
15. Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical
and electro-encephalographic study. Archives of Neurology 1976;33:696-705.
16. Simmons MA, Adcock EW 3rd, Bard H, Battaglia FC. Hypernatremia and intracranial
hemorrhage in neonates. The New England Journal of Medicine 1974;291:6-10.
17. Weil MH, Trevino RP, Rackow EC. Sodium bicarbonate during CPR. Does it help or
hinder? Chest 1985;88:487.
18. Wax PM, Hoffman RS. Sodium Bicarbonate in Contemporary Management in Critical
Care, 1991;1(3):81-108.
Phenytoin 227
31
Phenytoin
PHENYTOIN (FIG. 31.1)
Diphenylhydantoin and its precursor fosphenytoin are
membrane stabilizing agents. It inhibits post tetanic potentiation
INDICATIONS AND DOSAGE
For Cardiac Arrhythmias Associated with
Digitalis Intoxication
Dosage: The usual dose is 3.5 to 5 mg/kg body weight
administered by slow intravenous injection. This dose may
be repeated one more time, if necessary. Maintenance dose
is 4 to 8 mg/kg body weight daily (Flush with saline due to
high pH).
For Treatment of Seizures/Trigeminal
Neuralgia and Head Injury
Fig. 31.1: Phenytoin

sodium
In status epilepticus, it can be given as.

Continuous infusion: Initial loading dose of 10 to 20 mg/kg body-weight,
at a rate of 1 mg/kg/min. ECG and blood pressure are monitored during
infusion.
Slow intravenous injection (50 mg per min).
The maintenance dose is 5 mg/kg per day in two to three divided doses
(maximum of 300 mg daily). Fosphenytoin can be given much more rapidly,
as compared to phenytoin (Phenytoin and fosphenytoin modulate Na
channels).
Pedia Pearl: Fosphenytoin can be given much faster than phenytoin because it a
precursor of phenytoin and hence takes time to metabolize.

ADVERSE EFFECTS
Phenytoin is antifolate: Megaloblastic anemia

Phenytoin metabolizes vitamin D: Rickets may occur due to hepatic
microsomal enzyme induct ion by phenytoin (which metabolize vitamin D)
8 H:
Hyper- or hypo-reflexia
Hypotension
Hallucinations
Hirsutism
Hepatitis
Hyperplasia of gums
Hypersensitivity reactions like drug induced lupus
Hydantoin syndrome ( Fetal) is manifested by broad nasal bridge, wide
fontanelle, low hairline, cleft lip/palate, epicanthal folds, short neck,
microcephaly, low-set ears, small or absent nails, dislocated hip,
hypoplasia of distal phalanges, impaired growth, and congenital heart
defects.
Hyperglycemia (as it inhibits the release of insulin).
Dilantin-associated lymphadenopathy: Phenytoin can also cause
lymphadenopathy.
Anicteric hepatitis induced by diphenylhydantoin.
Dose related nystagmus and ataxia.
Avoid phenytoin in heart blocks.
BIBLIOGRAPHY
1. Berg MJ, Fischer LJ, Rivey MP, Vern BA, Lantz RK. Phenytoin and folic acid
interaction: A preliminary report. Therap Drug, 1983.
2. Carter BL, Small RE, Mandel MD, Starkman MT. Phenytoin-induced hyperglycaemia.
Am J Hosp Pharm 1981;38:1508-12.
3. Chaiken BH, Goldberg BI, Segal JP. Dilantin hypersensitivity: Report of a case of
hepatitis with jaundice, pyrexia, and exfoliative dermatitis. N Eng J Med 1950;242:8978.
4. Dilantin-associated lymphadenopathy. Spectrum of histopathologic patterns. Am J
Surg Pathol 19: 675- 86.
5. Folate deficiency after anticonvulsant drugs: An effect of hepatic enzyme induction?
Br Med J 1:279.
6. Natelli AA Jr. Phenytoin-induced gingival overgrowth: A case report. Compendium
1992;13:786.
7. Pezzimenti JF, Hahn AL. Anicteric hepatitis induced by diphenylhydantoin. Arch
Intern Med 1970;125:118-20.
Aminophylline 229
32
Aminophylline
INTRODUCTION
This is a bronchodilator drug combination that contains theophylline and
ethylenediamine in 2:1 ratio.
As a Bronchodilator
Used in the treatment of bronchitis, emphysema, asthma, etc. It is also used
for its steroid sparing effect.
As a Respiratory Center Stimulant
Used in treatment of apnea of prematurity.
As a Cardiotonic in Left Ventricular Failure (LVF)
It helps due to diuretic and cardiotonic action.
Dosage
Intravenous loading dose:
3 mg/kg is given to those who have received theophylline containing
products within 24 hours.
5 mg/kg, 6 hourly is given to those who have not received theophylline
containing products within 24 hours.
Recommended rate 25 mg/minute. It is diluted in 5 percent dextrose (1mg/
ml) and should be injected slowly.
Maintenance dose
Approx dosage is 2 mg/kg/dose 8 hourly. Ideally the dosage must be
individualized by monitoring theophylline plasma concentration.
Therapeutic index is very narrow (Normal -10-20 mcg/ml).
MECHANISM OF ACTION
Four Pronged Attack (mnemonic ABCD)
Anti-inflammatory action is due to adrenaline released by
phosphodiesterase inhibition which increases (cAMP) thereby releasing
epinephrine from the adrenal gland.
Bronchodilatation: It occurs because it can relax the involuntary muscles.

It is considered as the first choice remedy for intractable bronchial asthma.
CNS and cardiac stimulation in preterm infants, e.g. in apnea of prematurity.
Diuresis: This helps to reduce lung congestion.
Diaphragmatic contraction is improved.
Side Effects (Mnemonic ABCD)
Adrenaline release: This may cause flushing, nausea, vomiting and stomach
upset.
Brain (CNS) stimulation: This may cause apprehension, restlessness,
irritability and even seizures.
Cardiac stimulation: This may lead to rapid heart rate, irregular heartbeat and
even serious arrhythmias. Rapid IV administration may result in hypotension,
syncope, cardiac arrest, and death.
Dangerous metabolic problems: Hypokalemia and hyperglycemia.
BIBLIOGRAPHY
1. Bednarek FJ, Roloff DW. Treatment of apnea of prematurity with aminophylline.
Pediatrics.1976;58:335-9.
2. Blackbourne LH. Surgical Recall. Lippincott Williams and Wilkins, 2009.pp169.
3. Emerman CL, Crafford WA, Vrobel TR. Ventricular arrhythmias during treatment for
acute asthma. Annals of Emergency Medicine 1986;15(6):699-702.
4. Evans WV, Monie RD, Crimmins J, Seaton A. Aminophylline, salbutamol and
combined intravenous infusions in acute severe asthma. British Journal of Diseases
of the Chest 1980;74(4):385-9.
5. Hochwald C, Kennedy K, Chang J, Moya F. A randomized, controlled, double-blind
trial comparing two loading doses of aminophylline. J Perinatol.2002;22:275-8.
6. Jones RA, Baillie E. Dosage schedule for intravenous aminophylline in apnoea of
prematurity, based on pharmacokinetic studies. Arch Dis Child.1979;54:190-3.
7. Klein JJ, Lefkowitz MS, Spector SL, Cherniack RM. Relationship between serum
theophylline levels and pulmonary function before and after inhaled beta-agonist in
"stable" asthmatics. Am Rev Respir Dis. 1983 Apr;127(4):413-16.
8. Krzanowski JJ, Polson JB. Mechanism of action of methylxanthines in asthma. J
Allergy Clin Immunol. 1988 Aug;82(2):143-45.
9. Kuzemko JA, Paala J. Apnoeic attacks in the newborn treated with aminophylline.
Arch Dis Child.1973;48:404-6.
10. Littenberg B. Aminophylline treatment in severe, acute asthma. A meta-analysis.
JAMA. 1988 Mar 18;259(11):1678-84.
11. Svedmyr K, Svedmyr N. Does theophylline potentiate inhaled beta 2-agonists? Allergy
1982;37(2):101-10.
12. Svedmyr K. Beta 2-Adrenoceptor stimulants and theophylline in asthma therapy. Eur
J Respir Dis Suppl. 1981;116:1-48.
13. Wrenn K, Slovis CM, Murphy F, Greenberg RS. Aminophylline therapy for acute
bronchospastic disease in the emergency room. Annals of Internal Medicine 1991;115
(4):241-7.
Adrenaline 231
33
Adrenaline
ADRENALINE
This is a neurotransmitter of adrenergic nervous system. It has both and
activity:
1. Alpha adrenergic effects help in managing cardiac arrest. It causes
Vasoconstriction and hence decreases splanchnic intestinal, renal and skin
perfusion but diverts blood to myocardium and cerebrum.
2. Beta adrenergic agonist effects (Under 0.3 ug/kg/min)increase myocardial
contractility thereby heart rate and relax the bronchial smooth muscle.
Resuscitation in Pulselessness, Hypotension and/or Bradycardia
Resuscitation (bolus) in cardiac arrest, symptomatic bradycardia

unresponsive to ventilation and shock unrelated to volume depletion.
Post-resuscitation (Infusion) in hypotension despite intravascular volume
replacement or persistent bradycardia.
Refractory and persistant bradycardia in newborns.
Dosage
Resuscitation (bolus). In newborns:
Never use the 1:1000 concentration in newborns by any route. Give
Epinephrine (1:10,000) 0.1 to 0.3 ml/kg by IV or ET, route
Resuscitation (bolus). In children:
1. In children with Symptomatic bradycardia (with a pulse): 0.01 mg/kg IV
(0.1 ml/kg of 1:10,000)
2. In children with pulseless cardiac arrest Initial dose:
0.01 mg/kgIV (0.1 ml/kg of 1:10,000 solution).
3. In children with no effect of initial dose give High Dose:
0.1 mg/kg IV/IO (0.1 ml/kg of 1:1000 solution) Maximum dose: 0.2
mg/kg Repeat dose every 3 to 5 minutes, if needed.
Endotracheal Administration:
1. Children: 0.1 mg/kg (0.1 ml/kg of 1:1000).
2. Newborn: 0.1 mg/kg (1 ml/kg of 1:10,000).

Post-resuscitation (Infusion)
Draw up (0.6 x Weight) mg of Epinephrine

Add enough D5W or normal saline to epinephrine to make 100 ml total.
Now, infuse at a rate of 1 ml/h. This provides 0.1 ug/kg/hr
Start at high rate 20 ml/hour until tachycardia occurs which indicates that
drug has entered circulation. Now decrease rate by adjusting infusion rate at
every 5 min to desired rate of (0.1 - 1.0 ug/kg/min).
Anaphylaxis
In cases of acute allergic reactions to medications involving the respiratory
or cardiovascular systems. If the patient has had previous adverse reactions to
the same medication instant use of epinephrine should be considered, even if
the reaction is mild
Insect stings are prone to cause anaphylactic reactions.
Dosage
Subcutaneous (SC): 10 mcg/kg per dose:0.01 ml/kg of 1:1000 dilution

(maximum 3 doses every 20 minutes).
Slow intravenous( IV) bolus: 10 mcg/kg per dose: 0.01 ml/kg of 1:1000
dilution
Continuous infusion: If continued shock after volume resuscitation.
Status Asthmaticus
Dosage
Subcutaneous (SC): 10 mcg/kg per dose 0.01 ml/kg of 1:1000 dilution
maximum single dose, 300 mg (0.3 ml of 1:1000 dilution).
Croup/Bronchiolitis
Dosage
Racemic epinephrine inhalation aerosol is given in croup, bronchiolitis.
Adverse Effects/precautions
Diverts blood from kidneys and systemic circulation into lungs and brain
therefore, can cause renal ischemia and overperfusion of lungs and brain and
hence may cause: Pulmonary edema, Intracranial hemorrhage. Other side
effects are Ventricular Tachycardia, supraventricular tachycardia and Severe
hypertension. Remember three points:
Check concentration (1:1000 OR 1:10,000)
Extravasation may causes local necrosis
Do not mix with sodium bicarbonate containing fluids.
Adrenaline 233
BIBLIOGRAPHY
1. Alberta Medical Association. Guideline for the diagnosis and management of croup.
Alberta Clinical Practice Guidelines 2005
2. Barach EM, Nowak RM, Lee TG, et al. Epinephrine for treatment of anaphylactic
shock. JAMA. Apr 27 1984;251(16):2118-22.
3. Bochner BS, Lichtenstein LM. Anaphylaxis. N Engl J Med. Jun 20 1991;324(25):178590.
4. de Silva IL, Mehr SS, Tey D, Tang ML. Paediatric anaphylaxis: A 5 year retrospective
review. Allergy. Aug 2008;63(8):1071-6.
5. McDonogh AJ. The use of steroids and nebulised adrenaline in the treatment of viral
croup over a seven year period at a district hospital. Anaesth Intensive Care. Apr
1994;22(2):175-8.
6. Reisman RE. Insect stings. N Engl J Med. Aug 25 1994;331(8):523-7.
34
Furosemide
DIURETICS
The word diuretic comes from a combination of the Greek dia = thoroughly
+ ourein = to urinate which means to urinate thoroughly.
Types
1. Loop diuretics, e.g. furosemide.
2. Potassium-sparing diuretics, e.g. spironolactone.
FUROSEMIDEA LOOP DIURETIC
It is a potent loop diuretic that blocks the Na+, K+ and 2Cl- transporter in the
ascending loop of Henle, inhibiting their reabsorption.
Pulmonary Edema
This may occur in case of acute nephritis, cirrhosis,
respiratory distress syndrome (RDS) and bronchopulmonary dysplasia. Acute
improvement in lung function in infants is due to diuresis and pulmonary
decongestion caused by furosemide.
Congestive Heart Failure
Furosemide reduces the preload in CHF due to congenital heart diseases/acute
nephritis, etc.
Hypertension and Edema
Hypertension and edema secondary to cardiac/renal dysfunction may respond
to diuretic therapy.
During Poisoning
It is used for forced saline or alkaline diuresis.
Furosemide 235
In Premature Infants
For PDA closure: Continuous slow infusion or divided oral doses, reduce the
risk of ototoxicity. In neonates, loop diuretics may be used with indomethacin
to prevent NSAID-induced nephrotoxicity, during therapeutic closure of a
patent ductus arteriosus. However, these agents stimulate renal synthesis of
prostaglandin E and may interfere with closure of the PDA, when given to
premature infants.
For treatment of Bronchopulmonary Dysplasia: It is an oxygen dependent
state which responds to diuretics.
Dosage
Neonates: 1 to 4 mg/kg PO twice daily. IV/IM dose is 1 to 2 mg/kg/dose q 12
to 24 hours.
Children: 1 to 2 mg/kg/dose PO/IV/IM q 6 to 12 hours.
Adverse Effects
Fluid and electrolyte depletion: Monitor kidney function as hyponatremia

and hypokalemia and even dehydration may occur due to volume contraction
Diarrhea, vomiting, fatigue, light headedness muscle cramps,
photosensitivity, anemia, leukopenia, thrombocytopenia, hyperglycemia,
agranulocytosis, and various cutaneous eruptions are also seen
Allergy: Patients allergic to sulfa, may also be allergic to furosemide because
of a similarity in the chemical structure
Ototoxicity: Rarely tinnitus may occur
Neurotoxicity: More adverse effects are associated with loop diuretics, as
they are highly protein bound and displaces bilirubin bound to albumin,
predisposing to kernicterus due to free bilirubin.
SPIRONOLACTONEA POTASSIUM SPARING DIURETIC
This is not a potent diuretic but is potassium sparing type, because it is an

inhibitor of the action of aldosterone
Aldosterone enhances potassium secretion and sodium reabsorption by
the distal nephron
It is often used in treatment of ascites.
Dosage
Spironolactone is given PO 1.5 to 3.5 mg/kg/day divided 6 to 24 hourly.
Adverse Effects
Hyperkalemia
Vomiting
Abdominal cramp
Mild azotemia
Gynecomastia.

BIBLIOGRAPHY
1. Abman SH, Groothius JR. Pathophysiology and treatment of bronchopulmonary
dysplasia. Ped Clin North Am 1994;41(2):277-315.
2. Bailie MD. Diuretic treatment agents. Adv Pediatr 1993;40:273-85.
3. Baliga R, Lewy JE. Pathogenesis and treatment of edema. Ped Clin North Am
1987;34(3);693-748.
4. Beermann B, Dalen E, Lindstrom B. Elimination of furosemide in healthy subjects
and in those with renal failure. Clin Pharmacol Ther 1977;22:70-8.
5. Chemtob S, Kaplan BS, Sherbotie JR, et al. Pharmacology of diuretics in the newborn.
Ped Clin North Am 1989;36(5):1231-50.
6. Ellison DH. The physiologic basis of diuretic synergism: Its role in treating diuretic
resistance. Ann Intern Med 1991;114:886-94.
7. Feig PU. Cellular mechanism of action of loop diuretics: Implications for drug
effectiveness and adverse effects. Am J Cardiol 1986;57:14a-19a.
8. Green TP, Johnson DE, Bass JL, et al. Prophylactic furosemide in severe respiratory
distress syndrome: Blinded prospective study. J Pediatr 1988;112:605-12.
9. Kao LC, Durand DJ, McCrea RC, et al. Randomized trial of long-term diuretic therapy
for infants with oxygen-dependent bronchopulmonary dysplasia. J Pediatr
1994;124:772-81.
10. Kohr LM, O'Brien P. Current management of congestive heart failure in infants and
children. Nur Clin North Am 1995;30(2):261-90.
11. Lieberman PL. Anaphylaxis and anaphylactoid reactions. In: Adkinson NF, Yunginger
JW, Busse WW, Bochner BS, Holgate ST, Simons FER, (Eds). Middletons Allergy.
12. Olin BR (Ed). Diuretics. In: Drug Facts and Comparisons. St. Louis: Facts and
Comparisons, Inc., 1995;135a-138j.
13. Royall JA, Levin DL. Adult respiratory distress syndrome in pediatric patients. I.
Clinical aspects, pathophysiology, pathology, and mechanisms of lung injury. J Pediatr
1988;112(2):169-80.
14. Royall JA, Levin DL. Adult respiratory distress syndrome in pediatric patients. II.
Management. J Pediatr 1988;112(3):335-47.
15. Rupp W. Pharmacokinetics and pharmacodynamics of lasix. Scot Med J
1984;19(suppl):5-13.
16. Rush MG, Engelhardt B, Parker RA, et al. Doubleblind, placebo-controlled trial of
alternate-day furosemide therapy in infants with chronic bronchopulmonary dysplasia.
J Pediatr 1990;117:112-8.
17. Rybak LP. Pathophysiology of furosemide ototoxicity. J Otolaryngol 1982;11(2):12733.
18. Segar JL, Robillard JE, Johnson KJ, et al. Addition of metolazone to overcome
tolerance to furosemide in infants with bronchopulmonary dysplasia. J Pediatr
1992;120:966-73.
19. Sinaiko AR. Pharmacologic management of childhood hypertension. Ped Clin North
Am 1993;40(1):195- 212.
20. Sullivan JE, Yamashita TS, Wells TG, et al. Pharmacokinetics and pharmacodynamics
of bumetanide in critically ill children. Clin Pharmacol Ther 1995;57(2):180 (abstract).
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Card 1986;57:44a-53a.
Dopamine 237
35
Dopamine
INTRODUCTION
It is a precursor of norepinephrine and epi-nephrine and a neurotransmitter

as well
Dopamine is processed into norepinephrine by enzyme dopamine
betahydroxylase in certain neurons
It is produced in substantia nigra, parscompacta, ventral tegmental area
(VTA) and hypothalamus in the brain and peripherally in medulla of the
adrenals by hydroxylation of the L-tyrosine to L-DOPA using the enzyme
tyrosine hydroxylase and decarboxylated (dopadecarboxylase) to dopamine
Dopamine is enzymatically broken down by catechol-O-methyl
transferase (COMT) and monamine oxidase (MAO).
ACTIONS
In the brain, it activates dopamine receptors D1, D2, D3, D4, and D5.
It acts as a neuro-hormone which inhibit the release of prolactin from the
anterior pituitary. D1 and D4 receptors are responsible for the cognitiveenhancement.
Drugs like metoclopramide (a D2 antagonist) control vomiting via the
chemoreceptor trigger zone (CTZ).
Dopamine influences our pleasure system. It enhances:
Motivation
Creative drive
Decision-making and prioritization
Drugs like neuroleptics and antipsychotics reduce the dopamine levels
thereby retard motivation spirit, creativity and prioritization.
Dopamine dysfunction is seen in:
Parkinsons disease
Schizophrenia
Psychosis
Autism
Attention deficit hyperactivity disorder

Fibromyalgia.
Drugs like levodopa, a dopamine precursor are used to treat movement
disorders like:
Parkinsons disease
Dopa-responsive dystonia.
Fruit browning: The quinones and melanin brown pigments in damaged
fruits are derived from dopamine and protect fruits and vegetables against
bacteria and fungi.
DRUG EFFECTS
These drug effects are dose dependent

It acts on the sympathetic nervous system but cannot cross the blood-brain
barrier
L-DOPA, which is the precursor of dopamine. can cross the blood-brain
barrier.
DOSAGE (Intravenous Dosages have a Wide Range)
Low Dose: 2 to 5 g/kg/min is considered as the renal dose. It binds to

D1 receptors thereby dilating blood vessels, increasing renal, mesenteric
and coronary arteries perfusion.
Intermediate dose: 5 to 10 g/kg/min have more inotropic and chronotropic
effects via increased alpha 1 receptor activation. Hence, it is used in patients
with shock or heart failure to increase cardiac output and blood pressure
High dose: 10 to 20 g/kg/min causes vasoconstriction, increases systemic
vascular resistance, and increases blood pressure through alpha 1 receptor
activation (It is used in septic shock and after pheochromocytoma removal).
Adverse Effects
Tachycardia, ventricular arrhythmia and vomiting.
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1. Altier N, Stewart J. The role of dopamine in the nucleus accumbens in analgesia. Life
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cognitive performance in rats. Pharmacology, Biochemistry and Behaviour
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Dopamine 239
5. Chudler EH, Dong WK. The role of the basal ganglia in nociception and pain. Pain
1995;60(1):3-38.
6. Cervenka S, Plhagen SE, Comley RA, Panagiotidis G, Cselnyi Z, Matthews JC,
Lai RY, Halldin C, Farde L. Support for dopaminergic hypoactivity in restless legs
syndrome: a PET study on D2-receptor binding. Brain 2006;129(Pt 8):2017-28.
7. Coffeen U, Lpez-Avila A, Ortega-Legaspi JM, del Angel R, Lpez-Muoz FJ, Pellicer
F. Dopamine receptors in the anterior insular cortex modulate longterm nociception
in the rat. Eur J Pain 2008;12(5):535-43.
8. Flaherty AW. Frontotemporal and dopaminergic control of idea generation and
creative drive. Journal of Comparative Neurology 2005;493(1):147-53.
9. Heijtz RD, Kolb B, Forssberg H. Motor inhibitory role of dopamine D1 receptors:
Implications for ADHD (PDF). Physiol Behav 92(1-2):155-160.
10. Jskelinen SK, Rinne JO, Forssell H, Tenovuo O, Kaasinen V, Sonninen P, Bergman
J. Role of the dopaminergic system in chronic pain a fluorodopa- PET study. Pain
2001;15:90(3):257-60.
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dysphoric reaction under antipsychotic drugs - concepts, measurement and clinical
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12. Lpez-Avila A, Coffeen U, Ortega-Legaspi JM, del Angel R, Pellicer F. Dopamine
and NMDA systems modulate long-term nociception in the rat anterior cingulate
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13. Mayer, AM. Polyphenol oxidases in plants and fungi: Going places? A review.
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14. Mayer, AM. Polyphenol oxidases in plants and fungi: Going places? A review.
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Reduced presynaptic dopamine activity in fibromyalgias.
36
Oral Rehydration Solution
ORAL REHYDRATION SOLUTION (ORS) THERAPY (FIG. 36.1)
ORS has been hailed as one of the most
important medical advances by The Lancet
(1978, ii: 300301) calling it the most
important medical discovery of the 20th
century. It states that a simple therapy of water
with sugar and salt is a true miracle.
HISTORY
Dr Dilip Mahalanabis, participated in the
development of the oral rehydration therapy
as a staff member of the John Hopkins Centre Fig. 36.1: Oral rehydration solution
for Medical Research and Training, Kolkata.
During one of diarrhea outbreaks in Bangladesh war refugee camp the
intravenous fluids were in short supply. Dr Dilip Mahalanabis began giving
oral rehydration fluids to all patients who were not in urgent need of intravenous
therapy. The oral rehydration solution was administered by mothers and
relatives of children. They collected the solution in small cups from central
drums and gave to the suffering patients. Remarkably, the case-fatality rate in
Mahalanabiss camp was about 3 percent compared with 20 to 30 percent
rates in the camps that used only intravenous fluids.
But despite such efficacy, there was skepticism and it was not initially
accepted universally. Dr Barua an ardent crusader and supporter of Dr
Mahalanabis, applied unyielding pressure on medical fraternity which led to
formation of the Diarrheal Diseases Control Program, in 1978.
Advantages of ORS
Simplicity, low cost and remarkable ease of use.
Oral Rehydration Solution 241

PRINCIPLE OF ORS
Bad News
Nutrient-independent sodium absorption across the brush border membrane
of intestinal epithelial cells is impaired in patients with diarrhea.
Good News
Sodium-coupled glucose co-transport across gastrointestinal epithelium
against its concentration gradient remains largely intact and continues to
stimulate resorption of salt and water.
Sodium that enters the cell, is pumped into the blood by the Na+K+ATPase
(adenosine triphosphatase) pump in the basolateral membrane, maintaining
the sodium electrochemical gradient that drives the sodium-glucose cotransport
mechanism.
STANDARD WHO ORS
Glucose-electrolyte-ORT was a success, but in hope of reducing the stool
output, efforts to improve the efficacy of ORS continued. (especially with
respect to the sodium and glucose concentrations and thus, osmolarity).
WHO-recommended ORS contains:
90 mmol/L of sodium, 20 mmol/L of potassium, 80 mmol/L of chloride, 30
mmol/L of bicarbonate and 111 mmol/L of glucose, with an osmolarity of 311
mmol/L.
WHO recommended a revised formulation reduced osmolarity (245
mmol/L) ORS containing 75 mmol/L of sodium, 20 mmol/L of potassium, 65
mmol/L of chloride, 10 mmol/L of citrate and 75 mmol/L of glucose (1mol.
citrate=3 mol. bicarb).
The Concern: Sodium concentration of 90 mEq/L was too high for the
lower salt losses of childhood diarrhea. Efforts to improve ORS were made
with the development of rice-based ORS, which significantly reduced stool
output (being a super ORS containing amino acids).
Pedia Pearl: Supplementing intravenous potassium in IV Fluids may be dangerous in

dehydrated patient as one cannot clinically rule out the presence of intrinsic renal failure
as the cause of oliguria.

REDUCED OSMOLARITY ORS
What is reduced osmolarity ORS?
Typically 75 to 75 ORS is reduced osmolarity ORS (i.e. sodium ranges of
60-75 mEq/L and glucose ranges of 75-80 mmol/L), although some cerealbased ORS may also be of low osmolarity. These solutions generally preserve
the 1:1 molar ratio of sodium to glucose that is critical for efficient cotransport
of sodium, but present a lower osmolar load to the intestinal tract, than does
the original WHO ORS.
Expected Complications
Abnormalities, including chronic hyponatremia and hypokalemia, have been
hypothesized to occur with reduced-osmolarity ORS. But reduced-osmolarity
ORS given to patients with severe protein energy malnutrition have actually
shown improved clinical outcome and even absence of symptoms of
hyponatremia and hypokalemia. Reduced osmolarity ORS also appeared safe
and effective for children, even with cholera.
Also, in Infants with Persistent Diarrhea (duration >14 days), this new
ORS is more useful.
Indicators of Efficacy of ORS (Reduced osmolarity)
1. Reduced stool output.
2. Reduced vomiting.
3. Reduced need for supplemental IV therapy.
True Complications of Low Osmolarity ORS
Transient hyponatremia can occur in cholera but it can be rapidly corrected
when the normal diet is resumed.
Home Made ORS: (How to Prepare?)
Add two pinches of salt, one heaped tea spoon of sugar and half a lemon in
200 ml of water.
KILLER ORS
The addition of excess glucose in a solution of ORS can be a killer (due to
osmotic diarrhea).
Caution: Sugar, fruit juices, and cola can worsen diarrhea, as they have high
osmolar load.
Zinc-fortified ORS
This new ORS also reduces the duration and severity of diarrhea.

GUIDELINES
1. Use of oral rehydration solution (ORS) to correct estimated dehydration in
3 to 4 hours (i.e. fast rehydration).
2. Use of hyposmolar solution (New ORS).
3. Continuation of breastfeeding throughout.
4. Early refeeding, i.e. resumption of normal diet (without restriction of lactose
intake) after 4 hours of rehydration.
5. Prevention of further dehydration by supplementing maintenance fluids
with ORS (10 ml/kg/watery stool).
6. No unnecessary medications.
FAILURE OF ORAL REPLACEMENT THERAPY
This is likely in:
Shock
>10 percent dehydrated state
High purge rate and vomiting.
Caution: Hypernatremic dehydration needs careful management and requires
frequent reassessment. If ORS THERAPY does not work, then follow R3:
Resuscitate with IV normal saline/Ringer lactate
Rehydrate, but correct sodium levels slowly.
Oral or nasogastric rehydration using ORS or home available fluids is
tried. If it fails.
Replace the calculated deficit using N/2 (0.45%) saline in 5 percent dextrose
over 8 hours.
Cover ongoing losses as well.
Next step is to provide maintenance therapy using N/5 or (0.18%) saline
in 5 percent dextrose. Calculate for 24 hours from the end of replacement.
Add 10 mmol KCl to each 500 ml of IV fluid after the patient has passed
urine.
When the patient is rehydrated, start a normal diet including maintenance
fluids. Continue to supplement with ORS (10 ml/kg/watery stool) until
diarrhea stops.
BIBLIOGRAPHY
1. Barua D. Application of science in practice by the World Health Organization in
diarrhoeal diseases control. Journal of Diarrhoeal Diseases Research 1993;11:193-6.
2. Black RE, Morris SS, Bryce J. Where and why are 10 million children dying every
year? Lancet 2003;361:2226-34.
3. Booth I, Cunha Ferreira R, et al. Recommendations for composition of oral rehydration
solutions for the children of Europe. Report of ESPGAN Working Group. J Pediatr
Gastroenterol Nutr 1982;14:113-5.
4. Brown KH, Gastanaduy AS, Saavedra JM, et al. Effect of continued oral feeding on
clinical and nutritional outcomes of acute diarrhea in children. J Pediatr 1988;112:191200.

5. Brown KH. Dietary management of acute childhood diarrhea: Optimal timing of
feeding and appropriate use of milks and mixed diets. J Pediatr 1991;118 (suppl):
S92-8.
6. Brown KH, Peerson JM, Fontaine O. Use of nonhuman milks in the dietary
management of young children with acute diarrhea: A meta-analysis of clinical trials.
Pediatrics 1994;93:17-27.
7. Duggan C; Fontaine O; Pierce N F; Glass R I; Mahalanabis D; Alam N H; Bhan M K;
Santosham M. Bulletin of the World Health Organization, 2001; 79(5). Public Health
Classics Scientific Rationale for a Change in the Composition of Oral Rehydration
Solution, JAMA. 2004;291:2628-31.
8. Chung AW, Viscorova B. The effect of oral feeding versus early oral starvation on the
course of infantile diarrhea. J Pediatr 1948;33:14-22.
9. Farthing M, Walker-Smith, (Eds). Oral rehydration solutions for the children of Europe:
Proceedings of the workshop held at the XXI Annual Meeting of ESPGAN,
Copenhagen, May 20, 1988. Acta Paediatr Scand 1989; (suppl 364):1-50.
10. Hirschhorn N, Greenough WB 3rd. Progress in oral rehydration therapy. Sci Am
1991;264:50-6.
11. Hirschhorn N, Kinzie J, Sachar D, et al. Decrease in net stool output in cholera during
intestinal perfusion with glucose-containing solutions. N Engl J Med 1968;279:17681.
12. Hirschhorn N. Decrease in net stool output in cholera during intestinal perfusion with
glucose containing solutions. New England Journal of Medicine 1968; 279:176-80.
13. Hoghton MAR, Mittal NK, Mahdi G, et al. Continuous modified feeding in acute
gastroenteritis. J Gen Pract 1996;46:173-5.
14. Isolauri E, Juntunen M, Wiren S, et al. Intestinal permeability changes in acute
gastroenteritis: effects of clinical factors and nutritional management. J Pediatr
15. International Study Group on Reduced Osmolarity ORS. Multicentre evaluation of
reduced osmolarity oral rehydration salt solution. Lancet 1995;345:282-5.
16. Khin-Maung U, Nyunt-Nyunt-Wai, Myo Khin, et al. Effect on clinical outcome of
breastfeeding during acute diarrhoea. BMJ 1985;290:587-9.
17. King CK, Glass R, Bresee JS, Duggan C. Centers for Disease Control and Prevention.
Managing acute gastroenteritis among children: Oral rehydration, maintenance, and
nutritional therapy. MMWR Morb Mortal Wkly Rep 2003;52(RR-16):1-16.
18. Knudson KB, Bradley EM, Lecocq FR, et al. Effect of fasting and refeeding on the
histology and disaccharidase activity of the human intestine. Gastroenterology
1968;55:46-51.
19. Kosek M, Bern C, Guerrant RL. The global burden of diarrhoeal disease, as estimated
from studies published between 1992 and 2000. Bull World Health Organ.
2003;81:197-204.
20. Levine GM, Deren JJ, Steiger E, et al. Role of oral intake in maintenance of gut mass
and disaccharide activity. Gastroenterology 1974;67:972-82.
21. Lifshitz F, Wapnir RA. Oral dehydration solutions: Experimental optimization of
water and sodium absorption: I. Oral rehydration. J Pediatr 1985;106:382-9.
22. Lifshitz FI, Maggiori A. The nutritional management of acute diarrhoea in young
infants. J Ped Gastroenterol Nutr 1994;19:148-50.
23. Mahalanabis D, et al. Oral fluid therapy of cholera among Bangladesh refugees. The
Johns Hopkins Medical Journal 1973;132:197-205.
24. Molla AM, Rahman M, Sarker SA, et al. Stool electrolyte content and purging rates
or diarrhoea caused by rotavirus, enteropathogenic E. coli and V. cholerae in children.
J Pediatr 1981;98:835-8.

25. Nalin DR. Nutritional benefits related to oral therapy. In: Bellanti JA, Ed. Acute
Diarrhoea: Its Nutritional Consequences in Children. New York: Nestle, Levey/ Raven
Press 1983;185-91.
26. Nanulescu M, Condor M, Popa M, et al. Early feeding in childhood gastroenteritis. J
Pediatr Gastroenterol Nutr 1997;24:522-7.
27. Placzek M, Walker-Smith JA. Comparison of two feeding regimens following acute
gastroenteritis in infancy. J Pediatr Gastroenterol Nutr 1984;3:245-8.
28. Pierce NF, et al. Oral replacement of water and electrolyte loss in cholera. Indian
Journal of Medical Research 1968;57:848-55.
29. Parashar U, Hummelman E, Bresee J, Miller M, Glass R. Global illness and deaths
caused by rotavirus disease in children. Emerg Infect Dis 2003;9:565-72.
30. Pierce N, Banwell J, Mitra R, et al. Effect of intragastric glucose-electrolyte infusion
upon water and electrolyte balance in Asiatic cholera. Gastroenterology 1968;55:33342.
31. Report of a field trial by an international working group. A positive effect on the
nutrition of Philippine children of an oral glucose-electrolyte solution given at home
for the treatment of diarrhoea. Bulletin of the World Health Organization 1977;55:8794.
32. Rees L, Brook CGD. Gradual reintroduction of full strength milk after acute
gastroenteritis in children. Lancet 1979;2:770-1.
33. Samadi AR, Islam R, Huq MI. Replacement of intravenous therapy by oral rehydration
solution in a large treatment centre for diarrhoea with dehydration. Bulletin of the
World Health Organization 1983;61:471-6.
34. Santosham M, et al. Oral rehydration therapy for diarrhea: An example of reverse
transfer of technology. Pediatrics 1997;100(5).
35. Victora CG, Bryce J, Fontaine O, Monasch R. Reducing deaths from diarrhoea through
oral rehydration therapy. Bull World Health Organ 2000;78:1246-55.
36. Wapnir RA, Lifshitz F. Osmolarity and solute concentration-their relationship with
oral hydration solution effectiveness: An experimental assessment. Pediatr Res
1985;19:894-8.
37. Walker-Smith J, Sandhu BK, Isolauri E, et al. Recommendations for feeding in
childhood gastroenteritis. Medical position paper on behalf of ESPGAN. J Ped
38. Water with sugar and salt. Lancet 1978;2:300-1.
37
Digoxin
Digoxin is rapidly absorbed in children and is used for dysrhythmias/CCF, etc.
It is cardiotonic and has a positive inotropic and negative chronotropic action,
i.e. increases the catecholamine levels and vagal activity respectively (strengthens
the systole and lengthens the diastole). It also causes splanchnic, peripheral and
pulmonary vasoconstriction.
Congestive Cardiac Failure
Provided the myocardium is not involved, the heart muscle reponds to the
inotropic action of digoxin (In rheumatic myocarditis, digoxin has a
controversial role).
Tachyarrhythmias
As digoxin affects atrioventricular conduction tachyarrhythmias respond to
digoxin.
Digoxin Dosage (Therapeutic Levels are 1-2 ng/ml)
The total oral digitalizing dose = 0.04 mg/kg.

The IV doses are usually 2/3 rd of the oral doses. For preterms the dose is
slightly less.
The First dose is 1/2 the digitalizing dose. 8 hours later, give 1/4th the
digitalizing dose and after 16 hours the final 1/4 th digitalizing dose is
given.
Drug Interactions
Spironolactone decreases the digoxin clearance.
DIGOXIN TOXICITY
Toxicity often occurs from miscalculation of dose.

Toxicity is more likely if a child is on diuretics or has hypokalemia/
hypercalcemia.
Periodic ECG follow-up, helps to assess toxicity.
Digoxin 247
Adverse Effects
Lethargy, vomiting, diarrhea

Shortening of QTc interval
Prolongation of PR interval
Sagging ST segment
Sinus bradycardia or SA block
Diminished T-wave amplitude
Atrial or nodal ectopic beats
Slow heart rate and ventricular arrhythmias
Yellow vision occurs in toxicity.
Management of Toxicity
Acute Toxicity
1. Stop the digoxin.
2. Correct electrolyte problems.
3. Correct hypoxia and acid-base abnormalities.
Chronic Toxicity
A single vial (38 mg of the Fab fragments) adminstered if the weight > 20 kg
is usually adequate.
Each vial of Digibind contains specific antidigoxin antibodies produced by
sheep which will bind approximately 0.5 mg of digoxin and the Fab fragment
digoxin complex is excreted by the kidney.
For acute ingestions of unknown amounts 20 vials are adequate.
Contraindications of Digoxin
1.
2.
3.
4.
5.
Hypokalemia (as it enhances toxicity).

Renal diseases.
Thyrotoxicosis.
Myxedema (as it enhances toxicity).
Ventricular tachycardia (Digoxin may lead to ventricular fibrillation.
BIBLIOGRAPHY
1. DJ Goodman et al. (1975). "Effect of digoxin on atioventricular conduction. Studies in
patients with and without cardiac autonomic innervation". Circulation 51(2):251-6.
2. Flanagan RJ, Jones AL. "Fab Antibody Fragments: Some Applications in Clinical
Toxicology" (full text (subscription)). Drug Safety 2004;27(14):1115-33.
3. Jusko WJ, et al. Pharmacokinetic design of digoxin dosage regimens in relation to renal
function. J Clin Pharmacol 1974;14:525-35
4. Reuning RH, Garaets DR. "Digoxin", in Evans W, Schentag J, Jusko J (eds): Applied
Pharmacokinetics. Applied Therapeutics, Inc, San Francisco 1986;pp 908-43.
Pedia Pearl: Reverse hockey stick sign is seen in ECG in digitalis toxicity.
38
Steroids
INDICATIONS
A . Autoimmune Disorders
In the treatment of:
Acquired hemolytic anemias and ITP
Systemic lupus erythematosus
Nephrotic syndrome
Acute rheumatic fever (carditis).
B. Bronchial Asthma
In Bronchial Asthma, the treatment of persistent variety mandates the use of
steroids.
C. Cortisol Supplementation
Congenital Adrenal Hyperplasia (CAH)

Primary adrenal insufficiency
Adrenoleukodystrophy
Panhypopituitarism.
D. Dermatologic Diseases
Pemphigus, severe erythema multiform, Steven Johnson syndrome, herpes
zoster ophthalmicus, iritis, iridocyclitis and chorioretinitis.
E. Emergencies
Acute Adrenal Insufficiency with Shock
Perioperatively, the demand for steroids is high. The demand also increases
acutely if the steroids are abruptly stopped and in Meningococcemia/adrenal
hemorrhage. Hence, if steroids are not given. Addisonian crisis and shock
ensues.
Steroids 249
Anaphylaxis/Allergy
Treatment of hypersensitivity reactions including anaphylaxis.
Refractory Shock
Where standard therapy of fluid replacement has not been effective, there the
mineralocorticoid action increases the sensitivity of the vasculature to
epinephrine and norepinephrine. It also causes salt and water retention.
Refractory Hypoglycemia
In Weiddman Beckwith syndrome the steroids improve blood sugar.
Acute Attack of Ulcerative Colitis
Steroids help to reduce the inflammation.
F. Fevers
Typhoid in Toxic State
Children with typhoid fever often develop toxicity which may be serious
enough to warrant the use of steroids.
G. Granulomatous Inflammations
A typical example is that of non-caseating granulomas of sarcoidosis.
H. Hypotensive Low Birth Weight Babies
Prevention and treatment with glucocorticoids often helps prevent or relieve
this condition.
I. Inflammation
In Tuberculous involvement of serosal surfaces. (Effusion, tuberculous
meningitis with subarachnoid block or impending block) give steroids along
with appropriate antituberculous therapy.
J. Joint Inflammation
A typical example is rheumatoid arthritis.
K. Keeping Muscular Dystrophy Under Control
A typical example is the use of steroids in management of Duchennes Muscular
Dystrophy.

L. Lung Maturation
For fetal lung maturation, betamethasone is given 12 mg 12 hrly 2 days
prior to delivery.
Leukemias of Childhood: Prednisolone is given in treatments of ALL.
GLUCOCORTICOIDS
TYPES
Short acting glucocorticoid: Hydrocortisone

Intermediate acting glucocorticoids: Prednisolone, Methlyprednisolone
Long acting glucocorticoids: Dexamethasone, betamethasone.
Hydrocortisone
Hydrocortisone is the chemical form of cortisol which is a stress hormone,
produced in the response to stress. It is used as an anti inflammatory agent
and during emergencies.
Indications and dosage
1. Anti-inflammatory dosage of hydrocortisone is 5 mg/kg dose in most cases.
2. Dosage in shock is 10 mg/kg dose.
3. Dosage in Acute adrenal insufficiency:
Older children, Initial: 1 to 2 mg/kg by IV bolus; then, 150 to 250 mg/
kg/day IV is given in divided doses
Infants, initial: 1 to 2 mg/ kg by IV bolus; then, 25 to 150 mg/kg/day is
given in divided doses.
Oral Prednisolone
Usual dosage of prednisolone - 2 mg/kg day. Taper steroids if given for longer
than 1 week.
MINERALOCORTICOIDS
Aldosterone
Fludrocortisone
Desoxycorticosterone acetate.
Contraindication
In systemic fungal infections, steroids are contraindicated.
Interactions
Live vaccines, phenytoin and rifampin may increase the clearance of
corticosteroids.
Steroids 251
Adverse Effects
Anergy: Anaphylaxis may suppress reactions to skin tests.

Bone: Osteoporosis, pathologic fractures and aseptic necrosis.
Congestive cardiac failure in few susceptible patients.
Dermatologic: Impaired wound healing (at high doses), petechiae and
ecchymoses, facial erythema, increased sweating, pigmentation cutaneous
atrophy, sterile abscess, anaphylactoid reaction, etc.
Endocrine: Diabetogenic: Raising levels of blood sugar by increasing
gluconeogenesis. Cushingoid state, suppression of pituitary-adrenal axis,
suppression of growth in children.
Fluid and electrolyte disturbances: Steroids increase potassium and calcium
excretion.
Growth may be suppressed in children receiving long-term, daily-divided
dose glucocorticoid therapy.
Hypertension.
Immune system: Immunosuppressant: Masking of infections, latent
infections becoming active, opportunistic infections.
Just keeps the liver enzymes elevated.
Metabolic: Negative nitrogen balance due to protein catabolism.
Neurological
Myopathy, muscle weakness, and loss of muscle mass.
Raised intracranial pressure (pseudotumor cerebri).
Psychosis.
Ophthalmic: Cataracts, glaucoma, exophthalmos.
Peptic ulceration and esophagitis.
Steroid allergy, especially to topical steroids.
BIBLIOGRAPHY
1. 7-day treatment with low doses of hydrocortisone and fludrocortisone significantly
reduced the risk of death in patients with septic shock and relative adrenal insufficiency
without increasing adverse events. JAMA 2002;21:288(7):862-71.
2. Aberer W, Bircher A, Romano A, et al. Drug provocation testing in the diagnosis of
drug hypersensitivity reactions: General considerations. Allergy 2003;58:854-63.
3. Aranda A, Mayorga C, Ariza A, et al. IgE-mediated hypersensitivity reactions to
methylprednisolone. Allergy 2010.
4. Asakawa H, Araki T, Imai I, et al. Skin tests of steroid allergy. Allergy 1999;54:6456.
5. Borja JM, Galindo PA, Feo F, Gomez E. Urticaria to methylprednisolone sodium
hemisuccinate. Allergy 2001;56:791.
6. Bourhier. Bourchier D, Weston PJ. Randomised trial of dopamine compared with
hydrocortisone for the treatment of hypotensive very low bith weight infants 1997.
7. Brockow K, Romano A, Blanca M, et al. General considerations for skin test procedures
in the diagnosis of drug hypersensitivity. Allergy 2002;57:45-51.
8. Bourchier D, Weston PJ. Randomised trial of dopamine compared with hydrocortisone
for the treatment of hypotensive very low birth weight infants. Archives of Disease in
Childhood: Fetal and Neonatal Edition 1997;76:F174-8.

9. Bundgaard H. The possible implication of steroidglyoxal degradation products in
allergic reactions to corticosteroids. Arch Pharm Chem Sci Ed 1980;8:83-90.
10. Compalati E, Guerra L, Rogkakou A, et al. Angioedema after administration of
methylprednisolone to treat drug allergy. Allergy 2007;62:1346-8.
11. Efird, Efird MM, Heerens AT, Bose CL, Young DA. A randomized controlled trial of
prophylactic hydrocortisone supplementation for the prevention of hypotension in
extremely low birth weight infants. Journal of Perinatology 2005;25:119-24.
12. Elliot F, Ellis MD. Adverse effects of corticosteroid therapy. J Allergy Clin Immunol
1987;80:515-7.
13. Fernandez de Corres L, Urrutia I, Audicana M, et al. Erythrodermia after intravenous
injection of methyl prednisolone. Contact Dermatitis 1991;25:68-70.
14. Juren. Juren T. The effect of the early hydrocortisone administration on the blood
pressure in extremely low birth weight infants. Cesko-Slovenska Pediatrie.
2003;58:546-51.
15. Juren T. The effect of the early hydrocortisone administration on the blood pressure
in extremely low birth weight infants. Cesko-Slovenska Pediatrie 2003;58:546-51.
16. Kilpio K, Hannuksela M. Corticosteroid allergy in asthma. Allergy 2003;58:1131-5.
17. Klein-Gitelman MS, Pachman LM. Intravenous corticosteroids: adverse reactions
are more variable than expected in children. J Rheumatol 1998;25:1995-2002.
18. Lopez S, Torres MJ, Antunez C, et al. Specific immunological response to budesonide
in a patient with delayed-type hypersensitivity reaction. J Invest Dermatol
2010;130:895-7.
19. Mendelson LM, Meltzer EO, Hamburger RN. Anaphylaxis-like reactions to
corticosteroid therapy. J Allergy Clin Immunol 1974;54:125-31.
20. Padial A, Posadas S, Alvarez J, et al. Nonimmediate reactions to systemic
corticosteroids suggest an immunological mechanism. Allergy 2005;60:665-70.
21. Preuss ML. Allergic reactions to systemic glucocorticoids: A review. Ann Allergy
1985;55:772-5.
22. Pryse-Phillips WE, Chandra RK, Rose B. Anaphylactoid reaction to
methylprednisolone pulsed therapy for multiple sclerosis. Neurology 1984;34:111921.
Antibiotics 253
39
Antibiotics
Antibiotic Therapy
Which antibiotic is best indicated clinically, depends on the organisms, likely
to cause the infection (Educated guess), on the sensitivity patterns in the area,
the side effects and its cost. It antibiotic therapy is of three types:
Empiric therapy, Specific therapy and Prophylactic therapy.
Empiric Therapy
This is the treatment based only on clinical and laboratory data without any
information of culture and sensitivity report.
Steps in Empiric Therapy
First suspect clinical entity

Find the organisms causing this entity
Select an antibiotic which covers these organisms.
For example, cellulitis is usually associated with suppuration. Now, it is
preferable to select the antibiotic which shall act on pus, covering those organisms
likely to cause cellulitis.
Specific Therapy
This is based on the culture and sensitivity report. For example, if culture report
shows Staph. aureus, selection of an antibiotic with the most narrow spectrum
covering Staph. aureus shoud be done to reduce the likelihood of significantly
altering the patients normal flora.
Prophylactic Therapy
It is the use of antibiotics to prevent an infection, e.g. a child with vesicoureteral
reflux is at a greater risk for urinary tract infection. Children with rheumatic
fever/rheumatic heart disease are at risk of similar attacks. Such patients are
put on long-term treatment, e.g. long acting benzathine penicillin injections
to prevent another attack of Rheumatic Fever. This is called Prophylaxis.

COMMON ANTIBIOTICS AND ANTIBIOTIC GROUPS
Penicillin and Ampicillin
Action: Inhibits cell wall synthesis.
Uses:
1. Useful against gram-positive infections: Based on the premise that grampositive organisms are more dependent on peptidoglycan cell wall synthesis
(thats why they stain gram-positive), while gram-negative organisms are
not as dependent on peptidoglycan cell wall synthesis.
2. Useful in anaerobic infections like tetanus.
Side effects: Anaphylactic like fatal type-I reactions cross-reactivity with
cephalosporins and Jarisch Herscheimer reaction.
Points to note: Amoxicillin is metabolized to ampicillin.
Amoxycillin is a good drug for respiratory infections and Amoxyclavulinic
for complicated infections.
Cephalosporins
Action: Inhibits cell wall synthesis.
Uses
1. Lower generation cephalosporins cover Staphylococcus and Streptococcus
(hence useful for skin/soft tissue infection), e.g. cefazolin.
2. The higher generations of cephalosporins have extended coverage of gramnegative organisms. An example of a typical third generation cefalosporin
is ceftriaxone.
3. Special situations:
For meningitis: Cefotaxime and ceftriaxone, (third generation) penetrate
the blood-brain barrier easily.
For Pseudomonas coverage: Ceftazidime is used.
For Anaerobic coverage: Use cefotetan/cefoxitin.
For GI and GU infections: Cefixime is used.
Once a day concept: Ceftriaxone (long half-life) is used as once a day
therapy.
Side effects:
a. Hypersensitivity
b. Eosinophilia
c. GI disturbance and rash.
Antibiotics 255
Aminoglycosides
Action: Inhibit bacterial ribosomal function.
Uses: Aminoglycosides are generally directed at gram-negative organisms
(also cover gram-positive organisms such as Staph aureus and many
streptococci).
Side effects (Curare like action): They can cause respiratory depression or
apnea if given in Guillain-Barr syndrome, myopathies, etc. They are
nephrotoxic and ototoxic as well.
Metronidazole
Action: Against anerobes and parasites.
Uses: Metronidazole (Flagyl) is an antiparasitic (e.g. giardia) and antiamebic
drug and has almost complete coverage of anaerobes.
Side effects (Disulfiram like action): Disulphiram like reaction if taken with
alcohol. It has a metallic taste and can cause severe chest tightness if taken
even with a cough syrup containing alcohol.
Quinolones
Action: These drugs inhibit bacterial DNA synthesis by inhibiting B-subunit
of DNA gyrase.
Uses: This class of antibiotics are related structurally to nalidixic acid. They
are all rounders (excellent tissue levels and very broadspectrum), e.g.
norfloxacin. Newer quinolones have anaerobic activity as well.
Caution in Children
May affect cartilage function and growth.
Vancomycin
Action: Interferes with cell wall and RNA synthesis.
Uses: This belongs to glycopeptides used for treating MRSA (methicillin
resistant Staph. aureus) and Clostridium difficile colitis.
Side effects: They are nephrotoxic (must monitor blood levels) and ototoxic.
Rapid IV infusion can cause anaphylactoid reaction (red man syndrome).
Pedia Pearls:
Antibiotics may be given through oral, intramuscular, intravenous, intrathecal route
or in peritoneal dialysis fluid.
Antibiotics may diminish efficacy of vaccine like BCG and typhoid vaccines.
Aminoglycosides are preferably given once a day.
Gentamycin and penicillin group show synergy, hence added benefit is expected with
such combinations.

Sulfonamides
Action: Most sulfonamides inhibit folate metabolism, e.g. trimethoprimsulfamethoxazole (Bactrim/Septran).
Uses: In diarrheal diseases, upper respiration infection and Toxoplasmosis in
children.
Side effects: Adverse reactions include hemolytic reactions and Steven-Johnson
syndrome. They cause megaloblastic anemia due to folate deficiency.
Carbapenems
Action: This new class of antibiotic targets bacterial cell wall. It includes
imipenems and meropenems, etc.
Uses: In serious infections due to resistant organisms.
Side effects: Rash, eosinophilia, nausea, vomiting and even seizures.
Macrolides
Action: These drugs inhibit bacterial ribosomal function.
Uses: They cover most streptococci and some staphylococci and many
atypical organisms like Mycoplasma and Chlamydia. Once a day
azithromycin as a 5-day course of 10 mg/kg has 10 days efficacy, for pertussis,
etc.
Side effects: Azithromycin is ototoxic and nephrotoxic. Erythromycin estolate
may cause obstructive jaundice.
Tetracycline
Action:Binds to 30 S ribosomes and inhibit bacterial protein synthesis.
Uses: The tetracycline family, (e.g. doxycillin) are often used in cholera and
sinusitis.
Side effects: Staining of teeth, hypoplasia of dental enamel and abnormal bone
growth in children can occur.
Chloramphenicol
Action: Inhibits bacterial ribosomal function.
Uses: It crosses the blood brain-barrier well into the CSF. It was frequently
used to treat bacterial meningitis.
Side effects: It has potential to cause reversible dose dependant and irreversible
idiosyncratic bone marrow suppression.
Antibiotics 257
BIBLIOGRAPHY
1. Abramowicz M. Antimicrobial Prophylaxis in Surgery, Medical Letter on Drugs
and Therapeutics, Handbook of Antimicrobial Therapy, 16th edn. New York, NY:
Medical Letter, 2002.
2. Ahkee S, Smith R, Ritter GW. Once-daily aminoglycoside dosing in lower respiratory
tract tnfections. Pharm Therapeut 1995;20:226-34.
3. American Academy of Pediatrics Committee on infectious Diseases, Treatment of
Bacterial Meningitis, Pediatrics. 1988;81(6):904-7.
4. Boyce, John M. Epidemiology, prevention, and control of methicillin-resistant
Staphlyococcus aureus in adults. Up To Date (12.3). 2004
5. Cunha BA. Vancomycin, Med Clin North Am 1995;79(4):817-31.
6. Eliopoulos, GM. Current and new antimicrobial agents american heart journal
2004;147(4);587-592.
7. Frimat L, Hestin D, Hanesse B, et al. Acute Renal Failure Due to Vancomycin Alone.
Nephrol Dial Transplant, 1995;10(4):550-1.
8. Gilbert DN, Moellering RC, Eliopoulos GM, et al. (Eds): The Sanford Guide To
Antimicrobial Therapy, 36th edn. Hyde Park, VT: Antimicrobial Therapy, Inc, 2006;
6-7.
9. Linden P. Antibiotic Therapy in Critical Illness, Multidisciplinary Critical Care
Review, Zimmerman JL and Roberts PR, (Ed). Des Plaines, IL: Society of Critical
Care Medicine, 2003;192.
10. Luer MS, Hatton J. Vancomycin administration into the cerebrospinal fluid: A review.
Ann Pharmacother 1993;27(7-8):912-21.
11. Nielsen HE, Sorensen I, Hansen HE. Peritoneal transport of vancomycin during
peritoneal dialysis. Nephron 1979;24(6):274-7.
12. Quagliarello VJ, Scheld WM. Treatment of bacterial meningitis N Engl J Med. 1997;
336(10):708-16.
13. Richard, Grady. Safety profile of quinolone antibiotics in the pediatric population.
The Pediatric Infectious Disease Journal. 2003;22(12)1128-32.
14. Rossing TH, Fanta CH, McFadden ERJ. A controlled trial of the use of single versus
combined-drug therapy in the treatment of acute episodes of asthma. American Review
of Respiratory Disease 1981;123(2):190-4.
15. Roth DB, Flynn HW Jr. Antibiotic selection in the treatment of endophthalmitis: The
significance of drug combinations and synergy. Surv Ophthalmol 1997; 41(5):395401.
40
Vitamins and Minerals
Vitamin and mineral supplements are not necessary for healthy children who
follow a well-balanced, varied diet. Rather, encourage the consumption of
fruits, green and yellow vegetables. However, vitamin E, vitamin K, vitamin
B12, vitamin D and iron are needed in special circumstances.
AGEWISE INDICATIONS
Preterm Infants
Preterm infants have increased demands of catch up growth. Hence, during
the first week of life, a multivitamin supplement is given that contains equivalent
of Recommended Daily Allowance (RDA) for term infants. It should be
supplied till the baby achieves a weight of 2.5 kg to meet the extra demands of
preterm infants.
Iron supplementation is best delayed until after the first six weeks of life
because neonatal stores of iron are sufficient for erythropoiesis. The prophylactic dosage of elemental iron is 2 mg/kg per day.
All Newborn Infants
Vitamin K- prophylaxis against hemorrhagic disease of the newborn minimizes
the postnatal fall of the: vitamin K dependent coagulation factors (II, VII, IX,
and X).Vitamin K should be given as a single, intramuscular dose of 0.5 mg to
babies less than 2 kg and 1.0 mg for babies above 2 kg.
Side Effects
Vitamin K may cause hemolysis and displace bilirubin from its binding sites.
Older Infants
During the later part of infancy, once the child is on a good weaning diet of
cereal/milk/pulses, etc. in requisite amounts, he/she does not require extra
Vitamins and Minerals 259

supplements of vitamins and minerals. It is important, however, that the diet
includes an adequate source of vitamin C. Children and adolescents at nutritional
risks, are those from deprived families or on fad diets/vegetarian diets without
adequate dairy products or suffering from malabsorption due to cystic fibrosis,
etc. They need vitamin B12 and vitamin D supplementation as well.
For ToddlersVitamins A and Vitamin D Prophylaxis
Vitamin D is necessary in children with malabsorption, on anticonvulsants or
those on vegan diet and/or living in those areas where sunlight exposure is
very less (2 lac units above 1 year of age up to 3 years of age is given every
six months to these children).
Vitamin A prophylaxis at 9, 18, 24, 30 and 36 months is recommended for all
children to prevent nutritional blindness, while extra dose is indicated up to 5
years in measles and malnutrition. Dosage is 1 lac units at 9 months and 2 lac
units later.
For MothersFolic Acid Prophylaxis
Folic acid (0.4 mg) in periconceptional period is needed for prevention of
neural tube defects. A dose of 4 mg is given if she already has a child with
neural tube defect.
BIBLIOGRAPHY
1. Albertson AM, Tobelmann RC, Engstrom A, et al. Nutrient intakes of 2 to 10-yearold American children: 10-year trends. J Am Diet Assoc 1992;92:1492-6.
2. American Academy of Pediatrics. Pediatric Nutrition Handbook. 2nd edn. ElkGrove:
American Academy of Pediatrics, 1985.
3. Borowitz D, Wegman T, Harris M. Preventive care for patients with chronic illness.
Multivitamin use in patients with cystic fibrosis. Clin Pediatr 1994;33:720-5.
4. Bowering J, Clancy KL. Nutritional status of children and teenagers in relation to
vitamin and mineral use. J Am Diet Assoc 1986;86:1033-8.
5. Cook CC, Payne IR. Effects of supplements on the nutrient intake of children. J Am
Diet Assoc 1979;74:130-3.
6. Curtis DM. Infant nutrient supplementation. J Pediatr 1990;117:S110-8.
7. Filer LJ. Iron needs during rapid growth and mental development. J Pediatr
1990;117:S143-6.
8. Krebs-Smith SM, Cook A, Subar AF, et al. Fruit and vegetable intakes of children and
adolescents in the United States. Arch Pediatr Adolesc Med 1996;150:81-6.
9. Kumar A, Aitas AT, Hunter AG, et al. Sweeteners, dyes, and other excipients in
vitamin and mineral preparations. Clin Pediatr 1996;35:443-50.
10. Nelson M. Vitamin and mineral supplementation and academic performance in school
children. Proc Nutr Soc 1992;51:303-13.
11. Udall JN, Greene HL. Vitamin update. Pediatr Rev 1992;13:185-94.
41
Asthma Therapy
STEPS TO ASSESS THE DISEASE
Assess Severity
Take into consideration parents subjective impression regarding the severity
of obstruction, e.g. disturbance to sleep. Severity is also indicated by presence
of cyanotic episodes, altered sensorium bradycardia, diaphoresis and silent
chest.
Assess Progression
Assess progression of disease based on four factors, viz. wheeze, air entry,
SPO2 and pulsus paradoxus.
Assess Chronicity
Find out the stage of disease-whether intermittent or persistent (based on
the number of attacks).
DRUGS FOR PREVENTION AND MANAGEMENT
Prevention is better than cure. Avoid exposure/ contact with fur of animals,
pollen, dust mite, preservatives, beta-blockers and NSAIDs. Treat comorbid
conditions like gastrointestinal reflux, rhinitis/sinusitis, etc. Do not give
sedatives/ hypnotics/cough syrups/antihistamines as they dry up the secretions
and suppress expectoration, thus working against the bronchodilator action.
Preventors
Preventors are given for all asthmatics, except mild intermittent variety. They
maintain normal activity by causing prolonged bronchodilator action thereby
reducing mucosal swelling and secretions within the lumen.
Pedia Pearl: Mild intermittent asthma is characterized by nocturnal symptoms, not more
than twice a month, while persistent asthma has nocturnal symptoms more than twice a
month.
Asthma Therapy 261

Corticosteroids
Inhaled glucocorticoids like Beclomethasone and Budesonide are given twice
daily, preferably with spacers, which reduce the adverse effects and even a
lower dose suffices (800 g/day). Systemic steroids are given for severe
persistent asthma. If the physician is hesitant to hit hard with early use of
steroids then later the disease aggravates and much higher dosage of steroids
are needed (Rinse mouth after corticosteroids, to prevent fungal colonization).
Dose of oral prednisolone: 2 mg/kg/day.
Cromolyn Sodium (Mast Cell Stabilizer)
It is an anti-inflammatory drug which modulates mast cell mediator release
and the eosinophilic recruitment, prior to exercise or unavoidable exposure
to known allergens (stabilizes mast cell thereby preventing degranulation).
They attenuate/ prevent the early phase response. Similar action is seen
with ketotifen.
Dosage: 2 mg in 2 ml nebulizer solution.
Leukotriene Modifiers/Receptor Antagonists
Leukotrienes (released from mast cells), eosinophil and basophils attract the
inflammatory cells (the late phase). The leukotriene modifiers like Montelukast/
Zafirlukast attenuate this phase. They are given orally and have an additive
effect when used with inhaled steroids for children with mild persistent asthma,
above 12 years.
Dosage:
Monteleukast: 4 mg oraly HS (one dose suits all).
Preventor Plus Controller Drugs
Long-acting beta 2-agonists (Salmeterol, Formoterol) often combined with
steroids have this action.
They have a delayed onset but a sustained bronchodilator action, thereby they
relax airway smooth muscle for hours. These should not be used as monotherapy.
They prevent nocturnal and exercise-induced bronchospasm and give long-term
symptom control in moderate and severe pesistent asthma.
Dosage:
Salmeterol: 1 inhalation (Powder) 50 g 2 hourly.
Methylxanthines (Aminophylline, Theophylline)
They have a bronchodilatory, anti-inflammatory and diuretic action (by inhibiting
phosphodiesterase). They are used as add on therapy to inhaled steroids
especially for night symptoms. Long-acting theophyllines have fewer side
effects and give better response than the short-acting ones.
Dosage: Aminophylline 15 to 20 mg/kg/days in divided doses or as an infusion.

Relievers
Short-acting Beta 2-agonists (Salbutamol)
Dosage:
Oral salbutamol: 0.1 mg/kg day as tablets or syrup.
Meter dose inhalor: 0.1 mg/kg (100 g/puff) is given q15-20 min with a
spacer.
Nebulizer: 0.1 mg/kg in 2.5 ml normal saline.
Anticholinergics
Ipratropium bromide has atropine like action, but without its side effects.
It regulates the airway smooth muscle tone.
Systemic Steroids
In Acute Exacerbations
Both oral and IV steroids are potent in acute exacerbations.
Dosage:
Oral: Prednisone 60 mg/m2/day or 2 mg/kg/d.
Use short course early rather than long course later (Once a day dose)
Once good control occurs taper the oral steroids
When good control is achieved for more than 3 months, then reduce the
inhaled steroids.
In Steroid Dependence
These drugs reduce the steroid dosage requirement.
Cyclosporin
Methotrexate
Intravenous (IV) immunoglobulin
Hydroxychloroquine.
For Severe Cases.
Intravenous Methylprednisolone 30 mg/kg bolus administration is used.
Magnesium Sulfate and Heliox
Magnesium sulfate is used in refractory cases when hypomagnesemia

coexists.
Heliox (He:O2 mixture) utilizes the low density of helium to ventilate the
lung via a tight non-rebreathing mask.
Pedia Pearls:
Tobacco smoke, aspirin, infection and food additives may precipitate an attack of
asthma.
Goal of therapy is to maintain normal activity, without sleep disturbance and with
minimal adverse effects of medication.
Asthma Therapy 263

Preferable Mode of Drug Delivery
Inhalers/nebulizers
Inhalers with spacers are better than nebulizers in controlling asthma symptoms.
Outcomes that suggest efficacy of this inhalation therapy are:
1. Decreased hospital admission rates.
2. Improved asthma severity scores.
3. Improvement in pulmonary function scores.
Cochrane review and guidelines from the Global Health Initiative for Asthma,
recommend MDIs for children with asthma, due to good efficacy and less cost.
Recommendations
For infants: Use a spacer with face mask.
For preschool children: Use a mouthpiece and a spacer.
For school going children: Use a dry powder inhalor or a breath-activated
device (Rotahalers).
Summary of Treatment
1.
2.
3.
4.
For mild intermittent asthma: Use salbutamol.

For mild persisted asthma: Add Inhaled steroids.
For moderate persistent asthma: Add salmeterol theophylline.
For severe persistent asthma: Add oral steroids.
Definitions
1.
2.
3.
4.
Mild intermittent: <2 attacks at night per month

Mild persistent: 2-4 nights/month
Moderate persistent: minimum 2 nights/week
Severe persistent: every night attack.
BIBLIOGRAPHY
1. Ahrens R, Lux C, Bahl T, Havrr SH. Choosing the metered dose inhaler, sprayer or
holding chamber that matches the patients need: Evidence that the specific drug being
delivered in an important considerations. J. Allergen Clin Immunol 1995;96:288-94.
2. Anderson SD. Exercise-induced asthma. In: Kay AB (Ed): Allergy and allergic disease.
Oxford: Blackwell Scientific Publications 1997;99:692-711.
3. Barnes PJ, Pauwels RA. Theophylline in the management of asthma-time for
reappraisal? Eur Respir J 1994;7:579-91.
4. Barnes PJ, Pedersen S. Efficacy and safety of inhaled corticosteroids in asthma. Am
Rev Respir dis 1993;148:S1-S26.
5. Barnes PJ. Immunomodulation as asthma therapy where do we stand? Eur Respir J
1996;9:154-9.
6. Becker JM, Arora A, Scarfone RJ, et al. Oral versus, intravenous corticosteroids in
children hospitalised with asthma. J Allergy Clin Immunol 1999;103:586-90.

7. Bisgaard H. Leukotrine modifiers in pediatic asthma management. Pediatrics
2001;13(3):128-37.
8. Bloch H, Silverman R, Mancherje N, Grant S, Jagminas L, Scharf SM. Intravenous
magnesium sulphate as an adjunct in the treatment of acute asthma. Chest
1995;107:1576-81.
9. Calpin C, Macarthur C, Stephens D, Feldman W, Parkin PC. Effectiveness of
prophylactic inhaled steroids in childhood asthma. A systemic review of the literature.
J Allergy Clin Immunol 1997;100:452-7.
10. Cates CJ, Rowe BH, Bara A. Holding chambers versus nebulisers for beta-agonist
treatment of acute asthma (Cochrane Review). The Cochrane Library, Issue 2, 2002.
Oxford: Update Software, last updated February 21,2002.
11. Clough JB. Bronchodilators in infancy. Thorax 1993;48:308.
12. Deshpande A, Mckenzi SA. Short course of steroids in home treatment of children
with acute asthma. BMJ 1986;293:169-71.
13. Editorial. Acupuncture, asthma and breathlessness Lancet 1986;2:1427-8.
14. Evidence-Based Clinical Practice Guideline for Managing an Acute Exacerbation of
Asthma. Cincinnati, Ohio: Cincinnati Childrens Hospital Medical Center; 1998 (revised
2002). Available at: http://www.cincinnatichildrens.org/svc/dept-div/ health-policy/
ev-based/asthma.htm. Accessed on December 3, 2003.
15. Helms PJ. Wheezing infants. Clin Exper Allergy 1994;24:97-9.
16. Kemp JP. Making best use of todays bronchodilators. J Resp Dis 1994;15:521-7.
17. Lipworth BJ. Systemic adverse effect of inhaled corticosteroids therapy. ARCH interm
med 1999;159:941-55.
18. National Heart, Lung and Blood Institute (NHLBI), World Health Organization (WHO).
Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention.
2002. Available at: http:// www.ginasthma.com/workshop.pdf. Accessed on December
3, 2003. Updated from: NHLBI/WHO Workshop Report: Global Strategy for Asthma
Management and Prevention, issued January, 1995. NIH Publication No. 02-3659.
19. Newhouse MT, Delovich MB. Control of asthma by aerosols. N Engl J Med
1986;315:870-4.
20. Rees J, Prince J. Asthma in children: Treatment . BMJ 1995;310:1522.
21. Rees J, Prince J. Chronic asthmaGeneral management. BMJ 1995;310:1400.
22. Selvadurai H, Mallis C. Practical management of wheezy infants and toddlers. Modern
medicine 1998;41:18-32.
23. Singhal T, Garg H, et al. Efficacy of home made spacer for asthma. Indian J Ped
201;68(1):37-40.
24. Zorc JJ, Pusic MV, Ogborn CJ, Lebet R, Duggan AK. Ipratropium bromide added
asthma treatment in pediatric emergency departments. Pediatrics 1999;103:748-52.
Drugs in Seizure Therapy 265
42
Drugs in
Seizure Therapy
TYPES OF SEIZURES
1.
2.
3.
4.
Partial (simple or complex).

Generalized (absence, tonic, clonic, tonic clonic, myoclonic).
Special group like febrile seizures.
Syndromic epilepsy.
Mechanisms of Seizure
a. Ionic depolarization (Na channel, Ca channel and chloride channel induced)
b. Decreased inhibitory aminoacids (GABA, etc)
c. Increased excitatory amino acid transmission.
Aim of Treatment
To stabilize the membranes and prevent depolarization by action on ion channels
and/or to increase the GABAergic transmission and/or to decrease the excitatory
amino acid transmission.
DRUG TREATMENT OF EPILEPSY
Principles
1. Start with a single agent. Raise to the maximum tolerated dose before
shifting to another. Taper the first when starting the second. Raise dose of
the second drug to maximum tolerated dose needed to control seizures.
2. If therapy fails, one may use combination therapy (bi-therapy).
3. Compliance is a must (regular proper dose and never stop abruptly).
4. Duration of therapy is usually 2 years after last seizure, then taper and stop.
Pedia Pearls:
Rule out syncope, breath holding spells, migraine, jitteriness, night terrors and panic
attacks before starting treatment.
Specific signs of mennigitis may be absent in children less than 1 year. Hence, be
careful before labelling a seizure as a febrile seizure.
Presence of port wine stain, facial angiofibroma suggests a neurocutaneous syndrome.

Commonly Used Drugs and Dosages
Phenobarbital: 5 mg/kg Drug of choice for neonatal seizures.
Carbamazepine: 10 to 15 mg/kg. Drug of choice for partial seizures.
Ethosuximide: It was the drug of choice for absence seizures.
Valproic acid: 10 to 40 mg/kg. It is the drug of choice for refractory seizures
(Partial or generalized) and absence seizures.
Benzodiazepines (Sedative-hypnotic-anxiolytic):
Diazepam and lorazepam: Short-acting. for acute control.
Clonazepam for long-term treatment.
Fosphenytoin is a prodrug given IV or IM and is rapidly converted to phenytoin
in the body.
Phenytoin: 20 mg/kg loading and then 5 to 8 mg/kg in 2 divided doses. It is
the drug of choice for status and generalized seizures.
Newer Drugs
They stabilize the membrane and prevent depolarization with lesser side effects
and can be used for resistant cases: Lamotrigine, Felbamate, Topiramate,
Gabapentin, Vigabatrin, Oxycarbazepine, Levetiracetam and Fosphenytoin are
good examples.
Modes of Action and Side Effects
1. Metabolic action: Phenobarbital raises the seizure threshold and decreases
the metabolic requirement of brain and hence, drug of choice for neonatal
seizures.
2. Na channel blockers: For example, Carbamazepine and lamotrigine.
3. Inhibitors of calcium channels in the thalamus: For example, Ethosuximide.
4. Modulator of neuronal voltage-dependent sodium and calcium channels:
Phenytoin modulates neuronal voltage-dependent sodium and calcium
channels.
5. GABA increasers: They open chloride channels.
For example: Gabapentine is a GABA analog and vigabatrin is an
irreversible inhibitor of GABA transminase.
6. Modulators of GABA transmission: Valproic acid is effective in multiple
seizure types because it has multiple actions (blocks Na and Ca channels
inhibits GABA transaminase and increases GABA synthesis).
7. Multiple mechanisms: For example, Topiramate decreases EAA
transmission, as well.
Note: Most generalized tonic-clonic seizures respond to the drugs which
control partial seizures. Vice versa is not true.
Drugs in Seizure Therapy 267

Febrile Seizures: Preventive Drugs
1. Acetaminophen (15 mg/kg) to lower the temperature.
2. A controlled trial of diazepam given rectally or orally (0.3 mg/kg) during
febrile illness.
3. Long-term anticonvulsants may be needed if there are risk factors:
Family history of seizures, age less than 18 months
Previous neurological problems and/or prolonged seizures
Brief duration of fever < 1 hour
Low fever < 102 degrees
Phenytoin and carbamazepine are contraindicated in febrile seizures.
We can also use other drugs to prevent an acute attack of febrile seizures,
like frisium (clobazam).
Toxicity
Toxicity of Benzodiazepines:
Lethargy and drowsiness
IV administration can cause respiratory and cardiovascular depression.
Toxicity of Barbiturates (phenobarbitone):
Sedation, nystagmus and ataxia at higher dose.
In children paradoxical irritability, hyperactivity, behavioral changes and
serious leucopenia and SLE like illness, may occur.
Acute Toxicity (CVS and CNS) of Phenytoin:
Phenytoin binds nicely to the plasma proteins. Hence, drug interactions
occur due to competition for protein binding sites.
It is metabolized in liver High IV rate can cause cardiac arrhythmias
hypotension.
CNS depression in acute oral overdose: Cerebellar and vestibular effects
nystagmus, ataxia, diplopia vertigo.
Chronic Toxicity (9 H) of Phenytoin:
Hyperplasia of (Gingival) and (Lymphoid)
Hyperglycemia
Hyperactivity
Hirsutism
Hypersensitivity
Hypoprothrombinemia
Hypersegmented neutrophils in megaloblastic anemia.
Hydantoin (fetal) syndrome causing cleft lip, growth retardation
Hypoplasia of midface and fingers.
Pedia Pearl: Children with febrile seizure have 0.9% chance of getting epilepsy

Toxicity of Fosphenytoin:
Fosphenytoin has lesser side effects than those associated with phenytoin
vizvenous irritation, tissue damage, pain/burning at site, muscle necrosis
and there is no need for larger fluid volumes for dilution.
Toxicity of valproic acid:
Fulminant hepatitis especially, if polytherapy is given for >2 years.
Interactions: Phenobarbital and phenytoins metabolism is inhibited by
valproic acid.
Side effects of carbamazepine: Aplastic anemia and anti ADH.
Side effects of ethosuximide:
GI complaints
Drowsiness lethargy
Dopamine antagonist activity (Parkinsonian symptoms)
Rarely bone marrow toxicity and skin reactions may occur.
BIBLIOGRAPHY
1. Andriola MR, Ettinger AB. Pseudoseizures and other nonepileptic paroxysmal disorders
in children and adolescents. Neurology. 1999;53:89-95.
2. Bouma PAD, Bovenkerk AC, Westendorp RGJ, et al. The course of benign partial
epilepsy of childhood with centrotemporal spikes. Neurology. 1997;48(2):430-7.
3. Commission on Epiledmiology and Prognosis, International League Against Epilepsy.
Guidelines for epidemiologic studies on epilepsy. Epilepsia. 1993;37:592-6.
4. [Guideline] Expert Committee on Pediatric Epilepsy, Indian Academy of Pediatrics.
Guidelines for diagnosis and management of childhood epilepsy. Indian Pediatr. Aug
2009;46(8):681-98.
5. Hirtz D, Berg A, Bettis D, et al. Practice parameter: Treatment of the child with a first
unprovoked seizure: Report of the quality standards subcommittee of the American
Academy of Neurology and the Practice Committee of the Child Neurology Society.
Neurology. 60:166-75.
6. Holmes GL. How to evaluate the patient after a first seizure. Postgrad Med.
1988;83(2):199-209.
7. Musicco M, Beghi E, Solari A, Viani F. Treatment of first tonicclonic seizure does not
improve the prognosis of epilepsy. First Seizure Trial Group (FIRST Group).
Neurology. 1997;49(4):991-8.
8. Pillai J, Sperling MR. Interictal EEG and the diagnosis of epilepsy. Epilepsia.
2006;47(S1):14-22.
9. Rosman NP, Colton T, Labazzo J. A controlled trial of diazepann administered during
febrile illness to prevents recurrence of febrile seizures. N Eng J Med 1993;329:79-84.
10. Shinnar S, Glauser TA. Febrile seizures. J Child Neurol. 2002;17: 44-52.
11. Shinnar S, O'Dell C, Berg AT. Distribution of epilepsy syndromes in a cohort of children
prospectively monitored from the time of their first unprovoked seizure.subcommittee of
the American Academy of Neurology, The Child Neurology Society, and The American
Epilepsy Society. Epilepsia. 1999;40(10):1378-83.
12. Warren CR. Evaluation and management of febrile seizures in the out of hospital and
emergency department settings. Ann Emerg. Med. 2003;41(2):215-22.
Drug Treatment of Malaria 269
43
Drug Treatment
of Malaria
STEPS OF TREATMENT
1. First, identify malaria clinically and then confirm malaria based on signs,
symptoms and tests.
2. Next, assess the severity of malaria based on presence of prostration,
convulsions, hypoglycemia, hemoglobinuria, anemia, respiratory distress,
disseminated intravascular coagulation, jaundice or cerebral malaria.
3. Presumptive treatment is done without parasitological diagnosis to prevent
delay.
4. Radical treatment is done after parasitological diagnosis is made to eliminate
all forms of the parasite.
DRUG TREATMENT
1st line: Chloroquine.
2nd line: Amodiaquine, sulfonamides in combi-nation with pyrimethamine.
3rd line: Quinine, but it is 1st line drug irrespective of chloroquine resistance
status, in severe and complicated cases.
NATIONAL VECTOR BORNE DISEASE CONTROL PROGRAM:
SUGGESTIONS
First Line of Treatment
In Routine Cases (Presumptive treatment)
Dosage schedule (mg/kg Chloroquine base).
1st Day-10 mg/kg (600 mg max) Chloroquine base.
2nd Day-10 mg/kg (600 mg max) Chloroquine base.
3rd Day-5 mg/kg (300 mg max) Chloroquine base.
Other schizonticidal drugs used apart from Chloroquine for clinical and
parasitological cure are:
Amodiaquine, quinine, quinidine, pyrime-thamine, trimethoprim, proguanil,
sulfonamides in combination with pyrimethamine and mefloquine.

In Confirmed Cases (Radical Treatment)
Confirmation is done by microscopy or rapid diagnostic kit.
Gametocytocidal and antirelapse drugs are needed for radical cure. Chloroquine
followed by primaquine is given for eradication of liver forms (in P. vivax and
P. ovale infections).
Primaquine is the only compound having action on both gametocytes and
hypnozoites.
In Positive P. vivax Cases
They are treated with chloroquine in full therapeutic dose of 25 mg/kg over
three days. Primaquine can be given in dose of 0.5 mg/kg daily for 5 days,
under medical supervision. Actual dosage is 0.5 mg/kg for 14 days but Indian
Academy recommends only 5 days treatment.
It should be given to prevent the relapse. Primaquine is contraindicated in
infants and pregnant women and is available in 2.5 mg and 7.5 mg base.
Primaquine need not to be given with artesunate, as artesunate itself reduces
gametocyte carriage. Primaquine can cause hemolysis in G6PD deficient
children, hence G6PD screening is a must.
In Uncomplicated Falciparum +ve Cases
Chloroquine is given in total therapeutic dose of 25 mg/kg over three days and
single dose of Primaquine is given 0.75 mg/kg on the first day.
SECOND LINE OF TREATMENT
This is given to treatment failure cases, severe malaria cases and for mass treatment
(epidemics) in areas of high falciparum burden. The treatment includes Artesunate
+ Sulfapyrimethamine (ACT) combination.
ACT* in usual cases is a second line, any but becomes first line
antimalarial drug for treatment of confirmed P. falciparum (microscopically
or by rapid diagnostic kits) in chloroquine resistant areas. The dose is 4 mg/kg
of artesunate daily for 3 days + 25 mg/kg of sulphadoxine + 1.25 mg per kg of
pyrimethamine. Primaquine need not to be given with ACT combination as
artesunate reduces gametocyte carriage.
In areas with high disease burden:
If P. falciparum endemicity is high (Pf > 30%) and there is a poor clinical
response ACT may be given, based upon clinical diagnosis, after excluding
other common causes of fever.
However, it is necessary to take an approval of Directorate of NVBDCP
to change drug to Arte-sunate-Sulpha-Pyrimethamine (ACT) combination. The
policy is as follows:
*
ACT = Artesunate Combination Therapy.

NVBDCP = National Vector Bone Disease Control Programme
Drug Treatment of Malaria 271

If an area shows treatment failure in more than 3 cases out of the minimum
sample of 30 cases, switch over to. Artesunate-Sulpha-Pyrimethamine (ACT)
combination therapy.
Third line drugs are given if resistance to 1st line and [Artesunate +
Sulphapyrimethamine (ACT)] combination occurs or in severe and complicated
malaria.
THIRD LINE OF TREATMENT
In Severe and Complicated Cases
For example, P. falciparum (clinically/microsco-pically confirmed case). Use
the following options:
1. Quinine
Dosage schedule of quinine.
Quinine salt 10 mg/kg 8 hourly in 5 percent dextrose saline is preferred.
Patients should be switched over to oral quinine as early as possible and oral
dose is 10 mg/kg bw eight hourly (max 2 gm/day). Minimum 7 days total
therapy (parental and oral) should be given.
2. If Non-availability of Quinine, Use Chloroquine
Dosage schedule of chloroquine:
Chloroquine 10 mg/kg bw in saline should be given IV over 8 hours and 15
mg/kg over next 24 hours.
There is no need for primaquine as liver hypnozoites do not exist in
falciparum malaria.
RESISTANCE
It means that there has been no response within 3 days parasitologically. Hence,
giving ACT combination is justified.
If there is resistance to CQ* and SP-ACT, oral quinine with doxycline
may be given.
CHEMOPROPHYLAXIS (PREVENTION BY SUPPRESSION)
It is started a week before entering an endemic area. Chloroquine alone or
Chloroquine plus Proguanil or Mefloquine and Doxycycline may also be used.
In chloroquine sensitive areas, give Chloroquine at a loading dose of 10 mg/
kg followed by a weekly dose of 5 mg/kg. This is to continue till one month
after return from endemic area. The terminating dose should be radical treatment
*
CQ = Chloroquine
SP-ACT = Sulpha-pyrimethamine Artesunate combination therapy

for P.vivax, i.e. 25 mg/kg of chloroquine over 3 days along with 0.25 mg/kg
bw of primaquine for 5 days. Chemoprophylaxis with chloroquine is not
recommended for more than 3 years, as it causes Bulls eye retinopathy.
In chloroquine resistant areas Chloroquine 5 mg/kg is given weekly with
Proguanil daily.
RESERVE DRUGS IN TREATMENT
Artesunate
2.4 mg/kg IM/IV stat followed by 1.2 mg/kg bw after 12 hours, then 1.2 mg/
kg once daily for total duration of 5 days.
Artemether
1.6 mg/kg IM stat followed by 1.6 mg/kg daily for total of 6 injections or
1.6 mg/kg IM injection twice daily for 3 days for a total of 6 injections.
Artemisinin
10 mg/kg at 0 and 4 hours followed by 7 mg/kg at 24, 36, 48 and 60 hours.
BIBLIOGRAPHY
1. Look GC. Prevention and treatment of Malaria Lancet 1988;1:32-7.
2. Retrieved from http:nvbdcp.gov.in.
3. White NJ. The treatment of Malaria: N Engl J Med. 1996;335:800-06.
Drug Treatment of Tuberculosis 273
44
Drug Treatment
of Tuberculosis
CONSENSUS STATEMENT OF IAP WORKING GROUP

(Indian Pediatrics 1997;34:1093-1096)
Group 1 (Preventive Therapy)
Six months treatment of INH and Rifampicin [6HR].
For, asymptomatic individual, mantoux positive, < 5 years, untreated healed
TB or history of contact.
a. Asymptomatic individual Mantoux positive below three years of age.
Recent convertors, Immunocompromised or asymptomatic children.
Mantoux positive with grades III and IV. PEM (protein energy
malnutrition). below five years.
b. Healed TB lesion showing calcifications/ fibrosis who were not given
ATT previously.
c. A contact with adult taking treatment or who took treatment for TB in
the past two years.
Definition of Contact: Any child living with an adult who is on A.T.T or
who has taken ATT within last 2 years.
d. Symptomatic older children above five years of age having both Mantoux
and/or contact positive.
Group II (Mnemonic SIMPLE)
Six months treatment [2HRZ/4HR] for simple.
SIM = Symptomatic Individual Mantoux positive below three years.
Symptomatic individual Mantoux positive below five years with
Grades III and IV Protein Energy Malnutrition (PEM).
P
= Primary complex [Ghons complex].
L
= Lymphadenitis involving one group of lymph nodes only.
E
= Effusion (unilateral pleural).
Pedia Pearl: INH induced peripheral neuropathy is rare in children. Assess liver
function by doing LFT before starting ATT.

Group III
Six months treatment [2 HRZE/4HR]. For progressive disease.
a. Progressive primary complex having consoli-dation, collapse,
bronchiectasis.
b. Lymphadenitis involving multiple groups of lymph nodes.
c. Pleural effusion on both sides.
Continuation phase is extended by three months in event of non-resolution.
Group IV
For disseminated disease. (2 HRZE/7 HR).
Group V
For neurotuberculosis (2 HRZE/10 HR). Treat with two months INH,
rifampicin, pyrazinamide and ethambutol followed by 10 months of INH,
rifampicin and ethambutol. Also give steroids for six weeks and then taper.
Indications for Prednisolone
The Indications for prednisolone are those where there is
involvement of serous layers, so as to avoid fibrosis
Neurotuberculosis
Miliary tuberculosis, and other tuberculosis Involving serous layers
(peritoneal, etc.)
Endobronchial tuberculosis
Genitourinary tuberculosis
Sinus formation.
Give Prednisolone (1-2 mg/kg), which is to be tapered after 4 weeks (Total
6 weeks).
Essential drugs/side effects
Recommended dosages
in mg/kg 3 times weekly dosage
Isoniazid (H) S/E: Hepatotoxicity, peripheral neuritis,

rash, urticaria, interfere with metabolism of phenytoin.
10 mg/kg
Rifampicin (R) S/E: flu like syndrome, acute hemolytic

anemia, acute renal failure, hepatotoxicity.
15 mg/kg
Pyrazinamide (Z) S/E: Hepatitis, gouty arthralgia.
30 mg/kg
Streptomycin (S)S/E: Vestibular and renal toxicity, hearing loss
15 mg/kg
Ethambutol (E) S/E: Retrobulbar neuritis, pruritus, joint pain
25 mg/kg
Drug Treatment of Tuberculosis 275

Management of Pediatric Tuberculosis Under the Revised
National Tuberculosis Control Program.
Category I
New sputum positive lung Tb or Seriously ill extrapulmonary TB (sputum

negative). 2HRZE + 4HR.
CNS TB 2HRZS + 6HR.
Category II
Old sputum smear-positive relapse 2SHRZE + 1HRZE + 5HRE

Treatment failure /default 1H3R3Z3E3 + 5H3R3E3.
Category III
Sputum-negative and extrapulmonary TB, not seriously ill 2HRZ + 4HR.
Treatment of those who stop therapy earlier:
a) Within 4 weeks of therapy: (i) Resume the therapy as it is, if the duration
of stoppage is less than 2 weeks, (ii) However, if the duration of
discontinuation is more than 2 weeks, then restart therapy.
b) Between 4 to 8 weeks (i) Resume the therapy as it is, if the duration of
discontinuation is < than 2 week, (ii) If > 2 weeks then extend intensive
phase by 1 month.
c) After 8 weeks: Treat as category II defaulter.
Action for Major Antituberculous Drugs
Ripampicin: (R) It inhibits DNA dependent RNA synthesis and acts on
both intra and extracellular organisms (Bactericidal).
INH (Isoniazid) (H) It inhibits mycolic and synthesis and acts on intracellular
organisms (Bactericidal).
Pyrizinamide (Z) It also inhibits mycolic acid synthesis and acts on
intracellular organisms (Bactericidal for rapid multpliers).
Streptomycin (S) It inhibits protein synthesis and acts on 30S subunit of
ribosomes. It acts on extracellular organisms and cavities (Bactericidal).
Ethambutol (E) It inhibits incorporation of mycolic acid in the cell wall
(Bacteriostatic).
Pedia Pearls:
The newer drugs: Rifabutin, ciprofloxacin, clofazimine and clarithromycin.
Screen all babies born to mother with Tuberculosis. If negative for tuberculosis, give
INH prophyloxis for 6 months and if positive, give 2SHRZ + 4HR.

BIBLIOGRAPHY
1. Comped 2006 - Conference Abstracts. Pediatric Oncall [serial online] 2007 [cited 15
January 2007 (Supple-ment 1)];4. Available from: http://www.pediatriconcall. com/
fordoctor/Conference abstracts/comped/ Tuber.asp.
2. Mitchison DA. Baric mechanism of chemotherapy. Chest 1979;76:171-81.
3. Treatment of Childhood Tuberculosis Consensur Statement, IAP Cooking Group,
Indian Pediatrics 1997;34:1093-96.
4. Treatment of tuberculosis, Guidelines for National Programmes. Geneva 1993.
Oxygen 277
45
Oxygen
INTRODUCTION
Oxygen is one of the five basic elements of all life (oxygen, hydrogen, carbon,
nitrogen and sulfer). It is a colorless, tasteless and odorless gas.
Hypoxia
It is a pathological condition in which the body as a whole (generalized hypoxia)
or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply.
Hypoxemia
It is (PaO2 < 60 mm Hg or SaO2< 90%) and presents as altered mental state,
dyspnea, cyanosis, tachypnea, arrhythmias, and coma.
Response to Hypoxia
Initially, the child hyperventilates at a PaO2 of <40 mm of Hg.

Later, peripheral vasodilatation occurs along with consequent systemic
hypotension.
Eventually, coma may occur at PaO2 <30 mm of Hg.
If it is not treated, anaerobic metabolism sets in, causing metabolic acidosis
(Bicarb <18 mmol/L) and even cardiac/respiratory arrest occurs, eventually.
States of Hypoxia
1. Tissue hypoxia without arterial hypoxemia. This occurs in low cardiac
output states (anemia, cardiac failure and hypovolemic shock).
2. Tissue hypoxia + arterial hypoxemia. This occurs if either or both ventilation/
perfusion are inadequate or imbalanced, e.g. Low hemoglobin,
hemoglobinopathies and high carboxy hemoglobin in blood.
SOURCES OF OXYGEN
Oxygen cylinders
Oxygen concentrators
Liquid oxygen.

OXYGEN ADMINISTRATION
Low flow system:

Nasal catheter
Nasal prongs
Nasopharyngeal catheter
Tracheostomy oxygen adapters
Simple oxygen masks.
Partial-rebreathing masks
Nonrebreathing masks.
High flow system
Venturi mask
Air-entrainment nebulizers.
Enclosure systems
Oxygen hoods
Closed incubators
Oxygen tent.
USES OF OXYGEN
1. Oxygen in moderate amounts increases energy levels, aids restful sleep,
detoxification and digestion. It relieves headaches and nausea, enables
muscle recovery and boosts the immune system.
2. It is used to treat hypoxia: For example, in carbon monoxide poisoning,
severe uncorrected anemia and air or gas embolism. In general, oxygen
rapidly corrects arterial hypoxemia but improving ventilation must be
the goal.
3. For imminent respiratory arrest (PaO2 < 60 mm Hg PaCO2 > 40 mm Hg) give
ventilatory support urgently. For treating cardiac or respiratory arrest use 100
percent oxygen only.
4. During neonatal resuscitation, if no oxygen is available initially use air
but oxygen should be given, if no improvement occurs in 90 seconds.
5. Severe infection by anaerobic bacteria (such as gas gangrene) respond
favorably with oxygen.
Adverse Effects
1. Lung toxicity: High concentrations of oxygen damages the alveolar
membrane when inhaled for more than two days, causing Adult Respiratory Distress Syndrome (AIDS).
2. CNS toxicity: Breathing hyperbaric oxygen (for example, when diving)
can cause severe cerebral vasoconstriction and even epileptic fits.
3. Retinopathy of prematurity or bronchopulmonary dysplasia occur
secondary to the free radical damage (due to oxygen toxicity) in preterms.
Pedia Pearl: Pulse oximetry is better than conventional arterial blood gases for
monitoring arterial O2 saturation.
7
Problem-based
Learning
46
Anemia
PALLOR (PROBLEM-BASED LEARNING)
CASE PRESENTATION
History
Two-year-old boy was brought with a chief complaint of pallor. He was a poor
eater but used to drink bottle milk. Family history was normal. No past history
of splenectomy was noted. On examination: He was a pale, chubby toddler with
mild tachycardia and grades III/VI systolic ejection murmur. No
hepatosplenomegaly was found. BP 90/60 mm Hg, Height-50th percentile and
Weight -80th percentile.
Investigations
CBC: WBC 5400/cu.mm Hg 6g/dl, HCT-18 percent, Platelets 500,000/

cu.mm
MCV (Mean Corpuscular volume): 54 fL.
RDW (Red Cell distribution width): 17 percent.
Reticulocyte count: 1.8 percent.
Peripheral smear: Microcytosis, hypochromia, mild anisocytosis. There
was no basophilic stippling of RBCs.
Stool: Soft, negative for occult blood. No ova or cyst seen.
Diagnosis: Iron deficiency anemia.
DISCUSSION
The primitive pluripotent hematopoietic stem cell differentiate by an orderly
hierarchical process into multipotent progenitors which eventually become
circulating blood cells (hematopoiesis).
Anemia is alteration of this homeostasis and is defined as: Hematocrit
or hemoglobin below the lower limit of normal (11 gm/dl for children and
for neonates the value is 16 mg/dl). There may be reduction in red cell
mass and or reduction in the hemoglobin concentration.

IRON DEFICIENCY ANEMIA (IDA)
Etiology
Iron deficiency can be caused by:
Dietary iron deficiency (nutritional deprivation)
Malabsorption of iron
Blood loss, e.g. malignancies and inflammatory conditions and hookworm
infestation
Increased iron utilization, e.g. physiologic demands in infancy.
Iron Metabolism
Gastric acid converts iron to ferrous form, ten percent of iron is absorbed
in the duodenum and jejunum.
A protein (transferrin), then carries absorbed iron in the plasma to the
bone marrow, for uptake, by the erythroid precursors in the bone marrow,
which utilize iron and the young RBCs are released into the bloodstream
(lifespan of RBCS = 120 days).
The transport protein (transferrin) is normally saturated with iron up to 33
percent but percentage of transferrin saturation may decrease in iron
deficiency.
The uptake of iron into a developing red blood cell (erythroid precursor)
is by endocytosis.
The extra iron is stored as: (1) Hemosiderin in the bone marrow (visible
by a Prussian Blue stain) and as (2) Ferritin in the intestinal mucosa, as
well as in bone marrow (invisible by light microscopy).
Old RBCs are eaten-up by the spleen and bone marrow, which liberates
iron from the (Hb) hemoglobin. So, this iron is also transported by
transferrin (plasma iron transporting protein) and carried to bone marrow
for uptake.
Clinical Features
Children have fatigue, dyspnea, irritabilty headache or angina, poor logic and
reasoning and are weak in mathematics. Pica, breath holding spells, thrombosis
and restless leg syndrome are also seen.
Good Sources
Green vegetables
Jaggery
Meat, fish and liver
Although Cows milk contains modest amount of iron only little of it is
bioavailable.
Bottle fed babies often look chubby but are pale.
Anemia 283
Stages of Iron Deficiency
Fall in iron stores (FERRITIN) and increase in free transferrin (Total Iron
Binding Capacity) but no anemia. Child is irritable.
Fall in serum iron, no anemia.
Develop normocytic, normochromic anemia.
Develop microcytic, hypochromic anemia.
Investigations
Peripheral Smear
Microcytosis occurs as a result of a failure in hemoglobin production.

Early in the course of iron deficiency anemia, the red cells may be
normochromic and normocytic but as the condition progresses, we see a
microcytic, hypochromic picture.
Other Tests in Iron Deficiency and Their Expected Results
Low MCV (mean corpuscular volume), MCH and MCHC
Low hemoglobin and hematocrit
Low reticulocyte count
Elevated platelet count (often)
Low serum iron, transferrin saturation and ferritin
High total iron binding capacity (TIBC)
Elevated free erythrocyte protoporphyrin.
Treatment
Oral Therapy
The pediatric dose is 6 mg/kg of elemental iron per day in tablet or elixir
form. It usually corrects anemia within 4 to 6 weeks but one should continue
it for an additional 3 to 6 months to replenish stores as indicated by a return of
the serum ferritin concentration to a normal range of 50 to 100 mg/L. The
maintainance dose is 2 mg/kg of elemental iron per day.
Parenteral Iron
It may be considered in patients who fail oral therapy. Dose in mg = (Wt Hb
deficit 4.2).

APPROACH TO A CASE OF MICROCYTIC
HYPOCHROMIC ANEMIA
Differential Diagnosis
1. Iron Deficiency (Explained Above)
2. Thalassemia
It is caused by failure in globin chains synthesis. Hence, ineffective

erythropoiesis ensues and to compensate for ineffective erythropoiesis,
extramedullary hematopoiesis in liver, spleen and flat bones occurs.
This causes hepatosplenomegaly, hemolytic facies and a hair on end
picture on radiology of skull, due to increased production of cells in skull
bones, causing the space between inner and outer tables of skull to increase.
Thalassemia in contrast to iron deficiency has elevated reticulocyte count
and serum iron and low total iron binding capacity (TIBC).
3. Sideroblastic Anemias
They are characterized by:
Defective heme synthesis and consequent ineffective erythropoiesis.
Ringed sideroblasts are characteristic of sideroblastic anemia.
4. Lead Poisoning
This is a type of sideroblastic anemia but here globin synthesis is also

inhibited along with defective heme synthesis.
Lead poisoning inhibits porphobilinogin synthetase. Coproporphyrin and
ALA spill into the urine but not the porphobilinogen, as in congenital
porphyrias.
The anemia is usually microcytic, with basophilic stippling of RBCs and
ringed sideroblasts.
History
Clinical History
Sudden onset of pallor, fatigue, or exercise in tolerance suggest a more

acute anemia.
Anemia without symptoms may indicate a more chronic process.
Etiological History
Dark urine and icterus may be seen in G6PD* deficiency and hereditary
spherocytosis.
Splenomegaly and pallor indicate hemolysis.
G6PD stands for Glucose 6 phosphate dehydrogenase.
Anemia 285
Fatigue, dyspnea, headache, lightheadedness, angina, pica and breath

holding spells suggest iron deficiency.
Do enquire about menstrual losses as well.
Dietary History
Exclusive cows milk also suggests iron deficiency or even blood loss anemia
(as iron in cows milk is less bioavailable and excess cows milk intake exerts
a direct toxic effect on the intestinal mucosa of some infants, leading to
microscopic blood loss).
Family History
If a family member had his/her spleen taken out, it suggests a family history
of a hemolytic anemia (such as hereditary spherocytosis).
Childs ethnic origin may suggest thalassemias (more common in certain
ethnic groups, often in those of mediterranean descent).
Treatment History
History of frequent transfusions/splenectomy and iron chelation with
desferrioxamine suggest hemolytic anemias like thalassemia.
Examination
Look for Signs of Anemia
Look at the activity, playfulness, pallor and compare with his/her siblings/
parents.
Then look for tachycardia, orthostatic hypotension, heart murmur and
edema and signs of heart failure including tachypnea, rales, hepatomegaly
or edema to know the severity and acuteness of illness.
However, rarely heart failure or arrhythmias can occur in chronic iron
overload in thalassemias, due to myocardial damage.
Now Look, Palpate and Percuss for the Cause
Look (head to toe)
General appearance: Look for thalassemic facies- Frontal bossing,
maxillary prominence and protuding teeth (due to compensatory
extramedullary hematopoiesis, away from long bones, thus expanding the
marrow cavity in flat bones, i.e. frontal, parietal and maxillary bones).
Sudden acceleration of anemia after parvovirus B19 infection suggests
Aplastic crisis in a case of hemolysis.
Neurological abnormalitiesheadaches and paresthesias are seen in B12
deficiency.
Jaundiced sclera is seen in hemolysis.
Angular cheilitis, glossitis, smooth tongue and koilonychia is seen in iron

deficiency.
Retardation of growth and sexual maturity is seen in thalassemia. (Due to
ineffective erythropoiesis, the percentage of Hb F is more. Fetal hemoglobin
carries more oxygen but does not deliver it to the tissues, leading to hypoxia).
Hemoccult positive feces signify GI bleeding due to vascular malformations
or hookworms.
Palpate and Percuss
Liver span is reduced in iron overload (cirrhosis) and increased in CCF

(Congestive Cardiac Failure).
Splenomegaly is seen in hemolysis.
Feel for bone tenderness in leukemias and other malignancies.
Investigations to Evaluate the Cause

Basic Tests
First confirm anemia with hematocrit or hemoglobin.

Next do peripheral blood smear and describe, the characteristic
abnormalities:
Ringed sideroblasts are seen which suggest a diagnosis of sideroblastic
anemia
Microcytosis and Target cellsiron deficiency
PolychromasiaThalassemia
Red cell fragmentsin intravascular hemolysis (G6PD deficiency).
The RBCs are destroyed in the spleen in extravascular hemolysis.
Hence, red cell fragments are not seen, e.g. thalassemia.
Nucleated RBCsin sepsis and hemolysis
Microcytic RBCs, basophilic stippling of RBCs and ringed
sideroblastsin lead poisoning.
Also Check the Following

1. Serum Ferrritin: Low serum ferritin is diagnostic of iron deficiency. Its normal
level is misleading because ferritin is an acute phase reactant and is elevated
in any sort of inflammation.
Iron deficiency anemia and anemia of chronic disease are best
differentiated by ferritin levels which are low in iron deficiency anemia
while in chronic disease the marrow iron stores are usually normal.
2. RDW (red cell distribution width): In a fully established iron deficiency,
RDW (red cell distribution width) is wide. Wide red cell distribution width
(difference in size between the smallest and largest RBCs) indicates a dual
population of cells: Small (microcytic) iron deficient cells and some
normocytic cells with adequate iron.
Pedia pearl: Reticulocyte is a 1 to 2 day old blood cell released from bone marrow. The retic
count indicates marrow response.
Anemia 287
3. FEP (Free Erythrocyte Protoporphyrin not incorporated into Heme). It is
high in iron deficiency. Its determination is most useful in differentiating
between pediatric iron deficiency and lead poisoning.
4. Reticulocytosis: Reticulocytosis is commonly seen in hemolytic anemia
(Thalassemia) and also in iron deficiency, while on treatment with iron.
Marrow production is assessed by: Reticulocyte production index (RPI),
i.e. (reticulocytes as a percentage of the circulating RBCs). An RPI of less
than 2.0 indicates inadequate bone marrow response or hypoproliferation.
An RPI of greater than 3.0 represents appropriate bone marrow response.
5. Elevated LDH, AST, indirect bilirubin, decreased serum haptoglobin;
positive direct antibody test (Coombs test), high retic count are indicative
of hemolytic anemias.
6. Serum iron, TIBC and percentage iron saturation: They are used to differentiate
iron deficiency from Thalassemia. TIBC is more in iron deficiency.
7. Bone marrow stain for iron: This is a specific test as iron deficiency shows
no iron stores.
8. Pigmented gallstones: They are sometimes seen in hemolytic anemias.
9. X-rays: X-ray skull in thalassemia often show a typical crew cut or hair
on end appearance due to extramedullary hematopoiesis.
Treatment
Response to a therapeutic trial of iron is also acceptable as proof of iron
deficiency. Elemental iron is given at a dose of 6 mg/kg in iron deficiency.
Lead poisoning is managed by chelators like D penicillamine. In thalassemia,
hypertransfusion and bone marrow transplantation is the solution.
BIBLIOGRAPHY
1. Abshire TC. The anemia of inflammation. A common cause of childhood anemia.
Pediatr Clin North Am 1996;43(3):623-37.
2. American Academy of Pediatrics, Committee on Nutrition. The use of whole cows
milk in infancy. Pediatrics 1992;89(6):1105-9.
3. Blackwell S, Hendrix PC. Common anemias: What lies beneath. Clin Reviews
2001;11(3):53-62.
4. Booth IW, Aukett MA. Iron deficiency anemia in infancy and early childhood. Arch
Dis Child 1997;76(6):549-54.
5. Krantz SB. Pathogenesis and treatment of the anemia of chronic disease. Am J Med Sci
1994;307(5):353-9.
6. Markowitz M. Lead poisoning. Pediatr Rev 2000;21(10):327-35.
7. Piomelli S. Chapter 13 - Lead Poisoning. In: Nathan DG, Orkin SH (Eds). Hematology
of Infancy and Childhood, fifth edn. Philadelphia: WB Saunders 1998;480-96.
8. Sackey K. Hemolytic anemia: part 1. Pediatr Rev 1999;20(5):152-8.
9. Segel GB. Anemia. Pediatr Rev 1988;10(3):77-88.
10. Tong S, Baghurst PA, Sawyer MG, et al. Declining blood lead levels and changes in
cognitive function during childhood. JAMA 1998;280(22):1915-9.
11. Welch JC, Lilleyman JS. Anaemia in children. Br J Hosp Med 1995;53(8):387-90.
12. Wharton BA. Iron deficiency in children: Detection and prevention. Br J Haematol
1999;106(2):270-80.
47
Lymphadenopathy
LYMPH NODE ENLARGEMENT
(PROBLEM-BASED LEARNING)
CASE PRESENTATION
History
A 3-year-old female came to hospital with a chief complaint of a neck mass
that has been present and getting worse over four days. Swelling was painful,
and warm to touch with overlying redness. No recent skin infection, skin
rash, weight loss, dental problems or cavities, nausea, vomiting or diarrhea
were noted.
Examination
Examination revealed patches of exudate on both tonsils. 2 cm 3 cm tender,
warm anterior cervical lymph node on the right with overlying erythema was
observed. Consistency was fluctuant. No axillary or inguinal lymphadenopathy
was appreciated. Rest was normal.
Investigation
Throat swab showed -hemolytic streptococcus. An ultrasound study showed
abscess formation. CBC showed WBC of 25,000 per cubic mm with a left
shift.
DiagnosisBacterial abscess.
Pedia Pearl: (Medications That May Cause Lymphadenopathy):

Allopurinol, Captopril, Carbamazepine (Tegretol), Cephalosporins, Hydralazine,
Penicillin, Phenytoin (Dilantin), Pyrimethamine, Quinidine, Sulfonamides
Lymphadenopathy 289
APPROACH TO A CASE OF LYMPHADENOPATHY
Acute Cervical Lymphadenitis
This is commonly seen in toddlers. It may be bilateral in viral (adenovirus,
influenza and RSV) or unilateral in pyogenic lymphadenitis, a suppurative
bacterial (Staph. aureus and group A strep) infection and chronic cervical
lymphadenopathy. Mild cases need oral empiric therapy with cephalexin,
oxacillin or clindamycin. For abscess formation or cellulitis, I (Incision) and D
(Drainage) and Intravenous drugs like vancomycin or cloxacillin are
recommended.
Prolonged Cervical Lymphadenopathy
This is seen in infections such as atypical mycobacterial infections,

Mycobacterium tuberculosis, Cat scratch disease, EBV, CMV,
toxoplasmosis, histoplasmosis and HIV.
Noninfectious etiologies for chronic cervical lymphadenopathy include
malignancy such as leukemia, lymphoma, metastatic solid tumors such as
neuroblastoma, rhabdomyosarcoma and nasopharyngeal carcinoma.
Kawasakis disease is associated with a single, nontender, nonpurulent
enlarged cervical lymph node.
Lymphangitis
It can be:
Neoplastic (surrounding fibrosis takes place producing cords)
Benign or inflammatory
Seen at times, proximal to areas of cellulitis.
History
Find out:
Whether acute, chronic, localized or generalized.
Note history of any prolonged fever, weight loss, arthralgias, skin lesions/
infections or skin rashes, history of recurrent infections, immunization
status, contact with sick persons, recent travel, exposure to animals and
insects, URI symptoms (sore throat) and dental problems.
Examination
Look for palpable lymph nodes in the supraclavicular region, which often
reflects a mediastinal malignancy.
Hepatosplenomegaly, bruises, petechiae, conjunctivitis, pharyngitis are also
looked for.

Investigations
Screening
Do a PPD for tuberculosis screening.

A chest X-ray help to rule out mediastinal malignancy or tuberculosis and
HIV testing is done for selected cases.
Cultures and Counts

Throat culture, blood culture and CBC help to rule out an infective etiology.
Needle Aspiration/ Lymph Node Biopsy
This may be sent for Gram stain, acid fast stain and bacterial culture.
For fluctuant node where an abscess is suspected, ultrasound may be
helpful.
Biopsy of a lymph node is done if there is persistent enlargement despite
empiric therapy, with a -ve (negative) laboratory work up.
A solid fixed node, located in the supraclavicular area with symptoms of
fever and weight loss may require bone marrow aspiration as well.
Serologic Studies
Serology can be helpful in selected cases:
EBV (Epstein-Barr virus)
CMV (Cytomegalovirus)
HIV (Human immunodeficiency virus)
Treponema pallidum
Toxoplasma gondii
Brucella.
Treatment
Treat the cause.
BIBLIOGRAPHY
1. Liu JH. Chapter 15.5-Evaluation of Head and Neck Masses. In: Rudolph AM (Ed).
Rudolphs Pediatrics, New York: McGraw-Hill 2003;21:1279-81.
2. Peters TR, Edwards KM. Cervical Lymphadenopathy and Adenitis. Pediatr Rev
2002;21(12):399-405.
3. Twist CJ. Assessment of lymphadenopathy in children. Pediatr Clin North Am
2002;49(5):1009-25.
Muscle Disorders 291
48
Muscle Disorders
MUSCLE WEAKNESS
CASE PRESENTATION
History/Examination
A five-year-old boy presented with abnormal waddling gait and running on
his tiptoes. He had trouble getting up from a sitting position. Gowers sign
could be observed and calves were visibly enlarged with a firm, rubbery feeling.
Investigation
CPK MM (Creatinine phosphokinase-muscle) was very elevated.
Diagnosis
Duchennes muscular dystrophy (DMD).
DISCUSSION
Muscular Dystrophy (Figs 48.1A and B)
Delay in walking, waddling gait, walking unsteadily with frequent falling,
walking on toes, and difficulty at climbing stairs, positive Gowers sign and
pseudohypertrophy of the calves are typical of muscular dystrophy.
This dystrophy (abnormal trophy/nourishment/ growth) is a primary genetic
disorder causing an abnormal, absent or decreased dystrophin protein (normally
transcribed from gene on Xp21 locus) due to gene deletion, gene duplications
or point mutations. It is a progressive disease and children are wheelchair
bound by 13 years of age.
Pedia Pearls:
A normal CPK is incompatible with diagnosis of Duchennes muscular dystrophy
although CK may be lower in terminal stages as there is less muscle to degenerate.
Intellectual impairment occurs in all cases of DMD but does not correlate with
severity. Learning disabilities are less frequent in Beckers.
B
Figs 48.1A and B: Duchenne dystrophy (Gowers sign)
Inheritance
Duchenne muscular dystrophy (DMD), Becker muscular dystrophy and
Emery-Dreifuss muscular dystrophy are X-linked recessive.
Myotonic dystrophy, facioscapulohumeral dystrophy and limb girdle
muscular dystrophy are autosomal dominant.
Congenital muscular dystrophy is autosomal recessive.
Congenital myotonic dystrophy on the other hand is maternally transmitted
(mother has myotonia and child has hypotonia). Here, respiratory and
swallowing difficulties lead to early death.
Dystrophy is often congenital and slowly progressive and characterized
by bad growth of muscle fibers with replacement with fibrous tissue.
Types
Duchenne dystrophy: Here dystrophin is absent (Figs 48.1A and B).
Becker muscular dystrophy: Here, dystrophin is partially defective. Therefore,
patients with Becker muscular dystrophy have a slow progression.
Myotonic muscular dystrophy is due to an abnormal proteinkinase and has older
age of onset and presents with (FACE) facial weakness arrhythmias, cataracts
and cardiomyopathy and endocrine problems like diabetes, testicular atrophy
and menstrual irregularities. Distal muscle weakness is prominent.
Facioscapulohumeral muscular dystrophy presents in late childhood or
adolescence with facial weakness and weakness of the scapulohumeral muscles,
but the deltoid muscle is spared.
Pedia Pearls:
Epilepsy is more common in DMD than in general population.
After calves, the next most common sites are tongue and muscles of forearm.

Myositishere muscles are tender.

Dermatomyositis has positive Gowers maneuver and elevated aldolase and
CPK but have a heliotrope rash on the eyelids and rash on sunexposed areas.
Spinal muscular atrophies (SMA), present soon after birth with marked
hypotonia and weakness with fasciculations. Type 3 SMA (KugelbergWelander) disease also involves the proximal muscles but
pseudohypertrophy of calf is not seen. The DTRs are absent and muscle
fasciculations are present. Also fine tremors on outstretched hands are
present in the SMAs but are absent in muscular dystrophies.
Myopathies: They are most often acquired and progressive. Typically,
muscle degeneration is noted on histopathology.
Clinical Features
Wide Based Waddling
It is due to weakness of the gluteus medius and minimus. Lumbar lordosis also
occurs due to the weak gluteus maximus and walking on toes is due to imbalance
between the plantar and dorsiflexors.
Pseudohypertrophied Calves
Weak calves are due to necrosis of muscle (replaced by adipose), secondary
to its destruction, from the lack of dystrophin. Muscles that are affected first
are proximal muscles of lower extremities. Then upper extremities and finally
the muscles like masseters, deltoids, serratus anterior, and quadriceps are
affected.
Gowers Sign
The child climbs up on his thighs in order to extend his hips and push up his
trunk when going from a sitting to standing position (due to weakness of the
knee and hip extensors). Atrophy of the latissimus, even in the absence of calf
hypertrophy, presents as Valley sign (a dimple that is seen between Teres
major and deltoid muscle on abducting the arms).
Winging of the Scapulae
This is a late sign.
Complications
Pulmonary:Weakness of the intercostal muscles causes progressive and
restrictive type of respiratory difficulty. Ventilator may be required.
Cardiac: Progressive cardiomyopathies occur after first decade but EKG
changes can be seen in the early stages of the disease.
Neurological: Some children have low intelligence and emotional quotients.

Diagnosis
This is mainly clinical. Clues include:
Intact ankle reflexes without clonus.
Hyperreflexia.
Normal sensations and pseudohypertrophy.
Prenatal Diagnosis
PCR (Polymerase Chain Reaction)through amniocentesis or chorionic villus
sampling helps in prenatal diagnosis.
Investigations
Serum creatine phosphokinase (CPK or CK): It is released 100 times the

normal values in Duchenne and Becker muscular dystrophies (highest in
the early stages but then decreases with progression). Normal level total CPK
= 15 150g/l and the CPK MM fraction is 5 70g/l.
CPK can be elevated in spinal muscular atrophy, acute hypoxicischemic
encephalopathy, trauma and exercise as well.
Electromyography (EMG): Shows a myopathic pattern low-amplitude,
short-duration polyphasic action potentials.
PCR: It is done for gene defects.
Muscle biopsy: Look for muscle degeneration which is replaced by
connective tissue. Staining for dystrophin using immunocytochemical
techniques can be done as well.
Echocardiography: To screen for cardiomyopathy.
Dystrophin immunocytochemistry: This is better than PCR.
Treatment
The prognosis for Duchenne muscular dystrophy is not good. Slowly, they get
wheelchair bound or develop respiratory failure/cardiomyopathy. Give
physiotherapy night splints, bracing, orthopedic surgery and ventilatory
support, if necessary. Corticosteroids have proven to be beneficial.
HIGHLIGHT
Aggressive use of corticosteroids may delay need for mechanical ventilation,
and even the corrective surgery for scoliosis may be avoided.
Pedia Pearl: Girls are effected if normal X chromosome becomes inactive (Lyon hypothesis).
Also seen in girls with Turner syndrome in whom X chromosome has Xp 21 gene deletion.

BIBLIOGRAPHY
1. Emery AEH. Chapter 3 - Clinical Features. In: Emery AEH. Duchenne Muscular
Dystrophy, New York: Oxford University Press 1993;2:26-44.
2. Emery AEH. Chapter 5 - Differential Diagnosis. In: Emery AEH. Duchenne Muscular
3. Emery AEH. Chapter 10 - Pathogenesis. In: Emery AEH. Duchenne Muscular
4. Emery AEH. Chapter 11 - Prevention. In: Emery AEH. Duchenne Muscular Dystrophy,
New York: Oxford University Press 1993;2:209-50.
5. Haslam RHA. Part 26 - The Nervous System. In: Behrman RE, et al (Eds). Nelson
Textbook of Pedia-trics, Philadelphia: WB Saunders Company, 2000;16:1873-4.
6. Roland EH. Muscular Dystrophy. Pediatrics in Review 2000;21(7):233-7.
7. Sarnat HB. Chapter 616 - Muscular Dystrophies. In: Behrman RE, et al (Eds). Nelson
Textbook of Pedia-trics, Philadelphia: WB Saunders Company 2000;16:1874-5.
49
Bleeding Disorders
PETECHIAL RASH (PROBLEM-BASED LEARNING)
CASE PRESENTATION
Five-year-old girl presented with easy bruising and diffuse nonpalpable petechial
rash on neck, trunk and extremities for three days with no history of obvious
bleeding or hemarthrosis. She had upper respiratory infection symptoms almost
two weeks ago. Family history was negative. Examination was normal (including
neurologic status). There was no hepatosplenomegaly, either.
Investigations
Platelet count was low (5,000/cumm). The smear showed normal red blood and
white blood cell lines, but the platelets were reduced in number and the majority of
them were large in size. The bone marrow aspirate showed giant megakaryocytes.
Diagnosis: Immune thrombocytopenic purpura.
DISCUSSION
Immune Thrombocytopenic Purpura
Immune or idiopathic thrombocytopenic purpura (ITP) is a benign, self-limited
acquired bleeding disorder where the circulating antiplatelet anti bodies target
the epitopes on the platelet membrane following a viral infection or vaccination.
If the symptoms persist beyond 6 months, it is defined as chronic ITP.
Splenectomy is often necessary to raise the platelet counts in such cases.
There is usually no jaundice, pallor or any hepatosplenomegaly. However,
one should rule out HIV, systemic lupus erythematosus, or Evans syndrome.
Platelets are reduced in number and tend to be large. Bone marrow aspiration
is done if lymphadenopathy, hepatosplenomegaly or other peripheral smear
abnormalities are seen, to rule out leukemias.
Management
It includes reassurance, limitation of activities and avoidance of aspirin and
NSAIDs. If bleeding is significant, one may use oral or IV corticosteroid.
IVIG (intravenous immunoglobulin) inhibits phagocytosis, allowing
antibody-coated platelets to circulate freely. Anti-D can be given, which is the
anti-serum against Rh(D) antigen. This also decreases the platelet destruction.
Bleeding Disorders 297
APPROACH TO A CASE OF BLEEDING DISORDERS

PATHOPHYSIOLOGY
Bleeding Disorders Involve Primary Hemostasis
(Platelets, blood vessel and supporting matrix)
Bleeding defects include:
Quantitative defects (thrombocytopenia): They occur due to decreased bone
marrow production (leukemia, aplastic anemia) or increased platelet
destruction (giant hemangioma, spleen and foreign bodies in the
circulation).
Qualitative defects (poor platelet function): For example, Inherited platelet
aggregation defects like Glanzmann thrombasthenia (lazy platelets), BernardSoulier syndrome (Giant platelets), Storage pool defects, (Abnormal platelet
granules), ASA/NSAIDs (inhibit platelet granule release).
Clotting Disorders Involve Secondary Hemostasis
Congenital causes: Factor deficiency like hemophilia A and B.

Aquired causes like vitamin K deficiency (needed for the synthesis of factors
II, VII, IX and X) produces Hemorrhagic Disease of Newborn and Liver
failure results in incapacity to synthesize one or more clotting factors or
causes portal hypertension and platelet sequestration.
Mixed Disorders (Bleeding + Clotting Abnormalities) DIC

(Disseminated Intravascular Coagulation)
Disseminated intravascular coagulation (DIC) occurs in critically ill state
(hypotension, acidosis, oliguria or hypoxia, etc.) with evidence of
microvascular/large vessel thrombosis and decreased platelet count, due to
consumption and destruction.
In DIC, PT and PTT are prolonged due to consumption of factors V,
VIII, IX, and XI. Fibrinogen is decreased. Fibrin degradation products and
the D-dimers are increased.
von Willebrands Disease
von Willebrands factor is a cofactor for platelet adhesion and a carrier protein
for factor VIII. is inherited as an autosomal dominant trait:
Type 1: Quantitative defect (less factor)
Type 2: Qualitative defect
Type 3: Quantitative defect (absent factor).
The screening tests for suspected vWD are: Bleeding time, PTT and von
Willebrand factor activity called Ristocetin assay.
vWF is an acute phase reactant and therefore, studies for vWD can be affected
by cigarette smoking, stress, exercise, corticosteroids, etc.

DIFFERENTIATE BETWEEN BLEEDING
OR CLOTTING DISORDERS
History
Enquire Whether Spontaneous or Post-traumatic
Bruising with or without trauma can be due to platelet vascular or connective
tissue factors or even clotting disorder but deep palpable bruises are usually
due to a clotting factor defect and usually not spontaneous. Petechiae are
usually due to a platelet or blood vessel defect.
Enquire for Site of Bleeding
Mucosal bleeding (epistaxis, oral bleeding, gastrointestinal, genitourinary and
menstrual bleeding) often suggests bleeding disorder while bleeding after an
injury (circumcision, tonsillectomy) or musculoskeletal bleed is seen in clotting
defects.
Enquire about Age of Onset, Frequency and Severity of each
Bleeding Complaint
Extensive family history and medication history should also be obtained.
Children with severe hemophilia (a clotting defect) may present early.
Enquire About Inheritance
Hemophilia is an X-linked inherited clotting disorder transmitted from female
carriers to their male children (Males suffer).
Enquire about Prophylaxis
This is possible in clotting disorders only: Infuse factors two to three times a
week and/or prior to a sports activity in order to prevent spontaneous bleedings.
Examination
For signs of bleeding: Look for petechiae, bruising, mucosal bleeding, and
oozing from venipuncture sites (bleeding disorders manifest superficially).
For location: Superficial bruises versus deep palpable ecchymoses or deep tissue
bleeding, in joints and large muscle areas (suggest clotting disorder).
Laboratory Investigations
Complete blood count: This includes Hb, TLC, DLC and peripheral smear.
Platelet count is low in ITP and HUS as seen in Shigella gastroenteritis
(thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure).
Thrombocytopenia may also occur due to bone marrow aplasia or platelet
consumption.
Bleeding Disorders 299

PT evaluates: Extrinsic and common coagulation pathway (factors I, II, V,
VII, X) Hence it has a role in factor deficiency (I, II, V, VII, X), liver failure and
vitamin K deficiency.
PTT evaluates: Intrinsic and common pathway (factors I, II, V, X, VIII,
IX, XI, XII). Factor deficiency (I, II, V, X, VIII, IX, XI, XII), heparinization,
circulating anticoagulants, vWD affect PTT.
Platelet aggregation studies: Testing the aggregation of platelets in response
to several known agents adenosine diphosphate (ADP), epinephrine is collagen
is used to identify the cause of thrombasthenia.
PTT mixing study: If the prolonged PTT is due to a factor deficiency, then
the addition of factors from the normal plasma, will correct the PTT.
However, if the PTT is due to a circulating anticoagulant such as heparin or a
lupus anticoagulant, the circulating antibody will inhibit the normal factors
and the PTT will remain prolonged. Failure to normalize the PTT after the
addition of normal plasma, implies the presence of a circulating anticoagulants.
BIBLIOGRAPHY
1. Blanchette VS, Dean J, Lillicrap D. Chapter 31 - Rare Congenital Hemorrhagic
Disorders. In: Lilleyman J, Hann I, Blanchette V (Eds). Pediatric Hematology, London:
Churchill Livingstone Inc 1999;2:611-28.
2. DiMichele D Hemophilia. New approach to an old disease. Pediatr Clin North Am
1996;43(3):709-36.
3. Hardisty RM. Platelet Functional Disorders. In: Lilleyman J, Hann I, Blanchette V
(Eds). Pediatric Hematology, London: Churchill Livingstone Inc 1999;2:465-96.
4. Lillicrap D, Dean J, Blanchette VS. Chapter 30 - von Willebrand Disease. In: Lilleyman
J, Hann I, Blanchette V (Eds). Pediatric Hematology, London: Churchill Livingstone
Inc 1999;2:601-10.
5. Lusher JM. Chapter 29 - Hemophilia A and B. In: Lilleyman J, Hann I, Blanchette V
(Eds). Pediatric Hematology, second edn 1999, London: Churchill Livingstone Inc
1999;2:585-600.
6. Medeiros D, Buchanan GR. Chapter 47 - Disseminated Intravascular Coagulation
and Other Acquired Bleeding Disorders. In: Levin DL, Morriss FC (Eds). Essentials
of Pediatric Intensive Care, New York: Churchill Livingstone Inc 1997;2:473-82.
7. Medeiros D, Buchanan GR. Current controversies in the management of idiopathic
thrombocytopenic purpura during childhood. Pediatr Clin North Am 1996;43(3):75772.
8. Medeiros D, Buchanan GR. Idiopathic thrombocytopenic purpura: beyond consensus.
Curr Opin Pediatr 2000;12(1):4-9.
9. Medeiros D, Buchanan GR. Major hemorrhage in children with idiopathic thrombocytopenic purpura: immediate response to therapy and long-term outcome. J Pediatr
1998;133(3):334-9.
10. Werner EJ, Abshire TC, Giroux DS, Tucker EL, Broxson EH. Relative value of
diagnostic studies for von Willebrand disease. J Pediatr 1992;121(1):34-8.
11. Werner EJ. von Willebrand disease in children and adolescents. Pediatr Clin North
Am 1996;43(3):683-708.
50
Acute Rheumatic Fever
JOINT PAINS WITH FEVER
CASE PRESENTATION
History
A 10-year-old boy presented with moderate fever, joint pains and swelling
and shortness of breath for 5 days. Initially, the right knee was painful and
tender. Later the right ankle and left knee became tender, painful and swollen.
Examination
The child was apprehensive and had shortness of breath. The throat examination
revealed enlarged tonsils. The sleeping pulse rate was increased and there
was a holostolic grades III/VI murmur at the apex, radiating to the axilla. The
liver was five centimeters below the right costal margin. The right ankle and
left knee were very tender.
Investigations
Chest X-ray showed cardiomegaly. EKG done showed prolonged PR interval.
The erythrocyte sedimentation rate, CRP and ASO titer were high.
Diagnosis: Suspect Acute Rheumatic Fever (ARF).
DISCUSSION
Acute Rheumatic Fever typically occurs in school going, genetically
susceptible children, especially those living in overcrowded areas.
Acute Rheumatic Fever (ARF) is a term often used to describe the initial
or acute onset of the disease. The chronic heart disease as a sequelae of
carditis is called Rheumatic Heart Disease (when valvular scarring has set
in).
The initial valvulitis of ARF results in valvular insufficiency.
Acute Rheumatic Fever 301

Rheumatic Heart Disease (RHD)
Subsequently RHD sets in and enough inflammation may occur on the

leaflets of the mitral valve. Hence, the leaflets may scar and become
adherent to each other, resulting in mitral stenosis, etc.
The most common lesion is noted in mitral valve and aortic valve. The
classic mitral insufficiency presents with a pan systolic murmur (heard at
the apex) that radiates to the axilla. In Aortic insufficiency a diastolic
murmur is heard at (L) upper sternal border.
Clinical Diagnosis
Modified Jones criteria are categorized into major
and minor criteria. (Two majors or one major + two minor are required for
diagnosis).
Major Criteria
Carditis, migrating polyarthritis, chorea, erythema marginatum and
subcutaneous nodules.
Minor Criteria
Fever, arthralgia, elevated acute phase reactant (CRP or ESR) prolonged

PR interval (i.e., first degree AV block) and Echo evidence of Rheumatic
vegetation or regurgitant lesion, etc.
Leukocytosis used to be a minor criterion. All must have evidence of
streptococcal infection (positive ASO titer, Streptozyme and/or +ve
streptococcal throat culture).
Clinical Features
Correct order (most common to least common) is arthritis, carditis,
chorea and erythema marginatum.
Arthritis (Pain and Swelling of Joints)
In ARF, significant amount of pain is present with swelling which is very
tender and hyperesthetic, but child is fairly comfortable without movement
(swelling is seen in two or more joints it is considered polyarthritis). If the
polyarthritis is counted as a criteria, then one cannot use minor criteria of
arthralgia as well.
Pedia Pearls: Findings are sufficient to Label as Rheumatic fever if :
Syndenhams chorea present.
Nonexplainable insiduous or late onset carditis.
Rheumatic recurrence (if previously documented rheumatic fever or RHD).

Pancarditis (Rub, Tachycardia and Changing Murmurs)
If a rub is heard it indicates pericarditis

The murmur of mitral stenosis is a mid diastolic murmur, rather than later
in diastole as in aortic insufficiency. Changing murmurs indicate acute
activity (endocarditis).
For evidence of CCF: A gallop is an evidence of congestive heart failure
(often seen later in the course of illness, sometimes after repeated episodes
of ARF). Look at the point of maximal impulse. An enlarged PMI that is
displaced out indicates cardiomegaly. The enlarged liver size gives further
evidence of congestive heart failure, needing corticosteroids, diuretics,
digoxin, and occasionally inotropic agents. Sleeping pulse rate is useful
guide for tachycardia in myocarditis.
Sydenhams Chorea
This is a subacute phenomenon of rheumatic fever which usually resolves
with time. These are purposeless, involuntary movements present during
awake state with hypotonia, emotional lability and dysarthria. Lab tests are
normal.
Subcutaneous Nodules
Nodules are seen in fifth of patients with ARF and their presence heralds
severe carditis. They are located at the tips of the elbows, around the joints,
and the bony prominences of the spinal column.
Erythema Marginatum
The erythema marginatum also heralds severe carditis. It is an evanescent
pink eruption present over the trunk and almost never seen over the face. It
has irregular but well-demarcated borders and is seen in a few percentage of
cases only.
Juvenile rheumatoid arthritis: Joints swollen, without much tenderness,

with morning stiffness. Usually small joints are involved.
Systemic lupus erythematosus: Non-tender and lasting only for a few days.
Septic joint: Joint is tender swollen and painful even at rest and usually
unilateral single joint is involved.
Pedia Pearls: (Clinical markers of carditis)

Pericarditispericardial rub.
MycocarditisSoft S1, S3 gallop, CHF, Carey Coombs murmur.
EndocarditisChanging murmur.
Acute Rheumatic Fever 303

Treatment
If the carditis is mild, then salicylate therapy is usually given as Aspirin (80-100
mg/kg). However, if cardiomegaly is present then Corticosteroids (2 mg/ kg)
are indicated for 2 to 3 weeks followed by aspirin (80-100 mg/kg) while the
corticosteroids are being tapered over another 6 to 8 weeks (Total 8 to 10 weeks)
Crystalline Penicillin (1 lac unit/kg/day in 4 divided doses) is given for
streptococcal infections to prevent recurrence and further damage to the valves.
It is given for 10 days, intravenously.
Prophylaxis
Rheumatic Prophylaxis
For prevention of persistent cardiac disease and number of recurrences.
Benzathine penicillin is usually given up to 40 years. It is given upto 18 years
or 5 years after the last episode (6 lac below 27 kg and 12 lac units above 27 kg),
if carditis was mild.
Endocarditis Prophylaxis
Prophylaxis against alpha-hemolytic viridans streptococci (valvular infection)
is important prior to and following any procedure. The drug of choice is
Amoxycillin.
BIBLIOGRAPHY
1. Amigo MC, Martinez-Lavin M, Reyes PA. Acute rheumatic fever. Rheum Dis Clin
1993;19(2):333-47.
2. Berrios X, Campo E, Guzman B, Bisno AL. Discontinuing rheumatic fever prophylaxis
in selected adolescents and young adults. A prospective study. Ann Int Med
1993;118(6):401-06.
3. Cassidy JT, Petty RE. Chapter 12-Arthritis related to infection. In: Cassidy JT, Petty
RE (Eds). Textbook of Pediatric Rheumatology, Philadelphia: WB Saunders
1995;3:519-20.
4. Chun LT, Reddy DV, Yamamoto LG. Rheumatic fever in children and adolescents in
Hawaii. Pediatrics 1987;79(4):549-52.
5. Chun LT, Reddy DV, Yim GK, Yamamoto LG. Acute rheumatic fever in Hawaii:
1966 to 1988. Hawaii Med J 1992;51(8):206-11.
6. Forster J. Rheumatic fever: Keeping up with the Jones criteria. Contemp Pediatr
1993;3:51-60.
7. Kaplan EL. Global assessment of rheumatic fever and rheumatic heart disease at the
close of the century. Circulation 1993;88(4 Pt 1):1964-72.
8. Kurahara DK, Tokuda A, Grandinetti A, et al. Ethnic differences in risk for pediatric
rheumatic illness in a culturally diverse population. J Rheum 2002;29(2): 379-83.
9. Special writing group of the committee on rheumatic fever, endocarditis, and Kawasaki
disease of the council on cardiovascular disease in the young of the American Heart
Association. Guidelines for the diagnosis of rheumatic fever. JAMA 1992;268:2069-73.
10. Steer AC, Carapetis JR, Nolan TM, Shann F. Syste-matic review of rheumatic heart
disease prevalence in children in developing countries: The role of environmental
factors. J Paediatr Child Health 2002;38:229-34.
51
Nephrology Cases
EDEMA AND OLIGURIA
CASE 1
CASE PRESENTATION
Five-year-old boy, who recently recovered from a sore throat, was brought
with headache fever, edema of face and eyelids, for three days. Urine output
was decreased (passed urine twice in the past 24 hrs). Urine was reddish,
cloudy and dark cola colored. He also had dull back pain in the flanks with
headache. Physical examination revealed edema around the eyes and the ankle.
Blood pressure was 180/100 mm Hg.
Investigations
Urinalysis: Physical Appearance-Color:Yellow Hazy; Ph:6.5 Microscopic
Analysis-50 RBC/Hpf 10- WBC/Hpf, 5 RBC Casts/Hpf 2granular Casts/
Hpf Chemical Glucose: Nil, Ketones: Nil, Nitrite: Negative, Protein:2+,
Specific Gravity:1.015.
Serum: Electrolytes were normal. BUN 25 mg/dl and Cr 0.7. Dermatological
examination was negative for recent skin infection, although old healed
pyodermal lesions were seen.
Diagnosis: Suspect Acute Poststreptococcal Glomerulonephritis.
DISCUSSION
Acute Poststreptococcal Glomerulonephritis (APSGN) (Fig. 51.1)
It occurs commonly 2 to 4 weeks after streptococcal skin infection (impetigo,
pyoderma, etc.) due to group A -hemolytic streptococci, presenting as red
papules vesicles and pustules with honey colored crusts: Pyoderma may occur
secondary to insect bites, scabies, atopic dermatitis, etc. Family contacts need
to be treated with emulsion benzyl benzoate or 5 percent permethrin cream
before secondary infection develops in scabies.
Nephrology Cases 305

Pathophysiology
a. Structural damage to the glomerulus due to autoimmune inflammatory
processes. Hematuria is due to this structural damage.
b. Increased intravascular volume: Oliguria here is due to decreased GFR.
Hence, hyperaldosteronism and increased intravascular volume occurs due
to fluid retention. Hypertension is due to hyperaldosteronism and increased
intravascular volume (overload).
Components (Four)
Acute glomerulonephritis (GN) presents with (four) classic findings (Fig. 51.1):
1. Hematuria due to glomerular damage by antigen antibody complexes.
2. Oliguria due to decreased filteration.
3. Hypertension due to volume overload.
4. Edema due to volume overload.
Types of Glomerulonephritis (GN)
GN may be rapidly progressive (RPGN) or Chronic GN (CGN) which

implies that permanent damage has occurred.
The acute variety is poststreptococcal glomerulonephritis
It is frequent in males between 5 and 15 years after either an upper
respiratory tract or skin infection due to group A Hemolytic
Streptococcus.
Other causes are genetic/familial GN (Alport, X-linked) and other
autoimmune etiologies like SLE-lupus nephritis.
Fig. 51.1: Acute nephritis showing oliguria, edema and cola colored urine

Clinical Features
Many patients with APSGN are asymptomatic and do not seek medical care.
The presence of red cell casts on urinalysis almost always indicates the
presence of glomerulonephritis or renal trauma.
The presence of white cell casts on urinalysis can be seen in APSGN,
interstitial nephritis and pyelonephritis.
Complications (Four)
Increased intravascular volume may lead to complications like:
1. CCF (Congestive Cardiac Failure).
2. Pulmonary edema.
3. Hypertensive encephalopathy.
4. Acute renal failure and hyperkalemia due to structural damage to the
glomerulus.
Investigations
Serum:
1. Normal total protein level.
2. Serum complement C3 level is low C3 levels return to normal within a 6
to 8 week periods in APSGN. However, persistently low C3 levels suggest
a cause other than APSGN.
3. ASO titer is elevated.
4. Typically, there is increased specific gravity.
Urine:
1. Hematuria
2. Sterile pyuria.
3. Moderate proteinuria.
Erythrocyte casts/gross hematuria generally resolve within 1 to 2 weeks.
Microscopic hematuria may persist for a year or more.
Remember: Wilms will occasionally present with gross hematuria, so an
imaging study may be indicated to rule out this disorder.
Differentiate between nephritis and nephrotic syndrome before proceeding
for treatment (Table 51.1)
Treatment (Four)
1. Bedrest to prevent congestive heart failure even for hypertension. Give bedrest
and normalize blood pressure with diuretics and antihypertensive drugs.
2. Penicillin to eradicate Streptococcus. If it is poststreptococcal nephritis, give
benzylpenicillin 1 lac/kg /day in four divided doses for 10 days.
3. Weight monitoring loss of edema fluid and weight signifies improvement.
4. Lasix for volume overload (correct the over hydration with diuretics). For
hematuria alkalinize the urine to prevent acid hematin formation in tubules
which precipitates to block the tubules causing ATN.
Prognosis is excellent for APSGN with no relapse in later age.

Table 51.1: Differences between poststreptococcal nephritis
and nephrotic (minimal change)
Poststreptococcal nephritis
Nephrotic syndrome (minimal change)
1. Affects school going children

2. Often has hypertension and hematuria
due to glomerular damage
3. Usually has volume overload
Commonly affects children between 2-6 years.

Rarely has hypertension and hematuria due
glomerular damage
Usually has intravascular dehydration
4. Frusemide is commonly used

5. Complement (C-3) levels are low
Frusemide is used with caution

Complement (C-3) levels are normal
BIBLIOGRAPHY
1. Bergstein JM. Chapter 18 - The Urinary System, Nephrologic Diseases. In: Behrman
RE, et al (Eds). Nelson Textbook of Pediatrics, Philadelphia: WB Saunders Company
1992;14:1323-36.
2. Ruley EJ. Chapter 230 - Nephritis. In: Hoekelman RA (Ed). Primary Pediatric Care,
St Louis: Mosby-Year Book, Inc 1992;2:1379-86.
3. Travis LB. Chapter 19.6 - Glomerulonephritis. In: Rudolph AM (Ed). Rudolphs
Pediatrics, Stamford, CT: Appleton and Lang 1996;20:1351-66.
CASE 2
CASE PRESENTATION
History
A 5-year-old girl presented with swelling- first noticed around eyes (facial
puffiness) and decreased urine output. There was no history of sore throat,
rash, joint pain, diarrhea or trauma in recent past.
Examination revealed moderate periorbital edema and mild pitting edema of
hands and feet. Throat was normal. No hepatosplenomegaly was noted but
ascites was present. Urine color was normal.
Investigations
Urinalysis:
Physical appearance: Specific gravity of 1.030, Color yellow; pH: 6.5
Microscopic analysis: No rbc/hpf,1-2wbc/hpf, hyaline casts/hpf
Biochemical analysis: Glucose-nil; Ketones-nil; Nitrite-negative; Protein4+.
Blood chemistry
Protein of 2 g/dl, serum albumin of 1.4 g/dl
Cholesterol of 350 mg/dl
Blood urea nitrogen and creatinine were normal.
Diagnosis: Nephrotic syndrome.

DISCUSSION
Nephrotic Syndrome (Fig. 51.2)
Components: (NS) is a state characterized by:
Massive proteinuria (40 mg/m2/hr (or 1 gm/m2/d or 3 gm/day):
Nephrotic range of proteinuria = Urine Protein 3+ or 4+ or Urine protein/
creatinine ratio of > 2).
Qualitative assessment of proteinuria is by heat glacial acetic acid
method while Quantitative assessment is by Esbachs method done on
24 hour urinary sample.
Hypoalbuminemia (<2.5 g/dL):
Increased glomerulocapillary wall permeability (unknown antigen
enhances permeability) and the negatively charged glycoproteins are
lost within the capillary wall that usually repel negatively charged
proteins.
Albumin, immunoglobulins, thyroxine binding protein, cholecalciferol
binding protein and transferrin metal binding protein are lost in the
urine.
Hypercholesterolemia (>220 mg/dL):
It occurs secondary to hypoproteinemia which is thought to stimulate
protein synthesis in the liver, including the over production of
lipoproteins causing hyperlipidemia.
Also due to loss of lipoprotein lipase in urine (the main enzyme involved
in lipoprotein breakdown), the cholesterol level rises.
Edema: Children with minimal change disease usually present with edema
(localized or generalized).
Once albumin levels drop below 2 g/dL even pleural effusions, ascites
and decreased urine output may develop.
Fig. 51.2: Nephrotic syndrome showing facial puffiness and periorbital edema

Pathophysiology
Reduction of the intravascular volume:

It results in reduced renal perfusion thereby causing renin-angiotensinaldosterone system activation which leads to sodium and water
retention, further increasing edema.
Massive proteinuria causes hypoalbuminemia thereby plasma oncotic
pressure falls causing transudation of fluid from intravascular
compartment to interstitial space, leading to edema. This is similar to
what happens in protein calorie malnutrition and protein losing
enteropathy.
Types
1. Primary nephrotic syndrome (diseases limited to the kidney) is common
in two to six years age group.
2. Secondary nephrotic syndrome occurs due to (systemic diseases with kidney
involvement like systemic lupus erythematosus and Henoch-Schnlein
purpura, malignancies, drug or toxin exposures). It is seen in patients older
than six.
3. Autosomal recessive congenital form of nephrotic syndrome occurs due to
a defect in the nephrin gene on chromosome 19q13.1.
Primary Nephrotic Syndrome
The commonest primary nephrotic syndrome is Idiopathic Nephrotic
Syndrome.
Types
Minimal change disease: It is due to fusion and effacement of the foot
processes (Pseudovillus formation). There is increased permeability of the
basement membrane-podocyte system to albumin. The outcome is
decreased intravascular volume (hypovolemia induced decrease in urine
output).
Focal segmental glomerular sclerosis.
Membranoproliferative glomerulonephritis.
Membranous glomerulopathy.
Pedia Pearls: (Rule of two)

Massive proteinuria (40 mg/m2/hr (or 2 gm/day)
Hypercholesterolemia (>220 mg/dL):
Once albumin levels drop below 2 g/dL even pleural effusions, ascites and decreased
urine output may develop.

Complications
Infection
Escherichia coli sepsis, cellulitis, pneumonia and urinary tract infection.
Peritonitis/ pneumococcal sepsis is thought to be due to: IgG excretion,
decreased complement function, and diminished splanchnic blood flow.
Due to high possibility of S. pneumoniae, a polyvalent pneumococcal
vaccine should be administered to nephrotic children over two years
of age.
Investigate Blood culture.
Thromboembolic diseases:
For example, renal vein thrombosis occurs due to increased platelet
aggregation, increased fibrinogen concentration, decreased
antithrombin III concentrations, increased blood viscosity, decreased
blood flow and urinary losses of antithrombin III and Factors IX, X
and XI.
Investigate ultrasound abdomen.
Corticosteroid drug toxicity:
Gastric irritation, insulin resistance, growth retardation, elevated blood
pressure.
Hemorrhagic cystitis, sterility and leukopenia can be seen with
cyclophosphamide.
Various other causes of edema may confuse us, like those due to:
Impaired venous flow: Vana caval obstruction or hepatic vein obstruction
Impaired lymphatic flow like congenital lymph edema, Wuchereria
bancrofti infection, etc.
Increased capillary leakage in allergy and sepsis
Increased hydrostatic pressure in acute nephritic syndrome and congestive
cardiac failure.
Organ wise the various causes of edema are:
Renal: Look for periorbital edema with hematuria; hypertension; symptoms
of collagen disease (rash, joint pain); frothy urine; symptoms of uremia
(vomiting, nausea, pallor), convulsion, low urine output.
Cardiac: Look for symptoms like orthopnea, joint pain; palpitation; giddiness;
fainting episodes; bluish episodes.
Hepatic: Look for jaundice; ascites; prominent abdominal veins; neonatal umbilical
sepsis; spleenomegaly; purpura, etc.
Multisystemic: Collagen diseases (PPP) look for joint pain, pallor and
petechiae. In protein energy malnutrition. Look for diet, diarrhea and diseases
(DDD).

ISKDC Terminology
Remission
Urine albumin is Nil or Traces or < 4 mg /m2/hr for three consecutive early
morning specimens.
Response
Urine free of protein within eight weeks (Steroid sensitive). Most respond
with disappearance of proteinuria within two weeks.
Late response
A response beyond eight weeks.
Relapse
Proteinuria 3+ plus edema or 40 mg/m2/hr for three consecutive early
morning specimen(having been in remission previously). Relapse is often
precipitated by respiratory infection.
Early relapse
Initial early responders who relapse during eight weeks of therapy.
Frequent relapse
Two or more relapses in six months or > 4 relapses in 1 year.
Steroid dependent
Relapse while on alternate day steroid therapy or within 14 days of stopping
prednisolone therapy.
Steroid resistant
Either do not respond to the initial treatment with prednisolone within
eight weeks of therapy 60 mg/m2/d, or do so transiently and later/cease to
respond.
Principles of Investigation
1. Confirm presence of massive proteinuria, hypoalbuminemia and
hypercholesterolemia.
2. Investigate for presence of complications.
3. Invesgations to rule out nephritis (discussed earlier).
4. Renal biopsy.
Renal Biopsy
It is obtained in cases where there is poor or no response to corticosteroids,
or the patient is less than 1 year old (congenital nephrotic syndrome) or
over 10 years old.
In secondary nephrotic syndrome and corticosteroid toxicity, cytotoxic
agents are considered.
Patients with low serum complement levels or hypertension on presentation
may indicate nonminimal change renal lesion as serum C3 levels are normal
in cases of minimal change disease.

Treatment
Treat any associated infection.

Fluid Management
Intravenous fluids: Because of dynamic change of intravascular volume
in nephrosis, treatment should be tailored according to the volume state
(guided by blood pressure and CVP and daily weight loss which should
not exceed 1 kg).
Most commonly hypovolemia exists, so restore intravascular volume
with colloids and give Protein 1g/kg + losses.
Note: This type of protein diet decreases proteinuria and decreases the
compensatory lipoprotein synthesis of the liver (hypercholesterolemia).
Do not Give Diuretics, but:
If urine Na is low and hypovolemia/edema is life-threatening (severe
pleural, pericardial effusion): give Albumin <1 g/kg/day + diuretic
(furosemide 2 mg/kg)
Caution: Albumin hyperfiltration deteriorates kidney function and can
cause fluid and sodium overload.
If rarely hypervolemia exists, e.g. in secondary nephrotic syndromes
(nephrosonephritis) then diuretics are needed.
If normovolemia: Only restriction of sodium and fluid is required. ACE
inhibitors also decrease proteinuria.
Treat Complications
Electrolyte levels and renal function must be monitored. For hypokalemia,

an oral potassium supplement or spironolactone may be added.
Paracentesis is performed if there is respiratory compromise secondary to
severe ascites.
Antibiotic therapy is given, if there is evidence of bacterial infection.
Edema is managed with sodium restriction (the no added salt diet).
Monitor their weight closely, Consume adequate amounts of proteins.
Drug Therapy
In MCNS: Give steroids: In first attack (but first do chest X-ray to rule out
tuberculosis). Prednisone: 2 mg/kg/day (=60 mg/m2) (6) weeks then taper
to 1.5 mg/kg/2 day (=40 mg/m2) (6) weeks.
In Recurrence/Relapse
Prednisone: Give prednisolone 2 mg/kg/day, until urine is free of protein and
child is edema free for three consecutive days. Then give 1.5 mg/kg/alternate
days for four to six weeks.
In Frequent Relapser/Steroid Dependence
Give Methyl prednisolone or long-term alternate day steroid treatment. If
steroid toxicity develops then levamisole 2 mg/kg on alternate days for 6 to
12 months may be given.

In Continuing Relapses or Steroid Toxicity
Cyclophosphamide 2 mg/kg/day for (12) weeks is given to a lower the
corticosteroid dose, to prevent relapses and to increase the duration of
remission. Chlorambucil and cyclosporine have also been used. Biopsy is
indicated in such cases. Mycophenolate is a new promising drug.
BIBLIOGRAPHY
1. A Report of the ISKDC. The primary nephrotic syndrome in children. Identification
of patients with minimal change nephrotic syndrome from initial response to
prednisone. J. Pediatr 1981;98:561-4
2. A Report of the ISKDC. Nephrotic syndrome in children. Pediction of histopathology
from clinical and laboratory characteristic at time of diagnosis. Kidney Int.
1978;13:159-65.
3. British Association for Paediatric Nephrology. Levamisole for corticosteroid dependent
nephrotic syndrome in childhood. Lancet 1991; I:555.
4. Chin J, McLain PN, Drummond KN, a controlled prospective study of
cyclophosphamide in relapsing corticosteroid responsive, minimal lesion nephrotic
sundrome in childhood. J Pediatr 1973;82:607-13.
5. Giordano M, De Feo P, Lucidi P, et al. Effects of dietary protein restriction on fibrinogen
and albumin metabolism in nephrotic patients. Kidney Int 2001;60:235-42.
6. Ksiazek J, Wyszynska T. Short versus long initial prednisone treatment in steroid sensitive
nephrotic syndrome in children. Acta Paediatr 1995;84:889-93.
7. Koskimies O, Vilska J, Rapola J, Hallamn N. Long term outcome of primary nephrotic
syndrome. Arch Dis Child 1982;57:544-8.
8. Lewis MA, Baidom EM, Davis N, Houston IB, Postlethwaite RJ. Nephrotic syndrome:
From toddlers to twenties. Lancet 1989 I: 255-9
9. Matoo T. Kidney biopsy prior to cyclophosphamide therapy in primary nephrotic
syndrome. Pediatr Nephrol 1991;5:617-9.
10. Niaudet P, Broyer M, Habib R. Treatment of idiopathic nephrotic syndrome with
cyclosporin A in children. Clin Nephrol 1991;35 Suppl 1:S31-6.
11. Schulman SL, Kaiser BA, Polinsky MS, Srinivasan R, Baluarte HJ. Predicting the response
to cytotoxic therapy for childhood nephrotic syndrome: Superiority of response to
corticosteroid therapy over histopathologic patterns. J Pediatr 1988;113:996-1001.
12. Sharples PM, Poulton J, White RHR. Steroid responsive nephrotic syndrome is more
common in Asians. Arch Dis Child 1985;60:1014-7.
13. Ueda N, Chihara M, Kawaguchi S, et al. Intermittent versus long-term tapering
prednisolone for intial therapy in children with idiopathic nephrotic syndrome. J Pediatr
1988;112:122-6.
14. Ueda N, Kuno K, Ito S. Eight and 12 week courses of cyclophosphamide in nephrotic
syndrome. Arch Dis Child. 1990;65:1147-50.
15. White RHR, Glasgow EF, Mills RJ. Clinicopathological study of nephrotic syndrome
in childhood. Lancet 1970 I:1353-9.
8
Spotters
52
Turners Syndrome
SPOTTER
A normal female is labeled 46 XX (both X are fully functional).

In Turner female (Fig. 52.1) the chromosomal pattern is 45 XO. Only one
X chromosome is present (which is fully functional).
In lyonized X (rare cases) a second X chromosome is present but it is nonfunctional.
In mosaic, some cells have a second functional X chromosome and other
cells are without it. Normally, girls do not manifest X linked disorders
(like hemophilia) but due to lyonization they may manifest them.
Clinical Features
Imagine an adult that has been Compressed. From head to toe, everything
appears to have been compressed by nature.
Short stature maximum height is about 140 cm.
Low hairline and Low-set ears.
Small lower jaw and high-arch palate.
Fig. 52.1: Turners syndrome

Webbing of the neck. Thyroid disorders are also common.

Broad chest (shield chest), widely-spaced nipples and poor breast
development.
Truncal obesity and diabetes (due to compresson over the pancreas).
Turned-out elbows and (swelling) of the hands and feet (pedal edema in
newborn period).
Underdeveloped gonadal structures: (Female sexual characteristics are
present but generally underdeveloped). Even the Rudimentary ovaries/
gonadal streak and horseshoe kidney or abnormal urine-collecting system
seem to have been compressed by GOD.
Coarctation of the aorta: It is a congenital cardiovascular condition. Here,
aorta is compressed. Bicuspid aortic valve is also common.
Learning difficulties,Visual impairments and hearing loss may also be
present.
Antenatal Diagnosis
This is often recommended for families who have had a child with Turners
syndrome.
Diagnosis and Treatment
Suspect Turners in absence of secondary sexual characters/menarchy by the
age of 14 years
Confirm Turners syndrome by:
1. Karyotyping- 45XO (buccal smear).
2. Serum estradiol -Very low.
3. Serum FSH and LH are elevated (hypergonadotropic-hypogonadism).
Treatment
Estrogen replacement therapy prepares the uterus for assisted reproduction,

develops secondary sexual characteristics and improves bone density.
A donor egg can be used to create an embryo, which is carried by Turner
woman.
Growth hormone is effective in increasing height.
SUMMARY
1. In Turners syndrome there is complete or partial absence of second sex
chromosome
2. Short stature, premature ovarian failure and phenotypic female are
characteristic features
3. Intelligence is normal but verbal skills are better than other skills.
Turners Syndrome 319

BIBLIOGRAPHY
1. Davenport ML, Crowe BJ, Travers SH, Rubin K, Ross JL, Fechner PY, et al. Growth
hormone treatment of early growth failure in toddlers with Turner syndrome: A
randomized, controlled, multicenter trial. J Clin Endocrinol Metab 2007;92(9):340616.
2. Elsheikh M, Conway GS, Wass JA. Medical problems in adult women with Turners
syndrome. Ann Med. 1999;31(2):99-105.
3. Gravholt C. Clinical Practice in Turner Syndrome. Nature Clinical Practice
Endocrinology & Metabolism 2005;1:41-52.
4. Health supervision for children with Turner syndrome. American Academy of
Pediatrics. Committee on Genetics. Pediatrics. Dec 1995;96(6):1166-73.
5. Lippe BM. Primary Ovarian Failure. In: Clinical Pediatric Endocrinology. Philadelphia,
Pa: WB Saunders 1990;325-66.
6. Lyon AJ, Preece MA, Grant DB. Growth curve for girls with Turner syndrome. Arch
Dis Child 1985;60(10):932-5.
7. Mazzanti L, Prandstraller D, Tassinari D, Rubino I, Santucci S, Picchio FM, et al.
Heart disease in Turners syndrome. Helv Paediatr Acta 1988;43(1-2):25-31.
8. Medeiros CC, Marini SH, Baptista MT, Guerra G Jr, Maciel-Guerra AT. Turners
syndrome and thyroid disease: A transverse study of pediatric patients in Brazil. J Pediatr
Endocrinol Metab 2000;13(4):357-62.
9. Pai GS, Leach DC, Weiss L, Wolf C, Van Dyke DL. Thyroid abnormalities in 20
children with Turner syndrome. J Pediatr 1977;91(2):267-9.
10. Sas TC, de Muinck Keizer-Schrama SM, Stijnen T, van Teunenbroek A, HokkenKoelega AC, Waelkens JJ, et al. Final height in girls with Turners syndrome treated
with once or twice daily growth hormone injections. Dutch Advisory Group on Growth
Hormone. Arch Dis Child 1999;80(1):36-41.
11. Stephure DK. Impact of growth hormone supplementation on adult height in Turner
syndrome: Results of the Canadian randomized controlled trial. J Clin Endocrinol
Metab 2005;90(6):3360-6.
12. Turner HH. A syndrome of infantilism, congenital webbed neck, and cubitus valgus.
Endocrinology 1938;23:566-74.
53
Achondroplasia
SPOTTER
Achondroplasia (Fig. 53.1) is seen in the normally intelligent, circus dwarfs.
It has an autosomal dominant inheritance (fgfr3gene is involved).
CARDINAL FEATURES
Abnormal Skull Structure
An abnormally large skull and frontal bossing is common.
They have a relatively small skull base.
Large head may occur due to an abnormal skull structure or hydrocephalus.
Otitis media occurs frequently as there is abnormal drainage of the
eustachian tube.
Sometimes, central apnea occurs due to brainstem compression due to
abnormal skull structure. Hence, suboccipital decompression is indicated
in central hypopnea.
Fig. 53.1: Achondroplasia
Achondroplasia 321
Short Height
With increasing paternal age >35 years, a de novo mutation may occur in
FGFR3 causing disproportionate short arms and legs.
Rhizomelic (proximal) shortening of the arms and legs leads to orthopedic
deformities like genu varum (bow legs) and limitation of elbow extension.
Growth hormone (GH) therapy has been proposed as a possible treatment
for the short stature of achondroplasia.
Small Face Due to Mid-face Hypoplasia
Mid-face hypoplasia can cause:
Obstructive sleep apnea.
Overcrowding of the teeth
Adenotonsillectomy, weight reduction, continuous positive airway pressure
(CPAP) by nasal mask may help in treatment of obstructive sleep apnea.
Hypotonia
This leads to developmental delay in motor milestones and exaggerated lumbar
lordosis, which develops, when the child starts walking.
Orthopedic Deformities
They include limitation of elbow extension, trident configuration of hands
and genu varum (bow legs). Suboccipital decompression is indicated for lowerlimb hyperreflexia or clonus.
Genetics
It is an autosomal dominant disorder where advanced paternal age is a risk
factor.
Parents with normal stature and a de novo mutation have a low risk of
having another child with achondroplasia.
An adult with achondroplasia who has a normal reproductive partner has
a 50 percent risk in each pregnancy of having a child with achondroplasia.
When both parents have achondroplasia, the risk to their offspring of having
normal offspring is 25 percent; and that of having achondroplasia is 50
percent; while chance of a lethal condition is 25 percent.
Prenatal Testing
If one or both parents have achondroplasia, then amniocentesis or chorionic

villus sampling (CVS) is indicated.
Mothers with achondroplasia should have a cesarean section, because of
the small size of the pelvis.

Investigations
Radiological opinion and routine prenatal ultrasound examination may

identify short fetal limbs and also progressive discordance between the
length and biparietal diameter with gestational age.
The trident hand configuration may also be seen. MRI or CT of the Foramen
magnum region may be done for evaluation of severe hypotonia or signs
of spinal cord compression.
This includes Rickets where short stature, bow legs, hypotonia and large head
are common features. This is differentiated by:
Bone X-rays.
In rickets, the tubular bones are short and thick with cupping and flaring
and irregular growth plates.
The hand has broad wide wrists (bone - age delayed on X-ray).
General physical examination
The ribs are short with cupped anterior ends (rachitic rosary).
Treatment
Multidisciplinary Approach
They need a multidisciplinary approach for management of complications:
For management of frequent middle-ear infections and speech, evaluation
by ENT specialists is needed.
Orthopedic evaluation is necessary for truncal weakness or bowing of the
legs, if it interferes with walking. Spinal fusion may be done for kyphosis.
BIBLIOGRAPHY
1. Ain MC, Shirley ED. Spinal fusion for kyphosis in achondroplasia. J Pediatr Orthop
2004;24:541-5.
2. Bellus GA, Escallon CS, Ortiz de Luna R, Shumway JB, Blakemore KJ, McIntosh I,
Francomano CA. First trimester in couple at risk for achondroplasia. Lancet
1994;344:1511-2.
3. Hall JG. The natural history of achondroplasia. Basic Life Sci 1988;48:3-9.
4. Key LL Jr, Gross AJ. Response to growth hormone in children with chondrodysplasia.
J Pediatr 1996;128:S14-7.
5. Kitoh H, Kitakoji T, Kurita K, Katoh M, Takamine Y. Deformities of the elbow in
achondroplasia. J Bone Joint Surg Br 2002;84:680-3.
6. Krakow D, Williams J 3rd, Poehl M, Rimoin DL, Platt LD. Use of three-dimensional
ultrasound imaging in the diagnosis of prenatal-onset skeletal dysplasias. Ultrasound
Obstet Gynecol 2003;21:467-72.
7. Nelson FW, Hecht JT, Horton WA, Butler IJ, Goldie WD, Miner M. Neurological
basis of respiratory complications in achondroplasia. Ann Neurol 1988;24:89-93.
8. Richette P, Bardin T, Stheneur C. Achondroplasia: From genotype to phenotype.
Joint Bone Spine 2007;75:125.
9. Stoll C, Roth MP Bigel P. A re-examination on parental age effect on the occurrence
of for achondroplasia. Prog Clin Biol Res 1982;104:419-26.
Mucopolysaccharidosis 323
54
Mucopolysaccharidosis
SPOTTER
Mucopolysaccharides consist of glycosaminoglycans attached to a link protein
with a hyaluronic acid core. Lysosomal enzymes degrade them but defective
activity of the lysosomal enzymes blocks the degradation. Hence, heparan
sulfate, dermatan sulfate and keratan sulfate accumulate causing cellular
dysfunction. Mucopolysaccharidosis is common in Jews and French.
Age of Presentation
Most cases present in infancy. However, Morquio syndrome presents in toddlers
and MPS IS and MPS VI can present late in childhood.
CLINICAL FEATURES
Five major organs which utilize carbohydrates suffer:
1. CNS
Hydrocephalus, mental and neurologic retar-dation.
2. Heart
Angina ischemia hypertension, congestive heart failure and valvular
dysfunction.
3. Musculoskeletal
Short stature is seen in all except MPS IS (joint stiffness) or MPS IV
(hyperlaxity deformities, nerve entrapment, such as carpal tunnel syndrome
and atlantoaxial instability).
4. Liver
Liver enlargement is common in many.
5. Eye
Corneal clouding is seen (except in Hunter).
6. They also get respiratory diseases:
Obstructive airway disease is caused by a narrowed upper airway causing
sleep apnea and even cor pulmonale. Recurrent middle ear infections,
deformity of the ossicles and abnormalities of the inner ear are also seen.

TYPES
MPS 1H (H= hypothyroid, hydrocephalus, hepatosplenomegaly, hearing loss)
Hurlers syndrome looks like hypothyroid child, due to features like short stature
coarse facial features, large tongue, prominent forehead, inguinal and umbilical
hernias and mental retardation. Other features are corneal clouding,
hepatosplenomegaly, skeletal deformities (dysostosis multiplex) and joint stiffness.
They also have ear infections, nasal discharge, hearing loss and hydrocephalus.
Death usually occurs by ten years, due to cardiopulmonary complications.
Dysostosis multiplex and beaking of vertebrae are seen in several cases (Figs
54.1 and 54.2).
Fig. 54.1: Skeletal involvement in mucopolysaccharidosis

Beaking
Fig. 54.2: Mucopolysaccharidosis (beaking of vertebrae)
Mucopolysaccharidosis 325
MPS 1-H/S (H = heart disease, H = stiff joints, S = sensible with
normal intelligence).
Hurler-Scheie syndrome is a mild form of Hurlers syndrome (normal
intelligence) Micrognathia gives them a characteristic facies. Corneal clouding,
joint stiffness and heart disease develop late. Patients lives up to thirties.
MPS 1S (S = stiff joints, S = sensible with normal intelligence).
Scheie syndrome has onset after 5 years and have normal intelligence, normal
stature and a normal lifespan. These patients have aortic valve disease, corneal
clouding and joint stiffness.
MPS II (Hunter) X linked. Also Hunter needs to see for
hunting, hence no corneal clouding.
Hunters syndrome is X-linked recessive. (Hence patients are males. Remember
only boys hunt and hunters cannot be blind, so no corneal clouding). Other
mucopolysaccharidoses are autosomal recessive disorders. They have pebbly
ivory skin lesions on the back, arms and thighs. They have features of a primitive
Hunter, viz- coarse facial features, skeletal deformities (such as claw hand),
and joint stiffness is present, clear cornea and aggressive behavior. Death
occurs by 10 to 15 years.
MPS III (Sanfilippo syndrome flips here and there).
Sanfilippo syndrome is the most common of the MPS disorders:
Four subtypes A, B, C and D are not distinguishable clinically
(Mneumonickeep in mind Sanfilippo flips here and there, i.e. they are
restless due to central nervous system involvement).
Onset of the disease in preschool children presents with hyperactivity,
disturbed sleep aggressive social behavior, mental deterioration, enlarged
head and developmental delay.
Hepatosplenomegaly, mild dysostosis multiplex and joint stiffness are seen.
These patients die in twenties or thirties.
MPS IV Morquio syndrome
(they live up to 4th decade and present before 4 years).
Morquio syndrome presents between 2 to 4 years.
Skeleton is involved with preservation of intelligence.
Spondyloepiphyseal dysplasia is the hallmark of this disease. Spondylo
refers to spinal curvature, odontoid hypoplasia and Atlantoaxial instability
causing myelopathy Epiphyseal dysplasia refers to genu valgum, short
stature, and ligamentous laxity.
Severe form dies by fourth decade but mild forms have normal life-span.
MPS VI (Maroteaux-Lamy syndrome).
Maroteaux-Lamy syndrome has onset in todd-lers.
It is similar to Hurlers syndrome, including corneal clouding, coarse facies,
joint stiffness, skeletal deformities and heart valvular disease but
intelligence is normal.
Death usually occurs in the third decade due to cardiopulmonary

complications.
MPS VII (Sly syndrome) sly reminds of splenomegaly
Sly syndrome is associated with hydrops fetalis and hepatosplenomegaly. Other
features similar to Hurler syndrome.
TREATMENT
It includes supportive care and experimental modalities
Laronidase is useful for Type 1.
Hurler and Hurler scheie need synthetic form of L iduronidase, which is
deficient in these types.
Idursulfase is used to replenish Iduronate 2 sulfatase in MPS-II.
Bone marrow transplant in Hurler disease increases lifespan.
Hydrocephalus needs VP shunt.
Corneal clouding needs transplant of cornea in severe cases.
Tracheostomy may help in severe airway obstruction.
Orthopedic surgeries help in treatment of Dysostosis multiplex.
BIBLIOGRAPHY
1. Clarke LA. Idursulfase for the treatment of mucopolysaccharidosis II. Expert Opin
Pharmacother. Feb 2008;9(2):311-7.
2. Dupont C, Hachem CE, Harchaoui S, Ribault V, Amiour M, Guillot M. Hurler
syndrome: Early diagnosis and successful enzyme replacement therapy: A new
therapeutic approach. Case report. Arch Pediatr. Jan 2008;15(1):45-9.
3. Follow-up of nine patients with Hurler syndrome after bone marrow transplantation.
J Pediatr. Jul 1998;133(1):119-25.
4. Kasper DC, Iqbal F, dvorakova L, Zeman J, Magner M, Bodamer O, et al. Rapid and
accurate denaturating high performance liquid chromatography protocol for the
detection of alpha-1-duranidase mutations causing mucopolysacchridosis type 1. Clin
Chim Acta. Mar 2010;411(5-6):343-50.
5. Kottler U, Demir D, Schmidtmann I, Beck M, Pitz S. Central Corneal Thickness in
Mucopolysaccharidosis II and VI. Cornea. Mar 2010;29(3):260-2.
6. Muenzer J. Mucopolysaccharidoses. Adv Pediatr. 1986;33:269-302.
7. Menkies CJ, Rondot P. Idiopathic osteonecrosis of femur in adult Morquio type B
disease. J Rheumatol. Nov 2007;34(11):2314-6.
8. Tandon V, Williamson JB, Cowie RA. Spinal problems in mucopolysaccharidosis I
(Hurler syndrome). J Bone Joint Surg Br. Nov 1996;78(6):938-44.
9. Tolar J, Grewal SS, Bjoraker KJ, Whitley CB, Shapiro EG, Charnas L. Combination
of enzyme replacement and hematopoietic stem cell transplantation as therapy for
Hurler syndrome. Bone Marrow Transplant. Nov 26 2007.
10. Wraith JE, Scarpa M, Beck M, Bodamer OA, De Meirleir L, Guffon N.
Mucopolysaccharidosis type II (Hunter syndrome): A clinical review and
recommendations for treatment in the era of enzyme replacement therapy. Eur J
Pediatr. Mar 2008;167(3):267-77.
Neural Tube Defects 327
55
Neural Tube Defects
SPOTTER
INTRODUCTION
These birth defects are a spectrum which include anencephaly, encephalocele
and spina bifida. Commonest defect is in the lumbosacral area which occurs
due to incomplete closure or non-closure of the neural tube during the 3rd to
5th week of pregnancy. They may encompass the meninges and spinal cord in
addition to bony vertebral elements. Anencephaly is the severest form of neural
tube defect. It is more common in females.
Usual Scenario
History: 20-year-old unbooked case, a G1P0 mother delivered at 37 weeks.
She was not on any vitamins or folate supplements and had an ultrasound
done at 34 weeks which revealed a meningomyelocele with hydrocephalus
C-section was done and baby was delivered with Apgar scores of 7 and 8 at 1
and 5 minutes and the birthweight of 2.8 kg.
Examination: It revealed a translucent membrane sac overlying the mid-lumbar
region leaking yellowish fluid. Upper extremity movement was good but lower
extremity movement was moderate. Neuro-surgeon closed the
meningomyelocele defect over the lower back. Postoperative recovery in the
NICU was unremarkable. However, the (Ventriculoperitoneal) hydrocephalus
worsened on follow-up, so a VP shunt was surgically placed.
Diagnosis: Neural tube defect (meningomyelocele with hydrocephalus).
Etiology
It is due to failure of closure of neural tube (17-28 days, intrauterine). Presence
of abnormality in the gene producing 5, 10 methyl tetra-hydrofolate reductase
enzyme is critical. Predisposing factors include: (1) Trisomy 13 and 18. (2)
Exposure to valproic acid. (3) Thalidomide. (4) Increased maternal age and (5)
Maternal diabetes.

TYPES OF SPINAL DEFECTS
Myelodysplasia
It refers to defects of spinal cord development. It may occur with spina bifida;
but not necessarily associated, e.g. syringomyelia and diastematomyelia.
Myelodysplasias may experience spinal cord tethering due to stretching/traction
on the conus medullaris and cauda equine causing spasticity, weakness, decreased
sensation, urinary and bowel involvement, scoliosis and foot deformity.
Spina Bifida Occulta Closed Spina Bifida
It is failure of fusion of the spinal bony arches and the neural elements are
covered by skin. Overlying dimple, fistula, hairy tuft and hemangioma may
indicate NTD and the presence of lipoma or a dermoid cyst may indicate
tethering.
Spina Bifida Cystica Meningocele
It is a cystic transilluminant outpouching of the meninges but it has no neural
elements in it Lumbosacral region in the commonest site.
Meningomyelocele (Fig. 55.1)
It is a cystic outpouching of the meninges but with dysplastic neural elements in
it. It may be closed with skin or spinal fluid may leak outside (open
meningomyelocele). Lipomeningocele and lipomyelomeningocele are closed
with fatty tissue inside them.
Thoracic lesions present with flaccid paralysis of lower extremities with
variable weakness in abdominal and trunk musculature, frequently
associated with serious respiratory compromise.
High lumbar lesions (L1, L2) present with flaccid paralysis of knees and
ankles and may be able to walk with extensive braces and crutches.
Fig. 55.1: Neural tube defectmeningomyelocele

Midlumbar lesions (L3) present with paralyzed ankles and toes. These
children can accomplish independent ambulation with braces.
Low lumbar lesions (L4, L5) often have weak ankle and toe mobility. They
are particularly prone to ankle or foot deformities and often need orthosis
for independent ambulation.
High meningomyeloceles cause lower extremity paralysis but those with
low lying meningomyeloceles can manage with assistive devices.
Regardless of the level of lesion bladder and bowel problems are present
in nearly all children with meningomyelocele.
Complications
Bladder and bowel problems: Recurrent urinary tract infection and renal
failure may occur. In spinal bifida occulta however, the bladder function is
normal.
Lack of sensation and control over external sphincters makes these children
unable to control the passage of stool.
Major Association
Congenital malformations of the central nervous system.

Example:
Arnold-Chiari II malformation which can cause hydrocephalus (as the
cerebellum and medulla oblongata herniate into cervical spinal canal,
resulting in progressive hydrocephalus and dysfunction of the lower
cranial nerves). Treatment includes placement of a shunt.
Other Associations Include

1.
2.
3.
4.
5.
6.
Holoprosencephaly
Polymicrogyria
Club foot
Hip dislocation
Cerebellar abnormalities (decreased size)
GIT and genitourinary anomalies.
Investigations
1. MRI scan helps to identify the abnormality in case of occult spinal
dysraphism.
2. Ultrasonography, also has been increasingly accurate in prenatal diagnosis
of fetal anomalies (lemon sign, banana sign, etc.).
3. Alpha-fetoprotein (AFP) is normally produced by mothers to prevent graft
(that is the baby) being rejected by the host (that is the mother). Local
concentration of a variety of hormones, including alpha-fetoprotein provide
a blocking mechanism to prevent maternal cellular immune attack. This is

measured at (15 to 18 weeks of gestation) in: (1) Maternal serum (MSAFP)
and (2) Amniotic fluid (AFAFP):
It is elevated in open NTDs such as encephalocele, meningomyelocele
and anencephaly.
It is altered by gestational age, number of fetuses, maternal weight
(low in obese) and diabetes.
Amniotic fluid AFP level is more definitive than MSAFP(>2.5
milliosmoles in open NTDs).
4. Acetylcholinesterase assay is very specific in diagnosing neural tube defects.
Prognosis
It depends upon site of the lesion, its extent and association with anomalies
like hydrocephalus.
Higher lesions have worse prognosis.
Prevention
Pregnant women should consume 400 microgram of a dietary supplements of
folic acid to prevent NTDs, three months before and during the early weeks of
pregnancy, as folate supplementation prior to pregnancy and in early pregnancy
has been found to reduce the risk of neural tube defects. If the mother already
had a child with neural tube defect then the prophylactic dose of folic acid in
the subsequent pregnancy is 10 times the routine prophylactic dose = 4 mg/
day.
Treatment
Prone position
Prophylactic antibiotics in ruptured lesions
Cover the lesion with wet sterile saline dressing
If not ruptured surgery is done at 2 to 3 days of life.
Supportive Therapy
Mastery of bowel and bladder continence by early school age.

Intermittent catheterization and Individualized Education Programs (IEPs).
If possible, do early surgical closure of the defect.
Multidisciplinary approach is needed because of the multisystem
involvement (including pediatricians, nurses, neurologists, neurosurgeons,
urologists, orthopedists, physical therapists, occupational therapists, etc.).
Surgery generally does not help if lower limbs are paralyzed and if the
child also has hydrocephalus due to Arnold-Chiari malformation.
Children with meningomyelocele have a high risk of developing latex
allergy, therefore, they should not be exposed to latex from birth and
epinephrine should be kept ready at all times.

SUMMARY
1. NTDs are a spectrum disorder due to abnormal neurulation during
embryogenesis
2. They are preventable by folic acid supplementation during periconceptional
period
3. They can affect brain or spinal axis (lumbosacral commonest)
4. Open defects involve spine with meninges
5. Closed defects involve meninges only with fat, or cartilage
6. Can have paralysis with sensory loss in the legs, bowel, bladder involvement
and hydrocephalus.
BIBLIOGRAPHY
1. American Academy of Pediatrics Committee on Genetics. Folic acid for the prevention
of neural tube defects. Pediatrics 1999;104(2):325-7.
2. Ashwal S. Congenital structural defects. In: Swaiman KF, Ashwal S (Eds). Pediatric
Neurology: Principles and Practice, St. Louis: Mosby 1999;3:234-300.
3. Iqbal MM. Prevention of neural tube defects by periconceptional use of folic acid.
Pediatr Rev 2000;21(2):58-66.
4. Liptak GS. Neural tube defects in children with disabilities. In: Batshaw ML (Ed).
Children with Disabilities, Baltimore: Paul H Brookes Publishing Co 1997;4:52952.
Pedia Pearls:
Trimethoprim, Carbamazepine, Phenytoin, Phenobarbitone and Primidone increase
the risk of meningomyelocele if taken during pregnancy.
Neural tube defects (Dysraphism) lead to increased levels of fetoprotein (AFP)
and acetylcholinesterase in amniotic fluid.
56
Dental Caries
SPOTTER
CASE PRESENTATION
Three-year-old boy presented with tooth ache. He
was bottle fed at night (milk or juice) and has
decaying teeth and swollen gingival tissues.
Diagnosis: Dental caries (Fig. 56.1).
DISCUSSION
Dentition
There are 20 primary teeth (a through e) and 32
permanent teeth (1 through 8) on either side (both Fig. 56.1: Dental caries
upper and lower). As roots develop in the permanent
teeth, primary teeth are gradually resorbed by osteoclastic action. Primary
tooth bud starts at 6th week in utero, the primary central incisors erupt at 6 to
7 months, followed by the lateral incisors at 7 to 9 months, the first molars at
12 to 14 months, the canines at 16 to 18 months and the second molars at 20 to
24 months. By the time the child is 2-year-old, all 20 primary teeth should be
evident in the oral cavity. Number of teeth roughly = (Age in months -6).
Permanent teeth erupt in the following sequence: (mandibular) central incisor
and first molars at about age of 6 to 7, followed by the upper central incisor
and lateral incisors, the canines and premolars, second molars, and finally
third molars (wisdom teeth) during late teens up to the early twenties.
Structure of the Tooth (Fig. 56.2)
From outside to inside, the tooth has alveolar bone/cementum/dentin which
covered by enamel on top and has the pulp at the core. The commonest dental
disorder is dental caries. Untreated caries may lead to abscess, osteomyelitis
and even endocarditis in susceptible children. Dentigerous imperfecta (Weak
dentin) a hereditary defect, vitamin D-resistant rickets and hypoparathyroidism
Dental Caries 333
Fig. 56.2: Structure of the tooth
predispose to dental caries. Amelogenesis imperfecta is hereditary thin

malformed enamel susceptible to fracture and abrasions. Such an enamel allows
easy access to bacteria.
Dental Disorders
Dental caries: Oral bacteria are the acidogenic like Streptococcus mutans
a gram-positive bacteria, produces abundant acid which causes decay. The
pulp contains a neurovascular bundle. If caries advances, pain and sensitivity
result, due to pulpitis.
Bad eating habits predispose to caries. What is more important is frequency
of consumption and not the quantity of carbohydrate consumed, e.g. drinking
milk during sleep hours. The lower teeth are usually spared being near to
salivary glands.
Prevention of dental caries: Limit high sugar foods, e.g. candies, honey and
eating in between meals and bottle at bedtime. Brushing twice a day is
extremely helpful with a fluoride paste as high fluoride content makes the
teeth less soluble to the acid produced by bacteria. Supplemental fluoride is
needed only beyond 6 months ranging from 0.25 mg/day in toddlers to 1.0
mg/ day in adolescents, especially if the water fluoride concentration is less
than 0.3 ppm. Excessive fluoride, on the other hand can result in fluorosis
(white and brown spots on teeth).
Complications of Dental Caries
1. It predisposes to infective endocarditis, in children with an already damaged
heart.
2. Root abscess, osteomyelitis and lymphadenitis may also occur.
Pedia Pearl: Remember to give prophylaxis for infective endocarditis before dental
extraction if the heart is already damaged (e.g. due to rheumatic carditis).

Treatment
It includes dental filling and root canal treatment (if possible). Otherwise
extraction may be done.
Numerical Dental Disorders
Number of teeth in a child depend on the function of dental lamina. If the
dental lamina produces an increased number of buds or if embryonic dental
lamina is disrupted, extra teeth occur, most often between the upper central
incisors. In contrast, in congenital tooth absence, no tooth buds form (and
when a normal site is disturbed (e.g. in cleft palate) number of teeth may
become reduced (commonly third molars are absent).
Delayed Eruption vs Premature Eruption
Delayed eruption occurs in developmental, nutritional or systemic disorders
(e.g. hypothyroidism, trisomy 21, rickets, type I osteogenesis imperfecta), while
premature eruption is associated with precocious puberty or hyperthyroidism.
Large or Small Teeth
Large teeth are associated with hemifacial hyper-plasia and pituitary gigantism
while microdontia is seen in pituitary dwarfism.
Discoloration of Primary Teeth
Tea, coffee, iron, cholestatis, hemolytic anemia, neonatal hyperbilirubinemia,
tetracyclines and excessive fluoride cause discoloration of primary teeth.
BIBLIOGRAPHY
1. Ash MM. Development and Eruption of the Teeth. In: Ash MM (Ed). Wheelers
Dental Anatomy, Physiology and Occlusion, Philadelphia: WB Saunders Company
1993;7:24-45.
2. Dock M, Creedon RL. The Teeth and Oral Cavity. In: Rudolph CD, Rudolph AM
(Eds). Rudolphs Pediatric Textbook, New York: McGraw-Hill 2002;21:1283- 1304.
3. Dummett CO. Anomalies of the Developing Dentition. In: Pinkham JR, Casamassimo
PS, Fields HW, McTigue DJ, Nowak A (Eds). Pediatric Dentistry: Infancy Through
Adolescence, Philadelphia: WB Saunders Company 1999;3:43-54.
4. Johnsen D, Tinanoff N. The Oral Cavity. In: Behrman RE, et al (Eds). Nelson Textbook
of Pediatrics, Philadelphia: WB Saunders Company 2000;16: 1108-18.
5. Johnsen D. Early Caries: The Importance of Recognition for Prevention and Treatment.
In: Pinkham JR, Casamassimo PS, Fields HW, McTigue DJ, Nowak A (Eds). Pediatric
Dentistry: Infancy Through Adolescence, third edition. Philadelphia: WB Saunders
Company 1999;178-9.
6. Lunin M. Oral Pathology of the Child. In: Forrester DJ, Wagner ML, Fleming J (Eds).
Pediatric Dental Medicine. Philadelphia: Lea and Febiger 1981; 172-97.
7. Neville BW, Damm DD, Allen CM, Bouquot JE. Development and Eruption of the
Teeth. In: Neville BW, Damm DD, Allen CM, Bouquot JE (Eds). Oral and
Maxillofacial Pathology. Philadelphia: WB Saunders Company 1995;44-95.
9
Miscellaneous
57
Fever
APPROACH TO A CASE OF FEVER
First Confirm Fever
Documentation of Fever
Regular glass thermometer: Use this in the soft underarm (if < 6 years)
and orally (if > 6 years).
Rectal glass thermometer (for ages: 0-3 months).
Digital thermometer (oral, underarm or rectal). They are much faster, but
may not be very accurate.
Ear thermometer gives the idea of core temperature.
Next Grade the Fever

Low grade (oral reading of 99 to 100.4F [37.2 to 38 C])
Moderate (100.5 to 104 F [38 to 40 C])
High (above 104 F). [40 41.1 C].
Hyperpyrexia: A fever greater than 106F (41.1C). It can cause
unconsciousness and if sustained, permanent brain damage.
Now Establish the Type of Fever
A fever may be remittent, intermittent, sustained, relapsing, or undulant.
Intermittent fever: Drops into the normal range and then a rise (fluctuates
widely), above normal, typically producing chills and sweating.
Sustained fever involves persistent temperature elevation.
Relapsing fever consists of alternating fever and afebrile periods.
Undulant fever gradually increases in temperature that stays high for a few
days and then decreases gradually.
Note: No typical pattern may be seen in children.

History
Evaluate for:
General complaints, e.g. fever, weight loss, night sweats.
Previous illnesses
Nutrition, including consumption of dairy products.
Drug history
Immunization status,
Occupational history,
History of travel and recreational habits and
Sexual history.
Examination
Look for rashes, lymph nodes, arthritis, cardiac murmurs, abdominal
tenderness, fundoscopic changes and neurological deficits.
PYREXIA OF UNKNOWN ORIGINA DIAGNOSTIC DILEMMA
PUO is defined as temperature of more than 38.3C on several occasions.
This should be accompanied by more than three weeks of illness. There should
also be failure to reach a diagnosis, after 1 week of inpatient investigations.
The other types are:
Nosocomial PUO (unknown diagnosis after three days of investigation,while
in hospital).
Neutropenic PUO (<1 109 neutrophils with an uncertain diagnosis even
after three days).
HIV-associated PUO (HIV+ve patients with fever as above for four weeks as
outpatients, or three days as inpatient, with uncertain diagnosis after three
days, where at least two days have been allowed for cultures to incubate).
Remember
In infants, if fever is associated with lethargy and irritability, meningitis should
be kept in mind because typical features like Kernigs sign and other signs of
meningeal irritation may be missing.
Suspicion
Think of the following:
Common diseases, like. tuberculosis, endocarditis, gallbladder disease HIV
cancer, autoimmune disorders form the majority of cases.
1. Infections
Bacterial: Abscesses/Osteomyelitis (decreased movements of particular
area, e.g.) Tuberculosis (TB) (widespread), Brucellosis (in those who
Fever 339
2.
3.
4.
5.
consume raw milk products), Urinary tract infections (especially in

infants), Endocarditis (if previous heart disease), Hepatobiliary
infections (e.g. cholangitis, usually causes localized pain or discomfort
at least sporadically).
Viral infections usually have constitutional symptoms without any
prominent organ manifestations (e.g. HIV).
Fungi attack if there is immunosuppression, or use of broad-spectrum
antibiotics, intravascular devices or total parenteral nutrition.
Parasites, e.g. Toxoplasmosis presents with fever and lymph node
enlargement, while Psittacosis occurs due to contact with birds.
Neoplasms: They may have bone pains and pallor, e.g. in leukemias.
Drug fever is usually accompanied by rash, e.g. due to betalactam
antibiotics, procainamide and isoniazid. Recovery begins within 2 days of
stopping the drug.
Collagen vascular disorders: For example. vasculitides and autoimmune
diseases (High fevers, rashes, arthralgias, arthritis and myalgias, pharyngitis
and lymphadenopathy).
Endocrine disorders: For example. hyperthyroidism and subacute
thyroiditis (goiter).
Remember: Fever, sometimes remains undiagnosed despite extensive

investigations.
Investigations
Routine tests: CBC, ESR, Urine exam and CRP.
Cultures: Blood, urine, sputum, stool and CSF.
Serology: Rh factor, LE cell, ANA and ASO titer.
Aspirates: Gastric, (TB) bone marrow aspiration biopsy (In kala-azar and
malaria) liver biopsy if abnormal liver function tests lymph node aspiration/
biopsy (for lymphadenopathy) and skin biopsy (in rashes).
Radiology: Chest X-ray (TB, eosinophilia). Echo (endocarditis, rheumatic)
and CT/MRI (rarely).
Invasive procedures: Lumbar puncture (for meningitis). Laparotomy/
laparoscopy (for appendicitis, etc.).
Therapeutic trials: In TB and brucellosis, a labeled white cell scan helps to
identify areas of sepsis.
Management
This will depend on diagnosis:
Empirical treatment is not advocated, except if the criteria for culture
negative endocarditis, cryptic disseminated tuberculosis or temporal
arteritis (with vision loss) is fulfilled.
In neutropenic patients, the fever may be first and the only sign of
bacteremia (Start antipseudomonal penicillin plus aminoglycoside).
Deep fungal infection is also likely in fevers persisting for >72 hours:
Amphotericin B is drug of choice. Also if patient responds to initial
treatment, continue treatment for at least 7 days.
BIBLIOGRAPHY
1. Bryan CS, Ahuja D. Fever of unknown origin: Is there a role for empiric therapy?
Infect Dis Clin North Am 2007;21(4):1213-20.
2. Chan-Tack KM. Common causes of PUO. e-Medicine. March 2006.
3. Cunha BA. Fever of unknown origin: Focused diagnostic approach based on clinical
clues from the history, physical examination, and laboratory tests. Infect Dis Clin
North Am 2007;21(4):1137-87.
4. Durack DT, Street AC. Fever of unknown origin reexamined and redefined. Curr
Clin Top Infect Dis. 1991;11:35-51.
5. Ergonul O, Willke A, Azap A, et al. Revised definition of fever of unknown origin:
limitations and opportunities. J Infect 2005;50(1):1-5.
6. Evans RH. Grand Rounds University Hospital of Wales, Cardiff. Pyrexia of unknown
origin: The difficulty of establishing a diagnosis. BMJ. February 1997.
7. Gotzsche PC, Johansen HK. Routine versus selective antifungal administration for
control of fungal infections in patients with cancer. Cochrane Database Syst Rev
2000;(4):CD000026.
8. Meller J, Sahlmann CO, Scheel AK. 18F-FDG PET and PET/CT in fever of unknown
origin. J Nucl Med 2007;48(1):35-45.
9. Ozaras R, Celik AD, Zengin K, et al. Is laparotomy necessary in the diagnosis of
fever of unknown origin? Acta Chir Belg 2005;105(1):89-92.
10. Petersdorf RG, Beeson PB. Fever of unexplained origin: report on 100 cases. Medicine
(Baltimore) 1961;40:1-30.
11. Scagni P, Peisino MG, Bianchi M, et al. Kikuchi- Fujimoto disease is a rare cause of
lymphadenopathy and fever of unknown origin in children: Report of two cases and
review of the literature. J Pediatr Hematol Oncol 2005;27(6):337-40.
12. Schattner A. The patients history remains a powerful tool in the diagnosis of fever of
unknown origin. Eur J Intern Med 2005;16(1):63.
13. Vanderschueren S, Knockaert D, Adriaenssens T, et al. From prolonged febrile illness
to fever of unknown origin: The challenge continues. Arch Intern Med 2003;
12;163(9):1033-41.
14. Wagner AD, Andresen J, Raum E, et al. Standardised work-up programme for fever
of unknown origin and contribution of magnetic resonance imaging for the diagnosis
of hidden systemic vasculitis. Ann Rheum Dis 2005;64(1):105-10.
15. Zenone T. Fever of unknown origin in rheumatic diseases. Infect Dis Clin North Am.
2007;21(4):1115-35.
Pedia Pearl: Do not give round the clock paracetamol, but only as and when fever
appears.
Index
Page numbers followed by f refer to figure
A
Abdomen 16, 72
Abdominal
cramp 235
discomfort 69
X-rays 180
Abnormal
skull structure 320
sounds 66
Absent
breath sounds 85
QRS complex 151
Acanthocytes 119
Achilles reflex 52
Achondroplasia 320, 320f
Acid fast staining 128
Acquired
heart diseases 62
hemolytic anemias 248
Acute
adrenal insufficiency with
shock 248
attack of ulcerative colitis 249
cervical lymphadenitis 289
epidural hematoma 165
exacerbations 262
gastroenteritis 105
hyperkalemia 222
lymphoblastic leukemia 93
nephritis 135, 305f
poststreptococcal glomerulonephritis
304
renal failure and hyperkalemia 306
rheumatic fever 248, 300
toxicity 247
of phenytoin 267
Acyanotic CHD 61
Adenosine 215
Adenovirus parainfluenza 79
Adolescent vaccination 109
Adrenoleukodystrophy 248
Advantages of ORS 240
Adventitious sounds 85
Air
bronchograms 169
entrainment nebulizers 278
fluid levels 182
Airway obstruction 201
Aldosterone 250
Alkalinization of urine 224
Allergic rhinitis 79
Allogeneic transplants 148
Alopecia of eyebrows 95
Alpha-fetoprotein 329
Aminoglycosides 255
Aminophylline 261
Amodiaquine 269
Anacrotic pulse 64
Anaphylaxis 217, 232
Anatomical
face mask 211
peculiarities of children 78
Anemia 281
of chronic disease 118, 286
Anicteric hepatitis 228
Anorectal malformations 183
Anterior
limb of internal capsule 41
plagiocephaly 193
Anthropometry 15, 25
Antibiotic therapy 253
Anti-inflammatory dosage of
hydrocortisone 250
Antituberculous drugs 275
Anuria 133
Aorta 172
Aortic stenosis 66
Apex beat 67
Apgar scoring 11
Apoptosis 147

Appendicular stones 181
Aquired causes like vitamin K deficiency
297
Argyll-Robertson pupil 47
Artemether 272
Artemisinin 272
Arterial pulsations 68
Artesunate 272
Arthritis 301
Assessment of
autonomic nervous system 54
hypertrophy 153
tactile fremitus 83
Asymmetric head 193
Ataxia-telangiectasia 92
Atrial
fibrillation 156
flutter 156
septation 59
Atropine sulfate 219
Auditory evoked response 38
Auscultation of heart 71
Autoimmune disorders 248
Autologous transplants 148
Automatic reflex neurogenic bladder 43
Autonomic nervous system
and bladder 41, 42
testing 44
B
B12 deficiency 94
Babinskis
reflex 53
sign 53
Bacillus Calmette-Gurin 101
Back and lower limbs 70
Bacterial contamination 209
Bacteriuria 133
Bag and
mask ventilation 205
tube intubation/ventilation 205
Ballottment for enlarged kidneys 89
Balwadi Nutrition Programs 30
Basal metabolic rate 64
Basophilic stippling 119, 120
Beaus lines 96
Becker muscular dystrophy 292
Beckwith-Wiedemann syndrome 33
Bedside tests 74, 86
Benedicts test 135
Benzidine test 136
Biceps reflex 52
Bilateral choanal atresia 201
Bile
pigments 134
in urine 136
salts 134
in urine 136
Biliary calcification 180
Bilirubinuria 133
Biopsy imprints 145
Biots respiration 80
Birth asphyxia 192, 224
Bladder 41
stones 181
Bleeding
disorders 99, 296, 297
tendency 142
Blood
dyscrasias 105
flow 170
in urine 134, 136
pressure 68
Bone 169
age assessment 186
and soft tissues 181
marrow 146
aspirate 145
aspiration needle 144
biopsy 145
stain for iron 287
tests 144
trephine biopsy needle 145
X-rays 185
Bow legs 21f
Brachial neuritis 102
Brachioradialis reflex 52
Brachycephaly 193
Bradycardia 156
Bradypnea 80
Brain
abscess 69
calcification 194
edema 164, 164f
stimulation 230
Brainstem reflex 46
Breastfeeding promotion 28
Breathlessness 69
Bronchial
asthma 248
breathing 84
Bronchiectasis 85
Index 343
Bronchiolitis 79
Bronchodilatation 230
Bronchovesicular breath sounds 84
Brudzinskis sign 54
C
Caf au lait
macules 92
spots 51, 93f
Calcium 216, 221
Calcium
gluconate 221, 221f
stones 181
Calculation of QRS axis 151
Carbapenems 256
Cardiac
arrest 217
arrhythmias 227
stimulation 230
Cardiogenic region 58
Cardiomegaly on chest X-ray 171
Cardiotonic in left ventricular failure 229
Cardiovascular system 58
Cat scratch disease 289
Central
cyanosis 62
nervous system 39, 72
dysfunction 74
venous hum 9
Cephalosporins 254
Cerebellar
function assessment 54
testing 44
Cerebral palsy 3, 34, 35f, 55
Cerebrospinal fluid 164
examination 127
rhinorrhea 107
Chaddocks reflex 53
Check blood pressure 70
Chemoprophylaxis 271
Chest
compression 207
pain 63, 69
tissues 169
X-rays of newborn 175
Cheyne-Stokes respiration 80
Chickenpox 107, 109
Chloramphenicol 256
Chloroquine 269
Choanal atresia 205
Cholestatic liver disease 141
Chronic
granulomatous disease 94
headache 190
iron toxicity 95
obstructive respiration 80
renal failure 135
toxicity 247, 267
Closed incubators 278
Clostridium tetani 102
Clotting disorder 298
Club foot 329
CNS toxicity 278
Coarctation of aorta 62
Cold
agglutinin test 86
boxes 110
chain 110
Collagen vascular disorders 339
Collapsed lung 169
Collapsing pulse 64
Collection of urine sample 132
Colony forming units 134
Color of CSF 130
Combination vaccines 99
Complete blood count 298
Complex heart disease 62
Complications of
dental caries 333
intubation 207
NG feeding 209
percutaneous liver biopsy 142
Congenital
adrenal hyperplasia 248
heart disease 61, 169
immunodeficiency disorders 147
lobar emphysema 179
muscular dystrophy 292
myotonic dystrophy 292
Congestive
cardiac failure 62, 246, 251, 306
heart failure 63, 217, 234
Continuous
infusion 227
murmur 67, 72
positive airway pressure 176
Conventional phototherapy 210
Cord blood 146
Corticobulbar tracts 41
Corticospinal fibers 41
Corynebacterium diphtheriae 102
Costochondritis 63

Cough 81
Cracked lips 95
Cranial nerves 44, 46
Craniosynostosis 37f, 190, 192
Cromolyn sodium 261
Cross section of brain and skull 166f
Crystolluria 133
Cutaneous leukemic infiltrates 93
Cyanosis 69
Cyanotic
congenital heart disease and cardiac
fail 107
spells 224
Cyclosporin 262
Cystic fibrosis 79
Cystitis 125
Cytomegalovirus 290
Cytotoxic edema 164
D
Dacryocytes 119
Dandy-Walker syndrome 45
Dee-lee suction trap 202f
Deep
palpation 89
tendon reflexes 52
Deficit hyperactivity disorder 5
Degree of inflammation and fibrosis of
liver 141
Denatured hemoglobin 119
Dental caries 332, 333, 333f
Denver development screening test 38
Dermatologic diseases 248
Dermatomyositis 293
Desoxycorticosterone acetate 250
Development of sinusitis 79
Dexamethasone 218
Diabetes
insipdus 135
mellitus 107, 135
Diabetic ketoacidosis 218, 224
Diagnosis of cerebral palsy 34
Diaphragm 171
Diaphragmatic
contraction 230
excursion 83
hernia 177, 177f, 205, 206
Diarrhea 224
Diastolic murmur 72
Diazepam 219
Diazoxide 218
Digital thermometer 337
Digoxin 246
toxicity 246
Dilantin associated lymphadenopathy 228
Diphtheria toxoid 102
Discoloration of primary teeth 334
Disseminated intravascular coagulation
297
Documentation of fever 337
Documented metabolic acidosis 216, 224
Dolls eyes sign 54
Dopa-responsive dystonia 238
Dose of sodium bicarbonate 225
Downs syndrome 37, 55, 62
DPT vaccine 102
Drug treatment of
epilepsy 265
malaria 269
tuberculosis 273
Drugs in seizure therapy 265
Dry
beriberi 22
eyes 95
Duchenne
dystrophy 292
Ductus venosus 60
Dysdiadochokinesia 54
Dysmetria 54
Dysmorphisms 33, 195
Dyspnea 63, 81
Dystrophin immunocytochemistry 294
E
Eczematous dermatitis 94
Edema around lesion 163f
Ejection systolic murmur 67, 72
Elbow X-ray 188
Electromyography 294
Elicit reflexes 52
Embrace reflex 56
Embryonic stem cells 147
Emergency drugs 215
Emery-Dreifuss muscular dystrophy 292
Emphysema 174
Empiric therapy 253
Endobronchial tuberculosis 274
Endocarditis prophylaxis 303
Endocrine disorders 339
Index 345
Endotracheal tube 205, 206f
Enriched culture media 125
Epidural
anesthesia 129
hematoma 165
Epinephrine 217
Epithelial cell casts 134
Epstein-barr virus 290
Erythema
infectiosum 95, 96
marginatum 302
Erythrocyte cast 134
Ethambutol 275
Examination of
abdomen 25
eyes 24
joints and bones 25
mouth 24
nails 25
neck 24
skin 24
Exanthem with arthritis 96
Excessive
air loss 142
bile loss 142
bleeding 145
blood loss 142
External genitalia 17
Extracellular fluid 164
Extraluminal gas 182
Eyes 16, 323
F
Face mask 204, 211
Facial hemangioma 94
Facioscapulohumeral muscular dystrophy
292
Failure of oral replacement therapy 243
Fast regular
breathing 80
deep breathing 80
Fatty casts 134
Febrile seizures 267
Feeding intentions 10
Fehling test 135
Femoral pulses 65
Fencers stance 56
Fetal
alcohol 62
circulation 60
Fever 249
Fibromyalgia 238
Flapping tremor 88
Fludrocortisone 250
Fluid
and electrolyte disturbances 251
overload 217
Fluorescent in situ hybridization 37
Foersters sign 51
Folic acid prophylaxis 259
Foramen ovale 60
Foreign body aspiration 174
Formation of heart tube 59, 59f
Fournier test 51
Fractures 181, 193
Frontal
bossing 21
osteomyelitis 79
Furosemide 217, 234
G
Gastrulation 39f
Genitourinary tuberculosis 274
Giant cytoplasmic granules 120
GIT and genitourinary anomalies 329
Glucocorticoids 250
Glucose 216
Gordons sign 53
Gowers sign 51, 292f, 293
Grading of strength 50
Gram staining 121
Granular casts 134
Granulomatous inflammations 249
Grasp reflex 53
Growing skull fractures 162
Guillain-Barr syndrome 102
Guilland sign for meningeal irritation 54
Gynecomastia 235
H
Haemophilus influenzae 5, 79, 104, 112
type B vaccine 103
Hallucinations 228
Hand-foot and mouth disease 96
Hays sulfur test 136
Head
circumference 27
to-toe examination 11, 15
Hearing screening 38

Heart
blocks 157
borders and relations 60
embryology 58
failure 135
rates 150
sounds 65
Heinz body 119
Hemangioma 94
Hematopoietic stem cell transplantation
147
Hematuria 133, 306
Hemiplegia 52
Hemoglobin concentration 28
Hemoglobinuria 133
Hemoptysis 64
Hemorrhagic
cystitis 148
disease 23
Henoch-Schnlein purpura 96
Hepatitis 228
A 109, 112
B 109
immune globulin 98
vaccine 102
virus vaccine 102
Hereditary diseases 62
Herpes
encephalitis 163f
simplex virus 162
encephalitis 162
High
flow system 278
lumbar lesions 328
total iron binding capacity 283
Hilar vessels 172
Hip dislocation 329
Hirschbergs sign 53
Hodgkins disease 147
Hoffmans sign 53
Holosystolic murmur 67, 72
Horizontal eye movements 48
Horners syndrome 42
Howell-Jolly bodies 119, 120
HSV encephalitis 162
Human
immunodeficiency virus 290
papilloma virus immunization HPV
vaccine 109
Hunters syndrome 325
Huntington sign 52
Hyaline
cast 134
membrane disease 176, 176f
Hydantoin syndrome 267
Hydrocephalus 167
Hydrocortisone 250
Hydroxychloroquine 262
Hyperactive reflex 53
Hyperglycemia 12, 267
Hyperkalemia 235
Hyperoxy test 74, 86
Hyperplasia of gums 228
Hyperpyrexia 337
Hypersegmented neutrophils in
megaloblastic anemia 267
Hypersensitivity 267
Hypertension 66, 234
Hypertensive
crisis 218
encephalopathy 306
Hypocalcemia 12
Hypokalemia 247
Hypomagnesemia 12
Hypoplasia of
left heart 62
midface and fingers 267
Hypoplastic left heart syndrome 12
Hypoprothrombinemia 267
Hypotension 228
Hypotensive low birth weight
babies 249
Hypothermia 12
Hypotonia 321
Hypoventilation 80
Hypoxemia 277
Hypoxia 12, 277
I
Ice lined refrigerator 111f
Idioventricular rhythm 157
Immune
deficiency 107
system 251
thrombocytopenic purpura 296
Immunization 98
Immunodeficiency disorders 94
Inactivated
polio vaccine 101
poliomyelitis 112
Incubators 209
Index 347
Indications for
oral airway 201
prednisolone 274
Infant weighing scale 27f
Infection 142, 145
Infectious
rashes 95
vaccines 98
Inflammatory diseases 128
Influenza virus 112
Inhalers 263
Integrated child development services
scheme 30
Intermediate acting glucocorticoids 250
Intermittent fever 337
Interstitial edema 164
Intracerebral hematomas 166
Intracranial
calcification 194
hemorrhage in children 165
Intraluminal gas 182
Intramural gas 182
Intrasutural bones 193
Intravenous immunoglobulin 262
Iron
deficiency 118, 284
anemia 282, 286
supplementation 258
Isoniazid 275
J
Joint
inflammation 249
pains with fever 300
Jugular venous pressure 71
Junctional escape rhythm 157
Juvenile
onset systemic lupus erythematosis 3
rheumatoid arthritis 302
K
Kawasaki disease 95, 96
Kernigs sign 54
Ketone bodies 134
Killed
hepatitis A vaccine 108
ORS 242
King of blood tests 117
Klippel-Feil or Sprengels deformity 195
Knock knees 21f
Kochs original method of staining 123

Koilonychia 88, 96
Korotkoffs ausculatory method 68
Kwashiorkor 25
L
Lacunar skull 194f
Landau reflex 56
Laryngoscope 206f
Late diastolic murmur 72
Laurence Moon Bardet Beidel syndrome 37
Lead poisoning 118, 284
Left
atrial enlargement 153
ventricular hypertrophy 153
Leukocyte cast 134
Leukocytosis 9
Life threatening asthma 224
Light
palpation 89
touch 50
Linear skull fractures 162
Lipopolysaccharide endotoxin 121
Liquid oxygen 277
Live attenuated hepatitis A vaccine 108
Liver 323
biopsy 141
Looping of heart tube 59
Low
Apgar score 12
flow
devices 211
system 278
lumbar lesions 329
Lower motor neuron 41-43, 46
Lumbar puncture 127
Lung
abscess 85
maturation 250
parenchyma 169
toxicity 278
volumes 170
Lymph node 15
enlargement 288
Lymphadenopathy 288, 289
Lymphangitis 289
M
Macrocytes 119
Macrolides 256

Maculopapular eruptions 95
Magnesium sulfate and heliox 262
Malformation syndromes 192
Management of
pediatric tuberculosis 275
toxicity 247
Mandibular branch 47
Marasmus 25
Marfans syndrome 70
Maroteaux-Lamy syndrome 325
Mast cell stabilizer 261
Maxillary branch 47
Mean corpuscular
hemoglobin 28
volume 28, 281
Measles 95, 103
and MMR vaccine 103
Meconium aspiration 179, 206
syndrome 176
Mediastinal mass 171
Medulla 41
Meningomyelocele 328, 328f
Methotrexate 262
Methylxanthines 261
Metopic craniosynostosis 15f
Metronidazole 255
Microcytichypochromic anemia 284
Microscopic urine sediment tests 134
Mid upper arm circumference 27
Mid-day meal programs 30
Mid-systolic
click 66
murmur 72
Mild azotemia 235
Miliary tuberculosis 274
Mitochondrial disorders 55
Mitral valve prolapse 66
Mixed disorders 297
Moderate proteinuria 306
Monitor
blood pressure 55
heart rates 55
pupils 55
Moraxella catarrhalis 79
Moros reflex 54, 56
Morphine sulfate 218
Morquio sign 52
Motor system 44, 50
evaluation 50
Mucopolysaccharidosis 323, 324f
Mucus extractor 202
Muscle
biopsy 294
disorders 291
weakness 291
Muscular dystrophy 291
Mycobacterium tuberculosis 289
Myelodysplasia 328
Myelography 129
Myotonic
dystrophy 292
Myxedema 247
N
Naloxone 215
Nasal
cannula 211
catheter 278
endotracheal intubation 206
prongs 211, 278
Nasogastric tubes 207
Nasopharyngeal
catheter 278
discomfort 209
National
goiter control program 31
nutritional anemia prophylaxis
program 30
program for prevention of blindness
31
vector borne disease control
program 269
Nebulizers 263
Neonatal
circulation 61
incubator 209f
pneumonia 175
resuscitation 215
seizures 216
Nephrotic syndrome 248, 308f
Nerve
cell migration 40
conduction studies 38
Neural tube defect 327, 328f
Neurocutaneous disorders 92
Neurogenic bladder 43
Neuroregression 36, 55
Neurotuberculosis 274
Neurulation 39
Neutropenia 148
Niacin 22
Index 349
Night blindness 24
Nitroprusside
sodium 218
test 135
Noninfectious vaccines 99
Nonrebreathing masks 278
Normal
breath sounds 84
chest film of newborn 175
reflex 53
respiration 80
total protein level 306
Number of carpal bones 186
Numerical dental disorders 334
Nutritional
deficiencies 94
status 15
O
Obstruction below larynx 201
Oliguria 133
One-way fish mouth valve 204
Opening pressure 130
Oppenheims sign 53
Oppositional defiant disorder 5
Optional vaccines 104
Oral
cavity 16
polio vaccine 101
poliomyelitis 110
prednisolone 250
rehydration solution 240, 240f
therapy 240
salbutamol 262
Orbital cellulitis 79
Origin of pain 87
Oropharyngeal airway 201, 201f
Orthopedic deformities 321
Osmotic cerebral edema 164
Osteitis-erosion of tibia 188
Osteomyelitis 188
Otoacoustic emissions 38
Overview of cardiovascular system 58
Oxygen
concentrators 277
cylinders 277
hood 211, 278
supply devices 211
tent 278
P
Pain
and swelling of joints 301
in chronic bronchitis 63
Palmar
and plantar grasp reflexes 56
erythema and asterixis 88
Palmomental sign 54
Palpate trachea 71
Palpation of
liver 89
spleen 89
Pancreatic calcification 180
Panhypopituitarism 248
Parasites 339
Parasutural sclerosis 193
Parasympathetic nervous system 41
Parkinsons disease 237, 238
Passive
immunization 98
tone 56
Patellar reflex 52
Patent ductus arteriosus 9
Pathologies of autonomic nervous system
42
Pectus carinatum 82f
Peculiarities of
infection in children 79
respiratory rate 80
Peptic ulceration and esophagitis 251
Percussion 45, 71, 83
Perianal excoriation 95
Peripheral
blood 146
smear 28, 281, 283
Persistent pulmonary hypertension 75
Petechial rash 296
Phakomatosis 92
Phenobarbitone 267
Phenytoin 219, 227, 266
sodium 227f
Pierre-Robin syndrome 201
Pigeon chest 82f
Pigmented gallstones 287
Pleural friction rub 85
Pneumococcal vaccines 106
Pneumococcus 106
Pneumomediastinum 173
Pneumonia 85, 179
Pneumothorax 178, 179
Poikilocytosis 119

Poisonings 95, 219
Polio vaccine 101
Polymicrogyria 329
Port-wine stain 93
Posterior
fossa malformations 94
limb 41
plagiocephaly 193
Postnatal period 37
Potassium hydroxide 122
preparation 122
Potts puffy tumor 79
Prader-Willi syndrome 194
Premature infants 235
Pressure release valve 204
Preterm infants 258
Prevention of
dental caries 333
malnutrition on national scale 30
Primary
adrenal insufficiency 248
hemostasis 297
immunodeficiency 94, 99
Primitive reflexes 53, 56
Principle of ORS 241
Proper storage of vaccines 110
Prophylactic therapy 253
Protein energy malnutrition 25
Pseudo-Babinski's sign 53
Pseudohypertrophied calves 293
Psychogenic chest pain 63
Pulmonary
artery 172
blood flow 61
edema 69, 217, 234, 306
resistance 61
stenosis 66
Pulsus
alternans 64
bigeminus 64
bisferiens 64
differens 64
paradoxus 64, 86
Pyelonephritis 125
Pyrexia of unknown origin 338
Pyrizinamide 275
Q
QRS
amplitude 151
axis 151
complex 151
duration 157
Quadrivalent HPV vaccine 109
Qualitative defects 297
Quantitative defects 297
Quinckes sign 70
Quinine 269
Quinolones 255
R
Radiant warmer 210, 210f
Raised intracranial tension 218
Raynaud phenomenon pallor 51
Recognition of abnormal heart rhythms 154
Recommended
dietary allowance 20
vaccines for adolescents 109
Rectal glass thermometer 337
Red
blood cell 118, 134
casts 134
cell distribution width 281, 286
Reduced osmolarity ORS 242
Refeeding syndrome 209
Referred pain 42, 87
Reflex grading 52
Refractory
hypoglycemia 249
shock 249
Regular glass thermometer 337
Relapsing fever 337
Renal
calcification 180
diseases 247
stones 181
Respiratory
diseases 323
syndrome 234
system 72, 78
Resuscitation
bag 203
facemask 203f
Reticulocyte 119
count 281
Reticulocytosis 287
Retinopathy of prematurity 278
Retts syndrome 36
Rheumatic
fever 62, 70
heart disease 301
prophylaxis 303
Index 351
Rickets 25, 187
Right
atrial enlargement 153
ventricular hypertrophy 153
Rinne tuning fork test 49
Rombergs test 50, 51
Roseola infantum 95
Rotateq pentavalent vaccine 105
Rotation 168
Rotavirus 104
vaccine 104, 105
Rotheras test 135
Rubella 95
S
Sacral agenesis 195
Sail sign of thymus 175f
Salicylate poisoning 224
Scarlet fever 95
Schistocytes 119
Schizophrenia 237
Scurvy 23, 25
Seizure disorder 190
Sella turcica 194
Sense of smell 44
Sensory
extinction 50
inattention 50
paralytic bladders 43
system 44
Septic joint 302
Serum
creatine phosphokinase 294
ferrritin 286
iron 287
Severe hypersensitivity 105
Shakirs tape 28
Shock despite volume resuscitation 217
Short
acting glucocorticoid 250
spermatic cord 17
Sick sinus syndrome 156
Sickle cell 119
disease 107
Side effects of
carbamazepine 268
ethosuximide 268
Sideroblastic anemias 118, 284
Signs of meningeal irritation 44, 54
Silhouette signs 169
Silver beaten appearance 191f
Simple
face mask 211
oxygen masks 278
Sinus
arrhythmia 64, 156
bradycardia 156
disease 190
formation 274
tachycardia 154
tenderness 79
Sites of calcification 180
Skeletal disorders 192
Skin diseases 63
Skull
density 194
fractures 162
sutures 192
X-rays 190
Slow
intravenous injection 227
regular breathing 80
rhythms 156
Small head 192
Sodium bicarbonate 216, 224, 224f, 225
Soft tissues 181
Spastic bladder 43
Special nutrition program 30
Spherocytes 119
Spina bifida
cystica 328
occulta 328
Spinal
anesthesia 129
muscular atrophies 293
Spine X-rays 190, 195
Spironolactone 235
Splenic dysfunction 107
Split notochord syndrome 195
Spondyloepiphyseal dysplasia 325
Spot dyskinesias 34
Stage
hematologic disease 144
of iron deficiency 283
Stairs sign 51
Staphylococcus aureus 195
Status asthmaticus 232
Stem cell transplantation 144, 146
Steps
in empiric therapy 253
of treatment 269
Sterile pyuria 306

Steroids 248
Stills murmur 9
Streptococcus pneumoniae 106
Streptomycin 275
Structure of tooth 332, 333f
Struvite stones 181
Sturge-Weber syndrome 93
Subarachnoid hemorrhage 129, 165
Subcutaneous nodules 95, 302
Subdural
hematoma 165
hemorrhage 165
Subphrenic abscess 183
Sucking reflex 53, 56
Suction
apparatus 203
bulb 203
catheter 203
Sulfonamides 256, 269
Superficial reflexes 53
Superior vena cava 60
Supplementation in pubertal girls 222
Suppurative complications of pneumonias
85
Suprapatellar reflex 52
Suprapubic puncture 133
Supraventricular tachycardia 155, 215
Sustained fever 337
Sydenhams chorea 302
Syncope of cardiac origin 69
Syngeneic transplants 148
Systemic
lupus erythematosus 248, 302
steroids 262
Systolic
pulsations 67
recession 68
T
Tachyarrhythmias 246
Tachycardia 154
Tachypnea 80
Target cells 119
Tay-Sachs diseases 37
Tension pneumothorax 173, 173f
Testing intactness of brainstem function
54
Tetanus toxoid 102, 112
Tetracycline 256
Theophylline 261
Thick meconium stained babies 205

Thoracic lesions 328
Thyrotoxicosis 247
Timing of shunt closure 61
Tonic neck response 56f
Total
body irradiation 148
parenteral nutrition 30
Touch smear 145
Toxicity of
barbiturates 267
benzodiazepines 267
fosphenytoin 268
valproic acid 268
Toxoplasma gondii 290
Tracheal suction 206
Tracheostomy oxygen adapters 278
Transient tachypnea of newborn 177
Transposition of great arteries 13
Treacher-Collins syndrome 33
Treatment of urinary infection 132
Treponema pallidum 290
Triceps reflex 52
Tricuspid atresia 71
Tubercular meningitis 163
Tuberculoma 163f
Tuberous sclerosis 62, 93
Turners syndrome 317f
Two-finger technique 207
Types of
breathing 82
calculi 181
glomerulonephritis 305
renal anomaly 132
sacral agenesis 196
samples 145
seizures 265
spinal defects 328
stem cells 146
transplant 148
vaccine 98
Typical chest pain 63
U
Uncomplicated falciparum 270
Undulant fever 337
Unique phenomenon of womb 3
Upper motor neuron 41, 43, 46
Ureteric calcification 181
Index 353
Uric acid stones 181
Urine
culture 125, 134
examination 132
glucose 135
ketone bodies 135
microscopy 133
pH 134
protein 135
volume 133
Uses of
oxygen 278
stem cells 147
X-ray of bones 186
V
Vaccine carriers 110
Valsalva maneuver 9
Vancomycin 255
Varicella vaccine 107
Vascular anomalies 94
Vasogenic edema 164
Veno-occlusive disease 148
Venous pulsation 68
Ventricular
fibrillation 155, 155f
flutter 155
septation 60
tachycardia 155, 155f, 247
Venturi mask 278
Vertical suspension 56
Vesicular eruptions 96
Viral infections 79, 339
Visual acuity 46
Vitamin 20
A 20
prophylaxis 259
B1 22
B12 22
B2 22
B6 22
C 22
deficiency 25
D 20, 259
deficiency 25
E 21
K 21, 258
Vomiting 235
von Willebrands disease 297
W
Weber tuning fork test 49
Weiddman Beckwith syndrome 249
Wernicke-Korsakoff syndrome 22
Wet beriberi 22
Wheat-based nutrition program 30
White
blood cell 120, 134
casts 134
cell casts 133
Width of QRS complex 151
Winging of scapulae 293
Within bowel wall 182
Wolff-Parkinson White syndrome 156
Wrist X-ray 187
X
X-ray long bones 188
Y
Yellow fever 110
Z
Ziehl-Neelsen stain 123
Zinc
deficiency 94
fortified ORS 242

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Prelims_2.

Chapter-20_Bone Marrow Tests (Aspiration Biopsy Hematopoietic Stem Cell Transplantation).pdf

Pushpendra Magon MBBS DCH MD (Pediatrics)

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD.

Jaypee Brothers Medical Publishers (P) Ltd.

Jaypee-Highlights Medical Publishers Inc.

xiv Pearls in Clinical Pediatrics

SECTION 2: AN OVERVIEW OF BEDSIDE TESTING

SECTION 4: PEDIATRIC IMAGING

xvi Pearls in Clinical Pediatrics

SECTION 7: PROBLEM-BASED LEARNING

xviii Pearls in Clinical Pediatrics

Discussion 281 Iron Deficiency Anemia 282 Approach to a

Arterial Blood Gas

xx Pearls in Clinical Pediatrics

Tetanus Immune Globulin

xxii Pearls in Clinical Pediatrics

Chart - 1: Growth Chart for Boys

Chart - 2: Intrauterine Growth

MicrochimerismA unique phenomenon of the womb: In the womb, blood

DISEASE PRESENTATION, DIAGNOSIS AND MANAGEMENT

4 Pearls in Clinical Pediatrics

AGEWISE THEY ARE UNIQUE

Children are Unique 5

Preschooler (3-6 years)

School Goer (6-12 years)

They focus on achievement. Feelings of inferiority may occur due to high

UNIQUE PARENTING AND PSYCHOPATHOLOGY

6 Pearls in Clinical Pediatrics

WHY TO IDENTIFY WHAT IS NORMAL?

To identify variants of normal: One will not be able to recognize abnormal,

To allay parental anxiety

White blood-tinged discharge and mastitis due to withdrawal of maternal

8 Pearls in Clinical Pediatrics

Know What is Normal and What is Not? 9

Central venous hum is heard in toddlers as a continuous and soft,

STRUCTURE OF THE HISTORY

Antenatal history (Aim: To find out risk factors): Enquire about:

SGA small for gestational age weigh < 10th percentile

Essentials of History-taking and Examination in a Neonate 11

12 Pearls in Clinical Pediatrics

Assess development: Follow-up high-risk infants who are at risk of

Essentials of History-taking and Examination in a Neonate 13

STRUCTURE OF PEDIATRIC HISTORY

Chief complaint: Why was the medical attention sought?

Outline of Pediatric History and Examination 15

Measure oral temperature (Axillary below six years)

16 Pearls in Clinical Pediatrics

Outline of Pediatric History and Examination 17

In boys: Gently look for hernias, hydroceles, cryptorchidism/retractile

WHAT IS RAINBOW DIET = VIBGYOR

20 Pearls in Clinical Pediatrics

Vitamin D: In response to serum hypocalcemia regulates the mobilization

1 retinol equivalent (RE) = 1 mcg of retinol = 6 mcg of -carotene.

Fig. 5.1: Knock knees

Fig. 5.2: Bow legs

(For color version of Figures 5.1 and 5.2, see Plate 1)

22 Pearls in Clinical Pediatrics

Vitamin C: Facilitates the hydroxylation of procollagen

Calcium is present in Millets (like ragi, bajra) and milk

STRUCTURE OF NUTRITIONAL HISTORY

Dietary history is more important in mal-nutrition (obesity or undernutrition)

24 Pearls in Clinical Pediatrics