Escolar Documentos
Profissional Documentos
Cultura Documentos
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-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
Foreword
A Radhakrishna
Website: www.jaypeebrothers.com
Website: www.jaypeedigital.com
2013, Jaypee Brothers Medical Publishers
All rights reserved. No part of this book may be reproduced in any form or by any means
without the prior permission of the publisher.
Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com
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
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 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
47.
48.
49.
50.
51.
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
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
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
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
Charts xxiii
1
Clinical Pediatrics
1
Children are Unique
UNIQUE DEVELOPMENT AND GROWTH RIGHT
FROM THE WOMB
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
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 non- infectious
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.
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.
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.
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.
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.
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.
Know What is
Normal and What is Not?
Pedia Pearl: Erythema toxicum is rarely seen in preterms (scrapings show eosinophils).
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.
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
Pedia Pearl: Birth asphyxia is the most common cause of seizure on the first day.
*
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.
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.
Outline of Pediatric
History and Examination
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.
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.
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
Nutrition 21
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.
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
Examination of Eyes
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
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.
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.
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
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
BIBLIOGRAPHY
1. Batrum JL, Baxter PS. The Lasso-0 tape: Stretchability and observer reliability in head
circumference measurement. Archives of Disease in Childhood 2005;90(8):820-1.
2. Behrman. Nelson Pediatrics, Saunders, p 2000;1809.
3. Berson EL, Rosner B, Sandberg MA, et al. A rando-mized trial of vitamin A and
vitamin E supple-mentation for retinitis pigmentosa. Arch Ophthalmol
1993;111(6):761-72.
4. Blecker U, et al. Fat-soluble vitamin deficiencies. additional recommended reading for
good brief discussion of fat-soluble vitamins and deficiencies thereof. Pediatr Rev
1999; 20(11):394-5.
5. Christian P, West KP Jr. Interactions between zinc and vitamin A: An update. Am J
Clin Nutr 1998; 68(2 Suppl):435S-441S.
6. Fawsi W, et al. Vitamin A Supplements and Diarrheal and Respiratory Infections
Among Children in Dar es Salaam, Tanzania. J Pediatr 2000;137(5):660-7.
7. Fawzi WW, Chalmers TC, Herrera MG, Mosteller F. Vitamin A supplementation and
child mortality. A meta-analysis. J Am Med Assoc 1993;269:898-903.
8. Fawzi WW, Mbise R, Spiegelman D, Fataki M, Hertzmark E, Ndossi G. Vitamin A
supplements and diarrheal and respiratory tract infections among children in Dar es
Salaam, Tanzania. J Pediatr 2000;137:660-7.
9. Field CJ, Johnson IR, Schley PD. Nutrients and their role in host resistance to infection.
J Leukoc Biol 2002;71(1):16-32.
10. Food and Nutrition Board, Institute of Medicine. Vitamin A. Dietary Reference Intakes
for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese,
Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington DC: National Academy
Press 2001;65-126.
11. Hendler SS, Rorvik DR, (Eds). PDR for Nutritional Supplements. Montvale: Medical
Economics Company, Inc, 2001.
12. Hensrud DD. Nutrition screening and assessment. Med Clin North Am 1999;
83(6):1525-46.
13. Hussey GD, Klein M. A randomized, controlled trial of vitamin A in children with
severe measles. N Engl J Med 1990;323:160-4.
14. Kane AB, Kumar V. Food and Nutrition. In: Cotran RS, et al (Eds). Robbins Pathologic
Basis of Disease. Philadelphia: WB Saunders 1999;6:436-56.
15. Leleiko NS, Chao C. Nutritional Deficiency States. In: Rudolph AM, et al (Eds).
Rudolphs Pediatrics, Stamford, CT: Appleton and Lange 199620:1015-17.
16. Lynch SR. Interaction of iron with other nutrients. Nutr Rev 1997;55(4):102-10.
17. McCullough F, et al. The effect of vitamin A on epithelial integrity. Proceedings of the
Nutrition Society 1999;58:289-93.
18. Measles. In: Pickering LK, et al (Eds). Red Book: Report of the Committee on Infectious
Diseases, Elk Grove Village, IL: American Academy of Pediatrics 2000; 25:385-96.
Developmental
Assessment
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.
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
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
INVESTIGATION
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.
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)
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
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.
EXAMINATION
Summary of CNS Examination
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.
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
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.
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
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.
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.
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
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
Cardiovascular System 61
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, mild- moderate 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
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.
Cardiovascular System 63
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.
Cardiovascular System 65
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.
Cardiovascular System 67
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
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 System 69
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.
Cardiovascular System 71
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.
Cardiovascular System 73
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
Pedia Pearl: Apart from central, respiratory and cardiac causes of cyanosis,
methemoglobinemia due to any reason may produce cyanosis, as well.
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).
Cardiovascular System 75
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
BIBLIOGRAPHY
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9
Respiratory System
INTRODUCTION
In children, respiratory system has some peculiarities. They are:
DEVELOPMENTAL PECULIARITIES
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
LTB - Laryngotracheobronchitis
Respiratory System 81
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.
Respiratory System 83
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.
Respiratory System 85
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.
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
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.
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.
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
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
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.
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
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)
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
Most of these have a prodrome. Most involve face first followed by other
parts except roseola infantum where trunk is first involved. Eruptions common
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.
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.
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.
*
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
More than
6 weeks
Rotaviral vaccines
After 15
months
Varicella
After 18
months
Hepatitis A
Vaccines
Birth
BCG
OPV zero
Hepatitis B-1
6 weeks
OPV-1 + IPV-1/OPV-1
Note
DTPw-1/DTPa-1
Hepatitis B-2
Hib-1
10 weeks
OPV-2 + IPV-2/OPV-2
DTPw-2/DTPa-2
Hib-2
14 weeks
OPV-3 + IPV-3/OPV-3
DTPw-3/DTPa-3
Hepatitis B-3
Hib-3
9 months
Measles
2 years
Typhoid
5 years
OPV-5
DTPw booster-2 or
DTPa booster-2
MMR-2
10 years
Tdap
HPV
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).
Vaccination 103
Schedule
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
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.
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
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
Vaccination 111
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.
2
An Overview of
Bedside Testing
13
Blood
Peripheral Smear
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.
Contents
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.
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.
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
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
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
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.
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
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
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.
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.
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.
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.
18
Urine Examination
URINE
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.
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.
Urine Culture
CHEMICAL TESTS
Urine pH
Specific Gravity
Protein
Glucose
Ketone bodies
Blood in urine
Bile salts
Bile pigments.
pH
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.
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.
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.
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
To Diagnose
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.
20
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.
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.
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.
Pedia Pearl: Left axis deviation in first couple of monthssuspect endocardial cushion
defects or myocardial disease in later age (rarely L.V.H.)
QT Interval
RR Interval
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.
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.
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
CT Findings
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.
CT Scans 163
TUBERCULAR MENINGITIS
CT Findings
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
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 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
CT Findings
INTRACEREBRAL HEMATOMAS
CT Scans 167
SUMMARY
HYDROCEPHALUS
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)
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.
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
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.
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.
Chest X-ray Findings
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.
Fig. 23.8: Right side pneumothorax showing collapse of lung towards hilum
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.
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
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
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)
Fig. 25.1: Delayed bone age (bone age 2-3 years but chronological age 7 years)
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.
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.
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.
Fig. 26.1: Silver beaten appearance (sutural separation, lacunae, erosion of posterior
clinoid process can also be seen in raised intracranial tension)
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.
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
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
8. Skull Density
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.
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
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
5
Equipment
27
Equipment
(For Airway Obstruction/
For Circulation/For Poisoning/For
Supportive Care of Newborns)
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).
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
Diaphragmatic hernia
Thick meconium stained babies, (bag and mask ventilation may only be
done after tracheal suction)
Choanal atresia (Bilateral).
Relative Contraindications
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.
IV Cannula
IV Fluids
IV Set
Drugs
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
Equipment 209
Complications of NG Feeding
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.
Side Effects
Phototherapy may lead to:
Hot, dry, parched, or bronze skin.
Increased insensible water loss and diarrhea.
Bronze baby syndrome and hypocalcemia.
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.
1. Fluid overload.
3. Pulmonary edema.
Furosemide
Dosage: IV is : IV, IM: 1 - 2 mg/kg.
Side effects: Hypokalemia.
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.
INDICATIONS
Pedia Pearls:
On ECG hypocalcemia causes QT prolongation and hyperkalemia causes
t wave tenting.
In hypomagnesemia, the child may be refractory to calcium therapy.
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)
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).
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
Pedia Pearl: Fosphenytoin can be given much faster than phenytoin because it a
precursor of phenytoin and hence takes time to metabolize.
Aminophylline 229
32
Aminophylline
INTRODUCTION
This is a bronchodilator drug combination that contains theophylline and
ethylenediamine in 2:1 ratio.
INDICATIONS AND DOSAGE
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.
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.
INDICATIONS AND DOSAGE
Resuscitation in Pulselessness, Hypotension and/or Bradycardia
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).
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.
INDICATIONS AND DOSAGE
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
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.
Dopamine 237
35
Dopamine
INTRODUCTION
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
DRUG EFFECTS
Adverse Effects
Tachycardia, ventricular arrhythmia and vomiting.
BIBLIOGRAPHY
1. Altier N, Stewart J. The role of dopamine in the nucleus accumbens in analgesia. Life
Sci 1999;65(22):2269-87.
2. Brefel-Courbon C, Payoux P, Thalamas C, Ory F, Quelven I, Chollet F, Montastruc
JL, Rascol O. Effect of levodopa on pain threshold in Parkinsons disease: A clinical
and positron emission tomography study. Mov Disord 2005;20(12):1557-63.
3. Browman KE, Curzon P, Pan JB, Molesky AL, Komater VA, Decker MW, Brioni
JD, Moreland RB, Fox GB. A-412997, a selective dopamine D4 agonist, improves
cognitive performance in rats. Pharmacology, Biochemistry and Behaviour
2005;82(1):148-55.
4. Burkey AR, Carstens E, Jasmin L. Dopamine reuptake inhibition in the rostral agranular
insular cortex produces antinociception. J Neurosci 1999;15; 19(10):4169-79.
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.
11. Lambert M, Schimmelmann B, Karow A, Naber D. Subjective well-being and initial
dysphoric reaction under antipsychotic drugs - concepts, measurement and clinical
relevance. Pharmacopsychiatry 2003;36(Suppl 3):S181-90.
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
cortex. Pain 2004;111(1-2):136-43.
13. Mayer, AM. Polyphenol oxidases in plants and fungi: Going places? A review.
Phytochemistry 2006;67:2318-31.
14. Mayer, AM. Polyphenol oxidases in plants and fungi: Going places? A review.
Phytochemistry 2006;67:2318-31.
15. Renal Vasodilatory Action of Dopamine in Patients with Heart Failure: Magnitude of
Effect and Site of Action Circulation. 2008;117:200-5. http://www.circ.
ahajournals.org/cgi/ content/full/117/2/200. Retrieved 2009-04-20.
16. Merims D, Giladi N. Dopamine dysregulation syndrome, addiction and behavioral
changes in Parkinsons disease. Parkinsonism Relat. Disord 2008;14(4):273-80.
17. Pfaus J, Phillips A. Role of dopamine in anticipatory and consummatory aspects of
sexual behavior in the male rat. Behav Neurosci 1991;105(5):727-43.
18. Wood PB. Role of central dopamine in pain and analgesia. Expert Rev Neurother
2008;8(5):781-97.
19. Wood PB, Patterson JC 2nd, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL.
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.
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.
INDICATIONS AND DOSAGE
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)
Drug Interactions
Spironolactone decreases the digoxin clearance.
DIGOXIN TOXICITY
Digoxin 247
Adverse Effects
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.
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
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.
GLUCOCORTICOIDS
TYPES
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
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.
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
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.
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.
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
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.
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
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.
Definitions
1.
2.
3.
4.
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.
42
Drugs in
Seizure Therapy
TYPES OF SEIZURES
1.
2.
3.
4.
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.
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.
CQ = Chloroquine
SP-ACT = Sulpha-pyrimethamine Artesunate combination therapy
44
Drug Treatment
of Tuberculosis
Pedia Pearl: INH induced peripheral neuropathy is rare in children. Assess liver
function by doing LFT before starting ATT.
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
10 mg/kg
15 mg/kg
30 mg/kg
15 mg/kg
25 mg/kg
Category II
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.
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
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.
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
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
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).
3. Sideroblastic Anemias
They are characterized by:
Defective heme synthesis and consequent ineffective erythropoiesis.
Ringed sideroblasts are characteristic of sideroblastic anemia.
4. Lead Poisoning
History
Clinical History
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
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.
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.
Lymphadenopathy 289
APPROACH TO A CASE OF LYMPHADENOPATHY
Differential Diagnosis
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
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.
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.
48
Muscle Disorders
MUSCLE WEAKNESS
(PROBLEM-BASED LEARNING)
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)
(For color version, see Plate 6)
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.
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.
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.
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.
50
Acute Rheumatic Fever
JOINT PAINS WITH FEVER
(PROBLEM-BASED LEARNING)
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.
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
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).
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.
Differential Diagnosis
51
Nephrology Cases
EDEMA AND OLIGURIA
(PROBLEM-BASED LEARNING)
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.
Fig. 51.1: Acute nephritis showing oliguria, edema and cola colored urine
(For color version, see Plate 6)
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.
Poststreptococcal nephritis
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.
Fig. 51.2: Nephrotic syndrome showing facial puffiness and periorbital edema
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.
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.
Differential Diagnosis
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).
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.
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.
8
Spotters
52
Turners Syndrome
SPOTTER
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.
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
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.
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.
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
Differential Diagnosis
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.
Beaking
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.
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.
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
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
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
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
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.
Fever 339
2.
3.
4.
5.
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
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
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
muscular 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
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
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
Muscle
biopsy 294
disorders 291
weakness 291
Muscular dystrophy 291
Mycobacterium tuberculosis 289
Myelodysplasia 328
Myelography 129
Myotonic
dystrophy 292
muscular 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
endotracheal intubation 206
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
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
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
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