4th ea

r Anniversa
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Y
Edition

y
Fully

Tenth

Ed
Revised

ition
4 th
Scott's PEDIA-TRICKS

Scott's Edition

PEDIA-TRICKS
Written by the Students, for the Students

Written by the Students, for the Students

Srinivasa Raghavan R
Julius Scott

A comprehensive guide to pass the pediatric practical examination

for undergraduates and postgraduates

Julius Scott
Srinivasa Raghavan R
 CONTENTS
Dedication .................................................................................................................................................................. v
Foreword to the fourth edition ............................................................................................................................... vii
Preface to fourth edition .......................................................................................................................................... ix
Foreword to the first edition .................................................................................................................................... xi
Preface to the first edition...................................................................................................................................... xiii
Contributors ............................................................................................................................................................. xv

SECTION A: GENERAL
1. Exam cases ............................................................................................................................................................ 3
2. Some tips/ tricks for the exam preparation ............................................................................................................. 6
3. History taking ....................................................................................................................................................... 12
4. Nutrition history .................................................................................................................................................... 34
5. Pedigree charts ..................................................................................................................................................... 38
6. Assessment of development ................................................................................................................................. 41
7. General examination ............................................................................................................................................. 48
8. Abdomen examination .......................................................................................................................................... 82
9. Cardiovascular system examination ..................................................................................................................... 99
10. Respiratory system examination .......................................................................................................................... 111
11. Neurological examination ................................................................................................................................... 118
SECTION B: SYSTEMS
12. Neonatology ........................................................................................................................................................ 167
Cardiovascular system
13. Cardiovascular system disorders ........................................................................................................................ 205
Respiratory system
14. Bronchiectasis in children ................................................................................................................................... 242
15. Pleural effusion ................................................................................................................................................... 247
16. Pulmonary tuberculosis in children ..................................................................................................................... 252
Renal system
17. Nephrotic syndrome ........................................................................................................................................... 260
18. Post-infectious glomerulonephritis (PIGN) ......................................................................................................... 268
Abdomen
19. Approach to a child with fever and hepatosplenomegaly ................................................................................... 274
20. Afebrile hepatosplenomegaly without pallor/ jaundice/ hematemesis ................................................................. 287
21. Cirrhosis/Chronic liver disease and ascites ........................................................................................................ 291
22. Extra-hepatic portal venous obstruction (EHPVO) in children .......................................................................... 305
23. Neonatal cholestasis ........................................................................................................................................... 310
Neurology
24. Cerebral palsy ..................................................................................................................................................... 318
25. Post-meningitis/ post-encephalitis sequelae ........................................................................................................ 335
26. Acquired paraplegia - AFP, transverse myelitis, compressive myelopathy ........................................................ 346
27. Stroke in children ................................................................................................................................................ 371
28. Clinical approach to a child with neurodegenerative disorders including neuro Wilson ...................................... 379
29. Sub-acute sclerosing pan-encephalitis (SSPE) ................................................................................................... 391
30. Ataxia in children ................................................................................................................................................ 393
31. Approach to a floppy infant ................................................................................................................................ 398
32. Approach to a child with muscular dystrophy .................................................................................................... 402
33. Peripheral neuropathies ...................................................................................................................................... 410
34. Chorea ................................................................................................................................................................ 413
35. Facial palsy ......................................................................................................................................................... 417
36. Microcephaly, craniosynostosis .......................................................................................................................... 422
37. Macrocephaly, hydrocephalus ............................................................................................................................ 424
Nutrition
38. Undernutrition in children ................................................................................................................................... 430
39. Vitamin A deficiency........................................................................................................................................... 441
40. Breastfeeding ..................................................................................................................................................... 443
Genetics
41. Essential genetics for exams .............................................................................................................................. 450
42. Down syndrome ................................................................................................................................................. 457
43. Inborn errors of metabolism ............................................................................................................................... 461
Endocrinology
44. Short stature ....................................................................................................................................................... 474
45. Rickets ................................................................................................................................................................ 487
46. Congenital hypothyroidism .................................................................................................................................. 493
Hematology
47. Afebrile hepatosplenomegaly with pallor - hemolytic anemias ........................................................................... 501
48. Iron deficiency anemia ....................................................................................................................................... 512
49. Immune thrombocytopenic purpura (ITP) .......................................................................................................... 517
50. Approach to a child with lymphadenopathy ........................................................................................................ 521
51. Bleeding in children ............................................................................................................................................ 524
52. FAQs in Thalassemia major ............................................................................................................................... 527
Infections
53. Skin infections and infestations ........................................................................................................................... 532
54. Diarrhea .............................................................................................................................................................. 535
55. Fever with rash in children ................................................................................................................................. 543
Rheumatology
56. Approach to arthritis in children ......................................................................................................................... 550
Social programs
57. Social pediatrics: Various national programs for the welfare of children ........................................................... 556
SECTION C: VIVA VOCE

58. Nutrition, drugs, vaccines and instruments ......................................................................................................... 573

59. Radiology ............................................................................................................................................................ 603

SECTION D: MISCELLANEOUS

60. Model History Sheets ......................................................................................................................................... 633

61. Question Bank .................................................................................................................................................... 667

INDEX ............................................................................................................................................................... 683

 PREFACE TO FOURTH EDITION

The fourth edition of Scott’s Pedia-tricks continues in its tradition of being an essential resource, for both
undergraduate and postgraduate students in their preparation for the clinical examination. The huge success of the previous
editions had given us a responsibility to deliver a book that would live up to the student’s expectations. This edition hence
has been thoroughly updated, and edited to keep up with the growing data.
We live in the age of information. Almost anything can be learnt at the comfort of our study room. The internet has
made lives simpler by making knowledge accessible to everyone. With the advent of smartphones, access to information
has been made even simpler. It is no exaggeration to say that the world is in our hands. Any information is just a click
away. Yet, there is still a place for a good book. The very advantage of the internet can be its disadvantage as well - the
volume of information that is made available. It is difficult for a student to sift through the huge amount of data to find out
the information that he needs. Hence, a good book that provides the apt information is invaluable for the students preparing
for the exam. Often these days you may hear people saying - “The art of clinical medicine is becoming extinct”. These
aspects played on our mind when we set out to prepare this edition. During preparation of this edition, we wanted to ensure
that the book is comprehensive yet concise and student friendly, incorporating both the new advances and the time-
honored vintage art of clinical medicine that had been taught to us by the stalwarts of the previous generation. Hence you
may note that the contributors are a mix of both junior pediatricians as well as experts.
All the chapters have been thoroughly edited. Many chapters have been re-written totally. Must-know areas that
are considered as high-yield have been highlighted in green boxes. Nice-to-know category information has been highlighted
in yellow boxes. We feel this would help the students during a quick revision. To facilitate the student to answer questions
during the case discussion, relevant theory concepts have also been included in all the chapters. Model case sheets and
question bank sections have been revamped. We have also included simple flow charts and tables where ever relevant for
easier understanding. This book will help the students not only for their exams but also for their day to day work in the
hospital.
We thank all the contributors who have helped us realize this endeavour. We also thank all the expert reviewers who
have given their time and have taken pain-staking effort to go through all the chapters and have given their valuable
feedback. We are blessed to have such stalwarts as our guides and well-wishers. We also thank all our students who were
the driving force behind the book.
We sincerely hope this edition is useful to the students at large. We would love to hear your feedback about this
endeavour.

Dr. Julius Xavier Scott

Dr. Srinivasa Raghavan R

FOREWORD TO FOURTH EDITION

This much awaited “clinically oriented” and “student focused” 4th edition of Dr. Julius Scott’s
Pedia-Tricks is getting released by Paras Medical Books and there is absolutely no doubt in my
mind that it will go out of print within a few weeks after its release. Professor Julius Scott has
identified and roped in Dr. Srinivasa Raghavan as his associate editor, an able and competent
young pediatrician who shares the same degree of eagerness and enthusiasm to motivate young
generation and pass on and share unreservedly their knowledge and clinical skills in assessment,
management, communication and documentation. This team has identified other academically
competent and active, meritorious young contributors who have made themselves known to their
students as effective teachers and clinical trainers in their respective institutions and regions. The
result is obvious.
The initial few pages give relevant preparatory tips and tricks to tackle theory, clinical and oral
examinations. Whatever essential areas have to be emphasized in terms of history taking in various
clinical fields, clinical examination and assessment of a child’s (Neonates to Adolescents) status of
growth and development, nutrition, hydration, airway, breathing, circulation, integrity and functioning
of various organ systems, including genetic and immunological systems - are all appropriately
tailored and proportioned to the needs of the students with clinical examination oriented case
scenarios. Many new features and additions have been incorporated keeping in mind the needs of
examination going students in nutrition, genetics, inborn errors of metabolism, current emerging
infections, growth and development and other systemic disorders (GIT & Hepatobiliary, CNS,
Renal, Respiratory, Cardiovascular, Nutrition, Endocrinology, Preventive and Social Pediatrics).
The commonly asked questions in clinical bedside rounds, clinical, oral and OSCE examinations by
faculty, seasoned examiners and in quiz competitions are all appropriately answered. Even some
of the personalized, individualistic and idiosyncratic questions which are often used as trump cards
are given due attention. The book will be useful as an instant resource material even for well-
informed teachers and trainers to refer and re-equip themselves before lectures or clinical
discussions.
Reading this edition will definitely be a pleasurable experience to students who want to equip
themselves with essentials of pediatrics. The book will ensure their success, not only in examinations
but also in the delivery of meaningful professional health care to children. Whatever little margin of
profit that is accrued in the sales of this edition is going to help needy children get free anti-cancer
drugs, iron chelators, anti-hemophilic factor and anti-rejection drugs. My earnest request is not to
photocopy this well compiled and meticulously prepared book. My best wishes to all the students
who have rightly chosen this book as their essential companion for their academic progress and
professional success.

Dr. S. Srinivasan
Former Director-Professor of Pediatrics
JIPMER, Pondicherry
India
 Section - A: General

CHAPTER
7
General Examination Dr. Peter Prasanth
CHAPTER - 7

Dr. Kalyanakumar Guruswamy

GENERAL EXAMINATION C. Striking features

Of all the diagnoses that ever will be made, most are made The child’s level of consciousness is probably the most
during the history and the rest during the physical important part of examination of the acutely ill child, as
examination. alterations in the level of consciousness will often be the
(David L. Sackett, The Science of the Art of the Clinical first manifestation of a problem.
Examination.JAMA.1992;267 (19):2650-2652.) Describe level of consciousness. Expand on words like
TEN PRINCIPLES OF EXAMINATION IN A CHILD “lethargic”, “stuporous”, “obtunded” which mean different
things to different examiners. For example:
1. Gather as much data as possible by observation first.
• Child’s activity as you enter the room, such as talking,
2. Position: parent’s lap vs. bed (decide in which position
sleeping, posturing, etc.
child is more comfortable)
• Stimulus required to awaken the patient, such as calling
3. Include child - explain to the child what you are
her name.
going to do. Demonstrate what you are about to do on
a doll or teddy (e.g., auscultation or palpation). • Child’s best mental state seen, such as conversing well,
sluggish answers, semi-purposeful movements etc
4. Distraction is a valuable tool, especially in a sick child
• Child’s activity when you stop stimulating her, is the child
5. Stay at the child’s level as much as possible. Do
able to maintain alertness?
not tower over the child.
Some examples:
6. Order of exam. least distressing to most
distressing (e.g., do not start stripping a child straight • Three-month-old Nirmal appears alert, interested in his
away or examine painful area last ) surroundings and responds to my voice well. He was
lying in supine position with lower limbs abducted and
7. Rapport with child. Most important is to talk to the
externally rotated with supplemented oxygen via nasal
child and establish a rapport.
prongs and has a nasogastric tube in situ with a noticeable
8. Be honest. If something is going to hurt, tell in a calm see saw pattern of breathing.
fashion and reassure why it is important that you have
• Priya was very sociable and she enjoys playing with her
to examine. Don’t lie or you lose credibility!
mother.
9. Understand developmental stages’ impact on
child’s response. For example, stranger anxiety is a II. VITAL SIGNS
normal stage of development, which tends to make A. PULSE
examining a previously cooperative child more difficult.
Definition:
10. Be confident and extremely gentle. Always take
“Pulse” is the waveform generated by the left ventricular
permission before you start examining.
systole which traverses the arterial tree in a peripheral
I. GENERAL APPEARANCE AND POSTURE OF THE direction at a rate faster than the blood column.
BABY Assessment:
A. Level of consciousness and reaction of the child to the 1. Rate
environment 2. Rhythm
B. Level of attention and interaction with parents and others 3. Volume
in the room

48 Scott’s Pedia-Tricks
 7. General Examination

4. Character f. Femoral - Below inguinal ligament, midway between

5. Equality anterior superior iliac spine and pubic symphysis (not pubic
tubercle). It is best palpated with the examiner standing
6. Peripheral pulses on the ipsilateral side of the patient and the fingertips of
7. Radio-femoral/ radio-radial delay the examining hand pressed firmly into the groin.

CHAPTER - 7
How to feel the pulse: Auscultation should be performed in this area, as well.

The radial pulse is felt by the index (studies the artery), g. Popliteal - Flex knee before palpating. In midline, on
middle (measures the volume), and the ring finger (used to popliteal side of lower end of femur. Alternative method:
obliterate the pulse) (photos) Doctor’s one hand on patient’s knee, other hand under
knee. Push flexed knee downwards [into extension] until
Surface anatomy of pulses can feel popliteal.
a. Radial - Palmar side of wrist, between flexor carpi h. Posterior tibial - Posterior, inferior to medial malleolus,
radialis tendon and radius. The child’s forearm should be between flexor digitorum longus and flexor hallucis
supported in one of the examiner’s hands and his other longus. Posterior tibial lies just posterior to the medial
hand used to palpate along the radialvolar aspect of the malleolus. It can be felt most readily by curling the fingers
subject’s forearm at the wrist. This can best be done by of the examining hand anteriorly around the ankle, indenting
curling the fingers around the distal radius from the dorsal the soft tissues in the space between the medial malleolus
toward the volar aspect, with the tips of the first, second, and the Achilles tendon, above the calcaneus. The thumb
and third fingers aligned longitudinally over the course of is applied to the opposite side of the ankle in a grasping
the artery. fashion to provide stability. Again, obesity or edema may
b. Brachial - Cubital fossa, medial to biceps tendon. The prevent successful detection of the pulse at the location.
examiner supports the child’s forearm in his left hand, i. Dorsali spedis - Lateral to extensor hallucis longus, over
with the subject’s upper arm abducted, the elbow slightly tarsal bones. This is examined with the child in the
flexed, and the forearm externally rotated. The examiner’s recumbent position and the ankle relaxed. The examiner
right hand is then curled over the anterior aspect of the stands at the foot of the examining table and places the
elbow to palpate along the course of the artery just medial fingertips transversely across the dorsum of the forefoot
to the biceps tendon and lateral to the medial epicondyle near the ankle. The artery usually lies near the center of
of the humerus. The position of the hands should be the long axis of the foot, lateral to the extensor hallucis
switched when examining the opposite limb. tendon but it may be aberrant in location and often
c. Carotid - Just lateral to upper border of thyroid cartilage. requires some searching. This pulse is congenitally absent
Use index and middle fingers to feel the carotid pulse. in approximately 10% of individuals.
Caution: Do not palpate both the carotids at the same time. 1. RATE
d. Superficial temporal - Anterior to ear as crosses Count for one full minute (except during resuscitation) to
temporal bone’s zygomatic process. avoid missing an arrhythmia. A fast heart rate is called
e . Abdominal aorta - In midline, at umbilicus pressing into tachycardia. A heart rate that’s too slow is called
abdomen (Use caution if large aortic artery aneurysm to bradycardia.
avoid rupture). The abdominal aorta is an upper Table 7.1: Normal Heart Rate by Age (beats/minute)
abdominal, retroperitoneal structure which is best palpated Reference: PALS Guidelines, 2015
by applying firm pressure with the flattened fingers of
Age Awake Rate Sleeping Rate
both hands to indent the epigastrium toward the vertebral
column. For this examination, it is essential that the child’s Neonate (<28 day) 100-205 90-160
abdominal muscles be completely relaxed; such relaxation Infant (1 mon -1 yr) 100-190 90-160
can be encouraged by flexing the hips and by providing a
Toddler (1-2 yr) 98-140 80-120
pillow to support the head of the child. In extremely obese
individuals or in those with massive abdominal Preschool (3-5 yr) 80-120 65-100
musculature, it may be impossible to detect aortic School-age (6-11 yr) 75-118 58-90
pulsation. Auscultation should be performed over the aorta
Adolescent (12-15 yr) 60-100 50-90
and along both iliac vessels into the lower abdominal
quadrants.

Scott’s Pedia-Tricks 49
 Section - A: General

2. RHYTHM 4. CHARACTER OF THE PULSE

• The term “arrhythmia” refers to any change from A. Anacrotic (pulsus parvus et tardus)
the normal sequence of electrical impulses. The
electrical impulses may happen too fast, too slowly, • Low amplitude pulse with slow rising and late peak
or erratically – causing the heart to beat too fast, too • Seen in severe aortic stenosis
CHAPTER - 7

slowly, or erratically.
• It is important to take the pulse for one minute. Slurred gradual systolic upstroke Absent dicrotic notch

Otherwise rhythm abnormalities may be missed. 120

• A normal pulse is regular in rhythm and force. Narrowed pulse pressure

Pressure (mmHg)
• An irregular pulse may be due to sinus arrhythmia,
ectopic beats, atrial fibrillation, paroxysmal atrial 90
tachycardia, atrial flutter, partial heart block etc.

Time

Fig. 7.3
B . Dicrotic
Fig. 7.1 • A single pulse wave with one peak in systole and
• Intermittent dropping out of beats at pulse is called one peak in diastole
“intermittent pulse”. Examples of regular intermittent • Due to very low stroke volume and decreased
(regularly irregular) pulse include pulsus bigeminus, peripheral resistance
second-degree atrioventricular block. An example of
• Causes: Left ventricular failure, dilated
irregular intermittent (irregularly irregular) pulse
cardiomyopathy, cardiac tamponade.
is atrial fibrillation.

Fig. 7.2
3. VOLUME
Palpation should be done using the fingertips and intensity
of the pulse graded on a scale of 0 to 4 +:0 indicating no
palpable pulse; 1 + indicating a faint, but detectable pulse;
2 + suggesting a slightly more diminished pulse than
normal; 3 + is a normal pulse; and 4 + indicating a bounding
pulse.
Hypokinetic pulse Fig. 7.4
• Small weak pulse
• Small volume and narrow pulse pressure
• Causes: Shock and cardiac failure, mitral stenosis
and aortic stenosis
Hyperkinetic pulse
• High amplitude pulse with a rapid rise
• Large volume with wide pulse pressure
• Causes: High output states, mitral regurgitation,
Ventricular septal defect

50 Scott’s Pedia-Tricks
 12. Neonatology

SECTION - B : SYSTEMS

12. Neonatology ..................................................... 167 35. Facial palsy ....................................................... 417

Cardiovascular system 36. Microcephaly, craniosynostosis ....................... 422
13. Cardiovascular system disorders...................... 205 37. Macrocephaly, hydrocephalus ......................... 424
Respiratory system Nutrition
14. Bronchiectasis in children ................................. 242

C H A P T E R - 12
38. Undernutrition in children ................................ 430
15. Pleural effusion ................................................. 247 39. Vitamin A deficiency ......................................... 441
16. Pulmonary tuberculosis in children .................. 252 40. Breastfeeding ................................................... 443
Renal system Genetics
17. Nephrotic syndrome ......................................... 260 41. Essential genetics for exams ............................ 450
18. Post-infectious glomerulonephritis (PIGN) ...... 268 42. Down syndrome ............................................... 457
Abdomen 43. Inborn errors of metabolism ............................ 461
19. Approach to a child with fever and hepato- Endocrinology
splenomegaly ................................................... 274 44. Short stature ..................................................... 474
20. Afebrile hepatosplenomegaly without pallor/ 45. Rickets ........................................................... 487
jaundice/ hematemesis .................................... 287
46. Congenital hypothyroidism .............................. 493
21. Cirrhosis/Chronic liver disease and ascites ....... 291
Hematology
22. Extra-hepatic portal venous obstruction (EHPVO)
47. Afebrile hepatosplenomegaly with pallor - hemolytic
in children ......................................................... 305
anemias 501
23. Neonatal cholestasis ........................................ 310
48. Iron deficiency anemia ..................................... 512
Neurology
49. Immune thrombocytopenic purpura (ITP) ....... 517
24. Cerebral palsy ................................................... 318
50. Approach to a child with lymphadenopathy ... 521
25. Post-meningitis/ post-encephalitis sequelae ... 335
51. Bleeding in children ........................................... 524
26. Acquired paraplegia - AFP, transverse myelitis,
52. FAQs in Thalassemia major .............................. 527
compressive myelopathy .................................. 346
Infections
27. Stroke in children .............................................. 371
53. Skin infections and infestations ....................... 532
28. Clinical approach to a child with neurodegenerative
disorders including neuro Wilson ..................... 379 54. Diarrhea 535
29. Sub-acute sclerosing pan-encephalitis (SSPE) . 391 55. Fever with rash in children ................................ 543
30. Ataxia in children .............................................. 393 Rheumatology
31. Approach to a floppy infant ............................. 398 56. Approach to arthritis in children ....................... 550
32. Approach to a child with muscular dystrophy . 402 Social programs
33. Peripheral neuropathies ................................... 410 57. Social pediatrics: Various national programs for the
welfare of children ............................................ 556
34. Chorea ........................................................... 413

Scott’s Pedia-Tricks 165

 12. Neonatology

CHAPTER
12
Neonatology Dr. Umamaheswari B
Dr. Abiramalatha T

Usually newborn is either a short case or a spotter. HISTORY AND EXAMINATION

The usual newborn cases (for a short case) are: Introduction
• Well baby Baby name/ born to a __year old, primi/ G2 P1 L1 mother
• Neonatal jaundice at ___weeks gestation with a birth weight of ___grams by
• Prematurity ____mode of delivery

• Intrauterine growth restriction (IUGR) Day of life

C H A P T E R - 12
Additional topics that may be discussed are: Corrected gestational age (in preterms)

• Infant of diabetic mother (IDM) Informant, reliability

• Seizures Presenting Complaints

• Sepsis • In a well term or preterm or SGA baby, there will not be
any presenting complaints. You can start directly from
• Asphyxia
obstetric/ antenatal history
• Baby with systolic murmur
• In a jaundice newborn
Spotters include
- Complaints of yellowish discoloration of skin noticed
• Caput succedaneum and cephalohaematoma by the mother since day___ of life
• Large for gestational age (LGA)/ Small for gestational - Bilirubin levels (if the parents know)
age (SGA)
- No H/o of high colored urine/ pale stools
• Jaundice
- Mother’s blood group, baby’s blood group
• Benign skin conditions like erythema toxicum, Mongolian
- Signs of BIND (bilirubin induced neurological
spots, Epstein pearls, Milia etc.
dysfunction) - irritability/ lethargy, high-pitched cry,
• Erb’s palsy poor feeding, posturing/ seizures
• Cleft lip and palate - Details of treatment
• Meningomyelocele Obstetric/Antenatal History
• Sternomastoid tumor Mother is married since ____ years
• Congenital talipes equinovarus (club foot) 1st Child – Gestational age/ Birth weight/ Age of the child,
• Down’s syndrome Development
• Ambiguous genitalia G2 – Present pregnancy
• Umbilical sepsis/ granuloma Spontaneous conception
• Twins (probably twin to twin transfusion) Pregnancy confirmed by urine pregnancy test (UPT) at ___
gestation
You should be thorough with general and neurological Booked at---- _____. Regular antenatal visits
examination of newborn. You might be asked to demonstrate
I Trimester
neonatal reflexes, especially Moro reflex and asymmetric
tonic neck reflex (ATNR). • Hyperemesis

Scott’s Pedia-Tricks 167

 Section - B: Systems
• Fever with rash/ Drugs/ Irradiation Feeding
• Blood investigations • Type of feeding - DBF or spoon feeds
II and III Trimester • To assess whether the baby is getting adequate feeds
• Quickening - How many feeds per day?
• IFA and calcium tablets - Duration of each feeding?
• TT injections – at what months - Whether the baby sleeps for 2-3 hours after a feed?
• PIH/ GDM - How many times baby passes urine in 24 hours?
• Bleeding or spotting PV • Any problem in breast feeding (especially if baby’s weight
• Chorioamnionitis/ UTI loss is more) - The ideal way of assessing is to observe
the breastfeeding. Look for ‘positioning’ and
USGs – How many? When? Details – Dating scan, anomaly
‘attachment’.
scan, growth scan – AFI, Doppler
• Signs of good ‘Positioning’
Pre-pregnancy weight, weight gain during pregnancy
1. Head and body should be in straight line (neck should
Intrapartum History not be twisted)
C H A P T E R - 12

• Onset of labor 2. Whole body should be supported

• In preterms – Antenatal steroids 3. Baby face should face the breast
- Antenatal steroids are currently recommended from 4. Baby abdomen touching the mother’s abdomen
24-34 weeks of gestation; 2 doses of betamethasone
(12 mg) at 24 h interval or 4 doses of dexamethasone • Signs of good ‘Attachment’
(6 mg) at 12 h intervals. 1. Baby’s mouth wide open
• Meconium-stained or clear liquor? 2. Lower lip turned outwards
• Mode of delivery (Indication, if instrumental vaginal 3. Majority of the areola inside the mouth, with more
delivery or LSCS) areola visible above than below
• Cried at birth or not 4. Baby’s chin touches mother’s breast
• Details of resuscitation – PPV/ Intubation/ Chest
compressions/ Adrenaline/ Normal saline
• APGAR (If the mother knows)
• Birth weight
• Breastfeeding initiated when?
Neonatal History
• A brief description of any significant neonatal illness - Fig. 12.1
HMD/ Apnea/ PDA/ sepsis/ NEC/ seizures/
hypoglycemia Family History
• Jaundice (as described above) 1. Father’s age, literacy, occupation and income per month.
• If well newborn 2. Mother’s age, literacy, occupation and income per month.
- Whether passed urine and stools within 24 hours? 3. Any significant history among family members, especially
in elder siblings - neonatal deaths, congenital anomalies,
- Feeding (described below) neonatal seizures, developmental delay
- Any screening done, what’s the result? - Hearing, 4. Parents are consanguineous or not
thyroid, 17-OH P, IEM screen
Socioeconomic History
- Immunization
• Same as in pediatrics (not necessary in a short case)

168 Scott’s Pedia-Tricks

 12. Neonatology

Summary of the History There is another classification of neurobehavioral state by

Brazilton, which has a total of 6 states with the addition of
• For a baby with jaundice
a third state called ‘dozing’.
- Term baby/ ____ weeks gestation • Posture
- AGA/ SGA/ LGA Describe spontaneously, the posture of the baby at the
- Birth weight of ___ grams time of presentation as:
- Jaundice from ___ day of life (bilirubin level ___) ‘Baby is held in the mother’s lap in a universally flexed
posture’ (or)
- Treated with phototherapy for ___ hours
‘Baby is lying on the cradle in universal flexion’ or ‘
- Probable etiology being ____ lower limbs flexed and upper limbs extended’
• For a well newborn - A term newborn has a universally flexed posture.
- Term baby/ ____ weeks gestation by ___ delivery Preterm infants have varying degree of extension
depending on the gestational age.
- Birth weight of ___ grams
• Pallor/ Icterus/ Cyanosis/ Edema (Do not comment
- AGA/ SGA/ LGA about clubbing or lymphadenopathy in neonates)
- Passed urine and stools within 24 hours
Vital Signs

C H A P T E R - 12
- On exclusive breast feeds
• Normal range for term newborn infants
- Weight loss within normal limits
Table 12.1:
- Immunization done with BCG/ OPV/ HBV
Vital sign Normal range
- Screening (hearing, thyroid, etc.) results
Temperature 36.5-37.5oC
Examination Heart rate 120-160/ minute
Includes the following sub-headings: Respiratory rate 40-60/ minute
• General examination Blood pressure Mean BP should be above the corresponding
• Vital signs gestational age. Example: For a baby born
at 35 weeks, mean BP should be >35 mmHg.
• Anthropometry
• Gestational age assessment • Temperature - Must be measured in the axilla, using a
digital thermometer. Most examiners will not accept the
• Head to foot examination statement ‘baby is normothermic’.
• Systemic examination
General Examination
• Sensorium
Baby’s sensorium can be best described by Prechtl
Neurobehavioral state

Table 12.2:
Neurobehavioral state Eyes open/closed Extra-ocular movements Respiration Limb movements
State Description
1 Quiet sleep Closed Absent Regular Absent
2 Active sleep Closed Present Irregular Present
3 Awake, calm Open Absent Regular Absent
4 Awake, active Open Present Irregular Present
5 Fussy, crying Crying

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 20. Afebrile Hepatosplenomegaly without Pallor/ Jaundice/ Hematemesis

20
Afebrile Hepatosplenomegaly
CHAPTER

Without Pallor/ Jaundice

Dr. Sachitra Rathod
Hematemesis Dr. Srinivasa Raghavan R
Usually the child would have a history of incidentally detected • Congestive: Portal hypertension, congestive cardiac
organomegaly or would have been found to have an failure, Budd Chiari syndrome
organomegaly while being worked up for global
developmental delay. Rare presentations are as • Hematological causes: Mainly hemolytic anemias and
neuroregression/ pancytopenia. dyserythropoietic anemias have been dealt with in a
separate chapter on anemia with hepatosplenomegaly
Suspect storage disorder if there is organomegaly which has
infantile onset with minimal or no fever, no jaundice or other • Infiltrative disorders: Gaucher’s, Niemann Pick’s disease,
features of hemolysis, consanguinity with a similar illness in GM1 and 2 gangliosidosis, lysosomal storage disorders,

C H A P T E R - 20
the family and with associated coarse facies or skeletal or mucopolysaccharoidoses
neurological involvement. • Neoplasms: Hemangioma, hamartoma, leukemia
Splenomegaly: • Connective tissue disorders: Juvenile rheumatoid arthritis,
SLE
Spleen has to enlarge thrice for it to become palpable. Thus,
a palpable spleen always indicates splenomegaly, unlike liver. Causes of predominant hepatomegaly:
In newborns though spleen is normally felt 1-2 cm below 1. Infection - this subgroup is dealt with in fever with HSM
costal margin. chapter
Grading of splenomegaly: Hackett’s semi quantitative 2. Inflammation - this subgroup is dealt with in Fever with
assessment: HSM chapter
Table 20.1:
3. Congestive causes
Grade Class Palpation • Cardiac failure
Mild 0 Not palpable even on deep • Budd Chiari syndrome
inspiration
1 Palpable below costal margin
4. Infiltration
on deep inspiration • Hemochromatosis
2 Palpable but not beyond a • Extramedullary hematopoiesis
horizontal line halfway between
• Leukemia
costal margin and umbilicus
Moderate 3 Palpable more than halfway to • Lymphomas
umbilicus but not below a line • Primary liver tumors-hepatoblastoma
horizontally running through it
• Secondaries in liver
Massive 4 Palpable below umbilicus, but
not below a horizontal line half 5. Storage disorders
way between umbilicus and pubic • Glycogen storage disorders, Gaucher’s disease,
symphysis Neimann Pick disease, mucopolysaccharoidosis
5 Extending below class 4 6. Obstruction
Causes of predominant splenomegaly: • Hepatic vein thrombosis
• Infectious: This subgroup is dealt separately in fever with • Constrictive pericarditis
HSM chapter • Cardiac tamponade
• Congenital hepatic fibrosis

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 Section - B: Systems

Clues to Etiology: • Cardiac involvement in the form of hypertrophic

• Extramedullary hematopoiesis should be considered cardiomyopathy with hepatomegaly in neonate - Pompe’s
in an afebrile child with pallor, failure to thrive (not always disease.
necessary as in hereditary sphereocytosis), history of • Failure to thrive with massive hepatosplenomegaly in an
multiple transfusions beginning early in life (thalassemia infant with hypotonia, associated adrenal calcification-
and sickle cell anemia) abdominal distension, features of Wolman disease.
bone marrow expansion such as broad forehead,
Individual Disorders:
prominent cheek bones or features suggestive of
hemolysis like hemoglobinuria, jaundice, gall stones. • Glycogen storage disorders: Type 1, 3, 4 and 6 involve
Infections like TORCH and parvovirus also cause liver.
extramedullary hematopoiesis. Type 1 is the most common subtype. Hallmark of the
• Osteopetrosis: It is a condition resulting from defective disease is hypoglycemia, lactic acidosis, hyperlipidemia
bone resorption by osteoclasts. Severely affected infants and hyperuricemia. Some children have defective platelet
present with macrocephaly, hepatosplenomegaly, anemia, aggregability and defective neutrophilic function. Renal
failure to thrive, dental abnormalities and psychomotor involvement (renomegaly) is seen in type 1. They present
delay. Other features include pathological fractures and with proteinuria, hypertension, renal stones,
cranial nerve dysfunction (optic and facial more nephrocalcinosis, and altered creatinine clearance.
C H A P T E R - 20

commonly). Diagnosis is aided by history - typical early morning

seizures in later infancy, clinical examination - chubby
X-ray - Bone in bone appearance and increased mineral
cheeks, hepatorenomegaly and combination of
density and alternate bands of hyper and hypolucency-
biochemical abnormalities. With glucagon, blood sugars
sandwich appearance of vertebral bodies.
do not rise but lactate level increases. Mutation analysis
Treatment: Bone marrow transplantation if carried out gives the confirmatory test. Treatment is to give uncooked
before development of secondary complications. RANKL cornstarch, from which glucose is slowly released. Other
(Receptor activator of nuclear factor kappa-B ligand) associated conditions should be taken care of like
replacement therapy has also been found to be useful. hyperlipidemia and hyperuricemia with statins and
• Hereditary sphereocytosis (HS): Asymptomatic with allopurinol respectively. Liver transplantation is a potential
incidentally detected organomegaly to severe hemolysis cure but liver adenomas are known to occur even on
(anemia, jaundice, fatigue, expansion of extrameduallary transplanted liver. The prognosis is usually good if
spaces- skull, organs - isolated splenomegaly usually, identified early and treated appropriately with dietary
pigment gall stones). May have family history of similar therapy.
complaints (AD) or history of significant neonatal jaundice • Lysosomal storage diseases: Accumulation of
without ABO/ Rh incompatibility. sphingolipids in the cells of the body has two important
Investigations: Spherocytes on peripheral smear are seen, implications-cells of central nervous system resulting in
reticulocytosis is present. Osmotic fragility test is used neuroregression and in the viscera leading to
to confirm HS. Gel electrophoresis is used to identify the organomegaly, skeletal abnormalities and lung infiltrates.
specific protein deficiency in HS.
Treatment includes splenectomy as it is the major site of
hemolysis. Folic acid supplementation is recommended.
• Storage disorders: Suspected in a child with incidentally
detected organomegaly with associated skeletal problems
or neurological problems- developmental delay, seizures,
neuroregression etc. Anemia may be seen as a part of
all cell line suppression.
Clues to etiology:
• Hepatomegaly with hypoglycemia and early morning
seizures suggest glycogen storage disorders type I.

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 20. Afebrile Hepatosplenomegaly without Pallor/ Jaundice/ Hematemesis

• Gangliosidosis:
Table 20.2:
GM1 GM2 (Tay Sachs) GM2 (Sandhoff)
Infancy most common presentation Infancy Infancy
Neuroregression Neuroregression Neuroregression
Seizures Exaggerated startle reaction- Seizures
hyperacusis
Typical facies - broad forehead, Macrocephaly, ataxia and dysarthria Similar to Tay Sach but has associated
depressed nasal bridge, cherry red spot -juvenile forms, cherry red spot- splenomegaly
no splenomegaly usually

Gaucher’s disease:
• Type B has a variable clinical course. They present in
• Most common lysosomal storage disorder - Variable age either infancy or childhood with predominant
of onset- Characterized by multisystemic involvement – organomegaly, usually splenomegaly is the first to be

C H A P T E R - 20
hematological, skeletal and visceral. detected - May have pulmonary involvement (common
• Three types: Visceral non-neuronopathic (type 1), acute in older age group) which may progress to life threatening
neuronopathic (type 2), juvenile neuronopathic (type 3). bronchopneumonias and cor pulmonale in adults. Liver
involvement is so severe to cause cirrhosis, portal
• Clinical features are suggestive of suppression of all three hypertension and ascites and splenic involvement can be
cell lines-anemia, bleeding manifestations, fatigue, as severe as that needing splenectomy for hypersplenism.
infections; involvement of bone can present as bone pain CNS is not involved and they have a normal IQ.
due to fractures or pseudo-osteomyelitits
• Type C: Present as neonatal cholestasis - child may
• Examination - Hepatomegaly, splenomegaly or both - be normal appearing for initial 2 years after which
consistency of liver/spleen are firm to hard. They are neuroregression begins. Organomegaly is less severe.
non-tender with sharp edges
• Investigations: Presence of Niemann Pick cells in the
• Associated features: Bone deformitites- Erlenmeyer flask peripheral smear or bone marrow is diagnostic- Crumpled
deformity of femur can be seen. tissue paper/ Crumpled silk appearance. For subtype
• Bone marrow- Gaucher cells that stain strongly positive classification, enzyme analysis is important- type A and
with PAS are diagnostic B have enzyme levels of 1-10% but type C can have
• Gaucher type 2 and type 3: Neurodegenerative course normal levels of enzyme.
with hepatosplenomegaly. Type 2 can have neurogenic • Treatment of NPD: No treatment is available at present.
stridor and squint additionally and type 3 can have Bone marrow transplantation and amniotic cell
supranuclear gaze palsy, myotonia and dementia. transplantation have been tried for type A and B but the
• Treatment is available for Gaucher’s disease - enzyme has not been a success so far. For type B enzyme
replacement therapy (cerezyme) which reverses replacement therapy is under trial. Prenatal Diagnosis:
extraskeletal manifestations of the disease- useful in early it can be done by amniocentesis or chorionic villus biopsy.
type 1 • Mucopolysachharoidoses: These are progressive
Niemann Pick disease: Three types - Types A, B conditions caused by defect in the genes which code for
lysosomal enzymes degrading the mucopolysaccharides.
and C
Common features of MPS are coarse facies,
• Type A: Usually presents in infancy. Child is apparently organomegaly (liver and spleen), skeletal involvement with
normal at birth and acquires milestones appropriately for central nervous system features - they can also have
the age. By 8–10 months of age the child starts having corneal clouding, developmental delay and
loss of milestones with organomegaly and mucopolysacharoiduria. There are different sub-types of
lymphadenopathy. The disease progresses to death by 3 MPS - Hurler, Hunter, Scheie, Sanfilippo, Morquio,
years. Maroteaux-Lamy and Sly.

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 Section - B: Systems

CHAPTER
43
Inborn Errors of Metabolism
Dr. Uma Maheshwari

Introduction In India, the prevalence of IEM is one in 2497 newborns,

and in Andhra Pradesh, one in 1000 newborns. In the study
As communicable diseases are coming down, there is an
conducted in Hyderabad, the incidence of amino acid
increase in the burden of non-communicable diseases
disorder (protein metabolism) was 1 in 3600. In a study
including disorders of inborn error of metabolism (IEM).
conducted in Mumbai, the incidence was 1 in 1300.
Due to increase in healthcare facilities and diagnostic
facilities, metabolic conditions are being recognized What are inborn errors of metabolism (IEM)?
increasing in symptomatic babies. Though individually these
IEM are inherited disorders in which the body cannot
C H A P T E R - 43

disorders are rare, collectively they are common. The exact

properly turn food (protein, carbohydrate, lipid) into energy
incidences of these disorders in India are not known. In
due to deficiency of enzyme or its co-factor. The consequence
view of high consanguineous marriage and endogamous
of enzyme deficiency is depicted in the Figure 43.1.
population in India, these disorders are expected to be high.

Fig. 43.1 Theoretical consequences of an enzyme deficiency

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 43. Inborn Errors of Metabolism

When to suspect IEM? Eg. Pyruvate dehydrogenase def, pyruvate carboxylase def,
mitochondropathy
Advances in diagnostic facilities including Tandem mass
spectrometry (TMS), gas chromatography and mass Peroxisomal disorders
spectrometry (GCMS), and high performance liquid Presentation: Seizures, hypotonia, dysmorphism, cholestasis,
chromatography (HPLC) increase the chance of detection renal cysts, ocular abnormalities
of these disorders. It is imperative for the clinicians to
Eg. Zellweger syndrome
understand the ways to manifest IEM and when to suspect
these disorders so that appropriate management could be Lysosomal storage disorders
carried out. It is not only important for the treatment of Presentation: Presents with hepatomegaly, corneal clouding,
index child (affected child) but also important for predicting abnormal retinal pigmentary changes
the recurrence risk and genetic counseling as most are Eg. Mucopolysacchradosis
inherited as autosomal recessive disorder with 25%
recurrence risk.
Manifestation of IEM (System wise)
IEM can be broadly classified as:
CNS
1. Disorders that result in toxic accumulation
Acute metabolic encephalopathy: Presents with poor
(Micromolecule like amino acid, organic acid or
feeding, lethargy, seizures, coma urea cycle disorder, organic

C H A P T E R - 43
macromolecule like lysosomal storage disorder)
academia, biotinidase deficiency, MSUD.
2. Disorders of energy production/ utilization
Metabolic seizures: Occur with or without
Disorders that result in toxic accumulation encephalopathy. Characteristics of isolated metabolic
• Disorders of protein metabolism (e.g., amino seizures include seizures beginning prepartum, refractory
acidopathies, organic acidopathies, urea cycle defects) to conventional antiepiletics, progressive worsening clinical
and EEG abnormality and EEG indicative of burst
• Disorders of carbohydrate intolerance suppression, pyridoxine dependent seizures, cerebral folate
• Lysosomal storage disorders deficiency, molybdenum co factor deficiency, sulphite
oxidase deficiency, serine synthesis defect.
Disorders of energy production/ utilization
Neuroimaging: MRI indicative of brain atrophy, basal
• Fatty acid oxidation defects
ganglia lesions, cyst or dysgenesis and MRI indicative of
• Disorders of carbohydrate utilization, production (i.e., HIE without hypoxic insult at delivery.
glycogen storage disorders, disorders of gluconeo-
Developmental delay: 3-13% of children diagnosed to
genesis and glycogenolysis)
have developmental delay of unknown etiology are found
• Mitochondrial disorders to have treatable IEM.
• Peroxisomal disorders Cerebral palsy: Spasticity without evidence of perinatal
The presentations are summarized in the following table: asphyxia can occur in IEM.

Intoxication Other presentations: Dystonia, movement disorders,

ataxia, dementia, behavioral disturbance, stroke, hypotonia,
Presentation: Poor feeding, lethargy, respiratory distress, and neuropathy.
seizures after an initial symptom-free period
CVS
Eg. Protein metabolism
Cardiomyopathy: Occurs due to energy failure or other
• MSUD (Maple syrup urine disease)
causes.
• MMA, IA, PA (Organic acidemias)
Energy failure
• Disorder of urea cycle
• Fatty acid oxidation
Primary energy metabolic defects
• Mitochondriopathy
Presentation: Seizures, hypotonia, lactic acidosis, and other
systemic manifestations – Liver disease, cardiomyopathy, Others
cataract, hearing loss and renal tubular defects; May occur
without symptom-free period
• Pompe disease

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 Section - B: Systems

CHAPTER
44
Short Stature
Dr Dhivyalakshmi

Introduction Growth curve (Fig. 44.1) is a sigmoid shaped curve (bold

line). This is due to rapid growth occurring in infancy (dotted
Growth is defined as increase in the physical size of the
line), followed by a slow decelerating childhood growth
body as a whole or any of its parts associated with increase
(dotted line) and height spurt during puberty.
in cell number (hyperplasia) or cell size (hypertrophy).
Growth of child depends on interplay of various factors Normal growth rates in children: (Rules of "5")
starting from prenatal/fetal period to puberty. The following (See figure 44.3)
algorithm represents the various factors involved in growth.
Note: Pubertal height spurt occurs in Tanner stage 2 (breast)
C H A P T E R - 44

for girls and Tanner stage 4 (testicular volume) for boys.

Definition of short stature:
Short stature is classically defined as height below -2 SD
for age and gender within the population, or height below -
2 SD below the midparental target height.
Other definitions:
(i) Abnormally slow growth velocity (less than 25th
percentile on height velocity charts)
or
(ii) Height dropping across two major centile lines on the
growth chart
Dwarfism refers to more severe short stature, defined as
height below -3 SD for age and gender norms.

Fig. 44.1 Growth curve

Fig. 44.2 ICP (Infancy - childhood - puberty) model of somatic growth

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 44. Short Stature

Fig. 44.3 Normal growth rates in children

Causes of short stature:

C H A P T E R - 44

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 59. Radiology

CHAPTER
59
Dr. Lakshmanan Sakthikumar
Radiology Dr. Abinaya, Dr Latha M S
Dr. Vilvanathan V

General Points About Chest X-ray CONGENITAL DIAPHRAGMATIC HERNIA OF

The factors to be looked into in a chest x-ray are: NEWBORN
1. Technical data
• Right/Left marker
• Centering
• Penetration
• Depth of inspiration
2. Bones and soft tissues
3. Diaphragm
4. Lungs
5. Mediastinum
6. Upper abdomen
The Zones used in the chest x-rays do not represent the
lobes:
• Zone I - Extends from the apex of the lungs to a line
drawn through the lower borders of the anterior ends of

C H A P T E R - 59
the second costal cartilage.
• Zone II - From the 2nd to the 4th costal cartilage
• Zone III - Below the 4th costal cartilage
FIg. 59.1 Coils of air filled small bowel are seen in the left
The other terms used in a chest x-rays are: hemithorax with mediastinal shift to the right, the left dome of
• Opacity (homogenous or heterogeneous) the diaphragm is not seen.
• Hyperlucency (mention about lung markings)
• Emphysematous
Always comment on the following:
• Cardiophrenic angle
• Costophrenic angle
• Trachea
• Mediastinal shift

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 Section - C: Viva Voce

CONGENITAL CYSTIC ADENOMATOID MALFORMATION

FIg. 59.2 X-ray and CT show multiloculated cystic masses with a mediastinal shift
Differential Diagnosis includes: Cystic pulmonary airway malformation (CPAM), sequestration, congenital
diaphragmatic hernia.
BRONCHIECTASIS CT Chest BRONCHIECTASIS
C H A P T E R - 59

Fig. 59.3 Bronchiectasis (bronchial dilatation, signet ring sign)

in bilateral lower lobes (arrows).

FIg. 59.4 Hyperinflated lung fields, bronchopenumonia, dilated

bronchioles & marked linear streaking (railroad tracks) are
seen

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 59. Radiology

PULMONARY INTERSTITIAL EMPHYSEMA (PIE) LUNG ABSCESS

FIg. 59.5 Coarse opacities and small circular lucencies are seen
in both the lungs.
PIE is a complication of surfactant deficiency and mechanical
ventilation. In PIE, air dissects into the pulmonary interstitium.
EMPYEMA

C H A P T E R - 59
FIg. 59.6 Right hydropneumothorax which was later found to
be empyema FIg. 59.7 CT and X-ray show the presence of a large lung
Empyema is more common than pleural effusion in children. abscess
The most common organism is S. aureus and the antibiotic
of choice is cloxacillin.

Scott’s Pedia-Tricks 605

 TENTH YEAR ANNIVERSARY SPECIAL EDITION

Scott's Fully
Revised

PEDIA-TRICKS 4 th

Edition

Written by the Students, for the Students

Highlights of the current edition
 Inclusion of new authors - we have attempted to include both the younger generation medical teachers
as well the senior experts in the field
 The contents have been arranged according to systems for easier navigation
 Chapters have been designed such that key concepts are highlighted
 Many chapters have been added, completely revised or rewritten

Chapters that have been revised and updated New chapters that have been added

 History taking and systemic examination chapters  Child with cholestasis

 Nutrition history  Fever with hepatosplenomegaly
 Development  Afebrile hepatosplenomegaly
 Cerebral palsy  Extra-hepatic portal venous obstruction
 Stroke in children  Hepatosplenomegaly with pallor - hemolytic anemias
 Ataxia in children  Undernutrition in children
 Down syndrome  Breast feeding
 Nephrotic syndrome  Acute glomerulonephritis
 Viva-voce section  Social programmes

New sections that have been added

 Respiratory system chapters A comprehensive guide

to pass the pediatric
 Essential genetics for exams
practical examination
 Inborn errors of metabolism for undergraduates and
 Endocrinology section postgraduates
 Infections section
 Rheumatology section

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ISBN: 9789386480408