XIV KKCTH MILLENNIUM ENDOWMENT ORATION AND
POST GRADUATE CLINICAL TRAINING IN PEDIATRICS
20-09- 2013 & 21-09-2013
Under the auspices of
The CHILDS Trust Medical Research Foundation (CTMRF)
Kanchi Kamakoti CHILDS Trust Hospital &
The CHILDS Trust Medical Research Foundation
Post Graduate Clinical training in Pediatrics
September 20, 2013 (Friday)
8 00 - 8.15 AM Registration
8.15 - 8.30 AM Overview of the program - Dr.S.Balasubramanian
8.30 - 9.30 AM Cyanotic heart disease - Dr.Nalini Bhaskaranand / Dr.Riyaz
9.30 - 10.30 AM Acyanotic heart disease - Dr Andal / Dr Srinivasan
10.30 - 10.45 AM Coffee break
10.45 – 12 noon Rheumatic heart disease -Dr.Srinivasan / Dr.Vasanthi
12.00 – 1.00 PM Neurodegenerative disorders —Dr.Rana /Dr.V.Viswanathan
1.00 - 2.00 PM Lunch
2.00 - 3.00 PM Hepatosplenomegaly (Hemato-oncology) - Dr.Riyaz / Dr.Janani
3.00 - 4.00 PM Chronic liver disease - Dr.V.S.Sankaranarayanan/Dr.R.Ganesh
4.00 - 5.00 PM Bronchiectasis - Dr.Subbarao/ Dr N.Suresh
5.00 - 6.00 PM Hemiplegia - Dr.Kumaresan / Dr.LalithaJanakiraman
6.00 - 7.00 PM Cerebral palsy- Dr Rana /Dr T.Ravikumar
Post Graduate Clinical training in Pediatrics
September 21, 2013 (Saturday)
8.00 - 9.00 AM Differential diagnosis in Pediatric Neurology: Dr Rana
9.00 - 10.00 AM Nutrition& Anthropometry- Must know areas:
Dr Nalini Bhaskaranand
10.00 -11.00 AM Differential diagnosis of Hepatosplenomegaly: Dr John Matthai
11.00 - 11.15 AM Coffee break
11.15 - 12 Noon Inauguration function
12.00 – 1.00 PM Millennium oration—“Pneumococcal disease-
Past, Present & Future”
Prof Adam Finn
Consultant in Pediatric Infectious Disease
Royal Bristol children’s Hospital, UK
1.00 -2.00 PM Lunch
2.00 - 3.00 PM Case analysis in Respiratory system: Dr Subbarao
3.00 - 4.00 PM Approach to congenital heart disease: Dr Srinivasan
4.00 - 5.30 PM OSCE--Dr BalaRamachandran, Dr K.G.Ravikumar,
Dr.Radhika, Dr.Rahul Yadav
5.30 - 6.00 PM Feedback & wrap up
Dr Jayanthi Ramesh
Dr Lalitha Janakiraman
Dr S. Srinivas
Mr.Karthik Narayanan, Chairman,KKCTH
Dr.K.MathangiRamakrishnan, Chairman, CTMRF
Dr A.Andal, Medical Director, KKCTH
Finance & Administration
This book contains the academic materials covering the common clinical exam topics
in Pediatric Medicine. This material is prepared based on the information from the standard
Textbooks. However there is absolutely no assurance that any statement contained in this
material is precise, or up-to-date. Neither the individual contributors, nor anyone else
involved in the preparation of this material take responsibility for any errors in the text on this
material. We strongly recommend the readers to refer standard Textbooks in Pediatrics
On behalf of the CHILDS Trust Medical Research Foundation (CTMRF), I wish to
extend my hearty felicitation and best wishes to the organizing committee and the
participants of the “Millennium oration - Pneumococcal disease - Past, Present &
Future” to be held on 21st
I hope that this programme will help the delegates to update and enrich their
knowledge on Pneumococcal disease, a common and serious infection of childhood and it is
of utmost important for all pediatricians and pediatric postgraduates to keep up with recent
updates about this infection.
I also hope that the informative material in this sourvenir will be of immense help to
pediatric postgraduates in particular.
I wish the CME a grand success.
List of Millennium Orations
First Commemoration Oration & Seminar in Pediatric Neurology
02.10.2000 Newer Perspectives in Pediatric Neurology
Guest Oration given by Dr. Prem Puri
Our Lady’s Hospital for Sick Children,
Venue Hotel Chola Sheraton
Second KKCTH Commemoration Oration
02.10.2001 CME on Pediatric Gastroenterology
Guest Oration given by Prof V.I.Mathan,
Gastroenterologist & Senior Consultant,
UNAIDS / NACO, Bangladesh
Venue Hotel Savera
Third KKCTH Commemoration Oration
02.10.2002 CME & Refresher Update of Laboratory Medicine
in Pediatric Practice
Guest Oration given by Dr Kusum Verma,
Prof & Head, Dept of Pathology,
AIIMS, New Delhi
Venue Hotel Savera
Fourth Millennium Guest Oration
02.10.2003 Advances in Pediatric Surgery
Guest Oration given by Prof. Arnold G.Coran,
Prof. of Surgery &
Head of Section of Ped. Surgery
University of Michigan Medical School, USA
Venue Hotel Taj Connemara
Fifth Millennium Guest Oration
02.10.2004 National CME on Pediatric Critical Care
Guest Oration given by Dr. Brain Anderson,
Associate Prof. of Anaesthesia
Hospital, Auckland, New Zealand
Venue Hotel GRT Grand
Sixth Millennium Guest Oration
11.05.2005 Advances in Pediatric Surgery
Guest Oration given by Prof Klass N.Bax, Prof of Pediatric Surgery
Dept. of Ped. Surg., Wilhelmina Children’s
Hospital, University Medical Center Utrecht,
Venue Hotel Taj Coromandel
Seventh Millennium Oration & National CME on Pediatric Cardiiology
12.11.2006 Cardiac Surgery in Developing Countries
Guest Oration given by Dr.K.M.Cherian,
Cardio Thoracic Surgeon,
Frontier Lifeline Ltd, Chennai
Venue Hotel GRT Grand Days
Eighth Millennium Oration
03.12.2007 Cardiac Surgery in Developing Countries
Guest Oration given by Prof.Boix Ochoa
Professor in Pediatric Surgery,
University Barcelona, Spain
Venue Hotel Taj Coromandel
Nineth Millennium Oration & National CME
05.10.2008 National CME on Metabolic and Growth disorders
Guest Oration given by Dr.A.V.Ramanan
Consultant Pediatric Rheumatologist and
Hony. Senior Lecturer, University of Bristol,
Venue Hotel GRT Grand
Tenth Millennium Oration & National CME
04.10.2009 Clinical Approach to difficult problems
Guest Oration given by Prof.Y.K.Amdekar, Mumbai
Venue Hotel GRT Convention Centre
Eleventh Millennium Oration
03.10.2010 Bone Marrow Transplant
– Past, Present and Future
Guest Oration given by Prof.Anupam Sachdeva
Hemato Oncologist, Delhi
Venue Hotel GRT Convention Centre
Twelveth Millennium Oration
05.10.2011 State of the World’s Children
Guest Oration given by Prof Frank Shann
Prof. of Critical Care Medicine
Royal Children’s Hospital
University of Melbourne, Australia
Venue Hotel GRT Convention Centre
Thirteenth Millennium Oration
07.10.2012 Tuberculosis in Children – Past, Present & Future
Guest Oration given by Prof. S.Mahadevan
Venue Hotel GRT Convention Centre
Sl.No. Topic Page No.
01 Developmental Assessment 1
02 Cerebral Palsy 3
03 Acute flaccid paralysis 7
04 Aucte infantile Hemiplegia 11
05 Floppy Infant 16
06 Hydrocephalus 19
07 Neurodegenerative Disease 22
08 Tuberculous Meningitis 25
09 Rheumatic Heart Disease 28
10 Cyanotic Congenital Disease 31
11 Protein Energy Malnutrition (PEM) 33
12 Neonatal Cholestatsis 38
13 Hepatosplenomegaly with Anemia 44
14 Thalassemia 49
15 Approach to Short Stature 51
16 Approach to a child with rickets 58
17 Bronchiectasis 60
18 Tips to Post Graduates 62
Post Graduate Clinical Training in Pediatrics  Page 1
Dr. Ganesh, Dr.Suresh
Consulting Paediatrician KKCTH
Item/Age Gross motor Fine motor & vision Social Hearing &
6 weeks • Grasp reflex • Social smile • Cooing
3 months • Head control • Recognises
• Turns head to
4 months • Reaches for
7 months • Rolls over
• Sits with hands forward
• Palmar grasp
• Transfers objects
• Smiles at mirror • Babbling
10 months • Sits without support
• Pivoting-turns round to
pick up a toy without
• Pincer grasp • Waves bye-bye
• Plays pat-a cake
• Uses amma,
1 year • Can rise to Standing
• Walks alone
• Walks holding on to
• Bottom shuffling
• Holds two cubes
• Pincer grip
• Waves bye-bye
• Plays pat a cake
• Asks for objects
• Drinks from cup
• Turns to name
• Tells 2 words
1 ½ years • Goes upstairs & down
stairs using hand
• Carries toys while
• Walks backwards
• Kneels without support
• Makes tower of 3
• Turns 2-3 pages in
a book at a time
• Dry by day
• Holds spoon-takes
food to mouth
• Solitary play(
• Obeys simple
Close the door
• Points to parts
of the body
2 year • Goes upstairs & down
• Kicks the ball
• Makes tower of 6
• Copies vertical
• Turns page in a
• Turns door knob
• Unscrews lids
• Feeds with spoon
• Wears shoe and
• Gives name
• Obeys two step
the toy and put
in the basket)
Post Graduate Clinical Training in Pediatrics  Page 2
Item/Age Gross motor Fine motor & vision Social Hearing &
2 ½ year • Tip toe walking
• Copies horizontal
• Makes tower of 7
• Makes train
• Pretends play
• Names one
3 year • Goes upstairs -1
foot/step & down
• Pedals tricycle
• Stands on one foot for
• Can copy a circle
• Constructs a
• Begins to draw a
• Can construct a
block tower of ten
• Can thread large
beads on to a
• Cuts paper with
• Eats with fork and
• Dry by night
• Dresses and
• Knows own
name, age, and
• Knows some
• Names 3 colors
4 year • Stands on one foot for
• Walks heel-toe
• Goes upstairs & down
• Copies cross and
• Draws a man with
• Copies gate(6
• Threads small
• Dresses without
• Knows own
• Names 4 colors
5 year • Skips • Copies triangle
• Makes 10 cube
• Uses knife and
• Knows own
Post Graduate Clinical Training in Pediatrics  Page 3
Name : Age : Sex :
Not attained age appropriate mile stones since early infancy
Description of compliants.
Describe all 4 developmental domine important mile stones achieved by the child
o Gross motor
o Fine motor
o Social and adaptive mile stones.
Stiffness or floppiness of limbs
Convulsions - Generalised tonic clonic / myoclonic / focal /Infantile spasms.
Detailed birth history.
o Antenatal period - maternal drugs, Xrays, illnesses-like rash , PIH ,DM , fall
Milestone History Gross motor, fine adaptive, social, language (with rough DQ to
- Dystonia, tremors, chorea, dyskinesia.
- Limb dyskinesia , oromotor dyskinesia, jark in the box tongue.
Cranial nerve history:
Blindness (cortical/optic atrophy) / Squint / facial deviation / pseudobulbar palsy
(regurgitation, nasal twaning,) / tongue atrophy
Sensory symptoms: pain while vaccination/hot and cold water differentiation
Bladder, bowel involvement.
Post Graduate Clinical Training in Pediatrics  Page 4
For etiology :-
Birth details :Antenatal Infections, twins , trauma, drugs
Neonatal sepsis, kernicterus
Meconium, asphyxia, hypoglycemia.,NICU stay
Post meningitis / trauma.
Family history :-
Any neurological illness / convulsion in any sibling / family
any sibling deaths, any CPs in family.
H/O Complication :-
Feeding difficulty /constipation
Contractures, bed sores behavioral problems, injuries, falls.
H/O Treatment :-
Immunization:- ?? DPT
Detailed dietary history type of food, swallowing difficulties,
regurgitation, spitting, weight gain.
Anthropometry with interpretation
o Cataract, strabismus,
o Skull - Overriding of sutures.
o Shape of skull
o Anterior Fontanelle
o Neurocutaneous markers
o Eyes - cataract
Evidence of. malnutrition , bed sores, contractures - static/ dynamic
Post Graduate Clinical Training in Pediatrics  Page 5
• Higher Functions
• Cranial nerves
• Tone power reflexes
• Exaggeration of reflexes:- afferent spread. (Knee Jerk on tapping thigh)
efferent spill over (crossed adductor on knee jerk)
• Development :- supine, prone, pull to sit, ventral suspension, axillary
• Neonatal reflexes
• Fundus examination – choreoretinitis / optic atrophy / retinitis pigmentosa
• Primitive reflexes
Other systems (organomegaly/ murmurs)
Name-------------, aged---------- has static encephalopathy/ Spastic or
dyskinetic or atonic CP /hemiplegia or quadriplegia/microcephaly /seizures/Cranial
nerve dysfunction – squint, cortical visual blindness, hearing deficit, pseudo-bulbar
palsy,/with Gross motor functional classification of ---------/ with learning
disability/recurrent LRTI/ PEM / Contractures (dynamic or fixed) with probable
Post Graduate Clinical Training in Pediatrics  Page 6
Commonly asked questions :-
1) Early markers of CP
2) Functional grades of CP
3) Neonatal reflexes
5) MRI correlates in CP
6) Development - gross motor, fine motor, speech ,social
7) Drugs & Surgical procedure to reduce spasticity
8) Associated problems
9) What do you mean by perinatal depression
10) What is birth asphyxia
11) What are significance of primitive reflexes
12) What are differences between primitive reflexes and postural reflexes
13) What are poor prognostic indicators
14) Stages of kernictirus
15) Causes for feeding difficulties
Post Graduate Clinical Training in Pediatrics  Page 7
Acute flaccid paralysis/Guillian Barre Syndrome
Name : Age : Sex :
History of weakness in limbs :
• Unilateral /Bilateral weakness of limbs
• Bilaterally symmetrical or asymmetrical weakness
• Where does it start: From lower limbs and progresses upwards or vice versa
• Sudden or insidious onset
• Proximal or distal weakness
• Involvement of upper or lower limb
• Involvement of respiratory muscles: anxious expression, difficulty in breathing,
inability to speak without frequent pauses
• Involvement of bulbar muscles-pooling of secretions in mouth, nasal
regurgitation/nasal twang, dysphagia,dysarthria
Associated history/-ve history:
• Higher function abnormalities (sensorium, speech)
• Cranial nerve deficit:
o facial asymmetry,drooling saliva from angle of mouth(VII N);
o nasal twang,regurgitation (IX,X N)
o diplopia,eye movements (III,IV,VI N)
• Sensory disturbances-tingling, numbness, pain.
• Abnormal gait / posture( tripod sign)
• Bladder/bowel disturbance
• Autonomic disturbances : flushing, sweating, palpitations, postural hypotension
• Ataxia, involuntary movements
• Wasting of muscles
• History suggestive of increased intracranial pressure
Post Graduate Clinical Training in Pediatrics  Page 8
• Diarrhoeal /upper respiratory illness weeks prior to paralysis----GBS
• Immunisation -OPV, IM injection & fever prior to paralysis –(-Polio )
• Previous history or familial history of Paralysis - Periodic paralysis
• Throat pain, dysphagia,neck swelling(bull neck)---Diptheria
• Consumption of honey/tinned food ( botulism)
• H/O drug intake – vincristine, vinblastine
• H/O pica (heavy metal intoxication (lead))
• H/O trauma to spine
• H/O polyuria / polydipsia / weight loss (DM)
• H/O fever with exanthem(herpes, mumps, rubella, entero/ EBV)H/O pain swelling
Birth, Immunisation history (especially OPV),
Developmental, dietary history
Decubitus especially of lower limbs—Demonstrate flaccidity
Vital parameters: Heart rate, Blood pressure for autonomic dysfunction
Throat---patch for diphtheria
Anthropometry with interpretation
Blue line on gums, NC markers
• Drooping of shoulder s/o diaphragmatic paralysis
• Thickened nerves
• Reflexes Superficial – important as in case of transverse myelitis for level of the
• Signs of meningeal irritation
Post Graduate Clinical Training in Pediatrics  Page 9
Features suggestive of GBS are
• Ascending weakness, symmetrical involvement
• Lower limbs involved before upper limbs
• Proximal involvement earlier than distal
• Weakness progressing over days to weeks with peak maximally at 4 weeks
• Deep tendon reflexes absent even before paralysis.
• Cranial nerves: common VII nerve
• If abnormal gait(ataxia) with eye movements impaired (opthalmoplegia)---
Miller Fischer variant
• Bladder distension
• Involvement of respiratory muscles: increased respiratory rate , movements of alae
nasi and other accessory muscles of respiration, inability to cough or sniff with full
depth, Single breath count .Paradoxical abdominal movements due to diaphragmatic
immobility. Deltoid paralysis suggests impending respiratory paralysis
• Observation of patient’s capacity for thoracic breathing while abdominal muscles are
• Light manual splinting of thoracic cage helps assessment of diaphragmatic movts.
• PA see for phantom hernia on abdominal wall ( polio)
• CVS muffled heart sounds (viral myocarditis, diphtheria)
Post Graduate Clinical Training in Pediatrics  Page 10
Diagnosis : Differential diagnosis of GBS - shown in the table below
Traumatic neuritis Transverse myelitis
24 to 48 hours onset
to full paralysis
From hours to 10
From hours to 4 days From hours to
Fever at onset High, always present
at onset of flaccid
paralysis, gone the
Not common Commonly present
before, during and
after flaccid paralysis
and affecting only one
Acute, lower limbs,
Muscle tone Reduced or absent in
Global hypotonia Reduced or absent in
Acute, lower limbs,
Sensation Decreased to absent Globally absent Decreased to absent Absent in lower
backache, no sensory
palms and soles
Pain in gluteus,
Anesthesia of lower
limbs with sensory
Only when bulbar
VII, IX, X, XI, XII
Only when bulbar
In severe cases,
Rare Frequent blood
Normal Normal or mild in
Absent Transient Never Present
horn cell disease
(normal during the
first 2 weeks)
Normal or abnormal,
no diagnostic value
EMG at three
Abnormal Normal Normal Normal
and up to a
atrophy of distal
only in affected lower
atrophy after years
Post Graduate Clinical Training in Pediatrics  Page 11
ACUTE INFANTILE HEMIPLEGIA
Name : Age : Sex :
Consanguinity : Handedness :
Paucity of movements of right/left side of the body.
Progressive/ static/ improving
Involving the upper limb preferentially/equally
Detailed H/O CNS involvement –
H/O weakness, proximal/distal
H/O sensory involvement
H/O Cranial nerve involvement
H/O involuntary movements
H/O bladder / Bowel involvement
H/O speech abnormality
H/O gait abnormality
Bed sores/shortening of limbs/contractures /trophic ulcers
H/o Trauma - Head injury/Oral cavity injury
- Fracture (Fat embolism)
H/O pain in hand/foot/ abdomen (sickle cell crisis)
H/O bleeding from any site/petechae/purpura/ hematemesis / malena
H/O Fever/ bone pain /weight loss (leukemia)
H/O diarrhea/ vomiting oliguria/ hematuria (HUS) or, history of
Post Graduate Clinical Training in Pediatrics  Page 12
H/o fever with chills/ petechiae/hematuria (Infective Endocarditis)
H/o cyanosis /cyanotic spell (Cyanotic heart disease) (abscess/
H/o fever with joint pain/sore throat (Rheumatic)
H/o Cardiac surgery (Prosthetic heart valve)
H/o Hypertension-Headache/ Vomiting/Visual Disturbance
Collagen Vascular Disease
H/o fever with rash with joint pain (SLE)
H/O Claudication (Takayasus)
H/O sore throat (Pharyngeal abscess)
H/O Koch’s/Koch’s contact
H/O Viral exanthems (HSV Encephalitis/ mumps/chicken pox)
H/O Otorrhoea (brain abscess)
H/O Vaccination/ sera (Demyelination)
H/O Acute Gastroenteritis followed by seizures/ coma
(sagittal sinus thrombosis )
H/O recurrent attacks of TIA /hemi paresis
H/O post seizure transient paralysis (Todd’s paralysis)
H/O similar attacks in the family (Sickle cell/ homocystinurea/Hyperlipidaemia)
Preterm-Subependymal Hemorrhage-Intraventricular hemorrhage
Full-term- Breech/ Traumatic delivery/Birth Asphyxia
H/O Umbilical sepsis / Catheterization (Embolism)
H/o Rash/ fever/ petechae/jaundice (IU infection)
Post Graduate Clinical Training in Pediatrics  Page 13
General Examination-Routine examination plus look for dysmorphic features
Carotid pulses should be palpated as well as auscultated(Moya Moya,Takayasu)
US/LS & Length (homocystinurea)
Petechiae/Purpura/ Joint bleed/ Rash
Skull-Trauma/Crack pot/Bruit over the skull.
Higher Functions- Speech (dysphasia seen in involvement of dominant hemisphere)
Intellectual impairment (Meningitis, Encephalitis, Homocystinurea)
Gait (older child)/Gross motor assessment (infant)
Cranial nerve examination (3,4,6 ,7th
& gag reflex)
Motor examination -Tone/Power/Reflexes
Abdominal Reflexes & Plantars
Visual fields for field defects& partial visual neglect (A field defect infers a lesion at
or above the internal capsule)
Higher Centers-Test for dysphasia/ Agraphia/ astereognosis/ two point discrimination,
tactile localisation (these occur when the dominant side is involved)
1. Higher mental function
2. Cranial nerves
3. Motor system
Post Graduate Clinical Training in Pediatrics  Page 14
d. Involuntary movements
4. Sensory system
5. Meningeal signs
6. Spine and cranium
7. Primitive reflexes
LOCALIZATION OF THE LESION IN CASE OF ACUTE INFANTILE
A) If the cranial nerve palsy is on the same side as that of hemiplegia then the lesion is
above the level of brain stem-Ipsilateral hemiplegia
B) If the cranial nerve palsy is on the side opposite to that of hemiplegia then the lesion
is at or below the brain stem.-Contralateral hemiplegia
The lesion is either in the cortex , internal capsule or sub cortical region
A) Cortical lesion-
Hemi paresis-Mild involvement & not dense hemiplegia
Differential involvement (Upper limbs more than lower or lower limbs more
Altered sensorium may be present
Convulsions may be present
Cortical sensory loss may be present
Aphasia (if the dominant cortex is affected)
Involvement of the frontal lobe
o Altered behavior/personality
o Upper limb affected more than lower limb
o Motor aphasia
o Bladder/ bowel involvement
o Persistent neonatal reflexes on the opposite side
Post Graduate Clinical Training in Pediatrics  Page 15
Involvement of the parietal lobe
o Cortical sensory loss
Involvement of the Temporal lobe
o Temporal lobe epilepsy
o Sensory aphasia
o Memory loss
Involvement of occipital lobe
o Homonymous hemianopia
B) Internal capsule lesion
C) Subcortical lesion(Corona Radiata)
Same as cortical lesion but features such as convulsions & loss of cortical
sensation are absent
CONTRALATERAL HEMIPLEGIA- Lesion at or below the level of brain stem
A) Lesion in Midbrain
WEBER SYNDROME- 3rd
nerve palsy plus crossed Hemiplegia
nerve palsy + crossed hemiplegia +
Red nucleus affected (Tremor, rigidity, ataxia on the opposite side)
B) Lesion in Pons
MILLARD GUBLER SYNDROME-7th
nerve palsy +Crossed hemiplegia
nerve palsy + 7th
nerve palsy + contra lateral
C) Lesion in Medulla
nerve palsy + crossed hemiplegia.
Post Graduate Clinical Training in Pediatrics  Page 16
• Delayed motor and/ or mental milestones.
• Weakness of all 4 limbs and limpness noticed since birth.
• Abnormal posturing / contractures / arthrogyphosis.
ELABORATION OF C/C.
• H/O unilateral/ bilateral weakness of limbs, symmetrical or asymmetrical, sudden
onset /insidious,starting from lower limb and progressing upwards or vice versa. .
• Head holding achieved/ partial.
• H/O frog like posture
• H/O weak cry, h/o feeding difficulties
• H/O repeated cough/ cold/fever/ breathlessness
• H/O facial asymmetry, pooling of secretions,nasal regurgitation/nasal
twang,dysphagia(involvement of bulbar muscles)
• H/O sensory disturbances.
• H/O wasting of muscles, H/O fasciculations / fibrillations.
• H/O bladder/ bowel disturbances
• H/O exaggerated startle (Taysach’s)
• H/O Icterus, phototherapy, exchange transfusion (kernicterus)
• H/O constipation, prolonged neonatal jaundice (if MR, coarse facies for
• H/O cyanosis/ altered sensorium(respiratory muscle involvement)
• H/O mental development(hypotonic CP)
• H/O viral infection/ascending weakness(GBS)
• H/O recent vaccination /ring/ pulse polio
Post Graduate Clinical Training in Pediatrics  Page 17
• H/O flushing/sweating/ palpitation/ postural hypotension/ arrhythmias
• H/O maternal myasthenia like illness
• H/O diurnal variation (mysthenia gravis)
• H/O lump in abdomen,early morning hypoglycaemic convulsions with
breathlessness(GSD – Pompe’s)
• H/O prelacteal feeds like honey followed by bulbar weakness (botulism)
• H/O nonprogressive proximal muscle weakness-----congenital myopathies
• H/O involuntary movements------congenital cerebellar ataxia
• H/O obesity - Prader Willi
• H/O cataract/ MR- Lowes
H/o decreased fetal movements, fever with rash, irradiation, drug exposure (lithium/
phenytoin/ carbamazepine). ,polyhydramnios / prolonged labour / LSCS.
PERINATAL HISTORY - breech presentation, h/o birth asphyxia, h/o limpness, feeding
difficulties, breathlessness, convulsions in neonatal period, neonatal hyperbilirubinemia.
FAMILY HISTORY - h/o deaths in infancy in sibling
MILESTONES - motor +mental
DIET & IMMUNIZATION- last vaccine given (for GBS/ polio)
Decubitus - pithed frog position.
HR----/RR------/ regular, abdominothoracic, no e/o resp. distress/BP--------
ANTHROPOMETRY with interpretation
Obesity,dysmorphic facies (Prader- Willi)
Downy facies – Trisomy 21/ Zellweger’s syndrome
Doll like faces – GSD (Pompe)
V shaped face- myotonic dystrophy
Pallor, clubbing, cyanosis, icterus, lymphadenopathy, oedema feet
Post Graduate Clinical Training in Pediatrics  Page 18
Skull/ spine/ genitalia(hypogonadism in prader willi)
Conntractures ,CTEV, CDH
Higher functions---conscious, alert looking,recognizes others.
Ptosis with diurnal variation
Fundus---(cherry red spot in GSD type II)
Motor system- muscle wasting (SMA)
muscle hypertrophy(pompe/ congenital muscular dystrophy)
Hypotonia in all 4 limbs
Involuntary movements- ataxia, fasciculation/ fibrillation
Power--shoulder/ elbow/ distal/ hip/ knee/ distal
o Diaphragm/ intercostals
Superficial-------cremasteric/ gluteal/ paraspinal reflex
CVS-----cardiomegaly,murmur, abnormal heart sounds(pompe)
DIAGNOSIS--------month old child M/F gradually progressive/ static quadriparesis since
birth ,decreased fetal movements ,no MR, no significant pre/ perinatal events, generalized
hypotonia, areflexia, fasciculations. Most probable diagnosis
Post Graduate Clinical Training in Pediatrics  Page 19
Name : Age : Sex : DOB :
• History of progressive enlargement of head/large head noticed since (or)
• History s/o raised ICT (if the onset of hydrocephalus is more than 2 yrs (or)
• H/O abnormal eye movements (sunsetting / roving eye movements) (or)
• H/o developmental delay (or)
History of presenting complaints:
Abnormalities of higher functions - scholastic backwardness, altered sensorium,
History s/o cranial nerve palsy –diplopia,sunsetting.
History of blindness or hearing disturbance.
History of focal neurologic deficit.
H/S/O gait abnormalities (spastic gait with frequent falls)
History of bladder/bowel complaints
H/o involuntary movements
History of nausea/vomiting/head banging/headache.
History of occipital enlargement (Dandy Walker)
History of poor feeding/failure to thrive / stridor (nasal encephalocele)
ANTENATAL HISTORY - Infection (CMV, toxoplasma, mumps), Drugs-(vitamin A
toxicity-pseudo tumor), Irradiation , Antenatal detection, presentation
BIRTH HISTORY - Prematurity /Dystocia / PROM / Instrumentation
POST NATAL HISTORY – enquire - H /O trauma, H /O infection (meningitis), H/O
Koch’s contact, H/o prolonged hospitalization after birth, H/O hypo pigmented
macule with infantile Spasm ( Tuberous sclerosis), H/O swelling at the back &
Post Graduate Clinical Training in Pediatrics  Page 20
FAMILY HISTORY- In males Congenital aqueductal stenosis (XLR) ,
Any sibs having similar problem?
TREATMENT HISTORY – H/o treatment taken/shunt surgery
MILESTONES – delay OR regression?
Motor and mental milestones delayed. Weak head holding due to large head.
If there is neuroregression with large head then S/O ( Krabbe / Tay sachs, Alexander /
Canavan , Post TBM )
Diet history & socioeconomic history.
Vitals - BP (hypertension because of raised ICT)
Anthropometry with interpretation.
a) Head circumference & Shape of the skull noted- in terms of AP diameter, Biparietal
diameter, Frontal bossing& Occipital prominence.
b) Presence of dilated veins
c) Anterior & posterior fontanelle-(note their size, shape, borders, pulsation,tension in sitting
& supine position)
d) Sutural separation
e) Transillumination-more than 2 cm in frontal & more than 1 cm in Occipital (it is positive
only if the cerebral mantle is less than 1cm). It is positive in massive dilatation of the
ventricular system or in Dandy Walker syndrome.
f) Bruit over the head-It is positive in many cases of vein of Galen AV malformation.
g) Prominent occiput in Dandy Walker/post fossa tumor/arachnoid cyst
h) Flat occiput in achondroplasia/Arnold Chiary Malformation
Sunsetting (paralysis of upward gaze)
Spine-Neural tube defects. Look for tuft of hair
Post Graduate Clinical Training in Pediatrics  Page 21
Neurocutaneous markers-Hypo pigmented patches in Tuberous Sclerosis
Dysmorphic features/ coarse features.
Rhizomelic shortening (achondroplasia)
IU infection (Rash/lymphadenopathy/Hepatosplenomegaly/Cataracts)
Higher functions – sensorium, speech
Cranial nerves-Sixth nerve palsy, false localizing sign.
Vision & hearing
Motor -Spasticity is generally more in the lower limb than the upper limb.
Brisk jerks in the lower limb.
Gait-Truncal ataxia is seen in Dandy Walker.
Fundus- Papilledema , Optic atrophy, Chorioretinitis, Cherry red spot
Examination of spine
Shunt side, patency , Reservoir present or absent?
Post Graduate Clinical Training in Pediatrics  Page 22
Name : Age : Sex : DOB :
- loss of achieved mile stones
- progressive increase in size of head
- vision / hearing / speech regression
Narrative History :-
1. Convulsions :-
• Generalised tonic, clonic, myoclonic, tonic spasms, focal (convulsions suggest
that the disease involves grey matter degeneration)
• In certain epilepsy syndromes, convulsions are the hallmark which precede the
onset of regression.
o e.g. West Syndrome - Infantile spasms - Lennaux Gestaut syndrome - tonic
o Certain aminoacidopathies & organic acidurias patients / urea cycle defects
convulsions may be due to metabolic disturbances like hypoglycemia,
hyperammonemia etc )
o SSPE - Myoclonic jerks
2. Progressive dementia / personality changes-
o Scholastic backwardness - SSPE, HIV, encephalopathy Wilson’s disease.
o Behavioural changes - hyperactivity - sanfillipo, X linked ALD,
o Autistic behavioural - Autism, Rett's Syndrome
3. Loss of motor milestones
o eg. loss of head control, turning over.
o Period over which these milestones are lost in important.
o Progressive - Neuro degenerative disorders
o Sudden - Post encephalitis
o Mitochondrial disorders like MELAS
Post Graduate Clinical Training in Pediatrics  Page 23
White matter degeneration is characterised by focal neurological deficits / spasticity /
blindness or hypotonia (looseness of body).
4. Progressive disturbance of gait and co-ordination
- X linked Adrenoleuko dystrophy
- Progressive hydrocephalus
Focal neurological deficits - mitochondrial disorders
5. Vision problems :
1] Progressive loss of vision hydrocephalus, Tay sachs disease
Neuronal ceroid lipofuschinosis,
Wilson's disease ( Cataract)
2] Visual inattention - autistic spectrum disorders, Rett's syndrome
6. Speech abnormalities - Aphasia -
Expressive aphasia - Rett / autism
Dysarthria - cerebellar disorders ( Juvenile MLD)
7. Ataxia - MLD, ALD, Spasms mutan - pelizeus merchbacker
8. Involuntary Movements -
o Chorea, athetosis - Huntington , Wilson, pelizeus merchbacker
o Dystonia / Dyskinesis -
o Hand wringing, washing, tapping movement
o Sterotypy - Rett's syndrome
9. Increasing head size - progressive hydrocephalus, Alexander / Canavan
10. Sensory disturbances - trophic ulcers
o associated with peripharal neuropathy - MLD, INAD, krabbes
11. Progressive bulbar symptoms - feeding difficulties
12. H/o. Repeated vomiting, failure to thrive - neurometabolic disturbances
aminoacidopathies / organic acidemias
13. H/o. fever,, altered sensorium / convulsions Encephalitis
H/o. lethargy, constipation, neck swelling hypothyroidism.
14. H/o. Jaundice - Wilson's
15. H/o. Measles - SSPE
16. H/o. Self mutilation Lesch nyhan syndrome
Post Graduate Clinical Training in Pediatrics  Page 24
17. Family history of similor illness in other sib / sib death
18. Birth history
19. H/o. typical body / urine odor
20. H/o. complication - contractures / bedsore Repeated infections
21. Developmental history - Details of milestones - normal / delayed prior to onset
22. Diet history
23. Immunisation history
Temp. Pulse respiration BP
Anthropometry with interpretation
- size & shape of skull - overriding of sutures
- Anterior fontanelle
- Dysmorphic features - Grotesque features, Hypothyroid / MPS
- NC markers - Tuberous sclerosis, ataxia telengiectasia, café au lait spots
- Skin changes - Hypothyroidism - Xerodema pigmentosa
- Hair - menke's kinky hair
- Trophic ulcers - (peripharal neuropathy)
- Self mutilation - Lesch nyhan
- optic atrophy
- Cherry red spot
- Retinitis pigmentosa
- Central nervous system Examination
- PA - organomegaly
Post Graduate Clinical Training in Pediatrics  Page 25
Name Age Sex
1. Fever –
2. Convulsions :- focal / generalised seizures
3. Altered sensorium :- onset - sudden / insiduous.
5. Focal neurological deficit -
Hemiplegia / monoplegia / cranial neuropathies.
Complains in details.
H/o. Abnormality of higher functions - Lethargy, altered sensorium
Cranial nerve palsies - deviation of angle of mouth, drooling of saliva,
Focal neurological deficits ( hemiplegia /monoplegia).
Abnormal / involuntary movements tremors / chorea / hemiballismus
H/s/o increased intracranial pressure i.e. vomiting / headache / blurring of vision.
H/s/o meningeal inflammation i.e.neck pain, photophobia, restriction of neck
H/o bowel, bladder complaints.
History for etiology :-
H/o. head injury ( may precipitate TBM)
H/o. otorrhoea - (pyogenic meningitis )
H/o. any treatment taken outside in f/o intramuscular / intravenous injections
(Partially treated pyogenic meningitis)
H/o. vaccines / drugs / sera ( Acute disseminated encephalomyelitis)
H/o. rash, fever, altered sensorium, convulsions ( Viral encephalitis)
H/o. fever with rash (measles)
H/o. whooping cough.
Post Graduate Clinical Training in Pediatrics  Page 26
H/o. contact with tuberculosis.
H/o. diarrhoea, fever, chronic cough (HIV)
H/o. immunosuppressive drug intake.
Immunisation history – BCG , Measles.
History for complications :-
H/o bed sores, contractures, skin changes, bladder, bowel complications.
(constipation/ urinary infection )
H/o. decorticate / decerebrate posturing.
Drug history, procedure history.
H/o. any surgery, VP shunt / reservoir
Family history - of koch’s
Nutritional history - malnutrition may precipitate Tuberculous meningitis.
Birth History :-
Socio economic history - Overcrowding , sanitation.
General examination :-
2] Vitals - Temperature ,Pulse , Respiration , Blood pressure.
3] Anthropometry with interpretation.
4] Pallor, cyanosis, clubbing, icterus, lymphadenopathy, edema feet,
5] Stigmata of tubercolosis – Phlycten ,Scrofuloderma ,Sinuses, erythema nodosum
6] Anterior fontanelle
7] Size & heaviness of head
8] Crack pot sign
9] BCG scar - present / absent.
10] Neurocutaneous markers
11] Dysmorphic features
12] Presence or absence of IV line, Ryles tube
13] Skull, spine, scars
Post Graduate Clinical Training in Pediatrics  Page 27
14] Skin - bedsores
16] Signs of malnutrition & vitamin deficiency
17] Presence / absence & patency of VP shunt
Higher functions - state of conciousness
Corneal / conjunctival reflexes
Motor system examination
Hydrocephalus : Heavy head, crackpot or sutural seperation - Signs of increased
Fundus - papilloedema / choroid tubercules / optic atrophy.
---years old M/F child with chronic meningoencephalitis with / without
hemi / monoparesis with / without cranial nerve palsy with / without involuntary movement
with / without signs of increased intracranial pressure.
Probable etiology being TBM.
Post Graduate Clinical Training in Pediatrics  Page 28
RHEUMATIC HEART DISEASES
Four types of clinical scenarios usually present :
1. Acute rheumatic fever
2. Relapse /recurrence of acute rheumatic fever with chronic valvular heart disease.
3. Isolated Rheumatic valvular disease with H/o infective endocarditis
4. Combined chronic valvular disease
• H/o streptococcal pharyngitis –Fever , sorethroat - in the recent past (2-3 weeks back)
• H/o pallor, epistaxis , abdominal pain .
• H/o Joint pain, swelling, duration, joints involved,characteristics of pain and relief with
medications (arthritis),migratory or not
• H/o dyspnoea,palpitations easy fatigability ,exercise intolerance, chest pain, syncope ( s/o
• H/o skin rash, or nodes ( erythema marginatum , sub cutaneous nodes)
• H/o neurological symptoms- purposeless movements, emotional lability, ( Chorea)
• H/o complications ( PND, orthopnoea, hemoptysis, palpitations, syncope , edema ).
• S/o infective endocarditis (fever with chills,petechie, subcutaneous painful nodes ,
hemoptysis,hematuria ,skin lesions)
• H/o medications taken for fever and other symptoms .
• H/o previous similar such episodes,
• If RHD – h/o penidura injection – compliance & frequency .
• Family history of rheumatic fever / rheumatic heart disease.
• Immunization, dietary , development & socioeconomic status enquired .
General –Vitals, Growth parameters, Scars, Chest asymmetry, icterus, teeth- caries , lymph
nodes. Skin - erythematous rash & subcutaneous nodes over extensor surface of head, back
& limbs. Nails - pallor, clubbing, cyanosis. Joints - pain, swelling, tenderness & restriction of
Post Graduate Clinical Training in Pediatrics  Page 29
Cardiovascular examination –
Peripheral - Venous, major arterial pulses & Blood pressure (upper & lower limbs).
o Inspection – Scars, symmetry, apical pulsation
o Palpation – Apex position, point of maximal impulse (PMI), heaves,
(parasternal, substernal, apical) Thrills (Suprasternal, supraclavicular and over
precordium) Palpable S2- (pulmonary hypertension)
o Auscultation- (use diaphragm initially, then the bell)
Areas- Apex, parasternal border,pulmonary , aortic areas ( roll patient to
left to accentuate mitral murmurs).
o Heart sounds – intensity, splitting . Added sounds & Murmurs- systolic/
iastolic/ continuous – define intensity, character, grade , radiation of murmurs
& Variation of murmurs on sitting , inspiration and expiration.
Other Systems - Abdomen Liver – measure span, note pulsation and tenderness
Spleen – infective endocarditis
CNS Fundus and other signs of infective endocarditis.
Diagnosis - Investigations:
Sleeping pulse rate ( tachycardia - myocarditis/ CHF)
Complete blood count with ESR and CRP (Lab. Criteria)
Throat culture, ASLO – (second antibody titre/ rising titres if initial is normal)
Blood culture (if IE is suspected)
X ray chest for cardiomegaly, pericardial effusion and pulmonary oedema
ECG - PR interval and chamber enlargement
2 D Echo /CD– Status of cardiac –myocardial, valvular & pericardial involvement.
Differential Diagnosis for rheumatic fever- Arthritis - Juvenile Rheumatoid arthritis ,
Collagen vascular diseases, virus associated arthritis, Hematological disorders causing
Post Graduate Clinical Training in Pediatrics  Page 30
Commonly asked questions:
1. Jones criteria- original, modified, update and limitations of Jones criteria.
2. Conditions causing similar cardiac lesions:
3. Differentiation between rheumatic arthritis and rheumatoid arthritis .
4. Nonspecific criteria for rheumatic fever (abdominal Pain, anorexia, wt. loss, epistaxis,
pallor, chest pain,pneumonia , tachycardia)
5. Causes of diastolic murmur - Carey comb’s (active carditis) ,Flow murmur-severe
MR , Mid diastolic murmur of MS and AR murmur.
6. Differentiation between ARF and RHD.Signs of rheumatic activity .
7. Prognosis and sequelae of carditis, arthritis and chorea.
8. Causes of chorea and description of rheumatic chorea.
9. Surgical indications in various Rheumatic valvular heart disease.
10. Peripheral signs of Infective endocarditis and Aortic regurgitation.
11. Drugs for primary and secondary prevention of rheumatic fever if patient is allergic to
12. Other tests to prove streptococcal infection.
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CYANOTIC HEART DISEASE
a. Cyanosis age of onset,Distribution,precipitating and reliving factors.
b. Cyanotic spell frequency of episode, improving or worsening, drugs
c. Growth retardation/FTT
d. Dysmorphis facies conotruncal facies
e. History of vaccination due to association with Digeorge syndrome
(T cell def)
f. History of complication fever with altered sensorium (abscess)
g. Prolonged fever with chills and rigors IE
h. Older child syncope/chest pain/arthritis(gout)
i. Any iron supplementation
2. Antenatal history:
a. Mothers age Downs
b. Maternal drug intake
3. Development history
4. Dietary history
5. Immunization history: stress on T cell dependent vaccine
(ass. With Digeorge syndrome)
6. Family and socio economic history
7. Examination findings:
i. Precordial bulge
ii. Apical impulse will be normal in position
i. Parasternal heave
ii. Palpable murmurs
Post Graduate Clinical Training in Pediatrics  Page 32
i. P2 is delayed & soft ,it is inaudible
ii. S2 is single which is aortic component
iii. ESM at left 3rd
iv. Continuous murmur if collaterals / after shunt surgery
Diagnosis : case of cyanotic congenital heart disease/with decresed pulmonary blood
flow/single s2/no s/o CCF or IE/sinus rhythm/
Post Graduate Clinical Training in Pediatrics  Page 33
PROTEIN ENERGY MALNUTRITION (PEM)
Name: Age: Sex: Religion: Care taker: Address:
- Poor gain in weight / height
- Vomiting, loose motion
- Cough, breathlessness, cyanosis
- Difficulty in feeding, suck-rest-suck cycle
- Polyuria, Polydypsia
- Recurrent infections
- Questions should be asked pertaining to each system
- Age of expectant mother
- Maternal nutritional status
- Birth order, Birth weight
- Perinatal complications
- Calorie intake / day
- Protein gms / day
- Accurate assessment is difficult and good rapport with mother
- Assessment is done by a 24 hr recall method or a food frequency table, diet during
- Calculate calories and protein and calculate the calorie gap and protein gap as
compared to ICMR recommendation
H/O Breastfeeding ( to be taken in detail in infants )
- Time of initiation, duration, adequacy of breast milk.
- Breastfeeding to be continued till two years of life.
Post Graduate Clinical Training in Pediatrics  Page 34
- Breast milk is more advantageous as it is physiological, convenient, economical,
with optimum fluidity and warmth, besides being bio-chemically superior,
microbiologically sterile, immunologically safe, with psychological benefits of
ensuring mother-infant bonding.
- Epidemiologically breastfeeding decreases morbidity and mortality.
H/O Artificial / Top feeding
- Considered when either the mother is unavailable, critically ill or no more.
- Formula feeding / cow’s milk
-Dilution , bottle feeding. Over dilution and infection due to contamination are
common causes of malnutrition
- Weaning (meaning “to accustom to” ) / Complimentary feeding is started between
4 – 6 months of age. Breastfeeding must be continued during weaning.
- Preparation and storage of weaning foods should be done under hygienic
- Education of parents, occupation
- Monthly income, Housing, Sanitary facility
- Family size
- Toilet habits
- Safe drinking water
- Availability of electricity, recreation facility
- Kuppuswami scale – class I to V
- Closely spaced families,
- Working mother.
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On Examination –
1. Weight - Beam balance, electronic scale - simplest, most widely used, most reliable.
2. Height – Infantometer, stadiometer
3. US : LS ratio
4. MAC – between 1 –5 yrs of age, done on left arm midway between acromion &
olecranon. (<12.5 cms – severe PEM, 12.5 –13.5 – moderate PEM, >13.5 normal )
Not a good parameter for growth monitoring during 1 – 5 yrs of age.
5. Head circumference – maximum occipito frontal circumference
6. Chest circumference
7. Skin fold thickness
8. Somatic quotient – average of Wt, Ht head circumference, MAC expressed as % age
Age independent anthropometric indicators
1. The Bangle test – inner diameter of bangle of 4 cms crosses above elbow
2. The Shakir’s tape – green (13.5 cms), yellow ( 13.5 – 12.5 cms), red ( < 12.5 cms)
3. The Quac stick – Quacker’s arm circumference stick
4. Modified Quac stick
5. The Nabarrow’s thinness chart
6. The head circumference to chest circumference ratio ( > 1 - normal)
7. MAC to height ratio ( < 0.29 severe PEM , 0.32 to 0.33 - normal )
8. MAC to head circumference ratio 0.28 – 0.31 - mild PEM
0.25 – 0.279 - moderate PEM
< 0.249 - severe PEM
9. Ponderal index ( Wt / Ht3
) > 2.5 - normal
2.0 – 2.5 - borderline PEM
< 2.0 - sever PEM
10. Dughdale’s ratio ( Wt / Ht1.6
) > 0.79 - normal
< 0.79 - malnutrition
Post Graduate Clinical Training in Pediatrics  Page 36
11. Quatelet index ( Wt kg / Ht2
cm) X 100 > 0.15 - normal
12. BMI (Wt kg / Ht2
13. Mid arm muscle circumference - MAC – ( 3.14 X SFT) cm
Classification of PEM
(I) IAP classification (1972)
N - > 80 % (Wt for age – expected)
I - 71 – 80
II - 61 – 70
III - 51 – 60
IV - < 50 %
(II) Welcome Trust classification ( Boston Standard)
Wt for age ( % of Exp.) Oedema Type of PEM
60 - 80 + Kwashiorkor
60 - 80 - Under weight
< 60 - Marasmus
< 60 + Marasmic Kwashiorkor
(III) Gomez classification
Normal - > 90 %
deg PEM - 75 – 90
deg PEM - 60 – 75
deg PEM - < 60 %
(IV) Classification as per height for Age and Weight for age
Ht for age - Waterloo’s classification
Wt for age McLarein’s classification
Post Graduate Clinical Training in Pediatrics  Page 37
Ht for age Waterloo’s McLarein’s
Normal > 95 > 93
deg Stunting 90 - 95 80 - 93
deg Stunting 85 - 90 -
deg Stunting < 85 < 80
Wt for age Waterloo’s McLarein’s
Normal > 90 > 90
deg Wasting 80 - 90 85 - 90
deg Wasting 70 - 80 75 - 85
deg Wasting < 70 < 75
(V) WHO classification
Ht for age Wt for age HA & WH
> - 2 SD Normal Normal Normal
< - 2 SD Stunted Wasted Stunted & Wasted
Spectrum of PEM
- Kwashiorkor / Marasmus / Marasmic Kwashiorkor / Pre-Kwashiorkor/
- Nutritional dwarfing / Underweight /Invisible PEM
- Growth retardation
- Hair changes – Lack luster, thin , sparse ,Flag sign
- Hypochromotricia , Easily pluckable
- Skin changes-Hypo-pigmented, Hyper-pigmented, erythematous, jet black
- “Flaky paint dermatosis” , “Crazy pavement dermatosis”
- Eye Signs.- Pallor, xerosis, bitot's spot ,angular palpebreitis.
Post Graduate Clinical Training in Pediatrics  Page 38
- Mucosal changes- Glossitis, Stomatitis, chelosis
- Glands. -Parotid, thyroid gland enlargement
- Purpura or Bleeding
- Oedema – mooning of face
- Mental changes – Irritability, apathy
- Tremors – appear during treatment
- Hb, CBC, Platlet count, Priferal serum, RBS, BUN, S electrolytes, S protein, Alb,
CXR, MT, Urine – R & CS, LFT, RFT, CSF
Management …4 STEPS
- Resuscitation, Hospital care
- Prevention care
Treat medical emergencies
o What emergencies? Hypothermia, hypoglycemia, electrolyte disturbance,
sepsis , shock, dehydration, cardiac failure, Anemia
Achieve weight for height - How?
150-200Cal/actual weight , 3-4gm protein/actual weight , 150-165 ml fluid/ actual
weight and Multivitamins and minerals
Given as 2hrly feeds with a feed late night and early morning -Oral or gavage feeds
What type of feed?
Breast feeds, High energy milk
Isodense formulas ,Hyderabad mix, amylase rich food, Cereal pulse mix
Allow RDA as per ICMR recommendations
Supplementary through various national nutrition programmes…ICDS
Post Graduate Clinical Training in Pediatrics  Page 39
Prevent LBW babies….Antenatal care & Care of adolescent girls
NIMFES .. Nutrition, Immunization, Medical care, Family planning, Education,
NUTRITIONAL RECOVERY SYNDROMES
Gynecomastia, Parotid swelling, Hypertrichosis, Hepatomegaly, Ascites, Spleenomegaly,
Eosinophilia, "Kwashi shake" All are self limited but keep the baby under observation.
Commonly asked questions
Complications of PEM / Poor prognostic signs
National programmes in nutrition
Classifications of PEM
Nutritional recovery syndromes
Difference between marasmus / Kwashiorkor
Diet chart for PEM
To prevent malnutrition the “Three plank protein bridge”
by Jelliffe to prevent PEM
- Continue breastfeeding
- Introduce veg proteins
- Introduce animal proteins
Besides supplementary feeding, group eating and small frequent feeds.
Post Graduate Clinical Training in Pediatrics  Page 40
Name : Age : Sex : DOB :
Onset of Jaundice
Associated with high colored urine +/- clay colored stools (Obstructive jaundice)
Progressively increasing (organomegaly, Ascites)
Upper or lower abdomen
History of etiology
Maternal history of drug ingestion, jaundice / infection in pregnancy,
Neonatal umbilical catheterization
Associated skin rash, petechie, fever, cardiac disease
Full term or preterm
Family history of hemolytic anemia
History of complications
Bleeding from any site
Fundus for chorioretinitis
Signs for Vitamin Deficiencies
Post Graduate Clinical Training in Pediatrics  Page 41
Dysmorphic features (Chromosomal, Alagille)
Inspection : Localized bulge, distension (which quadrant is more affected)
Palpation : Superficial palpation: Guarding, tenderness, rigidity
o Hepatomegaly - Tender/Nontender
- Surface: Smooth/Nodular
- Span and Size
- Border: well felt/ sharp/diffuse
- Consistency: Soft/firm/hard
o Splenomegaly - Size (Grades of splenomegaly)
- Consistency: Soft/firm
- Splenic notch
Divarication of recti
Percussion: Shifting dullness/horseshoe dullness/fluid thrill. Puddle’s sign
Auscultation: Renal Bruit, Venous hum
Other systems: Cardiac murmur, hydrocephalus, Meningitis
Neonatal jaundice With/without hepatosplenomegaly,
With/without dysmorphic features
With/without associated anomalies
Most likely etiology being :
Neonatal Hepatitis / Biliary atresia / Inborn error of
Metabolism / Galactosemia/ Chromosomal disorder
Post Graduate Clinical Training in Pediatrics  Page 42
Special Etiological Tests Morphological
Other tests Histopathology
(Both of child and mother)
Test for Galactosemia
Thyroid function tests
Staining with HE
Jaundice in newborn
Conjugated jaundice Unconjugated jaundice
Infective: Viral :CMV, Rubella, Reovirus III, Hep B
Bacterial: E. Coli, Listeria,
Inherited : Niemann-Pick Type C, Galactosemia,
Alpa-1 antitrypsin deficiency, Biliary Hypoplasia (Syndromic),
Progressive intrahepatic cholestasis
Chromosomal Anomalies: Trisomy 13/18/21
Biliary atresia – Neonatal Hepatitis
Miscellaneous: TPN, Hypothyroidism, Maternal alcohol
Ingestion, Erythromycin estolate, Frusemide
Post Graduate Clinical Training in Pediatrics  Page 43
Proper nutrition and multivitamin supplementation in cholestatic doses
Vitamin K supplementation
Toxoplasmosis: Sulphamethaxazole, pyrimethamine
Galactosemia: Galactose free diet
Biliary Atresia: surgical intervention
Choledochal cyst: Surgical intervention
Post Graduate Clinical Training in Pediatrics  Page 44
HEPATOSPLENOMEGALY WITH ANEMIA
Name: Age : Sex :
Complaints : Abdominal distension
Associated with lump elsewhere
• H/o Icterus, pallor, petechie, purpura.
• H/o anorexia, nausea, vomiting, dysphagia, diarrhea, constipation, clay colored stools,
worms, mucus in stools.
• No h/o Koch’s/ Koch’s contact or swelling of PPD given in hospital.
• No h/o chronic fever with rigors (Chronic malaria/ Kala Azar)
• No h/o jaundice in the past, hematemesis / malena / hematochezia / dilated veins on
abdominal wall (portal hypertension)
• No h/o umbilical catheterization/ History /s/o umbilical sepsis in neonatal period
(Extrahepatic portal hypertension)
• No h/o altered sensorium/ unconsciousness/ coma/ convulsions (hepatic
• No h/o blood transfusions, other sibs affected (Hepatitis B/ Hepatitis C / Chronic
• No h/o petechie, purpura/ ecchymosed (leukemia/ hypersplenism)
• No h/o breathlessness/ edema feet/ increased precordial activity/refusal to feed (CCF)
• No h/o delayed milestones/myoclonic convulsions/incoordination (storage disorder-
Niemann-Pick disease, Gauchers)
• No h/o defective vision/ hearing (Mucopolysacchridosis, Osteopetrosis)
Post Graduate Clinical Training in Pediatrics  Page 45
• No h/o fever / rash in mother during pregnancy (intrauterine infection)
• No h/o fractures (Osteopetrosis)
• Acutely ill or chronically ill
• Patient is conscious, irritable.
• PRESENCE/ABSENCE: pallor, icterus, cyanosis, clubbing, significant
lymphadenopathy, edema feet, increased JVP (CONSTRICTIVE PERICARDITIS)
• Vital signs.
• Anthropometry measurements – with percentiles.
• Abdominal girth (in c/o ascites)
• Look for platynychia / koilonychia, petechie, purpura / ecchymosis, xanthomas,
pruritus marks, hemolytic facies, and phylecten.
• Signs of liver cell failure
• BCG mark, abdominal tap mark, liver biopsy mark.
• Skull/ spine
• Dental cavity- dentition, fetor hepaticus
• Distended/not if so upper or Lower or both; more on right or left
• Distended with everted stretched umbilicus with fullness in flanks.
• There are scars, abdominal tap marks, liver biopsy, sinuses or dilated veins.
• Hernial orifices and genitalia are normal.
Post Graduate Clinical Training in Pediatrics  Page 46
There is edema of abdominal wall/ doughy abdomen.
Superficial palpation: tenderness/guarding/ rigidity.
Deep palpation :
Liver : Enlarged ------- cms in Right midclavicular line and --------- cms in midline below the
xiphisternum; upper border of liver dullness is in --------- Right Intercostal space; span -------
cm. The edge is sharp/ round/ leafy. The surface is smooth/nodular/ tender/nontender.
Consistency----soft/firm/hard. Moves with respiration. Pulsations-Rub/bruit over the liver.
SPLEEN is--------cm from the left subcostal margin; is non tender; smooth in consistency;
soft/firm or hard; anterior notch is felt; there is/ is no bruit.
PERCUSSION : S/o free fluid in the form of puddle sign (120cc)/ Shifting dullness (>1
litre)/ Fluid thrill (>2 litres).
AUSCULTATION : Bowel sounds, Bruits
Per rectal examination
-------Yr old M/F born of a-------marriage with hepatosplenomegaly with pallor/ icterus/
hematemesis/ malena/ IU infection/ umbilical vein catheterization with, failure to thrive, with
vitamin deficiency A/D/E/K. with s/s of liver cell failure, with s/s of Portal hypertension with
s/s of hypersplenism with dysmorphic features, or s/s of congenital infection/ cataracts or s/s
of storage disorder.
• Infection - Disseminated Koch’s, malaria, kala azar, SBE, IU infection, Neonatal
• Hematological - Chronic hemolytic anemia, leukemia, Hodgkin’s lymphoma.
• Congestive - CCF, constrictive pericarditis, Budd-Chiari, Portal hypertension.
• Storage - Niemann pick disease, Gaucher, GSD, MPS.
• Gaucher’s disease type 1 to 4
Post Graduate Clinical Training in Pediatrics  Page 48
Childhood – spherocytosis, Infection, JRA, SLE, Cirrhosis with portal hypertension,
Hepatosplenomegaly with ascites:
• Disseminated Koch’s
• Cirrhosis of liver- post hepatitis, Indian childhood cirrhosis, Wilson’s Disease, portal
• Congestive- Constrictive pericarditis, Budd-Chiari, pericardial effusion.
• Malignancy-rarely ascites.
Post Graduate Clinical Training in Pediatrics  Page 49
Name: Age : Sex :
• Presented with c/c of increasing pallor
• Abdominal distension
• Failure to thrive
Elaboration of complaints:
Increasing pallor: easy fatigability, palpitation, fast breathing, edema.
Only symptoms pertaining to RBC or combined RBC+WBC(repeated
H/o repeated transfusions—transfusions started at what age, regularity
and frequency of transfusions.
H/o receiving any regular injections/ medications.
H/o discoloration of skin
H/o not achieving adequate weight and height.
Older child-----h/o having achieved puberty.
H/o repeated chest infections/ breathlessness
H/o deafness (sensorineural deafness due to Desferrioxamine toxicity
or bony expansion and compression of the eight cranial nerve.)
H/o complications of blood transfusion------ blood transmitted disease,
FAMILY HISTORY - OF Sibling/ relatives receiving transfusions
DIET HISTORY - to check the iron consumption in food
Rest of the history as usual.
• Position patient,Vital parameters, Growth Parameters –Height, Weight with Percentiles,
Tanner staging for puberty ,
• Skin Colour , Pigmentation, Pallor, Jaundice
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• Facial features-Frontal bossing/Parietal bossing/Chipmunk facies / Maxillary
Overgrowth/ Dental malocclusion /Prominent malar eminence/ Broadened nasal bridge
• Hands- Finger tip pricks / Pallor, pigmentation
• Peripheral stigmata of chronic liver disease
• Pulse – Slow (hypothyroid) ,Irregular (cardiomyopathy) , Alternans (CCF),
• Head & neck- Conjuctival pallor ,Scleral icterus ,Cataracts(desferrioxamine)
Retinopathy(desferrioxamine) , Teeth:dental malocclusion, Neck/goiter
• Heart-Full precordial examination to detect cardiomyopathy, CCF, haemic murmurs
• Abdomen - Distension, Splenectomy scar
Injection sites –Desferrioxamine/ Insulin
• Lower limbs and gait- Leg ulcers , Ankle odema (CCF), Bony tenderness
• Gait examination for long tract signs-----due to vertebral bony expansion and cord
• Delayed ankle jerk relaxation
• Back examination for lordosis, tenderness
• Others-Urinanalysis for glucose
• Chvostek’s and Trousseau’s signs(hypoparathyroidism)
• Hearing(sensorineural deafness)
Commonly asked questions:
Differential Diagnosis of Hemolytic anemias.
Ideal transfusion regime.
Complications of Thal major and Blood transfusions.
Diagnosis of hypersplenism.
Recent advances in management of Thal major.
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APPROACH TO SHORT STATURE
Chief complaint :- Child is not gaining in height.
• To ascertain that the child is indeed short, measure height/ length with infantometer
till 2 years of age and with stadiometer later on by appropriate technique. This
parameter is plotted on growth charts. Different growth charts are available like
NCHS, Tanners, ICMR , K.N.Agrawal .
A child is said to have short stature if his/her height is below the 3rd
percentile or more
than 2SD below the mean for the reference population.
A child is said to have growth retardation if his growth ( height) velocity is below 25th
centile of reference population.
• Age of onset …since when is the child not growing.
• School, home or physician records of previous heights and weights must be sought and
charted on growth charts.
• Associated complaints …(suggestive of systemic cause),
Polyuria----- Chronic renal failure, renal tubular acidosis(RTA)
Polyuria, Polydypsia ---- RTA , Diabetes insipidus
Shortness of breath, cyanosis, cough, fever----Congenital heart
disease, asthma, cystic fibrosis, other chronic respiratory illness,TB
Headache, vomiting, visual problems------pituitary /hypothalamic mass
Diarrhoea, steatorrhea, abdominal pain-------malabsorption
Constipation ,weight gain, inadequate growth-------Hypothyroidism
Psychosocial disturbances-------psycosocial dwarf
• Past history of illnesses.
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• Antenatal history …
maternal medical illnesses during pregnancy , maternal exposure to
teratogens, irradiation, maternal infections
• Birth history …
Type of delivery (breech), Mode of delivery,
Full term / preterm/ post term . Birth weight
Neonatal period.. Seizures , prolonged hyperbilirubinemia, feeding
difficulties, hypoglycemic episodes, delayed cry.
• Family history ..
Pedigree, Consanguinity , height of parents, Age at onset of puberty
in parents, Presence of similar complaints in other family members.
• Developmental milestones
• Dietary history
Calories and proteins intake.
• Psycosocial history.
A well taken history can give clues to aetiology of short stature like:
• H/o antenatal substance abuse, medication, birth weight-------IUGR
• Edema hands and feet at birth---------Turners syndrome
• Breech delivery, neonatal hypoglycemia, jaundice, micropenis----Growth hormone
• Dietary intake (caloric and protein intake) ,sunlight exposure-------malnutriiton, rickets
• Family h/o short stature, delayed puberty in parents----familial short stature,
constitutional delay in growth
• Prolonged intake of steroids, amphetamine derivatives----drugs as cause of short
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On Examination :
Anthropometric measurements like weight, standing and sitting height, upper to lower
segment ratio, arm span, rhizo, meso and acromelic lengths , head circumference, must be
• Growth points should be charted and growth velocity should be recorded.
Normal growth velocity:
In the first year of life a child grows by 25cm, 12.5 cm in 2nd
year, 6-7cm in 3rd
5cm per year from 5-9 years with a nadir of 3.5 cm per year in pre pubertal age group.
During pubertal growth spurt 10-30 cm height is gained , with peak height velocity of 9-11
cm per year in boys and 7-9 cm per year in girls.
Upper to lower segment ratio helps to differentiate between proportionate and
disproportionate causes of short stature.
Body proportions (upper segment: lower segment) change from 1.7 at birth to 0.98-1 by 13-
14 years of age and to 1 in adult hood.
• Plot the height against mid parental height range .Mid parental height (MPH) is
calculated by adding 6.5cm to the average of mothers and fathers height in boys and
by subtracting 6.5cm in case of girls. This should be plotted on growth chart with a
range of about 8.5 cm below or above MPH. If a child lies within this range he has a
genetic cause of short stature.
• Thorough general and systemic examination needs to be performed to look for
dysmorphism, skeletal and non-skeletal anomalies, signs suggestive of malnutriiton
and vitamin deficiencies and chronic infections.
Signs of chronic systemic disease and endocrine abnormality is to be sought for.
Pubertal development to be assessed by Tanners sexual maturity rating.
Clinical examination can give certain clues to the aetiology like:
• Dysproportionate short stature------skeletal dysplasia, rickets, congenital
• Dysmorphism------congenital syndromes
• Midline defects-------hypopituitarism
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• Pallor ---------Chronic anemia ,chronic renal failure, hypothyroidism
• Vitamin deficiency signs----PEM ,malabsorption
• Hypertension-----chronic renal failure
• Cherubic facies ,frontal bossing, depressed nasal bridge--------growth hormone
• Jaundice, clubbing------chronic liver disease
• Goitre ,impalpablethyroid, coarse skin------hypothyroidism
• Central obesity ,striae ,proximal muscle weakness------Cushing’s
• Round face ,short 4th
metacarpal, mental subnormality---pseudohypoparathyroidism
• Frontal bossing ,beading ,wrist widening------rickets
• Visual field defect, optic atrophy, optic nerve hypoplasia, papilledema-----
pituitary/hypothalamic tumour ,septooptic dysplasia
Bone age is done to study the skeletal maturity IT IS DONE BY TAKING HAND AND WRIST
X-RAY OF LEFT HAND. Two systems for reading bone ages are available-Greulich and
Pyle’s Atlas method and Tanner and Whitehouse scoring method.
Normal ranges of bone age range:
Range + 2SD Chronological age
+/- 3-6 mo 0-1yr 0-1yr
+/- 1-1.5 yr 3-4 yr 2-3yr
+/- 2yr 7-11yr 6-10yr
+/- 2yr plus 13-14yr 12-13yr
Familial short stature: H.A< B.A=C.A; Constitutional growth delay: H.A=B.A.<C.A
If height is normal for national standards and midparenteral height and growth velocity is
normal on follow up then reassurance is needed without any further investigations.Normal
bone age at outset usually rules out pathological cause of short stature.
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Laboratory tests can be requested if clinical findings are suggestive of a disease. Chest
x-ray ,2-D Echo for cardiac defect, Thyroid functions for hypothyroidism, skeletal
survey for skeletal dysplasias etc. However where there is no clue on history and
examination and with delayed bone age and low growth velocity screening
investigations are needed.
Weight for height gives an important clue for investigations i.e. poor weight for height can
suggest malabsorption or other systemic illnesses while good weight for height may mean
growth hormone deficiency.
Screening investigations for finding cause of short stature are:
• Complete blood count, ESR----Anemia ,chronic infection
• Sr.calcium, phosphorus, alkaline phosphotase ---- Rickets, pseudohypoparathyroidism
• Sr.proteins, SGPT-------Chronic liver disease
• Venou blood gas, S.Electrolytess------------RTA
• Urine routine ,microscopy, pH-----RT , chronic pyelonephritis, glomerulonephritis
• Stool routine microscopy--------malabsorption , giardiasis
• X-ray hands --------bone age ,rickets
If screening tests are normal suspect Turner syndrome, GHD, malabsorption .Other
investigations like karyotyping, provocative assays for growth hormone and special tests for
malabsorption need to be done.
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APPROACH TO EVALUATION OF SHORT STATURE
Is the child short ?
( Ht less than 3rd
*Reassurance 1) Is the height within midparental height (MPH) range
*Assess growth velocity
2) Assess bone age (BA)
Elicit history to rule out
Systemic diseases, malnutrition, IUGR,
Dysmorphic / chromosomal syndromes BA= CA >HA BA =HA <CA
Familial short stature CDGP
Assess growth velocity (over 6/12 mon)
CBC, Hb, ESR ( anemia ,infection),
Renal, Liver function test (CRF, CLD)
Total proteins, albumin (Nutrition)
S.Ca, P, AlkPo4ase ( rickets, pseudohypoparathyroidism)
Blood gas , serum electrolytes ( metabolic acidosis, RTA)
Coeliac screen , malabsorption workup
Genetic studies (Turner,Russel Silver, Trisomy )
(BA- Bone age , CA – Chronological age , HA- Height age , CDGP- Constitutional Delay in
Growth and Puberty, RTA- Renal Tubular Acidosis, CRF- Chronic renal failure, CLD-
Chronic Liver Disease)
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• Measurement of height should be done on a well calibrated stadiometer / infantometer
• Height velocity is measured over a period of 6 to 12 months.
• KN Agarwal charts are used as the reference curve .
• Mid Parental Height (MPH) ( All heights measured in cms. )
= (( Mother’s height +13) + Father’s height )/ 2 ( BOYS)
= ((Mother’s height +( Father’s height-13) )/ 2 ( GIRLS)
MPH Range = MPH +/- 8.5cm
• Upper segment, lower segment ratio should be calculated in all short children to check
for disproportionate short stature.
Causes of disproportionate short stature-
• Skeletal dysplasia, Rickets, Congenital hypothyroidism , Mucopolysaccaridosis
• Calculation of weight for height is helpful in differentiating wasting (malnutrition,
systemic illnesses), obesity (cushing’s syndrome) and stunting ( GHD).
Commonly asked questions :
1] Discussion of differential diagnosis
2] Stages of coma
3] Stages of TBM & prognosis in each stage.
4] Signs of meningeal irritation.
5] Signs of increased intracranial pressure
6] Types of herniation
7] Management of TBM - supportive + definitive
8] Types of shunt & complications of shunt
9] Complication of TBM
10] Pathology in TBM & lesion localization
11] CT correlates in TBM
12] Precipitating factors in TBM
13] Poor prognostic factors in TBM
14] Role of steroids
15] Newer modalities of diagnosis of TBM
Post Graduate Clinical Training in Pediatrics  Page 58
APPROACH TO A CHILD WITH RICKETS
Progressive bony deformity
Bone pains, Fractures
Seizures in young infants, Carpopedal spasm in older children
Delayed dentition, dental deformities
Proximal muscle weakness
Delayed motor development
Polyuria, polydypsia (Renal rickets, RTA)
Recurrent diarrhoea, steatorrhoea ( Malabsorption..fat)
Jaundice, distension abdomen (Chronic liver disease, Cholestatic jaundice)
Pallor (Nutritional, Wilson’s disease, Chronic renal failure)
Visual problems (Lowe’s syndrome, Cystinosis)
Alopecia - Patchy, totalis (Vit. D Dependent Rickets Type II)
Hearing affection ( RTA)
Recurrent respiratory infection
Drugs ingestion- Anticonvulsants,anti tubercular drugs
Calcium supplement in expectant mother
Consanguinity (Autosomal recessive disorder)
Preterm /Full term (Osteopenia of prematurity)
IUGR (may manifest with rickets during catch up growth)
Breast feed/ top fed
Vit D or Calcium supplement
Exposure to sunlight
Family history of similar complaints (X linked hypophosphatemic rickets)
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Anthropometry - Short stature, Disproportionate short stature
Bony features of rickets
Craniotabes (young infants)
Wide open / persistent open anterior fontanelle
Fronto parietal bossing giving a hot cross bun appearance
Widening of wrists
Bowing of long bones
Genuvarus / genu valgus
Coxa vera/ coxa valga deformity.
Dental feature: -
Delayed eruption of teeth, dental abcess, pulp defects, dental problem usually affect the
Muscle and ligament: -
Proximal muscle weakness causing waddling gait, difficulty in climbing stairs, difficulty in
getting up squatting position. Visceroptosis, laxity of ligaments.
Associated problems: -
Pallor, Icterus, other vitamin deficiencies, hypertension, alopecia, hepatosplenomegaly,
cataracts, glaucoma, sensorineural hearing loss.
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Name : Age : Sex :
PRESENTING COMPLAINT: Patients typically present with fever, chronic cough,
purulent sputum, weight loss and loss of appetite.
A) RESPIRATORY SYSTEM
o Impaired exercise tolerance
o Cough-frequency/severity/nocturnal/exercise induced/change in
o Sputum-volume/color/blood tinged/recent change
o Fatigue/Dyspnea/Chest pain
o Chronic sinusitis
o Wheezing might point towards allergic bronchopulmonar aspergillosis
o Bronchodilators required and response to their use
PAST COMPLICATIONS : pneumothorax/hemoptysis
INVESTIGATIONS DONE : Sputum culture, chest x-ray, pulmonary function tests,
THERAPY RECEIVED - exercise, physiotherapy, nebulised saline, bronchodilators
B) GASTRO INTESTINAL SYSTEM : Generally GI symptoms are present in cystic
fibrosis or in IgA deficiency. Liver is affected in alpha 1 antitrypsin deficiency.
History of weight loss/pain abdomen/vomiting/loss of appetite
History of oily, bulky or offensive stools.
History of meconium ileus or rectal prolapse
C) Recurrent pyogenic infections are suggestive of immunodeficiency. Recurrent middle
ear infections are suggestive of ciliary dyskinesia or immunodeficiency.
FAMILY HISTORY: History of tuberculosis or cystic fibrosis in the family.
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IMMUNIZATION: History of receiving BCG or measles or pertussis vaccine.
A) General Examination
a) Pubertal status (Tanner staging) - A delay in puberty may be seen.
b) Nutritional status parameters –Weight, height, head circumference, percentiles.
c) Vitals- Pulsus paradoxus (severity of airway obstruction)
Pulses Alternans (congestive cardiac failure)
Bounding pulse (hypercarbia)
d) Look for clubbing/ cyanosis
e) Ears –Secretory otitis media
f) Nose – Nasal polyps
g) Mouth- cyanosis/thrush
B) Affected system
Inspection - Note the increase in AP diameter.
Cough-Moist/productive/ foul smelling
Perform peak flow measurement if possible.
Palpation - Measure the AP diameter (hyperinflation), Tracheal position, position of
apex, palpable pulmonary valve closure
Percussion - Hyperinflation /consolidation
Auscultation - Coarse leathery crepts over the affected region (First heard in the upper
lobes in cystic fibrosis)
Wheeze may be present
Loud second heart sound in pulmonary hypertension
Gallop rhythm in cor pulmonale
Dextrocardia in Kartagener syndrome
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TIPS FOR STUDENTS
Firstly, exams are just a phase in life. It too will pass. So, do not make it a do-or-die
Set realistic goals.
Work towards your goals.
Keep motivating yourself.
Remember, it is just an examination.
The real test, is your daily routine--- saving lives of kids. So
don’t lose focus on that.
If you are sincere and hard working at taking care of kids
under your care, you will know what to do in the exams.
Look at the exams as stepping stones. Do what you need to do to reach the top. Don’t
think of the difficult nature of the stones.
People have cleared the exams. So it is not impossible.
Start with a positive attitude.
Preparing for theory examination:
Make a schedule that is realistic and covers every chapter in Nelson.
Post Graduate Clinical Training in Pediatrics  Page 63
You may jumble up systems or sit with a single system till that is over, that is a
personal choice. But do not omit any system.
Prepare notes in your own style and revise them whenever possible.
You must know the salient points in each topic, not necessarily every point.
Work out previous question papers.
You will get an idea of the pattern of questions and will be a good guide to your
Do not forget community medicine, vaccination, recent advances.
If possible, formulate your own questions in each topic. Think about how you would
Prepare algorithms and flowcharts for questions like –approach to a disease or a
condition, line of treatment.
Make a list of questions you want to revise the day before.
On the night before the exam, stop reading by dinner time, have a good dinner, relax
and give your body time to ease out the tension. Try to get a good night sleep.
Do not worry about the questions, it is not in our hands. Do not think about all the
“what if” questions the fill our heads with fear.
It is just another day of your life. Face it with courage, determination and a will to
Writing the theory paper:
Answer in the given order.
During presentation of an answer, highlight the salient points either by using a
different colour or by underlining.
Post Graduate Clinical Training in Pediatrics  Page 64
Use different colour / capitals/ underlining , to show the different parts of the same
question. Marks are being allotted in parts. Ensure they know what is where.
Space out neatly and write, let it not go on for pages.
Make the answers neat, precise and legible.
There is a high probability that you may not know the answer to a question or you are
not sure of it completely. Do not panic.
Face questions one at a time. Focus on the answer you are writing. Do not think and
worry about a question you do not know.
If you do not know the answer, leave out a few pages, write the remaining, come back
to that question at the end when you will be able to think and write.
For clinical questions, you can imagine what you would do, how you would approach
a child with the given condition in the ER / OP.
Do not think about the paper you have written and submitted. It is done. You cannot
change. Focus on the next paper. That is the best thing to do.
Relax for a few days / weeks after theory exams and then start preparing for
Prepare a list of systems and diseases that are commonly kept in the clinicals.
Write a fake case sheet for each disease ,so that you know what all needs to be
covered in history, clinical examination.
Present the entire history to your colleagues and teachers, don’t worry about making
errors, it is better to make them now than in the exam. Learn from your mistakes and
Try to finish taking history and clinical exam within 45 minutes.
Post Graduate Clinical Training in Pediatrics  Page 65
Request your teachers and friends to correct you / show you how to elicit signs and do
Do not make errors in the basics.
Be sure of the order of presentation.
Be thorough in anthropometry, nutrition and immunization. These are what separate
the kids from adults, pediatrics from general medicine. There is no excuse if you falter
in these areas.
Prepare for osce (objective structured clinical examination) parallelly.
There are certain topics that need to be covered compulsorily for osce preparation.
Wear a coat with long sleeves.
Take some toys / chocolates / biscuits to befriend the kid who is helping you in the
exam (by being your patient)
Do not panic if they ask you a question to which you do not know the answer. Try to
think and answer or else respectfully say you do not know. But don’t make it a habit.
Be loud and clear while you talk.
They are only making you do what you have been doing daily in the hospital—take
history, do clinical examination, derive at a differential diagnosis, plan the line of
You need to talk, converse and not keep quiet because by not doing that you are
making it hard for them to help you.
Do not worry about the reputation of the teachers / examiners. At the end of the day,
you have to perform.
Be at your best.
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