PG Clinical Training in Pediatrics 2013

i
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)
ii
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
iii
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 orationPneumococcal diseasePast, Present & Future

by
Prof Adam Finn
Consultant in Pediatric Infectious Disease
Royal Bristol childrens 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
iv
Organizing Committee
Patrons
Organizing Committee:
Mr.Karthik Narayanan, Chairman,KKCTH
Dr Jayanthi Ramesh
Dr.K.MathangiRamakrishnan, Chairman, CTMRF
Dr.Kalpana Gowrishankar
Dr A.Andal, Medical Director, KKCTH
Dr Lalitha Janakiraman
Dr.LakshmiSundararajan
Academic coordinators
Dr.Major K.Nagaraju
Dr.V.S.Sankaranarayanan
Dr.S.Muralinath
Dr.S.Balasubramanian
Dr.S.Namasivayam
Dr BalaRamachandran
Dr.PriyaRamachandran
Organizing secretaries:
Dr.RahulYadav
Dr.Janani Sankar
Dr K.G.Ravikumar
Dr.R.Radhika
Dr.T.Ravikumar
Dr T.Vasanthi
Dr.V.Viswanathan
Finance & Administration
Dr.Arathi Srinivasan
Mr.Sivakumar
Dr.AmrutaKanjani
Mr.Ananthanarayanan
Dr.Eswararaja
Dr.R.Ganesh
Dr.M.Lakshmi
Dr.Padma Balaji
Dr.SenthilGanesh
Dr S. Srinivas
Dr.N.Suresh
Disclaimer
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
vi
vii
FOREWORD
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 August 2013.
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.
Prof.Dr.K.Mathangi Ramakrishnan
Chairperson-CTMRF
viii
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 Ladys Hospital for Sick Children,
Dublin, Ireland
Venue
Hotel Chola Sheraton
Second KKCTH Commemoration Oration

02.10.2001
CME on Pediatric Gastroenterology
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
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
Prof. Arnold G.Coran,

Prof. of Surgery &
Head of Section of Ped. Surgery
University of Michigan Medical School, USA
Venue
Hotel Taj Connemara
ix
Fifth Millennium Guest Oration

02.10.2004
National CME on Pediatric Critical Care
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
Prof Klass N.Bax, Prof of Pediatric Surgery

Dept. of Ped. Surg., Wilhelmina Childrens
Hospital, University Medical Center Utrecht,
Netherlands
Venue
Hotel Taj Coromandel
Seventh Millennium Oration & National CME on Pediatric Cardiiology

12.11.2006
Cardiac Surgery in Developing Countries
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
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

in Children
Dr.A.V.Ramanan
Consultant Pediatric Rheumatologist and
Hony. Senior Lecturer, University of Bristol,
United Kingdom
Venue
Hotel GRT Grand
Tenth Millennium Oration & National CME

04.10.2009
Clinical Approach to difficult problems
Prof.Y.K.Amdekar, Mumbai
Venue
Hotel GRT Convention Centre
Eleventh Millennium Oration

03.10.2010
Bone Marrow Transplant

Past, Present and Future
Prof.Anupam Sachdeva
Hemato Oncologist, Delhi
Venue
Twelveth Millennium Oration

05.10.2011
State of the Worlds Children
Prof Frank Shann

Prof. of Critical Care Medicine
Royal Childrens Hospital
University of Melbourne, Australia
Venue
Thirteenth Millennium Oration

07.10.2012
Tuberculosis in Children Past, Present & Future
Prof. S.Mahadevan
JIPMER, Pondicherry
Venue
xi
Contents
Sl.No.
Topic
Page No.
01
Developmental Assessment
02
Cerebral Palsy
03
Acute flaccid paralysis
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
xii
Developmental Assessment
Dr. Ganesh, Dr.Suresh
Consulting Paediatrician KKCTH
Item/Age
Gross motor
Fine motor & vision
Social
Hearing &
language
6 weeks
3 months
Grasp reflex
Head control
Social smile
Cooing
Recognises
Turns head to
mother
4 months
sound
Reaches for
objects
7 months
Rolls over
Palmar grasp
Crawling
Transfers objects
Sits with hands forward
Smiles at mirror
Babbling
(ba,da,ka)
from hand-hand
for support
10 months
Sits without support
Pincer grasp
Waves bye-bye
Plays pat-a cake
Pivoting-turns round to
Uses amma,
appa
pick up a toy without

overbalancing
Creeping
1 year
Can rise to Standing

Walks alone
Walks holding on to
furniture (cruising)
Holds two cubes

and bangs
Casting
Pincer grip
Goes upstairs & down

stairs using hand
held/rails
Carries toys while
walking
Turns to name
Plays pat a cake
Tells 2 words
Asks for objects
with meaning
by pointing
Drinks from cup
Bottom shuffling
1 years
Waves bye-bye
Makes tower of 3
cubes
Turns 2-3 pages in
a book at a time
Scribbles
Dry by day
Holds spoon-takes
Close the door
Solitary play(
Points to parts
plays alone)
of the body
when asked
Echolalia
Kneels without support

stairs-both foot/step.
Runs
Kicks the ball
command:
food to mouth
Walks backwards
2 year
Obeys simple
Makes tower of 6
cubes
Copies vertical
line
Turns page in a
Feeds with spoon

safely
Wears shoe and
socks
Gives name
Obeys two step
commands(pick
the toy and put
in the basket)
book singly
Turns door knob
Unscrews lids
Post Graduate Clinical Training in Pediatrics [2013]
Page 1
Item/Age
Gross motor
Fine motor & vision Social
Hearing &
language
2 year
Tip toe walking

Jumps
Copies horizontal
line
Makes tower of 7
cubes
Recognize
themselves in
Names one
color
photos
Pretends play
Makes train
3 year
Goes upstairs -1
foot/step & down
stairs-two foot/step.
Pedals tricycle
Stands on one foot for
one second
Can copy a circle

Constructs a
bridge
Begins to draw a
man
Can construct a
block tower of ten
Eats with fork and

spoon
Knows own
name, age, and
Dry by night
gender
Dresses and
(boy/girl)
undresses if
helped with
buttons
Knows some
nursery rhymes
Names 3 colors
cubes
Can thread large
beads on to a
string
Cuts paper with
scissors
4 year
Stands on one foot for

five second
Walks heel-toe
Hops
Copies cross and

square
Dresses without
supervision
(boy/girl) and
three parts
Copies gate(6
stairs-one foot/step.
cube steps)
name, age,
gender
Draws a man with
Knows own
address
Names 4 colors
Threads small
beads
Right-left
discrimination
5 year
Skips
Copies triangle
Makes 10 cube
steps
Uses knife and

fork
Knows own
name, age,
gender
(boy/girl)
address and
birthday
Page 2
CEREBRAL PALSY
Name :
Age :
Sex :
Complaints :
Not attained age appropriate mile stones since early infancy
Convulsions.
Description of compliants.
Describe all 4 developmental domine important mile stones achieved by the child
o Gross motor
o Fine motor
o Language
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
each category).
Involuntary movement
-
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
Mannerisms, stereotypies.
Bladder, bowel involvement.
Page 3
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 :
Convulsions
Feeding difficulty /constipation
Recurrent LRTI
Contractures, bed sores behavioral problems, injuries, falls.
H/O Treatment :
Immunization:- ?? DPT
Detailed dietary history type of food, swallowing difficulties,
Diet History
regurgitation, spitting, weight gain.

Examination :
Vitals
Anthropometry with interpretation
General- pallor
o Cataract, strabismus,
o Skull - Overriding of sutures.
o Shape of skull
o Anterior Fontanelle
o Dysmorphism
o Neurocutaneous markers
o Eyes - cataract
Dentition
Evidence of. malnutrition , bed sores, contractures - static/ dynamic
Page 4
CNS :
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

suspension
Neonatal reflexes
Hearing
Vision
Fundus examination choreoretinitis / optic atrophy / retinitis pigmentosa
Primitive reflexes
Other systems (organomegaly/ murmurs)
Diagnosis
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

etiology being-----------------
Page 5
Commonly asked questions :1)
Early markers of CP
2)
Functional grades of CP
3)
Neonatal reflexes
4)
Audiometry
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
Page 6
Acute flaccid paralysis/Guillian Barre Syndrome

Name :
Age :
Sex :
Complaint:
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
Page 7
Etiological history:
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
Examination:
Decubitus especially of lower limbsDemonstrate flaccidity
Vital parameters: Heart rate, Blood pressure for autonomic dysfunction
Throat---patch for diphtheria
Blue line on gums, NC markers
Spine
CNS
Drooping of shoulder s/o diaphragmatic paralysis
Fasciculations
Thickened nerves
Reflexes Superficial important as in case of transverse myelitis for level of the

lesion
Signs of meningeal irritation
Page 8
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
Respiratory system
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 patients capacity for thoracic breathing while abdominal muscles are
splinted manually
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)
Page 9
Diagnosis : Differential diagnosis of GBS - shown in the table below

Polio
Guillain-Barr
syndrome
Traumatic neuritis
Transverse myelitis
Installation of
paralysis
24 to 48 hours onset
to full paralysis
From hours to 10
days
From hours to 4 days
From hours to
4 days
Fever at onset
High, always present

at onset of flaccid
paralysis, gone the
following day
Not common
Commonly present
before, during and
after flaccid paralysis
Rarely present
Flaccid
paralysis
Acute, usually
asymmetrical,
principally proximal
Generally acute,
symmetrical and
distal
Asymmetrical, acute
and affecting only one
limb
Acute, lower limbs,

symmetrical
Muscle tone
Reduced or absent in
affected limb
Global hypotonia
Reduced or absent in
affected limb
Acute, lower limbs,

symmetrical
Sensation
Decreased to absent
Globally absent
Decreased to absent
Absent in lower
limbs early
hyperreflexia late
Deep-tendon
reflexes
Severe myalgia,
backache, no sensory
changes
Cramps, tingling,
hypoanaesthesia of
palms and soles
Pain in gluteus,
hypothermia
Anesthesia of lower
limbs with sensory
level
Cranial nerve
involvement
Only when bulbar

involvement is
present
Often present,
affecting nerves
VII, IX, X, XI, XII
Absent
Absent
Respiratory
insufficiency
Only when bulbar

involvement is
present
In severe cases,
enhanced by
bacterial
pneumonia
Absent
Sometimes
Autonomic
signs &
symptoms
Rare
Frequent blood
pressure
alterations,
sweating, blushing
and body
temperature
fluctuations
Hypothermia in
affected limb
Present
Cerebrospinal
fluid
Inflammatory
Albumin-cytologic
dissociation
Normal
Normal or mild in
cells
Bladder
dysfunction
Absent
Transient
Never
Present
Nerve
conduction
velocity: third
week
Abnormal: anterior
horn cell disease
(normal during the
first 2 weeks)
Abnormal: slowed
conduction,
decreased motor
amplitudes
Abnormal: axonal
damage
Normal or abnormal,
no diagnostic value
EMG at three
weeks
Abnormal
Normal
Normal
Normal
Sequelae at
three months
and up to a
year
Severe, asymmetrical
atrophy, skeletal
deformities
developing later
Symmetrical
atrophy of distal
muscles
Moderate atrophy,
only in affected lower
limb
Flaccid diplegia
atrophy after years
Page 10
ACUTE INFANTILE HEMIPLEGIA

Name :
Age :
Sex :
Address :
Consanguinity :
Handedness :
CHIEF COMPLAINTS
Paucity of movements of right/left side of the body.
Convulsions
Onset-Catastrophic/acute/sub acute/chronic/static/episodic
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
H/O Complications
Bed sores/shortening of limbs/contractures /trophic ulcers
ETIOLOGICAL HISTORY
H/o Trauma
Head injury/Oral cavity injury
Fracture (Fat embolism)
Hematological causes

H/O pallor
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

nephrotic syndrome
Page 11
Cardiac causes

H/o fever with chills/ petechiae/hematuria (Infective Endocarditis)
H/o cyanosis /cyanotic spell (Cyanotic heart disease) (abscess/

Thrombosis )
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 Kochs/Kochs 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
Infectious Causes
Dehydration
(sagittal sinus thrombosis )

H/O recurrent attacks of TIA /hemi paresis

(Migraine/Moya-Moya/alternating hemiplegia)
H/O post seizure transient paralysis (Todds paralysis)
FAMILY HISTORY
H/O similar attacks in the family (Sickle cell/ homocystinurea/Hyperlipidaemia)
BIRTH HISTORY
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)
Page 12
EXAMINATION:
General Examination-Routine examination plus look for dysmorphic features
Carotid pulses should be palpated as well as auscultated(Moya Moya,Takayasu)
Anterior Fontanelle
Head Circumference
US/LS & Length (homocystinurea)
Pallor/Cyanosis/Clubbing
Xanthomas
Petechiae/Purpura/ Joint bleed/ Rash
Eyes-Ectopia lentis
Neurocutaneous Stigmata
Skull-Trauma/Crack pot/Bruit over the skull.
CNS
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)
CVS Examination
1. Higher mental function
2. Cranial nerves
3. Motor system
a. Tone
b. Power
c. Bulk/Nutrition
Page 13
d. Involuntary movements
e. DTR
4. Sensory system
5. Meningeal signs
6. Spine and cranium
7. Primitive reflexes
LOCALIZATION OF THE LESION IN CASE OF ACUTE INFANTILE

HEMIPLEGIA
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
IPSILATERAL 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
than upper)
Altered sensorium may be present
Convulsions may be present
Cortical sensory loss may be present
Astereognosis
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 Convulsions
o Bladder/ bowel involvement
o Persistent neonatal reflexes on the opposite side
Page 14
Involvement of the parietal lobe

o Cortical sensory loss
o Astereognosis
Involvement of the Temporal lobe

o Temporal lobe epilepsy
o Sensory aphasia
o Memory loss
Involvement of occipital lobe

o Homonymous hemianopia
B)
C)
Internal capsule lesion

Dense Hemiplegia
Hemianaesthesia
Homonymous hemianopia
Dysarthria
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
BENEDICTS SYNDROME-3rd 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
FOVILLE SYNDROME-6th nerve palsy + 7th nerve palsy + contra lateral
Hemiplegia
C)
Lesion in Medulla
JACKSON SYNDROME-12th nerve palsy + crossed hemiplegia.
Page 15
FLOPPY INFANT
Complaints :
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 (Taysachs)
ETIOLOGY
H/O Icterus, phototherapy, exchange transfusion (kernicterus)
H/O constipation, prolonged neonatal jaundice (if MR, coarse facies for
hypothyroidism)
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
Page 16
H/O flushing/sweating/ palpitation/ postural hypotension/ arrhythmias

(dysautonomia)
H/O maternal myasthenia like illness
H/O diurnal variation (mysthenia gravis)
H/O lump in abdomen,early morning hypoglycaemic convulsions with

breathlessness(GSD Pompes)
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
ANTENATAL HISTORY
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)
EXAMINATION
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/ Zellwegers syndrome
Doll like faces GSD (Pompe)
V shaped face- myotonic dystrophy
Pallor, clubbing, cyanosis, icterus, lymphadenopathy, oedema feet
Anterior fontanelle
Cataracts(Lowe syndrome)
Page 17
ENT
Skull/ spine/ genitalia(hypogonadism in prader willi)
Conntractures ,CTEV, CDH
CNS EXAMINATION
Higher functions---conscious, alert looking,recognizes others.
Cranial nerves
Tongue fasciculations
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
o Reflexes
Superficial-------cremasteric/ gluteal/ paraspinal reflex
Deep reflexes
Sensory system
P/A-----hepatomegaly----GSD
CVS-----cardiomegaly,murmur, abnormal heart sounds(pompe)
RS--------r/o LRTI
Orthopedic examination
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
Page 18
HYDROCEPHALUS
Name :
Age :
Sex :
DOB :
Complaints :
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,

convulsions
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)
Etiological History
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
Kochs contact, H/o prolonged hospitalization after birth, H/O hypo pigmented
macule with infantile Spasm ( Tuberous sclerosis), H/O swelling at the back &
limb weakness
Page 19
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.
EXAMINATION
Vitals -
BP (hypertension because of raised ICT)

Bradycardia
Shallow respiration
Anthropometry with interpretation.
Skulla) 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
i) Craniotabes
Sunsetting (paralysis of upward gaze)
Spine-Neural tube defects. Look for tuft of hair
Page 20
Others Neurocutaneous markers-Hypo pigmented patches in Tuberous Sclerosis

Dysmorphic features/ coarse features.
Rhizomelic shortening (achondroplasia)
IU infection (Rash/lymphadenopathy/Hepatosplenomegaly/Cataracts)
Crackpot sign.
CNS Examination 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
Neonatal reflexes.
Examination of spine
Shunt side, patency , Reservoir present or absent?
DIAGNOSIS
Page 21
NEURODEGENERATIVE DISEASE
Name :
Age :
Sex :
DOB :
Informant :
Chief complaints:-
loss of achieved mile stones
convulsions
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
spasms .
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 changeso Scholastic backwardness - SSPE, HIV, encephalopathy Wilsons 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

Page 22
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
Page 23
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
of regression.
22. Diet history
23. Immunisation history
EXAMINATION
General examination
Decubitus
Temp.
Pulse
respiration
BP

-
size & shape of skull - overriding of sutures
Anterior fontanelle
Dysmorphic features - Grotesque features, Hypothyroid / MPS
NC markers - Tuberous sclerosis, ataxia telengiectasia, caf au lait spots

Chediac Higashi
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
Fundus
Diagnosis:
Page 24
TUBERCULOUS MENINGITIS
Name
Age
Sex
Address
Handedness
Complains:
1. Fever
2. Convulsions :- focal / generalised seizures
3. Altered sensorium :- onset - sudden / insiduous.
4. Vomiting
5. Focal neurological deficit Hemiplegia / monoplegia / cranial neuropathies.
Origin/Duration/Progress
Complains in details.
H/o.
Abnormality of higher functions - Lethargy, altered sensorium

Convulsions
Cranial nerve palsies - deviation of angle of mouth, drooling of saliva,

squinting, diplopia.
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

movement.
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.
Page 25
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. seizures.
H/o. decorticate / decerebrate posturing.
Drug history, procedure history.
H/o. any surgery, VP shunt / reservoir
Family history - of kochs
Nutritional history - malnutrition may precipitate Tuberculous meningitis.
Birth History :
Developmental history.
Socio economic history - Overcrowding , sanitation.
Examination :General examination :1]
Decubitus
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
Page 26
14] Skin - bedsores

15] Contractures
16] Signs of malnutrition & vitamin deficiency
17] Presence / absence & patency of VP shunt
CNS : Higher functions - state of conciousness
Gag reflex
Eye movements
Pupillary reflexes
Corneal / conjunctival reflexes
Motor system examination
Sensory system
Cerebellar signs
Meningeal signs
Hydrocephalus : Heavy head, crackpot or sutural seperation - Signs of increased
intracranial pressure.
Involuntary movements
Fundus - papilloedema / choroid tubercules / optic atrophy.
Diagnosis :---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.
Page 27
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
History:
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
Carditis)
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 .
Examination :
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
movements.
Page 28
Cardiovascular examination
Peripheral - Venous, major arterial pulses & Blood pressure (upper & lower limbs).
Precordium
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.

Choreiform movements
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
arthritis.
Page 29
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 combs (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
Penicillin.
12. Other tests to prove streptococcal infection.
Page 30
CYANOTIC HEART DISEASE
Checklist:
1. Complaints:
a. Cyanosis age of onset,Distribution,precipitating and reliving factors.
b. Cyanotic spellfrequency 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 complicationfever with altered sensorium (abscess)
g. Prolonged fever with chills and rigorsIE
h. Older childsyncope/chest pain/arthritis(gout)
i. Any iron supplementation
2. Antenatal history:
a. Mothers ageDowns
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:
a. Cyanosis,clubbing,Polycythemia
b. Anthropometry
c. Inspection:
i. Precordial bulge
ii. Apical impulse will be normal in position
d. Palpation:
i. Parasternal heave
ii. Palpable murmurs
Page 31
e. Auscultation:
i. P2 is delayed & soft ,it is inaudible
ii. S2 is single which is aortic component
iii. ESM at left 3rd & 4th ICS
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/
Page 32
PROTEIN ENERGY MALNUTRITION (PEM)

Name:
Age:
Sex:
Religion:
Care taker:
Address:
Presenting complaints
-
Poor gain in weight / height
Associated complaints
-
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
Birth History
- Age of expectant mother
-
Maternal nutritional status
Birth order, Birth weight
Prematurity
IUGR
Perinatal complications
Dietary history
- 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

illnesses
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.
Page 33
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 / cows milk
-Dilution , bottle feeding. Over dilution and infection due to contamination are
common causes of malnutrition
H/O Weaning.
-
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

conditions.
SOCIO-ECONOMIC HISTORY
- 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.
Psychosocial history
Cultural practices
Page 34
On Examination
Anthropometry
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
of expected
Age independent anthropometric indicators
1. The Bangle test inner diameter of bangle of 4 cms crosses above elbow
2. The Shakirs tape green (13.5 cms), yellow ( 13.5 12.5 cms), red ( < 12.5 cms)
3. The Quac stick Quackers arm circumference stick
4. Modified Quac stick
5. The Nabarrows 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
> 2.5
- normal
2.0 2.5
- borderline PEM
< 2.0
- sever PEM
> 0.79
- normal
< 0.79
- malnutrition
9. Ponderal index ( Wt / Ht3 )
10. Dughdales ratio ( Wt / Ht1.6 )
Page 35
11. Quatelet index ( Wt kg / Ht2 cm) X 100
> 0.15
- normal
12. BMI (Wt kg / Ht2 m)

13. Mid arm muscle circumference - MAC ( 3.14 X SFT) cm
Classification of PEM
(I) IAP classification (1972)
N
> 80 % (Wt for age expected)
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
(IV)
Normal
> 90 %
1st deg PEM
75 90
2nd deg PEM -
60 75
3rd deg PEM
< 60 %
Classification as per height for Age and Weight for age

Ht for age
- Waterloos classification
Wt for age
McLareins classification
Page 36
Ht for age
Waterloos
McLareins
Normal
> 95
> 93
1st deg Stunting
90 - 95
80 - 93
2nd deg Stunting
85 - 90
3rd deg Stunting
< 85
< 80
Wt for age
Waterloos
McLareins
Normal
> 90
> 90
1st deg Wasting
80 - 90
85 - 90
2nd deg Wasting
70 - 80
75 - 85
3rd 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
Clinical Signs
-
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
Xerosis, hyperkeratosis
Eye Signs.- Pallor, xerosis, bitot's spot ,angular palpebreitis.
Page 37
Mucosal changes- Glossitis, Stomatitis, chelosis
Glands.
Hepatomegaly
Purpura or Bleeding
Oedema mooning of face
Mental changes Irritability, apathy
Tremors appear during treatment
-Parotid, thyroid gland enlargement
Investigations
- 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
-
Restoration,
Rehabilitation
Prevention care
Resuscitation..
Treat medical emergencies
o What emergencies? Hypothermia, hypoglycemia, electrolyte disturbance,
sepsis , shock, dehydration, cardiac failure, Anemia
Restoration.
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
Rehabilitation
Allow RDA as per ICMR recommendations
Supplementary through various national nutrition programmesICDS
Growth monitoring
Developmental stimulation
Page 38
Prevention
Prevent LBW babies.Antenatal care & Care of adolescent girls
NIMFES .. Nutrition, Immunization, Medical care, Family planning, Education,
Stimulation
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.
Page 39
NEONATAL CHOLESTASIS
Name :
Age :
Sex :
DOB :
Consanguinity :
C/O
Jaundice
Onset of Jaundice
Associated with high colored urine +/- clay colored stools (Obstructive jaundice)
Abdominal distension
Progressively increasing (organomegaly, Ascites)
Upper or lower abdomen
Urine output
Stool history
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
Dysmorphic features
Family history of hemolytic anemia
History of complications
Bleeding from any site
Altered sensorium
Ascites
Examination
General examination
Jaundice,
Fundus for chorioretinitis
Signs for Vitamin Deficiencies
Page 40
Edema, anasarca
Anemia
Dysmorphic features (Chromosomal, Alagille)
Cataracts
Abdominal examination:
Inspection : Localized bulge, distension (which quadrant is more affected)
Palpation : Superficial palpation: Guarding, tenderness, rigidity
Deep Palpation
o Hepatomegaly
o Splenomegaly
Tender/Nontender
Surface: Smooth/Nodular
Span and Size
Border: well felt/ sharp/diffuse
Consistency: Soft/firm/hard
Size (Grades of splenomegaly)
Consistency: Soft/firm
Splenic notch
Kidneys
Divarication of recti
Hernial sites
Percussion: Shifting dullness/horseshoe dullness/fluid thrill. Puddles sign
Auscultation: Renal Bruit, Venous hum
Other systems: Cardiac murmur, hydrocephalus, Meningitis
Diagnosis
Neonatal jaundice
With/without hepatosplenomegaly,
With/without ascitis
With/without dysmorphic features
With/without anemia
With/without associated anomalies
Most likely etiology being :

Neonatal Hepatitis / Biliary atresia / Inborn error of
Metabolism / Galactosemia/ Chromosomal disorder
Page 41
Investigation:
Jaundice in newborn
Conjugated jaundice
Unconjugated jaundice
Infective: Viral :CMV, Rubella, Reovirus III, Hep B

Bacterial: E. Coli, Listeria,
Protozoal: Toxoplasma
Inherited : Niemann-Pick Type C, Galactosemia,
Alpa-1 antitrypsin deficiency, Biliary Hypoplasia (Syndromic),
Progressive intrahepatic cholestasis
Chromosomal Anomalies: Trisomy 13/18/21
Idiopathic
Biliary atresia Neonatal Hepatitis
Choledochal cyst
Miscellaneous: TPN, Hypothyroidism, Maternal alcohol
Ingestion, Erythromycin estolate, Frusemide
Biochemical/
Special Etiological Tests
Morphological
Tests
Routine tests
Other tests
LFT including
Blood culture
USG abdomen
X-ray spine:
Bilirubin
Urine culture
Hepatobiliary
(Alagille)
SGOT/SGPT/GTP/
Alk.PO4
Stool culture
Scan
X-ray chest:
CRP
Cholangiogram
(Cardiomegaly)
PT/PTT
VDRL
(Peroperative/
Fundoscopy:
Total proteins
TORCH titres
Laproscopic)
(Chorioretinitis)
RFT
(Both of child and mother)
Hemogram
HbsAg, HIV
S.electrolytes
Test for Galactosemia
S.Ammonia
Antitrypsin levels
VBG
UAA/PAA
RBS
Thyroid function tests
Histopathology
Staining with HE
and PAS.
Page 42
Treatment:
General measures:
Proper nutrition and multivitamin supplementation in cholestatic doses
Vitamin K supplementation
Phenobarbitone
Cholestyramine/Urodeoxycholic acid
Specific measures
Toxoplasmosis: Sulphamethaxazole, pyrimethamine
Galactosemia: Galactose free diet
Biliary Atresia: surgical intervention
Choledochal cyst: Surgical intervention
Page 43
HEPATOSPLENOMEGALY WITH ANEMIA
Name:
Age : Sex :
Religion:
Address:
HISTORY:
Complaints
Abdominal lump
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.
Etiological history:
No h/o Kochs/ Kochs 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
encephalopathy)
No h/o blood transfusions, other sibs affected (Hepatitis B/ Hepatitis C / Chronic

hemolytic anemia)
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 disorderNiemann-Pick disease, Gauchers)
No h/o defective vision/ hearing (Mucopolysacchridosis, Osteopetrosis)
Page 44
No h/o fever / rash in mother during pregnancy (intrauterine infection)
No h/o fractures (Osteopetrosis)
EXAMINATION:
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
Genitals
BCG mark, abdominal tap mark, liver biopsy mark.
Skull/ spine
Dental cavity- dentition, fetor hepaticus
SYSTEMIC EXAMINATION
Abdominal system:
INSPECTION:
Abdomen:
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.
Page 45
PALPATION:
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

Diagnosis
-------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.
Differential diagnosis:
Hepatosplenomegaly:
Infection - Disseminated Kochs, malaria, kala azar, SBE, IU infection, Neonatal

Hepatitis syndrome.
Hematological - Chronic hemolytic anemia, leukemia, Hodgkins lymphoma.
Congestive - CCF, constrictive pericarditis, Budd-Chiari, Portal hypertension.
Storage - Niemann pick disease, Gaucher, GSD, MPS.
Splenohepatomegaly:
Gauchers disease type 1 to 4
Page 46
Hepatosplenomegaly with lymph nodes:
Disseminated Kochs, leukemia, lymphoma, infectious mononucleosis.
Splenomegaly with pallor/ icterus:
Hemolytic anemia, cirrhosis, Portal hypertension, hypersplenism.
Splenomegaly with petechie / ecchymosis:
Acute leukemia, SBE, ITP, hypersplenism.
Hepatomegaly:
TB, kwashiorkor, CCF, leukemia, lymphoma, congenital hepatic fibrosis, Storage

disorders (glycogenosis, MPS, Gauchers disease, Niemann-pick disease), tumors
(hepatoblastoma, wilms, neuroblastoma).
Splenomegaly:
Infections- malaria, kala-azar, TB, SBE, CMV, EBV, Toxoplasmosis.
Hematological -hemolytic anemia, hemoglobinopathies.
Congestive - PHT, cirrhosis, chronic CCF, constrictive pericarditis.
Infiltrative- Niemann-pick disease, Gauchers disease.
Neoplastic -leukemia, lymphoma.
Miscellaneous-Rheumatoid arthritis, SLE.
Massive splenomegaly-disseminated Kochs, malaria, kala-azar, Extrahepatic portal

hypertension, tropical splenomegaly, spherocytosis, osteopetrosis.
Moderate splenomegaly- above+ leukemia, Hodgkins lymphoma, hemolytic anemia.
Mild splenomegaly -above+ typhoid, SBE, septicemia.
Hepatosplenomegaly with anemia:
Neonatal-Isoimmune hemolytic anemia, congenital spherocytosis, alpha thalassemia,

TORCH, TB, congenital malaria, congenital leukemia, histiocytosis, neuroblastoma,
osteopetrosis.
Infancy- Thalassemia, sickle cell anemia, Malignancy, Malaria, Kala-azar, TB,

Gauchers, Niemann-Pick disease, GSD.
Page 47
Childhood spherocytosis, Infection, JRA, SLE, Cirrhosis with portal hypertension,

Malignancy
Hepatosplenomegaly with ascites:
Disseminated Kochs
Cirrhosis of liver- post hepatitis, Indian childhood cirrhosis, Wilsons Disease, portal
hypertension
Congestive- Constrictive pericarditis, Budd-Chiari, pericardial effusion.
Malignancy-rarely ascites.
Page 48
THALASSEMIA
Name:
Age : Sex :
Religion:
Address:
Complaints:
Presented with c/c of increasing pallor
Failure to thrive
Elaboration of complaints:
Increasing pallor: easy fatigability, palpitation, fast breathing, edema.
Only symptoms pertaining to RBC or combined RBC+WBC(repeated

infection)+Platelet(bleeding manifestations)
H/o repeated transfusionstransfusions 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,

iron overload
FAMILY HISTORY - OF Sibling/ relatives receiving transfusions

DIET HISTORY - to check the iron consumption in food
Rest of the history as usual.
ON EXAMINATION
GENERAL INSPECTION
Position patient,Vital parameters, Growth Parameters Height, Weight with Percentiles,

Tanner staging for puberty ,
Skin Colour , Pigmentation, Pallor, Jaundice
Page 49
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),
Hyperdynamic(anaemia)
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
Hepatosplenomegaly
Lower limbs and gait- Leg ulcers , Ankle odema (CCF), Bony tenderness
Gait examination for long tract signs-----due to vertebral bony expansion and cord
compression
Delayed ankle jerk relaxation
Back examination for lordosis, tenderness
Others-Urinanalysis for glucose
Chvosteks and Trousseaus signs(hypoparathyroidism)
Hearing(sensorineural deafness)
Commonly asked questions:

Differential Diagnosis of Hemolytic anemias.
Ideal transfusion regime.
Complications of Thal major and Blood transfusions.
Penatal diagnosis.
Diagnosis of hypersplenism.
Chelation therapy
Recent advances in management of Thal major.
Page 50
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.
History :
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.
Page 51
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

deficiency
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

stature
Page 52
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
taken.
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 & 4th year,
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 1314 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
hypothyroidism
Dysmorphism------congenital syndromes
Midline defects-------hypopituitarism
Page 53
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

deficiency
Jaundice, clubbing------chronic liver disease
Goitre ,impalpablethyroid, coarse skin------hypothyroidism
Central obesity ,striae ,proximal muscle weakness------Cushings
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
Pyles Atlas method and Tanner and Whitehouse scoring method.
Normal ranges of bone age range:
Range + 2SD
Chronological age
Male
Female
+/- 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.
Page 54
Investigations
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.Creatinine------CRF
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.
Page 55
APPROACH TO EVALUATION OF SHORT STATURE

Is the child short ?
( Ht less than 3rd centile)
No
*Reassurance
Yes
1) Is the height within midparental height (MPH) range
*Assess growth velocity

No
Yes
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
Hormone deficiency
Assess growth velocity (over 6/12 mon)

Screening tests
CBC, Hb, ESR ( anemia ,infection),
Bone age
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
IGF1
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, CLDChronic Liver Disease)
Page 56
Note
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. )

= (( Mothers height +13) + Fathers height )/ 2 ( BOYS)
= ((Mothers height +( Fathers 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 (cushings 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
Page 57
APPROACH TO A CHILD WITH RICKETS

Complaints:
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
Associated symptoms(etiology)
Polyuria, polydypsia (Renal rickets, RTA)
Recurrent diarrhoea, steatorrhoea ( Malabsorption..fat)
Jaundice, distension abdomen (Chronic liver disease, Cholestatic jaundice)
Pallor (Nutritional, Wilsons disease, Chronic renal failure)
Visual problems (Lowes syndrome, Cystinosis)
Alopecia - Patchy, totalis (Vit. D Dependent Rickets Type II)
Hearing affection ( RTA)
Recurrent respiratory infection
Mental retardation
Drugs ingestion- Anticonvulsants,anti tubercular drugs
Antenatal history
Calcium supplement in expectant mother
Consanguinity (Autosomal recessive disorder)
Preterm /Full term (Osteopenia of prematurity)
IUGR (may manifest with rickets during catch up growth)
Dietary history
Breast feed/ top fed
Vit D or Calcium supplement
Weaning
Balanced diet
Exposure to sunlight
Family history of similar complaints (X linked hypophosphatemic rickets)
Page 58
Examination
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
Rachitic rosary
Harrison sulcus
Pectus excavatum
Widening of wrists
Double malleolus
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
secondary detention.
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.
Diagnosis:
Page 59
BRONCHIECTASIS
Name :
Age : Sex :
Address :
HISTORY:
PRESENTING COMPLAINT: Patients typically present with fever, chronic cough,
purulent sputum, weight loss and loss of appetite.
A) RESPIRATORY SYSTEM
SYMPTOMS
o Impaired exercise tolerance
o Cough-frequency/severity/nocturnal/exercise induced/change in
pattern.
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,
pulse oximetry.
THERAPY RECEIVED - exercise, physiotherapy, nebulised saline, bronchodilators
or antibiotics.
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.
Page 60
IMMUNIZATION: History of receiving BCG or measles or pertussis vaccine.

EXAMINATION:
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
RESPIRATORY 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
Auscultation -
Hyperinflation /consolidation
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
DIAGNOSIS:
Page 61
TIPS FOR STUDENTS

Dr. Ranjitha
Registrar, KKCTH
Firstly, exams are just a phase in life. It too will pass. So, do not make it a do-or-die
experience.
Be systematic.
Plan ahead.
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
dont 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. Dont
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.
Page 62
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
progress.
Do not forget community medicine, vaccination, recent advances.
If possible, formulate your own questions in each topic. Think about how you would
answer that.
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
win.
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.
Page 63
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.
Practical examination:
Relax for a few days / weeks after theory exams and then start preparing for
practicals.
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, dont worry about making
errors, it is better to make them now than in the exam. Learn from your mistakes and
others too.
Try to finish taking history and clinical exam within 45 minutes.
Page 64
Request your teachers and friends to correct you / show you how to elicit signs and do
the examination.
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.
Dress neatly.
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 dont make it a habit.
Be loud and clear while you talk.
Be confident.
They are only making you do what you have been doing daily in the hospitaltake
history, do clinical examination, derive at a differential diagnosis, plan the line of
management.
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.
Page 65
Page 66

PG Clinical Training in Pediatrics 2013

Încărcat de

Informații document

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

PG Clinical Training in Pediatrics 2013

Încărcat de

Drepturi de autor:

Formate disponibile

i

XIV KKCTH MILLENNIUM ENDOWMENT ORATION AND

20-09- 2013 & 21-09-2013

Under the auspices of

Kanchi Kamakoti CHILDS Trust Hospital &

Overview of the program - Dr.S.Balasubramanian

Cyanotic heart disease - Dr.Nalini Bhaskaranand / Dr.Riyaz

Acyanotic heart disease - Dr Andal / Dr Srinivasan

Rheumatic heart disease -Dr.Srinivasan / Dr.Vasanthi

Neurodegenerative disorders Dr.Rana /Dr.V.Viswanathan

Hepatosplenomegaly (Hemato-oncology) - Dr.Riyaz / Dr.Janani

Chronic liver disease - Dr.V.S.Sankaranarayanan/Dr.R.Ganesh

Bronchiectasis - Dr.Subbarao/ Dr N.Suresh

Hemiplegia - Dr.Kumaresan / Dr.LalithaJanakiraman

Cerebral palsy- Dr Rana /Dr T.Ravikumar

Post Graduate Clinical training in Pediatrics

Differential diagnosis in Pediatric Neurology: Dr Rana

Nutrition& Anthropometry- Must know areas:

Differential diagnosis of Hepatosplenomegaly: Dr John Matthai

12.00 1.00 PM Millennium orationPneumococcal diseasePast, Present & Future

Case analysis in Respiratory system: Dr Subbarao

Approach to congenital heart disease: Dr Srinivasan

OSCE--Dr BalaRamachandran, Dr K.G.Ravikumar,

Feedback & wrap up

Mr.Karthik Narayanan, Chairman,KKCTH

Dr.K.MathangiRamakrishnan, Chairman, CTMRF

Dr A.Andal, Medical Director, KKCTH

Finance & Administration

On behalf of the CHILDS Trust Medical Research Foundation (CTMRF), I wish to

List of Millennium Orations

Newer Perspectives in Pediatric Neurology

Guest Oration given by

Dr. Prem Puri

Hotel Chola Sheraton

Second KKCTH Commemoration Oration

CME on Pediatric Gastroenterology

Guest Oration given by

Third KKCTH Commemoration Oration

CME & Refresher Update of Laboratory Medicine

Guest Oration given by

Fourth Millennium Guest Oration

Advances in Pediatric Surgery

Guest Oration given by

Prof. Arnold G.Coran,

Hotel Taj Connemara

Fifth Millennium Guest Oration

National CME on Pediatric Critical Care

Guest Oration given by

Dr. Brain Anderson,

Hotel GRT Grand

Sixth Millennium Guest Oration

Advances in Pediatric Surgery

Guest Oration given by

Prof Klass N.Bax, Prof of Pediatric Surgery

Hotel Taj Coromandel

Seventh Millennium Oration & National CME on Pediatric Cardiiology

Cardiac Surgery in Developing Countries

Guest Oration given by

Hotel GRT Grand Days

Eighth Millennium Oration

Cardiac Surgery in Developing Countries

Guest Oration given by

Hotel Taj Coromandel

Nineth Millennium Oration & National CME