PG Clinical Training in Pediatrics 2013

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ii

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)

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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

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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”

by

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

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Organizing Committee

Organizing Committee:

Dr Jayanthi Ramesh

Dr.Kalpana Gowrishankar

Dr Lalitha Janakiraman

Dr.LakshmiSundararajan

Dr.Major K.Nagaraju

Dr.S.Muralinath

Dr.S.Namasivayam

Dr.PriyaRamachandran

Dr.RahulYadav

Dr K.G.Ravikumar

Dr.T.Ravikumar

Dr T.Vasanthi

Dr.V.Viswanathan

Dr.Arathi Srinivasan

Dr.AmrutaKanjani

Dr.Eswararaja

Dr.R.Ganesh

Dr.M.Lakshmi

Dr.Padma Balaji

Dr.SenthilGanesh

Dr S. Srinivas

Dr.N.Suresh

Patrons

Mr.Karthik Narayanan, Chairman,KKCTH

Dr.K.MathangiRamakrishnan, Chairman, CTMRF

Dr A.Andal, Medical Director, KKCTH

Academic coordinators

Dr.V.S.Sankaranarayanan

Dr.S.Balasubramanian

Dr BalaRamachandran

Organizing secretaries:

Dr.Janani Sankar

Dr.R.Radhika

Finance & Administration

Mr.Sivakumar

Mr.Ananthanarayanan

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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

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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

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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,

Dublin, Ireland

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

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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,

Netherlands

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

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Nineth Millennium Oration & National CME

05.10.2008 National CME on Metabolic and Growth disorders

in Children

Guest Oration given by 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

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


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


Thirteenth Millennium Oration

07.10.2012 Tuberculosis in Children – Past, Present & Future

Guest Oration given by Prof. S.Mahadevan

JIPMER, Pondicherry


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Contents

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 [2013] Page 1

Developmental Assessment

Dr. Ganesh, Dr.Suresh

Consulting Paediatrician KKCTH

Item/Age Gross motor Fine motor & vision Social Hearing &

language

6 weeks • Grasp reflex • Social smile • Cooing

3 months • Head control

• Recognises

mother

• Turns head to

sound

4 months • Reaches for

objects

7 months • Rolls over

• Crawling

• Sits with hands forward

for support

• Palmar grasp

• Transfers objects

from hand-hand

• Smiles at mirror • Babbling

(ba,da,ka)

10 months • Sits without support

• Pivoting-turns round to

pick up a toy without

overbalancing

• Creeping

• Pincer grasp • Waves bye-bye

• Plays pat-a cake

• Uses amma,

appa

1 year • Can rise to Standing

• Walks alone

• Walks holding on to

furniture (cruising)

• Bottom shuffling

• Holds two cubes

and bangs

• Casting

• Pincer grip

• Waves bye-bye

• Plays pat a cake

• Asks for objects

by pointing

• Drinks from cup

• Turns to name

• Tells 2 words

with meaning

1 ½ years • Goes upstairs & down

stairs using hand

held/rails

• Carries toys while

walking

• Walks backwards

• Kneels without support

• Makes tower of 3

cubes

• Turns 2-3 pages in

a book at a time

• Scribbles

• Dry by day

• Holds spoon-takes

food to mouth

• Solitary play(

plays alone)

• Obeys simple

command:

Close the door

• Points to parts

of the body

when asked

• Echolalia

2 year • Goes upstairs & down

stairs-both foot/step.

• Runs

• Kicks the ball


cubes

• Copies vertical

line

• Turns page in a

book singly

• Turns door knob

• Unscrews lids

• Feeds with spoon

safely

• Wears shoe and

socks

• Gives name

• Obeys two step

commands(pick

the toy and put

in the basket)


Item/Age Gross motor Fine motor & vision Social Hearing &

language

2 ½ year • Tip toe walking

• Jumps

• Copies horizontal

line


cubes

• Makes train

• Recognize

themselves in

photos

• Pretends play

• Names one

color

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

cubes

• Can thread large

beads on to a

string

• Cuts paper with

scissors

• Eats with fork and

spoon

• Dry by night

• Dresses and

undresses if

helped with

buttons

• Knows own

name, age, and

gender

(boy/girl)

• Knows some

nursery rhymes

• Names 3 colors

4 year • Stands on one foot for

five second

• Walks heel-toe

• Hops

• Goes upstairs & down

stairs-one foot/step.

• Copies cross and

square

• Draws a man with

three parts

• Copies gate(6

cube steps)

• Threads small

beads

• Right-left

discrimination

• Dresses without

supervision

• Knows own

name, age,

gender

(boy/girl) and

address

• Names 4 colors

5 year • Skips • Copies triangle

• Makes 10 cube

steps

• Uses knife and

fork

• Knows own

name, age,

gender

(boy/girl)

address and

birthday


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.


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

Diet History

� Detailed dietary history � type of food, swallowing difficulties,

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


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-----------------


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


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


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 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

� 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


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 patient’s 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)


Diagnosis : Differential diagnosis of GBS - shown in the table below

Polio Guillain-Barré

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


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


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)

Infectious Causes

� 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)

Dehydration

� H/O Acute Gastroenteritis followed by seizures/ coma

(sagittal sinus thrombosis )

� H/O recurrent attacks of TIA /hemi paresis

(Migraine/Moya-Moya/alternating hemiplegia)

� H/O post seizure transient paralysis (Todd’s 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)


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


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


� 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) Internal capsule lesion

� Dense Hemiplegia

� Hemianaesthesia

� Homonymous hemianopia

� Dysarthria

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

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.


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 (Taysach’s)

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


• 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 – 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

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/ Zellweger’s syndrome

� Doll like faces – GSD (Pompe)

� V shaped face- myotonic dystrophy

� Pallor, clubbing, cyanosis, icterus, lymphadenopathy, oedema feet

� Anterior fontanelle

� Cataract’s(Lowe syndrome)


� 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


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

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 &

limb weakness


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.

Skull-

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

i) Craniotabes

Sunsetting (paralysis of upward gaze)

Spine-Neural tube defects. Look for tuft of hair


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


NEURODEGENERATIVE DISEASE


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 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


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


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

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

Chediac Higashi

- Skin changes - Hypothyroidism - Xerodema pigmentosa

- Hair - menke's kinky hair

- Trophic ulcers - (peripharal neuropathy)

- Self mutilation - Lesch nyhan

Fundus

- optic atrophy

- Cherry red spot

- Retinitis pigmentosa

- Central nervous system Examination

- PA - organomegaly

Diagnosis:


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.


� 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 koch’s

� 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


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.


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.


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.


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

Penicillin.

12. Other tests to prove streptococcal infection.


CYANOTIC HEART DISEASE

Checklist:

1. Complaints:

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:

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


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/


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.


- 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

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


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 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


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)

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 %

1st deg PEM - 75 – 90

2nd

deg PEM - 60 – 75

3rd

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


Ht for age Waterloo’s McLarein’s

Normal > 95 > 93

1st deg Stunting 90 - 95 80 - 93

2nd

deg Stunting 85 - 90 -

3rd

deg Stunting < 85 < 80

Wt for age Waterloo’s McLarein’s

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.


- Mucosal changes- Glossitis, Stomatitis, chelosis

- Glands. -Parotid, thyroid gland enlargement

- Hepatomegaly

- Purpura or Bleeding

- Oedema – mooning of face

- Mental changes – Irritability, apathy

- Tremors – appear during treatment

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 programmes…ICDS

� Growth monitoring

� Developmental stimulation


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.


NEONATAL CHOLESTASIS


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


� 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 - 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

� Kidneys

� Divarication of recti

� Hernial sites

� Percussion: Shifting dullness/horseshoe dullness/fluid thrill. Puddle’s 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


Investigation:

Biochemical/

Routine tests

Special Etiological Tests Morphological

Tests

Other tests Histopathology

LFT including

Bilirubin

SGOT/SGPT/GTP/

Alk.PO4

PT/PTT

Total proteins

RFT

Hemogram

S.electrolytes

S.Ammonia

VBG

RBS

Blood culture

Urine culture

Stool culture

CRP

VDRL

TORCH titres

(Both of child and mother)

HbsAg, HIV

Test for Galactosemia

Antitrypsin levels

UAA/PAA

Thyroid function tests

USG abdomen

Hepatobiliary

Scan

Cholangiogram

(Peroperative/

Laproscopic)

X-ray spine:

(Alagille)

X-ray chest:

(Cardiomegaly)

Fundoscopy:

(Chorioretinitis)

Staining with HE

and PAS.

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


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


HEPATOSPLENOMEGALY WITH ANEMIA

Name: Age : Sex :

Religion: Address:

HISTORY:

Complaints : Abdominal distension

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 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

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 disorder-

Niemann-Pick disease, Gauchers)

• No h/o defective vision/ hearing (Mucopolysacchridosis, Osteopetrosis)


• 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.


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 Koch’s, malaria, kala azar, SBE, IU infection, Neonatal

Hepatitis syndrome.

• Hematological - Chronic hemolytic anemia, leukemia, Hodgkin’s lymphoma.

• Congestive - CCF, constrictive pericarditis, Budd-Chiari, Portal hypertension.

• Storage - Niemann pick disease, Gaucher, GSD, MPS.

Splenohepatomegaly:

• Gaucher’s disease type 1 to 4


Hepatosplenomegaly with lymph nodes:

• Disseminated Koch’s, 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, Gaucher’s disease.

• Neoplastic -leukemia, lymphoma.

• Miscellaneous-Rheumatoid arthritis, SLE.

• Massive splenomegaly-disseminated Koch’s, malaria, kala-azar, Extrahepatic portal

hypertension, tropical splenomegaly, spherocytosis, osteopetrosis.

• Moderate splenomegaly- above+ leukemia, Hodgkin’s 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.


Childhood – spherocytosis, Infection, JRA, SLE, Cirrhosis with portal hypertension,

Malignancy

Hepatosplenomegaly with ascites:

• Disseminated Koch’s

• Cirrhosis of liver- post hepatitis, Indian childhood cirrhosis, Wilson’s Disease, portal

hypertension

• Congestive- Constrictive pericarditis, Budd-Chiari, pericardial effusion.

• Malignancy-rarely ascites.


THALASSEMIA

Name: Age : Sex :

Religion: Address:

Complaints:

• 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

infection)+Platelet(bleeding manifestations)

� 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,

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


• 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

• 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.

� Penatal diagnosis.

� Diagnosis of hypersplenism.

� Chelation therapy

� Recent advances in management of Thal major.


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.


• 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


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 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

hypothyroidism

• Dysmorphism------congenital syndromes

• Midline defects-------hypopituitarism


• 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------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

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.


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.


APPROACH TO EVALUATION OF SHORT STATURE

Is the child short ?

( Ht less than 3rd

centile)

No Yes

*Reassurance 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

Hormone deficiency

Familial short stature CDGP

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, CLD-

Chronic Liver Disease)


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. )

= (( 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


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, 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

� 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)


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:


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.


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 - 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

DIAGNOSIS:


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

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.


� 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.


� 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, don’t 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.


� 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 don’t 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 hospital—take

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.


Date post:	26-Dec-2015
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PG Clinical Training in Pediatrics 2013

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