Dr. B.

R Ambedkar Medical College and Hospital

DEPARTMENT OF PEADIATRICS

Paediatrics Clinical
Guide for Under Graduates

Ready reckoner

Jan 2019

By: Dr. M. Govindaraj (Prof&HOD)

Dr. Prabhavathi .R
Dr. Sandhya

Special thanks to Pediatric team of Dr.B.R.AMCH for their

contribution for students.
Dr. S.M. Prasad, Dr. Madhusudan.S.R, Dr. Ranganath.K.R,Dr. Suman,
Dr. Pallavi Hiremath, Dr. Sameeta Mercy Prabhu,
Dr. Zala Pranaliba Dharmendra Singh , Dr Srinidhi M,Dr.Pavan kumar
Interns : Tejaswini K.N,Pooja M.V,Anil Chowdary,Abhishek N.R
Priyanka .V, Aishwarya Lohidakshan,Uma Devi ,K M Angurajakumari
Gayathri Devi,D. Ekta Priyadarshini ,Adnan Ahmed.,Anishaw reddi
TOPICS

1) Steps of pediatrics model case sheet

2) Detail History Elicitation

a) Developmental Milestones
b) Immunization Schedule
c) Diet History and Diet Chart

3) General Physical examination

a) Vitals
b) Anthropometry
c) Head to toe examination

4) Common pediatric symptoms

a) Fever
b) Cough
c) Diarrhea
d) Vomiting
e) Pain Abdomen

5) Respiratory system

i) History taking and examination

ii) Model case sheet
6)Gastrointestinal tract

i) History taking and examination

ii) Model case sheet- acute GE
iii) Per abdomen model case sheet
iv) Nephrotic syndrome model case sheet

7)Cardiovascular system

I) History taking and examination

II) Acynotic congenital heart disease model case sheet
III) Cyanotic congenital heart disease model case sheet(TOF)
8)Central nervous system

CNS examination
a) Higher mental functions
b)Head to toe examination
c)Cranial nerve examination
d) Reflexes
e)Motor system examination
f)Proprioceptive sensation
g)Cerebellar signs
h)Types of gait.
i)Signs of meningeal irritation
j)Signs of raised ICT
k)Areas of the brain
A) Cerebral Palsy History taking and notes
B) Seizure model case sheet
c) Downs syndrome-notes

9)Protein energy malnutrition model case sheet

!0)Anaemia model model case sheet

11)Thalassemia notes

12) Neonatology

a) New born model case sheet

b) New born viva questions
c) Neonatal resuscitation steps
d) APGAR Scoring system
e) New ballards scoring system

13) Viva Spotters

a) X-ray spotters
b) Nutrition spotters
c) Immunization spotters
d) instruments
PAEDIATRIC MODEL CASE SHEET

NAME : Informant :
AGE : Reliability :
SEX :
ADDRESS :

1. Presenting Complaints:

2. History of presenting illness :

3. Past History :

4. Family History :

5. Birth History :

 Antenatal :

 Natal :

 Postnatal :

6. Developmental Milestones

7. Diet History

8. Immunization History

9. Socio Economic Status

Summary :
 General Physical Examination

Alert , Conscious, Comfortably lying on mother lap

Vitals

HR/Pulse rate

RR

B.P

CFT

Anthropometry

Present Expected Percentage %

Weight
Height
MAC
US/LS Ratio
Arm span

Classification any One of

Comment

Head to toe examination

Systemic examination

CVS

RS

PA

CNS

Diagnosis
 DETAIL HISTORY ELICITATION

1) INFORMANT

Person who takes care of the child and gives history regarding the child,
(reliability of the informant is based on his/her intellectual level,
awareness of the problem and emotional reaction to the disease)

2) NAME:
Identification, to develop rapport with the patient & parents

3) AGE : Pediatrics age - birth to 18 years

Importance of age

BIRTH AND NEONATES

Chromosomal Anomalies Genetic Syndromes, IUGR, Sepsis,
Jaundice , etc..

INFANCY :
Marasmus, Iron Deficiency Anemia, Rickets, Bronchiolitis,
Gastroenteritis, Bronchopneumonia, Measles.

EARLY CHILDHOOD:
Kwashiorkor, Gastroenteritis, Measles, Mumps
Acute Glomerulonephritis, Rickets.

CHILDHOOD:
Typhoid, T.B, Mumps Rheumatic Fever, congenital heart disease

4) IMPORTANCE OF SEX:

Males only : Hemophilia, Duchenne Muscular Dystrophy

Females only : Incontinentia Pigmenti,
Predominantly in males: Congenital Hypertrophic Pyloric stenosis,
Transposition of Great Arteries, G6PD deficiency
Predominantly in Females : Congential dislocation of hip , Rheumatic
Chorea, Patent Ductus Arteriosus.
5) FAMILY HISTORY :

1) Age of mother Down’s

Father Marfan’s Syndrome, Achondroplasia.

2) Number of siblings, Deaths, Abortions,

3) Familial illness, Genetic Disorders, Allergy , Asthma, Seizures, IEM

4) Contact the TB

5) Scabies, Infectious Diseases

6) Consanguinity

1st Degree - Parents, Siblings, Brother & Sisters - 50% (½ ) genes.

2nd Degree - Aunts, Uncles, Nephew, Nieces - 25% (¼) genes.
3rd Degree - 2nd Degree Cousins, 12.5% (1/8) genes.
4th Degree - Distant Relation

GENETIC DISORDER:

A) Autosomal Dominant - Achondroplasia, Marfans Syndrome,

Neurofibromatosis, Tuberous Sclerosis, WVD, Osteogenesis
imperfecta, Retinoblastoma, Hereditary spherocytosis

B) Autosomal Recessive:
Thalassemia, Sickle cell Anemia, Wilsons Disease, Glycogen Storage
Disorders, Cystic fibrosis, Phenylketonuria, Galactosemia,
Homocystinuria, Congenital adrenal hyperplasia, Ehler Danlos
Syndrome, Friedrich ataxia, Spinal muscular atrophy

C) X linked Recessive - Alports syndrome, Becker’s muscular

dystrophy, Duchenne muscular dystrophy, G6PD deficiency
Hemophilia A, B, Hunters disease, agammaglobulinemia, Brutons
disease, Wiscott Aldrich syndrome

D) X linked Dominant - Alport syndrome, incontinentia pigmenti,

RETT syndrome, Fragile X syndrome, hypophosphatemic rickets,
familial hypophosphatemia
 DEVELOPMENTAL MILESTONES

I : KEY GROSS MOTOR DEVELOPMENTAL MILESTONES

Sl. no AGE MILESTONES

1 3 Months Neck holding
2 5 Months Rolls over
3 6 Months Sits in tripod fashion (sitting with own support )
4 8 Months Sitting without support
5 9 Months Stands holding on ( with support)
6 12 Months Creeps well , Walk but falls , stands without support .
7 15 Months Walks alone , creeps upstairs.
8 18 Months Runs , explores drawers .
9 2Years Walks up and downstairs (2 feet /step), jumps .
10 3 Years Rides tricycle , uses alternate feet going upstairs
11 4 Years Hops on one foot, alternate feet going down stairs

II : KEY FINE MOTOR DEVELOPMENTAL MILESTONES

Sl. no AGE MILESTONE

1 4Months Bidextrous reach ( reaching out for objects with both
hands)
2 6 Months Unidextrous reach ( reaching out for objects with one
hand), transfers object.
3 9 Months Immature pincer grasp , probes with forefinger.
4 12 Months Pincer grasp mature .
5 15 Months Imitates scribbling, tower of 2 blocks.
6 18 Months Scribbles , tower of 3 blocks.
7 2Years Tower of 6 blocks, vertical and circular stroke.
8 3 Years Tower of 9 block, copies circle .
9 4 Years Copies cross, bridge with blocks.
10 5 Years Copies triangle , gate with blocks.
III : KEY SOCIAL AND ADAPTIVE MILESTONES

Sl. no AGE MILESTONE

1 2 Months Social smile (after being talked to).
2 3 Months Recognizes mother , anticipates feeds .
3 6 Months Recognizes stranger, stranger anxiety.
4 9 Months Waves ‘’Bye Bye’’ .
5 12 Months Comes When called, plays simple ball game.
6 15 Months Jargon .
7 18 Months Copies parents in task (Ex : Sweeping ).
8 2 Years Asks for food , drink, toilet, pulls people to show
toys.
9 3 Years Shares toys , knows full name and gender
10 4 Years Plays co- operatively in a group, goes to toilet alone.
11 5 Years Helps in household tasks, dresses and undresses.

IV: KEY LANGUAGE MILESTONES

Sl. no AGE MILESTONE

1 1 Month Alerts to sound.
2 3 Months Coos (musical vowel sounds ).
3 4 Months Laughs loud.
4 6 Months Mono-syllables (ba, da, pa), ah –goo sounds
5 9 Months Bi-syllables (mama,baba,dada)
6 12 Months 1-2 words with meaning.
7 18 Months 8-10 word vocabulary.
8 2Years 2-3 word sentences , uses pronouns ‘‘I’’, ‘‘Me’’,
‘‘you’’.
9 3 Years Ask questions, knows full name and gender.
10 4 Years Says song or poem, tells stories.
11 5 Years Asks meaning of words .
V : VISION

Sl. no AGE MILESTONE

1 Newborn  Pupillary reactions to light
 Blinking to light stimulus
 Conjugate horizontal gaze development
2 1 week Vestibule-ocular reflex
3 2 weeks Follows horizontal moving objects
4 1 month Can watch mother’s face for prolonged time
5 2 months Pursuits and convergence movements
Conjugate vertical movements
6 3 months Watches movements of own hands and reaches out
for interesting objects
7 5 months Grasps and explores objects
Stereopsis begins to develop
8 6 months Accommodation well developed
9 9 months Picks up small objects
10 3 years Best visual acuity approaches near to adult levels

VI : HEARING

Sl. No AGE MILESTONE

1 New born Responds to sound by startle , blink or cry.
2 3-4 months Turns his head towards the source of sound.
3 5-6 months Turns head to one side and then downwards if sound
is made below the level of ears.
4 10Months Child directly looks at the source of sound diagonally.
 National Immunization Schedule (NIS) for Infants, Childern and
Pregnant Women in Karnataka
Version Date : 08 th , March, 2016

Vaccine When to give Dose Route Site

For Pregnant Women

TT – 1 1 st visit to ANC 0.5ml Intra -muscular Upper Arm

TT – 2 4Weeks after TT-1* 0.5ml Intra -muscular Upper Arm

TT -Booster If received 2TT dose in a Single dose

pregnancy within the last
3yrs*
For Infants
At Birth – BCG-0.1ml ,intradermal
Opv-0 dose ,oral 2 drops
Hep B - 0.5 ml ,im

6,10,14 weeks- DPT,Hep B, Hib (Pentavac), 0.5ml I.M,

OPV, 14 weeks, ^IPV-0.1 ml ,intradermal

9 MONTHS - MR 1st dose,0.5ml ,S.C

Vit A 1st dose 1 ml (1 lakh IU)

15 MONTHS – MR 2nd dose,0.5ml,S.C

18 MONTHS – DPT (1st Booster),im

OPV

5 YEARS – DPT (2nd booster )

10 YEARS & 16 YEARS-TT (0.5 ml, I.M)

^ Inactivated polio virus vaccine at 14 weeks under National

Immunization program
 IAP Immunization Time Table
I IAP Recommended Vaccines For Routine Use
3
AGE VACCINE
- BCG
Birth - OPVo
- Hep –B1
- DTaP1/ DTwP1 Hib 1
6 WEEKS - IPV 1 Rotavirus1
- Hep – B2 PCV 1
- DTaP2 / DTwP 2 - Rotavirus2
10 WEEKS - IPV 2 - PCV 2
- Hib 2
- DTaP 3/ DTwP 3
14 WEEKS - IPV 3 - PCV 3
- Hib 3
6 MONTHS - Flu vaccine I dose
7 MONTHS - Flu vaccine II dose
- OPV 2
9 MONTHS - MMR1
9 - 12 MONTHS - Typhoid conjugate vaccine single dose
12MONTHS - Hep – A1

15 MONTHS - MMR2
- Varicella
- PCV Booster
- DTwP B1/DTap B1
16 to 18 MONTHS - IPV B1, Hib B1
18MONTHS - Hep –A2

4to 6 YEARS - DTwP B2 /DTap B2,MMR 3

- Varicella2
- OPV 3

10to 12 YEARS - Tdap /Td

GIRLS -HPV 2 Doses (9-14 years) 3doses(15-18 years)

 6) DIET HISTORY:
Methods:
a) 24 hours recall method
b) Food frequency questionnaire method
c) Food diary
d) Weighing the raw food method

BEDSIDE CALCULATION OF CALORIES

HOLIDAY AND SEGAR FORMULA

up to 10 kg 100 cal/kg
10-20kg 1000+50cal for each kg
> 20kg 1500+20cal
or
Energy Requirement: 1000 Kcal at 1 Year & add 100 Kcal every year.
Protein Requirement: 2 gm \Kg\Day

MODEL DIET CHART- 10kg Baby

Time Food item Quantity Calories Protein (g)

(kcal)
7.00am MILK 100ml 65 1.1

9.00am Idli 2 150 4

1.00pm Rice ½ cup 4 tsp 85 2

4.00pm Biscuit + Banana 2 20+90 0.4 + 2

8.00PM Rice ½ cup 4 tsp 85 2

Total 490 11.5

(observed)
Required 1000 20
(for a 10 kg
child)
Deficit 510 8.5

Comment on Diet History

 DIET CHART

Energy Requirement: 1000 Kcal at 1 Year & add 100 Kcal every year.
Protein Requirement: 2 gm \Kg\Day

RAW ITEMS
Item Quantity Protein(gms) Energy (Kcal)
CEREALS
(1) Rice 100 7 350
(2) Ragi 100 7 330
(3) Wheat 100 11 350
(4) 100 11 340
Maize(Corn) 100 10 350
(5) Jowar
PULSES
(1) Bengal gram 100 17 360
(2) Black gram 100 24 350
(3) Green gram 100 24 340
(4) Red gram 100 22 340
(5) Soya bean 100 43 430
(6) Horse gram 100 22 320
NUTS SERVING CALORIES
Almonds 10 Nos 85
Cashew nuts 10 Nos 95
Peanuts 50 Nos 90
Ground nut 100 gms 560 Kcal
Dates 100gms 317
FRESH FRUITS
Fruits Serving Calories
Apple 1 Medium 65
Banana 1 Medium 90
Grapes 30 Nos 70
Guava 1 Medium 50
Mango 1 Medium 180
Mosambi 1 Medium 43
Orange 1 Medium 48
Papaya 1 Piece 80
Pineapple 1 Piece 50
Chikku 1 Medium 80
Watermelon 1 Slice 15
 NUTRITIVE VALUE OF COOKED FOOD

Cereal Quantity Calories Protein

(1) Cooked Rice 1 cup 170 4

(2) Ragi ball Medium(6 tsp) 100 2

(3) Idli 1 no 75 2

(4) Dosa 1 no 75 2

(5) Upma(Uppitu) 1 cup 270 6

(6) Puri 1 no 80 1

(7) Bread 2 slice 170 2

(8) Phulka\Roti 1 no 80 2

(9)Khichidi and Pongal 1 cup 200 6

Wheat Porridge( Gangi) 1 cup 220 6

NUTRITIVE VALUE OF MILK ( 100ML) & MILK

PRODUCTS
Milk Protein Fat Calories

Human Milk 1.1 3.4 65

Buffalo Milk 4.3 6.5 117

Cow’s Milk 3.2 4.1 67

Skimmed 38 0.1gm 357

milk(100gm)powder
Goat’s Milk 3.3 4.5 72
PULSE QUANTITY KCALORIES
Plain dhal 1\2 cup 100

Sambar 1 cup 110

Vegetable with gravy 1 cup 170

Dry 1 cup 150

Savoury Snacks 2 70
Bajji
Vada 2 140

Potato bonda 2 200

Samosa 1 200

Sandwich(butter) 2 tsp 2 200

Veg puff 1 200

Pizza(cheese & 1 slice 200

Tomato
Masala dosa 1 200

Non-Veg QUANTITY CALORIES

1) Egg Boiled 1 egg ---60gms, 6gm protein
(Contains all nutrients 6 gm fat, 30mg calcium
except carbohydrate 1.5mg Iron
& Vitamin C ) 60 Kcal
Omlet 1 160Kcal

Mutton curry 3\4 cup 260

Chicken curry 3\4 cup 240

Fish fried 2 big piece 190

SWEETS AND DESSERTS
Sl.No Name Quantity Calories
1) Besan Barfi 2 pieces 400
2) Chikki 2 pieces 290
3) Halwa(Kesari) 1\2 cup 320
4) Jelly\Jam 1 tsp 20
5) Milk Chocolate 25g 140
6) Ice Cream 1\2 cup 200
BEVERAGES
1) Tea(2 tsp sugar+50ml 1 cup 75
toned milk)
2) Coffee (2 tsp sugar + 1 cup 110
100ml toned milk)
3) Cow’s milk(2 tsp 1 cup 180
sugar)
4) Buffalo milk(2 tsp 1 cup 320
sugar)
5) Lassi(2 tsp sugar 1 glass(200ml) 110
6) Cold Drinks 1 bottle(200ml) 150
7) Fresh Lime Juice 1 glass(200ml) 60
NIN --- HYDERABAD MIX
Ingredients Quantity Energy Protein
Whole Wheat-Roasted 40gm
Bengal Gram – Roasted 16gm
Groundnut – Roasted 10gm
Jaggery 20gm
Total 86gm 330Kcal 11.39
DAVANGERE – MIX
Ragi 25gm
Bengal gram 25gm
Ground nut 25gm
Jaggery 25gm
Total 100gm 411.75 14.09
OUR HOSPITAL KANJI
Rice(2 tsp) 10gm 34 Kcal 0.85g
Bengal gram(1 tsp) 5 gm 18 Kcal 1.04g
Oil ( 1tsp) 5g 45Kcal
Sugar(1 tsp) 5g 20Kcal
Total 25gm 117Kcal 1.89g
SAT MIX
Rice 20
Wheat 20
Black Gram 20
Sugar 40
Total 100g 380kcal 8g
 PEM DIET
STARTER DIET :

F – 75 MILK BASED

COW,S MILK 30ml

SUGAR 9 gm
VEGETABLE OIL 2gm
WATER (Make up to ml ) 100ml
ENERGY (Kcal ) 75 Kcal
PROTEIN 0.9gm
LACTOSE 1.2gm

F – 75 CEREAL BASED
Example :- 1Example :- 2

Cows ,milk : 30 ml 25 ml
Sugar : 6 gm 3 gm
Powder Puffed Rice : 2.5 gm 6 gm
Vegetable Oil : 2.5 gm 3 gm
Water (make up to) : 100 ml 100 ml
Energy : 75 Kcal 7.5 Kcal
Protein : 1.1 gm 1.2 gm
Lactose : 1.2 gm 1 gm

CATCH UP DIET

F – 100 MILK BASED CEREAL BASED

PUFFED RICE – 7gm
COWS MILK 95 ml 75 ml
SUGAR 5 gms 2.5 gms
VEGETABLE OIL 2 gms 2 gms
WATER TO MAKE 100 ml 100 ml
ENERGY 101 Kcal 100 Kcal
PROTEIN 2.9 gms 2.9 gms
LACTOSE 3.8 gms 3 gms

General physical examination

VITALS
1) Temperature
Temperature Degree centigrade Degree Fahrenheit
Normal 36.6-37.2 98-99
Febrile/Pyrexia > 36.6 > 98
Hyperpyrexia > 41.6 > 107
Hypothermia < 35 < 96

2) Pulse
Characteristic features of the pulses
Feature Artery Findings
Rate Radial artery Bradycardia & tachycardia
Rhythm Radial artery Regular, irregular, regularly
irregular, irregularly
irregular
Character Carotid artery Slow rising, water hammer,
pulsus alternans
Volume Carotid artery Normal, low or high
Radiofemoral delay Radial artery, Seen in coarctation of aorta
femoral artery

Normal pulse rate at various ages:

Age Beats/min
<6months 120-160
6-12months 110-120
1-5yrs 95-100
6-12yrs 80-110
>12yrs 60-100

3) Respiratory rate
Normal respiratory rate at various ages
 Age Normal respiratory rate
(breaths/min)
<2months 30-50
2-12 months 20-40
12 months to 5 yrs 20-30
5-10yrs and >10 years 15-20

4) Blood pressure
Normal ranges in children
Age Blood pressure mm/hg)
Systolic Diastolic
Newborn 50-70 25-45
Upto 6 months 60-80 30-50
6months-1yr 60-90 50-70
1-6yrs 70-100 40-70
7-12 yrs 90-110 50-70

Formulae:
Systolic BP (99th centile) = 90 + (2 X age in years)
Systolic BP (5th centile) = 70 + (2 X age in years)
Diastolic BP = 55 + (2 X age in years)
[For the purpose of Hypotension]
Pulse pressure = systolic BP – diastolic BP
{ narrow pulse pressure – 20 or less
Wide pulse pressure – 40 or more }
Mean arterial pressure = diastolic pressure + 1/3 of pulse
pressure.[For management of shock in children]

ANTHROPOMETRY

Weight :-
Birth Weight : 3kg
5 Months : 6kg (Double)
1Year : 9kg (Triple)
2Year : 12 kg (Quadriple)

Baby lose 10% of the baby weight after birth and regains its birth weight
by 10th day of life.
later gains weight at the rate of 25 - 30 gm Per day till 3 months of age
10 - 15 gm Per day from 3 – 6 months of age

Weight formulas

3 – 12 months Age (in months) + 9

2
1 - 6 Years Age ( in years ) x 2 + 8

7 - 12 Years Age ( in years) x 7 - 5

2

LENGTH UP TO 2 YEARS
(to be checked in infantometer)

HEIGHT AFTER 2 YEARS

LENGTH
BIRTH 50 cms
3MONTHS 60 cms
9 MONTHS 70 cms
1 YEARS 75 cms
( length increases by 2 cms every month upto 1 year )
2 YEARS 90 Cm
Formula

2 - 12 years 6 X A + 77
12 TO 18 Years Percentile Chart
HEAD CIRCUMFERANCE

BIRTH 33 - 35 Cm

1 - 3 MONTHS 2 Cms / month

Growth
3 - 6 MONTHS 1 Cm / month

6 MONTHS - 1 YEAR 0.5 Cm / month

NORMAL H.C

3 MONTHS 40 Cm
6 MONTHS 43 Cm
1 YEAR 47 Cm
2 YEARS 48 Cm
4 YEARS 50 Cm
Adult head circumference reaches at 5 years =52-54 cms

Chest Circumference : About 3 cms less than the Head

Circumference at birth ,equal to H.C by 1year, Chest Circumferance
exceeds the Head Circumference after 1 year.
Body Surface Area :
Grading of malnutrition according to weight for age :

- IAP Classification – most commonly used

- Gomez’s Classification
- Jeliffe's Classification
- Welcome Classification

Grading of malnutrition according to weight for age :

- Water low’s Classification

- Maclearer's Classification Mac – Claren’s
- Visweshwara rao’s Classification

WHO Classification considers

a) Weight for age
b) Height for age
c) Weight for height

IAP Classification
Nutritional status Weight for age(% of expected)

Normal > 80

Grade I PEM 71 – 80

Grade II PEM 61 - 70

Grade III PEM 51 - 60

Grade IV PEM < 50

WHO Classification of under nutrition in under five children

ModerateSevere
Under nutritionunder nutrition

Symmetrical edema NO YES

Weight for Height 0-79 % of < 70 %

expected
(Measures wasting ) expected wasting severe wasting

Height for age 85%- 89% of < 85 % of expected

(Measures stunting) expected stunting Severe stunting

WHO Classification :

Weight / age Height / age Weight /

Height
Acute
Malnutrition ↓ N ↓

Chronic ↓ ↓ Normal
Malnutrition

Acute on chronic ↓ ↓ ↓
Malnutrition
Other important anthropometric measurements

Mid arm circumference (MAC)

Upper segment : lower segment ratio (US : LS)
Midparental height (MPH)

MAC

-Done between 1yrs – 5 yrs

- Age independent anthropometric index
- Measured on left arm midway b/n acromion & olecranon
- Shaker’s tape is used which is color coded
Green >13.5 cm – normal
Yellow 12.5 cm – 13.5cm - moderate PEM
Red < 12.5 cm – Severe PEM
< 11.5 cm – SAM Severe acute malnutrition

Us : Ls ratio :
LS - measured from symphysis pubis is to toes
US - total length – LS
At birth - 1.7 : 1
6 month - 1.6 : 1

1 year - 1.5 : 1
2 years - 1.4 : 1

4 years - 1.2 : 1

By 7 years - 1 : 1

MPH

- It is a good prediction of adult height ( height at 18 years of age)

- Used in growth retardation & short stature

MPH for male child = Father Ht + Mother Ht +13

2

MHP for female child = Father Ht + Mother Ht -13

2
MHP + 8cm is plotted at 18 years on growth chart , which given the
expected adult height of the child.

BMI : Body mass index < 13 - sereve under weight

Quetlet index < 15 – modulate under nutrition

BMI = Wt in kg18 - 25 - Normal

Ht in m2 > 25 - Over Weight

BMI also expected in percentiles> 30- obese

< 5th cantle - Under Weight

5th -85th - Normal
> 85th - Over Weight
> 95th - Obesity

Age independent anthropometric indicators

Can be used Irrespective of age

a) The Bangle Test

B) The Shakers’ Tape
C) The Quackery Arm Circumference Stick
WHO DEFINITION OF SAM
SEVERE ACUTE MALNUTRITION

1) Weight For Below – 3 SD On WHO Growth Charts

2) Visible Severe Wasting

3) Presence Of Bipedal Edema

4) Mid Upper Arm Circumference

MUAC < 11.5 cm

MAC :

>13.5 Cm – Normal – Green

12.5 cm – 13.5cm – Moderate PEM – Yellow

< 12.5 cm – severe PEM – Red

< 11.5 cm – SAM-Severe acute malnutrition

 HEAD TO TOE EXAMINATION

1) Head : Shape, Size, Anterior fontanalle/PF, Deformity, Frontal

Bossing

2) Eyes : Epicanthal Fold, Mongolian Slant, Hyper/Hypotelorism,

Microphthalmia, Cataract, Features of Vitamin A Deficiency
(Bitots Spot,Corneal Xerosis, Corneal ulceration),
LischNodules,

3) Ears : Low set ears, Pre-Auricular Sinus/Skin tags, Discharge,

Otoscopic Examination

4) Nose : Depressed nasal bridge, DNS, Sinuses,

5) Oral Cavity : High arched palate, Cleft lip, Cleft palate,

Dentition (formula), Tooth caries

6) Throat : Pharyngeal Congestion, Tonsillar Enlargement

7) Facies : Hemolytic Facies, Moon facies, Adenoid facies,Triangular

facies ( Silver russel syndrome)

8) Neck : Short neck, Webbing of neck, Low hair line

9) Chest : Pectus excavatum, Pectus carinatum,

Costochondral beads, Harrison sulcus

10) Skeletal anomaly : Polydactyly, Syndactyly, Bow legs, Knocknee,

Club feet, Scoliosis

11) Nail changes : Koilonychias, Leuconychia, knuckle pigmentation

12)Hair changes : Sparseness, Depigmentation, Flag sign Brittleness

13)Skin: Haemangioma, Neurocutaneous Markers, Petechae,Purpura,

Rashes, Fibroma, Dryness

14)Genitalia: Testicular volume, Penile length, Undescended testes,

Hypospadiasis, Phimosis, Ambiguity

12) Pallor, Icterus, Cyanosis, Clubbing, Lymphadenopathy

FEVER CASE PRESENTATION TIPS

 DEFINITION: Elevation of body temperature above normal circadian

range, as a result of change in thermoregulatory mechanism(due to
infection, metabolic derangement or increased cell destruction)
 Normal body temperature: 97.5F-98.9F(36.4-37.2C)
In newborns 97.7F- 99.4F (36.5-37.5c)
 Evening temperature (0.5 to 1C) > morning.
 RECTAL >ORAL>AXILLARY
 HYPERPYREXIA: Elevation of core temperature above 41C (106F).
Seen in heat stroke, Pontine Haemorrhage, Malaria, Epticemia,
Meningitis, Malignant Hyperthermia.

HISTORY:

 ONSET :
Acute – Ex: Pyelonephritis, Pneumonia
Insidious – Ex: Typhoid, Infective Endocarditis, TB, Brucellosis.
 DURATION
 CHARACTER : Continuous, Remittent, Intermittent
 SEVERITY : Mild, Moderate, Severe.
 CHILLS & RIGOR : In infectious process like malaria, UTI,
Septicemia, Lobar pneumonia.
 Localising Symptoms: (Indicates system involved)

 CHARACTER OF FEVER:
1) Continuous fever : fever doesn’t touch baseline, fluctuates <1C in 24
hours.
Ex: Enteric fever, bacterial endocarditis, viral pneumonia, UTI.

2) Remittent fever : fluctuates >1C in 24 hrs, without touching

baseline.
Ex: Infective Endocarditis, Brucellosis, Malignancy, Kawasaki
Disease.

3) Intermittent fever : Fever touches baseline for few hours during the
day.
Ex : Malaria, Acute Pyelonephritis, Local boils, Furuncle
 Quotidian : Daily occurring (Ex: juvenile RA)
 Tertian : Fever occurring on alternate days (Ex: Vivax malaria)
 Quartan : Fever occurring at 2 days intervals (Ex:Malariae
malaria)
4) Step ladder fever : Temperature gradually increases to higher level
with
every spike, so that new plateau is higher than preceding one.
Ex: Enteric fever

5) Relapsing fever : fever for 2-9days,afebrile period for 2-9 days and
cycle repeats
Ex: Borrelia infection.

6) Pel Ebstein fever : Fever 3-10 days, Afebrile 3-10 days.

Ex: Hodgkins Disease, Other Lymphomas

NOTE: Because of widespread use of antipyretics and antibiotics,

classical
pattern of fever is no longer seen.
 Fever in infant <3 months considered as
 bacterial, until proved otherwise.

Common causes for fever in children:

1) Infection : Bacterial,Viral,Rickettsial, Fungal, Parasitic

2) Neoplasms : Hypernephromas, Lymphoproliferative Malignancies,

CA Pancreas, CA lung, Hepatoma.

3) Immunological Diseases : SLE, RA, Collagen vascular diseases and

other allergic reactions.

4) Drugs: Penicillin, Sulphonamides, Cephalosporins, ATT,

Anticonvulsants (Phenytoin), Vaccines (Hep B, Typhoid, DPT )
APPROACH TO CHILD WITH FEVER:

1) Respiratory Symptoms :
 Sore throat, nasal discharge,sneezing – URTI
 Sinus pain,headache – sinusitis
 Cough, sputum, breathlessness – LRTI
 Ear ache, ear discharge – Otitis Media
 Post tussive vomiting – Pertussis

3)Abdominal Symptoms :
 Diarrhoea – Gastroenteritis, Enteric fever, Bacillary Dysentry etc.,
 Vomiting & pain abdomen – Hepatitis, Appendicitis, Enteric fever,
Amoebiasis.
 Projectile Vomiting : Meningitis
 Jaundice – Hepatitis
4)Genito- urinary Symptoms :
 Burning micturition/cry during micturition, increased frequency of
urination – UTI
5)CNS symptoms :
 Neck rigidity, headache – Meningitis

6)Headache : Sinusitis, Otitis media, Meningitis

7)Lymphadenopathy : TB, Toxoplasmosis, IM, Brucellosis, HIV,

Lymphoma
8) Fever with Skin rash :
 Measles and Roseola infantum- rash comes on 3rd day of fever.
 Rubella- rash on 1st day of fever.
 Viral hemorrhagic fevers(like dengue), Rickettsial fever,
Varicella,meningococcaemia,Kawasaki disease,toxic shock
Syndrome.

9) Night sweats : TB, Leukaemia, Autoimmune diseases

10) Myalgia : Viral fever, malaria, brucellosis

11) Associated seizures : Febrile seizures

12) Evening rise of fever : TB, Juvenile RA.

* FEBRILE SEIZURES :
“ seizures during fever, occurring between 6 months to 5 years of age, in
the absence of infection of CNS in a neurologically normal child.’’
Types : a)Simple, Benign
b) Atypical, complex
 Genetically determined, Family history + ve
 Always associated with fever
 Normal developmental milestones, no signs of neurological
involvement.
 Neuroimaging, EEG – normal.
 TREATMENT :
a) Tepid sponging
b) Antipyretics: oral- 15mg/kg, Suppository-10 mg/kg
c) c)Inj.Lorazepam (0.5- 1mg/kg/dose) slow iv for controlling
seizures.

 PROPHYLAXIS :
a) Intermittent prophylaxis : during first 3 days of fever.
Clobazam 1mg/kg/day in 2 divided doses given.

b) Continuous prophylaxis : advocated in the event of failure of

intermittent therapy; Antiepileptic drug therapy given.
Sodium valproate 10-20mg/kg/day OR
Phenobarbitone 3-5mg/kg/day
For 1-2 years or until 5 years of age, which ever comes earlier.
 APPROACH TO COUGH

 DEFINITION : Cough is an explosive expiration that provides a

normal protective mechanism for clearing the tracheobronchial tree, of
secretions and foreign material.
 HISTORY:
1) Onset - Acute, Chronic (>3weeks)
2) Type of cough – Dry, Productive/Post tussive vomiting
3) Relation to posture, time of day.
4) Association with chest pain
5) Aggravating and relieving factors
Examples:

ACUTE cough CHRONIC cough

Acute Respiratory infections. Passive smoking
Acute Bronchiolitis Post nasal drip
Asthma Asthma, Allergic bronchitis
Pneumonia Bronchiectasis
Foreign body TB, HIV
Cystic fibrosis, Hiatus hernia
Laryngeal Stenosis, Tracheomalacia.

TYPES OF COUGH & CLINICAL DIAGNOSIS :

1) Runny nose, purulent discharge in posterior pharynx, cough at night
and early morning – Postnasal drip
2) Hoarse voice, stridor, croupy cough – laryngitis,laryngeal edema,
foreign body in larynx
3) Wheezing;initially dry later productive – Asthma, Bronchitis
4) Paroxysmal whoop, post tussive vomiting – Whooping cough
5) Brassy cough - Tracheitis
6) Early morning cough,copious,thick and purulent,foulsmelling
sputum – Bronchiectasis, lung abscess, foreign body.
7) Dry hacking,nocturnal cough – Tropical Eosinophilia
8) Night & early morning cough with wheeze – Bronchial Asthma
9) Dry hacking, very noisy, disappears when attention diverted –
Psychogenic cough
10) Cough on changing posture- Bronchiectasis or lung abscess
11) Cough on lying down – Left ventricular failure, GERD.
 DIARRHEA
Definition :
1) Passage of watery stools, at least 3 or more episodes in a 24
hours period .
2) Changes in frequency, volume & fluidity as related by the
mother is also considered as diarrhea
3) Other criteria – age < 3yrs water loss > 15g/kg/day
> 3yrs water loss > 200g/day

1) Acute Diarrhea - Starts suddenly, lasts for 3-7 days, can be

acute watery diarrhea or acute bloody diarrhea

2) Persistent Diarrhea - Starts as an acute episode, lasts for at

least14 days, secondary to aninfection

3) Chronic Diarrhea - Primary condition associated with abnormal

stools, last more than 15 days, also associated with weight loss and
tenesmus. Commonly seen in malabsorption

4) Transitional Diarrhea -Self limited acute fluid diarrhea, occurring

soon after birth caused due to failure of adaptation to enteral feeding and
microbial colonization during this transitional period

5) Parenteral Diarrhea - Diarrhea caused due to infection seen

outside the gastrointestinal tract. Eg: Pneumonia, UTI and CSOM

Difference between VIRAL & BACTERIAL Diarrhea

VIRAL BACTERIAL
Involved site More Commonly involves More Commonly involves
Small intestine Colon

Diarrhea Watery Bloody, mucoid

Vomiting More common Less common

Abdominal pain Less common More common

Tenesmus(pain while Absent More common

passing stools
Anorexia Less common More common

Systemic illness symptoms Less common More common

 WHO CLASIFFICATION:

No Dehydration Some Severe

Dehydration Dehydration
Look
1) Condition of the Alert well Restless , irritable Lethargic /
child unconscious

2) Eyes & Tears Normal , tears Sunken , tears not Very sunken/tears
present present absent

3) Mouth &Tongue Moist Dry Very dry

4)Thirst Drinks normally, Drinks eagerly , Drinks poorly

not thirsty thirsty

Feel

Skin Pinch Goes back quickly Goes back slowly Does not go back or
tenting
Status Treatment plan A Treatment plan B Treatment plan C

TYPES OF DIARRHEA :
1) Infective 2) Inflammatory 3) Hemorrhagic 4) Chronic Diarrhea
5) Secretory Diarrhea 6) Malabsorptive Diarrhea

CAUSES :
1) Viral –Ex: Norwalk virus, Rota virus, adenovirus,
cytomegalvirus
2) Protozoa- Ex:Giardia lamblia, Cryptosporidium
3) Bacterial- Staphylococcus aureus, E. coli , Shigella,
Salmonella, Yersinia, Campylobactor, Bacillus cereus,
Clostridium difficle, Vibrio cholera
5) Medication - Including antibiotic use (cefixime, Amoxicillin,
6) Laxative use
7) Fecal impaction
8) Pancreatic insufficiency
9) Malabsorption

MANAGEMENT :
Oral rehydration therapy to prevent dehydration( plan A)
2 Packets of ORS to be given to the mother.
Explain about Method of preparation of ORS
About danger* signs

*Danger signs include 1) Watery stools >3 times/hour

>5 times/day
 2) Vomiting >3 times/hour
>5times/day
3) Fever and blood in stools
4) Abdominal distention

Give a tea spoonful of ORS every 1 to 2minutes for a child less than 2
years
Give frequent sips from a cup of for an older child.
If the child vomits, wait for 10 minutes then give the solution more
slowly.
If diarrhea continues after the ORS packets are used up tell the mother to
give homemade fluids.

For treating patients with some dehydration (plan B)

75 Ml/Kg/Body Wt of ORS is given over 4 hours hourly
monitoring look for signs of dehydration For every one stool give
100ml of ORS.
Encourage breast feeding.
For infants under 6 months who are not breast feed also give 100 to
200ml clean water during this period.

Fluid therapy in severe dehydration (plan c) (RL/NS)

Age First give Then give

< 12 months 30ml /kg in one hour * 70 ml/kg in 5 hours
12 months up to 5 years 30ml/kg in 30minutes * 70ml /kg in 2 hours
30minutes

* Repeat again if the radial pulse is still very weak or not detectable
Antibiotics are started only for : Shigella, Vibrio , Entamoeba , Giardia
Antibiotics used are : Cotrimoxizole, Nalidixic acid, Amoxicillin,
Ciprofloxacin

ORS
INGREDIENTS Gm /litre of ORS Solution
Sodium chloride 3.5
Trisodium citrate 2.9
Potassium chloride 1.5
Glucose 20

WHO ORS conc Low osmolarity ReSoMal

solution (mmol/L) ORS(mmol/L) Rehydration
(old) (new) solution for
malnutrition
Sodium 90 75 45
Chloride 80 20 70
Potassium 20 65 40
Citrate 10 10 7
Glucose 111 75 125
Magnesium 3
Zinc 0.3
Copper 0.045
Total 311 245 300

Super ORS
1) Replacement of glucose by starch or maltodextrin or aminoacids
2) Does not increase osmolality
3) More Caloric
When to stop ORS when the child is active and refuses to take
ORS

Oral Rehydration Therapy (ORT)

1) To prepare ORS solution at home (1 fist of sugar,3 finger pinch

salt,2 finger pinch baking soda and half a lemon (K+))
2)sugar and salt solution* in half a litre of water (Sugar-40mg, salt-
4mg)
3) rice water* with salt (rice approximately 50mg, salt 40mg)
4) lassi (butter milk) with salt
5) plain water, lemon water, coconut water, soups,
6) thin rice ganji, dal water (salt can be added for taste).

*May be used for treatment of dehydration when ORS is not available

and while the child is being taken to a facility where ORS is available

What is not ORT?

Glucose water without salt
Fluids without starch or sugar and salt in children who are starved.

Advice on discharge: One extra meal for 15 days to prevent viscious

cycle of malnutrition-diarrhea

Other additional therapies for diarrhea

1) Zinc 20mg/kg/body weight – children >6 months for 14 days
10mg/kg/body weight _ children <6 months for 14 days
 VOMITING

Vomiting – Forceful oral expulsion of gastric contents associated with

contraction of the abdominal and chest wall musculature.

HISTORY:
1) Age of the patient
Causes-
a. Neonatal pyloric atresia/stenosis,
- Inborn errors of metabolism - Malrotation
- Bacterial meningitis - Volvulus
- Birth asphyxia - Necrotizing enterocolitis
- Hydrocephalus - Meconium plug
- Faulty feeding technique
- Gastroesophageal reflux

b. Infancy
- Congenital hypertrophic pyloric stenosis ,Peritonitis,
Malrotation ,CNS space occupying lesions, Volvulus, Cow milk
protein allergy, Intussusception , Over feeding-UTI ,Inborn errors
of metabolism

c. Childhood
- Gastroenteritis ,pneumonia, Intestinal obstruction
- CNS space occupying lesion
- Gastroesophageal reflux
- DKA
- UTI
- Psychogenic
- Hepatitis
2) Duration/Frequency
 Severity is indicated by dehydration in acute cases and weight
loss in chronic cases

3) Onset and association with food intake
 Instantly – oesophageal obstruction
 After a while - stomach or duodenal obstruction
 Tracheo - esophageal fistula- excessive frothing and chokes on
attempted feeding
  Achalasia cardia – vomiting relieved on feeding popped up
position

4) Nature
 Projectile - in cases of raised ICT- meningitis, encephalitis,
hydrocephalus, head injury
 Non projectile

5) Colour
 Bilious – lesion distal to 2 nd part of duodenum - duodenal atresia,
paralytic ileus, peritonitis
 Non bilious – lesion proximal to 2nd part of duodenum – achalasia
cardia, pyloric stenosis

6) Contents
 Non digested food – proximal obstruction
 Semi digested food – distal obstruction
7) Time of vomiting
 Early morning vomiting in intracranial space occupying lesion
8) History of drugs
 Digoxin, theophylline, aspirin, iron, metronidazole induce vomiting
9) Associated symptoms
 Diarrhea – Acute gastroenteritis
 Fever and urinary symptoms – UTI
 Vertigo and ear symptoms – labrynthitis
 Jaundice – hepatitis
 Headache – migraine
 Cough – post tussive vomiting common after paroxysmal cough in
pertussis and asthma

10) Recent history of change in food habits
 Cow milk allergy / Food allergy

11)Associated with blood

 Hematemesis - vomiting of frank blood or altered blood (coffee –
ground colour)

 Causes of hematemesis
 Oesophageal – oesophagitis, oesphageal ulcer
 Gastric – gastric ulcer, duodenal ulcer, gastritis due to NSAID,
Mallory Weiss syndrome
 Liver – portal hypertension, liver cell failure
 Septicemia
 Swallowed blood
 Bleeding disorders
 

 History to be asked in hematemesis

 h/o epigastric pain – acid peptic disease
 h/o bleeding diathesis – bleeding from other sites
 h/o drug ingestion – e.g. aspirin other NSAID steroids
 h/o liver disease – cirrhosis, portal hypertension
 whether preceded by a series of vomiting (Mallory Weiss
syndrome)
 enquire about blood clots in vomitus, giddiness or syncope
following episode, which indicates heavy loss
 h/o neonatal umbilical catheterization or intra-abdominal infections
(e.g. appendicitis)
 Approach to abdominal pain in children
1) ONSET: Acute,chronic.

ACUTE CHRONIC
 Single episode, lasts for hours to days.  Recurrent episodes,lasts for days to
 Sharp, shooting/stabbing pain. weeks.
 Ex: Abdominal colic, perforated peptic  Dull, diffuse, poorly localized pain.
ulcer, appendicitis, diverticulitis etc.,  Ex: Constipation,Lactose
intolerance,food allergies, IBD etc.,

2) DURATION: If lasting for >2-3months,defined as chronic

3) SITE : to be ideally pointed with 1 finger.
 Localised – as shown in table below.
 LINES DIVIDING THE ABDOMEN
INTO 9 QUADRANTS
Right Hypochondrium Epigastrium Left

 Gall stones  Oesophagitis/ gastritis Hypochondrium

 Cholecystitis  Perforated peptic ulcer  Splenomegaly
 Hepatitis  pancreatitis  Splenic abscess
 Pneumonia/ empyema  Sickle cell crisis


 Right Lumbar Umbilical Left Lumbar
 Renal stones  Early appendicitis  Renal stones
 Pyelonephritis  Pancreatitis  Pyelonephritis
 Ischaemic colitis  IBD  IBD
 Infective colitis  Gastroenteritis
Right Iliac Hypogastrium Left Iliac
 Appendicitis  UTI  Constipation
 Constipation  Cystitis  IBD
 IBD  Diverticulitis  Inguinal hernia
 Inguinal hernia  IBD

Type or character of pain

 Dull, diffuse, poorly localized  chronic/ visceral pain

 Sharp/ stabbing pain  somatic pain, trauma
 Appendicitis  sharp stabbing pain
 Peptic ulcer  dull pain rather than burning in children
 Biliary colic, intestinal obstruction  colicky pain
 Peritonitis  diffuse pain with board like rigidity
4) Radiation (because of same dermatome)
Eg: appendicitis earlier pain in umbilical region, later migrates
to right iliac fossa
Pancreatitis, cholecystitis referred to the back
5) Aggravating and relieving factors
 Food  peptic ulcer + Duodenal ulcer
 Medication  Antacids relieve pain in peptic ulcer
 Movement aggravates pain in peritonitis ( patient lies flat on
bed with little or no movements
6) Associated symptoms
 Vomiting and diarrhea gastroenteritis, food poisoning, enteric
fever
 Constipation
 Irregular/ altered bowel habits  IBD, irritable bowel syndrome
 Fever, fatigue, jaundice  viral hepatitis
 Dysuria, increased frequency of micturition  UTI
 Cough, shortness of breath  pneumonia, empyema
 Blood in stools  ulcerative colitis, NEC, dysentery, constipation.
 Hematemesis  gastritis, peptic ulcer disease
 Bilious emesis  small bowel obstruction
 Joint pain, swelling & skin lesion IBD, HSP
 Testicular pain  testicular torsion
 Weight loss  TB, malignancy
  Palpable mass  tumors, round worm infestation, chronic
constipation, TB abdomen, intussception

7) Travel history  viral hepatitis, infectious gastroenteritis.

Consumption of outside food  GE, food poisoning.

8) Past/other medical history :

 Sickle cell disease/ cystic fibrosis – prone for gall stones
 Spina bifida, mental retardation, CP – constipation
 DM1 – DKA

10)Family History : Useful in IBD

OTHER CAUSES OF PAIN ABDOMEN :

 Psychogenic pain- Ex: school phobia, attention seeking behavior.

 Infantile colic - <3months of age, usually in evening hours. No
specific cause
 Lead poisoning (H/o recurrent abdominal pain, H/o PICA)
 Parasitic infestation
 Obstructed hernia
 Abdominal migraine
 Sickle cell crisis

RED FLAG SIGNS :

 Bilious vomiting
 Blood in stools/ haemetemesis
 Night time waking with pain
 Haemodynamic instability
 Weight loss

RESPIRATORY SYSTEM

Importance of history taking

Age :
Preterm baby- respiratory distress syndrome
bronchiolitis - infancy
Cystic fibrosis - Usually present in newborns and infants.
Foreign body aspiration – m/c in infants and toddlers
Fibrosis of lungs ( due to Tuberculosis) – rare in children

Gender :
Smoking and its related complications – m/c in adolescent males.
Place :
Tuberculosis – m/c in India.

Cardinal symptoms in history taking :

a) Cough
b) Difficulty in breathing/ fast breathing
c) Chest pain
d) Haemoptysis
e) Noisy breathing- Wheeze or stridor
f) Others – Hoarseness of Voice
Halitosis ( Lung abscess, Bronchiectasis)
Cyanosis ( Hypoxia )
Haemoptysis

Cough
 Onset
 Sputum
a) Productive/Non productive ( Usually the child swallows the
sputum,ask for post tussive vomiting)
b) Character and consistency ( in older children)
Types of Consistency : Mucopurulent - Bronchitis
Purulent - Broncheictasis
Frothy - Pulmonary oedema

c) Smell : Foul smelling – Infections with anaerobes, Staphylococci,

Klebsiella and Pseudomonas.
 Aggravating and relieving factors
 Diurnal variation
 Seasonal variation
Symptoms due to infections of the respiratory tract/ENT (
Sinusitis/Rhinitis)
 Cough
 Running nose
 Ear discharge
  Ear pain
 Sore throat

HISTORY OF PAST ILLNESS :

 Exanthematous fever : Measles – decreases the immunity hence
vulnerable to infections of lung and gut and it also causes giant
cell pneumonitis.
 Whooping cough, diphtheria
 Aspiration
 Change in voice ( Associated with palatal paralysis predisposing to
aspiration)
 Nasal regurgitation
 Failure to thrive
 Asthma/Allergy
 Recurrent RTI
 Previous hospitalization/treatment
 Bad child-rearing practices

ANTENATAL HISTORY
 Booked/Unbooked case
 Immunization – 2 TT doses
 Intrauterine infections
 USG – rule out congenital anomaly

BIRTH HISTORY
 Gestational age - full term/pre term
 Birth weight - LBW, small/large/appropriate for gestational age
 Mode of delivery - natural/caesarean/forceps
 Birth asphyxia – if not cried soon after birth

NEONATAL HISTORY
 Respiratory distress syndrome
 Breath difficulty
 Feeding problems, duration of feeding
 Weight gain

GROWTH AND DEVELOPMENT HISTORY

Delay in growth is seen in children with chronic cough.
NUTRITIONAL HISTORY
IMMUNISATION HISTORY
 Details of immunization should be enquired.
 If age<5 Y, details of pulse polio should be noted.

FAMILY AND SIBLING HISTORY

 Consanguinous marriage
 Asthma
 Family h/o of hereditary diseases – Eg: Cystic fibrosis
 Diabetes Mellitus
 Maternal age at conception
SOCIOECONOMIC HISTORY
Summary

GENERAL PHYSICAL EXAMINATION

 Level of consciousness
 Facies- Eg: Down’s syndrome – Frequent RTI due to
immunodeficiency
 Nutritional status – failure to thrive in long standing lung disorders
 Decubitus – i.e. the position in which the child is lying
Pleural effusion – prefers to lie down on the side of the
effusion because when the patient lies on the opposite side, the
effusion compresses the opposite lung and compromises the lung
volume.
 Dyspnoea
 Hydration status
 Pallor
 Cyanosis-chronic lung disease
 Clubbing is seen in suppurative lung disorders
 Palmar erythema – due to polycythaemia as a result of hypoxia
 Flap – flap in hands due to CO2 retention in respiratory failure
 Dental caries, oral hygiene and odour of breath
 Neck veins – Engorged or not
Look for JVP
 Skeletal deformities- kyphosis and scoliosis
 Signs of cardiac failure – Pedal edema and hepatomegaly
  Lymph nodes – Cervical lymph nodes are m/c enlarged and
matted in pul. Tuberculosis
 Skin : Look for sinuses ( Tubercular sinus), mantoux test, BCG scar,
Surgical scars, boils & eczema.

VITAL SIGNS
 Temperature
 Pulse
 Blood pressure
 Heart rate
 Respiratory rate – Count for a minute by observing the chest wall
movements or the abdominal movements

ANTHROPOMETRY – Ht, Wt, MAC, HC, CC

EXAMINATION OF RESPIRATORY SYSTEM

Examination consist of two parts:
Upper respiratory tract
Lower respiratory tract

Examination of upper respiratory tract

Consist of:
1. Nose
2. Air sinuses
3. Pharynx
4. Larynx
The ear should also be examined for the signs of infection.
Nose:- anatomical defects- deviate nasal septum, polyp
Congestion
Rhinorrhea
Foreign body
Air sinuses: tenderness
Frontal sinus
Maxillary sinus
Pharynx : cleft palate, post nasal drip, pharyngitis
Movement of the uvula
Tonsils- inflammation and enlargement
Adenoids- enlargement
 Examination of lower respiratory tract

Inspection

SURFACE MARKINGS
1)LUNG MARKING: 6th,8th,10th ribs along the mid clavicular line,mid
axillary line and scapular lines.\
Apex of the lung extends upto 1-1.5 inch above the clavicle.
2)MARKING OF PLEURA: 8th,10th and 12th ribs along the mid
clavicular line,mid axillary line and scapular line.
3)MAIN FISSURE: Extends from 2nd dorsal verterbra i.e T2 to 5th rib in
the mid axillary area,to 6 th costochondral junction.
4)On the right side: horizontal fissure is at the 4th costal cartilage.
BRONCHOPULMOMNARY SEGMENTS
RIGHT LEFT
UPPER: 1)Apical 2) posterior 3) UPPER:1) Apical 2)anterior 3)
anterior posterior
4)Superior lingual 5)
inferior lingual
MIDDLE:1) Lateral 2)Medial
LOWER: 1)Apical 2) Anterior LOWER : 1)Apical 2)Anteroir
basal 3)Posterior basal 4)lateral basal 3)Posterior basal 4)lateral
basal 5) Medial basal. basal.
No medial basal

ANGLE OF LOUIS importance:

1)Bifurcation of aorta
2)2nd costal cartilage
3)Arch of aorta
4)Left atrium.
Coastal angle measures upto 90degress, noramally 45-90 degress.
 a) Types of respiration: abdomino thoracic – seen young children
Thoracic- seen in children 7-8 yrs
abdominal- seen in infants
abnormal types of respiration:
 Periodic breathing
 Cheyne stokes breathing
 Biots breathing
 Kausmauls breathing
 Paradoxical breathing
b) Respiratory efforts-
Findings:
- intercostal recession
-Subcostal recession
-Diaphragm – paradoxical abdominal movement
-Flaring of alae nasi
-Accessory muscles of respiration- sternomastoid, latissimus
dorsi,pectoralis major, -serratus anterior trapezius, abdominal
muscles.
-wheeze or stridor
-grunting
c) Examination of chest
- shape of the chest- symmetrical/asymmetrical
-Movement of chest wall- symmetrical/asymmetrical
Decreased in pleural effusion/ collapse.

-deformities of chest wall – pectus excavatum ,barrel shaped chest,

pegion shaped chest ,crowding of ribs.
-apical impulse
-fullness of chest wall- due to trapping of air as in asthma.
- flattening of intercostal spaces on chest wall.

d)Examination of the back

- vertebral deformities: kyphosis or scoliosis
- Gibbus in caries of the spine.
- drooping of the shoulders on the side of the collapse of the lungs.
- winging of the scapula on the opposite side of the collapse of lung
-movements are symmetrical or not
- interscapular distance.

e)tracheal position
- normally lies in the midline or slightly deviated to the right side.
- trail’s sign: undue prominence of the lower part of the c;lavicular head
of the sternomastoid muscle on the side of which the trachea is shifted.

Palpation:
Done with warm hands.
Inspectory findings are confirmed.
1. Position of trachea- normally central or slightly right.
Head should be fixed straight with patient sitting or standing.
Second and fourth fingers of the examining hand should be placed
on each side of the sternal notch. Now with the third finger in the
midline the position of the travhea should be assessed.
Next, the index finger is slid in the angle between the trachea and
the sternomastoid muscle.

2. Chest expansion and symmetry:

measured by placing both the hands on either side of the chest
wall.
Diminished movements: pleural effusion, collapse.
Measure the chest circumference in full inspiration and full
expiration using a measuring tape.

3. Chest tenderness must be noted.

4. Crepitus seen in pneumothorax due to subcutaneous emphysema.
5. Other palpable findings: pericardial rub, palpable ronchi.
6. Vocal fremitus: vibration detected by palpating the chest with the
palm placed flat on the chest wall. The patient is asked to repeat
some common words like one-one and the palm is placed on the
chest wall.
The vibrations are felt on the palm. This is known as vocal
fremitus.
It should always be examined on the both the sides of the lung
fields.

Auscultation:

The following areas are auscultated in a systematic order on both

the sides:
Supraclavicular
Infraclavicular
Inframammary
Axillary
Infra axillary
 Suprascapular
Interscapular
Infrascapular
The following to be noted:

1.Breath sounds: present/ absent

Intensity- increased/decreased/normal
Quality-bronchial/vesicular

2. Vocal resonance: resonance perceived by the examiner during

auscultation of the chest while the child is repeating words like
one-one. Note the intensity and character.

Types of breath Character pitch Respiratory

sounds conditions
Vesicular Inspiration more than low normal
Typ expiration
No pause
es of
Bronchial Inspiration tubular high Consolidation
voca equal to Collapsed lung
l expiration with patent
reso with a bronchus
nan pause Cavernous low Thick walled
ce: present cavity with
connecting
~Br bronchus
onc amphoric Low, metallic Tension
hop quality pneumothorax
hon Bronchopleural
y: fistula
Hea Bronchovesicular Expiration more than High/low Bronchial asthma
breathing inspiration with no emphysema
rd in pause in between
cons
olid
ation.
~Whispering pectoriloquy: seen in consolidation and a large cavity
communicating with a bronchus
~aegophony-due to dilatation of lungs.
Adventitious sounds:
Wheeze: (ronchi) are continuous prolonged musical sounds that arise in
the bronchi.
May be high pitched as in bronchitis and asthma
Low pitched as in bronchiolitis.
Crepitations discontinuous crackling or bubbling sound of short duration.
Stridor may be inspiratory or expiratory. Seen in partial obstruction of to
the bronchus by a mass or a foreign body.
Pleural rub heard in pleurisy due to rubbing of both layers of pleura.
Seen in inflammation of the pleura.
Other findings:
Post tussive suction
Succution splash

RECURRENT RTI >/ = 6 INFECTIONS per year with each infection

lasting for atleast a week.

Wheeze
 Inspiratory wheeze : Prolonged inspiration due to larynx or
tracheal obstruction
 Expiratory wheeze : Prolonged expiration due to obstruction of
the bronchioles

RESPIRATORY SYSTEM MODEL CASE SHEET

Name: XYZ
Age: 6 years
Sex: Male
Address: ABC
Informant: Mother, reliable

Chief complaint:
1. Fever – since 1 week
2. Cough – since 6 days
3. Hurried breathing – since yesterday
4. Chest in drawing – since yesterday
5. Noisy breathing – since yesterday
6. Decreased appetite
7. Pain abdomen**
8. Neck stiffness**
9. Photophobia**
10. Headache**
11. Vomiting**
12. Chest pain **
**rare symptoms/involved in other diseases

History of present illness

Six years old male child, was apparently well when developed fever since
one week. Fever was sudden in onset, moderate grade, associated with
chills and rigor (lobar pneumonia). Fever was intermittent; subsided
temporarily on medications. Child was inactive in the inter febrile period
(bacterial etiology). Child had h/o cough, insidious in onset; a/w post
tussive vomiting(productive cough).

Child had h/o hurried breathing and lower chest in drawing since
yesterday (increased respiratory efforts and involvement of lower
respiratory tract).
H/o grunting/noisy breathing present since yesterday. (Grunt is due to
expiration against a partially closed glottis to increase the end expiratory
pressure to prevent collapse of alveoli-indicates severe pneumonia).

*Wheeze maybe seen in bronchopneumonia

A/w h/o decrease in appetite and decreased food intake. (Poor feeding
and excessive crying in infants) – complication on pneumonia Child was
treated with oral antibiotics and other symptomatic treatment for the
above complaints. The symptoms persist despite this.

No h/o of pain abdomen. (Pain abdomen can be seen in lower lobe

pneumonia – referred pain due to proximity to the diaphragm and also
due to repeated abdominal contractions due to excessive cough).

No h/o recurrent headache, neck stiffness, photophobia, projectile

vomiting ( very rarely seen in upper lobe pneumonia- meningitis like
symptoms)
No H/o chest pain. (Chest pain aggravated on deep inspirationindicates
pleural irritation).

No h/o sore throat, nasal discharge, ear pain, ache or discharge.

No history suggestive of foreign body inhalation
No h/o choking, regurgitation of feeds or vomiting (GERD)
No h/o halitosis/mouth breathing/snoring (adenoids)
No h/o weight loss/evening rise of temperature/Tb contact (rule out TB)
No h/o rashes (measles associated pneumonia)
No h/o skin infections(staphylococcal infections which can lead to
pneumonia)

Past history:
No h/o recurrent episodes of pneumonia(more than 1 per year may
indicate immunodeficiency)
No h/o fever with rashes in the past(measles)

Antenatal/natal/postnatal history
Immunisation history
Important to ask regarding the following vaccines in respiratory illnesses
a) BCG (mention scar)
b) Pertussis
c) Measles
d) Pneumococcal vaccine
e) Influenza
f) Developmental history
These children are prone to pneumonia:
a) Cerebral palsy – repeated aspirations
b) Down’s syndrome – hypotonia of oesophageal muscles cause
repeated aspirations

Dietary history

Family history
H/o Tb contact
H/o similar complaints in the family

Socioeconomic history

Summary : A six year old male child, who is second in order to a non
consanguineous marriage, is immunised appropriately, has achieved all
appropriate milestones, with no significant birth, family or past history
presented with sudden onset, intermittent fever which was associated with
chills and rigor. Child was inactive in the inter febrile period. Child also
had insidious onset cough which was associated with post tussive
vomiting, hurried breathing, chest indrawing, decreased appetite and
decreased food intake.
With the above history I would like to conclude that child has a lower
respiratory tract infection with a bacterial etiology, most likely
Pneumonia.

General examination :
 Level of consciousness
 Facies (eg. Down’s syndrome – may suffer from recurrent
respiratory infections)
 Nutritional status: (malnutrition or FTT predispose to recurrent
infections)
 Pallor,cyanosis, clubbing, lymphadenopathy, edema
 Vitals
 Anthropometry
 Head to toe examination
a) Palmar erythema ( hypoxia causes polycythemia)
b) Flap in the hands (carbon dioxide retention in resp failure)
 Systemic examination – respiratory
Inspection
  Nasal discharge
 Flaring of alae nasi
 Foreign body
 Sinus tenderness
 Throat
 Tonsils
 Position of trachea
 Type of respiration: abdominal in infant, abdominothoracic
in young children and thoracic in children after 7-8 years of
age
 Shape of chest
 Chest movements(decreased in pleural effusion or collapse)
 Apical impulse
 Type of breathing
 Chest retractions
 Grunting
 Examination of spine

Palapation
 Position of trachea
 Chest expansion and symmetry
 Chest tenderness
 Vocal Fremitus

Percussion
 Different areas

Auscultation
 Different areas
 Listen for breath sounds – bronchial breath sounds in
pneumonia
 Vocal resonance – increased in consolidation
 Added sounds – crepitations (fine in early consolidation and
coarse in late consolidation), occasional rhonchi maybe seen
in bronchopneumonia

Differential diagnosis :
1) Pneumonia
2) FB inhalation

DISCUSSION:

VIVA ON PNEUMONIA

1) Define pneumonia?
It is an inflammatory process which involves the lung parenchyma.
2) Classification of pneumonia
 o Anatomical : lobar/lobular, interstitial, bronchopneumonia and
multilobar pneumonia
o Duration : persistent: symptoms and X-ray findings for more than
4 weeks; recurrent: two episodes in one year or more than three at
any time.
Aetiology : infective, non-infective
o
o Source of infection : community acquired(s.pneumoniae,
h.influenzae, s.aureus, mycoplasma, chlamydia, legionella),
hospital acquired(e coli, proteus, klebsiella, s.aureus,
Pseudomonas), opportunistic (p.carinii, CMV, varicella Zoster)

3) Causes of bacterial, atypical and viral pneumonia?

Bacterial  St. Pneumoniae
 H.influenzae
 St. aureus
 M. TB
 Pseudomonas aeruginosa
Atypical pneumonia  Chlamydia
 Mycoplasma
 Legionella
Viral  RSV
 Parainfluenza virus
 Influenza virus
 Rhinovirus
 Adenovirus

4)Differences between bacterial and viral pneumonia

Features Bacterial pneumonia Viral pneumonia

Onset Abrupt Gradual
Epidemic Not seen Common
Associated conditions Other site infections, Associated URI, coryza
septicaemia
Fever High grade Maybe absent
Toxaemia Common Absent
Respiratory distress Common Common in neonates
Lung signs Crepitations Wheeze
X-ray Confluent infiltrates Diffuse in peripheral areas
Pleural involvement Maybe seen Not common
Prognosis Complications such as Self limiting.
empyema, pneumatocele,
septicemia
4) What are the organisms common in different age group?

Organisms Neonates 1 month to 5 years Above 5 years

Bacteria  Grp B  S. Pneumoniae  S.pneumoniae
streptococcus  S.aureus  S.aureus
 Ecoli  H.influenzae  H.influenzae
 Klebsiella  Grp A strep  M.tb
 Listeria  Klebsiella
 S.aureus  Pseudomonas
 M.tb
Viruses  CMV  CMV  Influenza
 Herpes  RSV  Varicella
 Influenza
 Adenovirus
Atypical  Chlamydia  Mycoplasma  Mycoplasma
Organisms  Legionella
 Chlamydia

5) What are the common organisms that cause pneumonia in

immunocompromised children?
 P.carinii
 S.pneumoniae
 S.aureus
 Klebsiella
 Pseudomonas
 H.influenzae
 Legionella
 CMV
 Varicella zoster
 Measles giant cell pneumonia
 RSV
 Herpes simplex
 HIV
 Candidiasis
 Aspergillus
6) Investigations in pneumonia?
 Chest X-ray
  Complete blood count
 Serological tests for viruses and bacteria
 PCR for M.TB
 Sputum and blood culture

7) What is recurrent pneumonia?

 Two episodes of pneumonia in a year or more than three at
any time with X-ray clearance between two episodes of
illness.

8) What is persistent pneumonia?

 Symptoms and X-ray abnormalities or more than 4 weeks.

9) Complications of pneumonia
 Suppurative lung diseases – lung abscesses following
staphylococcus and klebsiella infections
 Collapse
 Bronchiectasis
 Parapneumonic effusion
 Empyema
 Pneumothorax
 Pyopneumothorax
 Pericarditis
 Endocarditis
 Meningitis

10) What are the different types of sputum?

i. mucopurulent in bronchitis
ii. purulent in bronchiectasis
iii. frothy in pulmonary edema
iv. foul smelling in infections with anaerobes, staphylococci,
klebsiella and pseudomonas infection

11) Radiological findings in different pneumoniae

Radiological changes Type of pneumonia

Lobar involvement Pneumococcal
pneumoniae
Right middle lobe Aspiration pneumonia

Upper lobe pneumonia, cavitations, bronchopneumonia with Tuberculous pneumoniae

hilar lymphadenopathy
Lower lobe pneumonia Chemical pneumonitis

Multiple abscesses Staphylococcal/klebsiella

Bilateral interstitial pneumonia Viral

Bilateral interstitial pneumonia in immunosuppressed Pneumocystis carinii

children

12) Antimicrobial therapy

Infective agent Drugs Dosage

Group B stretoccci, Ecoli Ampicillin+ 100mg/kg/day + 3-5mg/kg/day
gentamicin
S.aureus Cloxacillin+gentamicin 100mg/kg/day+ 3-5mg/kg/day
H. Influenza type B Penicillin/Ampicillin 1 lakh units/kg/day
100mg/kg/day
S.pnemoniae Penicillin  1month to 1 year: 1 lakh
Cefotaxime units/kg/day for 2-3 weeks
Ampicillin  Older than 1 year: 50,000
to 1,00,000 units/kg/day
100mg/kg/day
100mg/kg/day
Chlamydia Erythromycin 40mg/kg/day

APPROACH TO COUGH

 DEFINITION : Cough is an explosive expiration that provides a

normal protective mechanism for clearing the tracheobronchial
tree, of secretions and foreign material.

 HISTORY:
1) Onset - Acute, Chronic (>3weeks)
2) Type of cough – Dry, Productive/Post tussive vomiting
3) Relation to posture, time of day.
4) Association with chest pain
5) Aggravating and relieving factors
 TYPES OF COUGH & CLINICAL DIAGNOSIS :

a. Runny nose, purulent discharge in posterior pharynx, cough at

night and early morning – Postnasal drip

b. Hoarse voice, stridor, croupy cough – laryngitis,laryngeal edema,

Foreign body in larynx

c. Wheezing;initially dry later productive – Asthma, Bronchitis

d. Paroxysmal whoop, post tussive vomiting – Whooping cough

e. Brassy cough - Tracheitis

f. Early morning cough, copious, thick and purulent, foul smelling

sputum- Bronchiectasis, lung abscess, foreign body.

g. Dry hacking, nocturnal cough – Tropical Eosinophilia

h. Night & early morning cough with wheeze – Bronchial Asthma

i. Dry hacking, very noisy, disappears when attention diverted-

Psychogenic cough

j. Cough on changing posture- Bronchiectasis or lung abscess

k. Cough on lying down – Left ventricular failure, GERD.

15) What’s ARI?

For pneumonia
GASTROINTESTINAL SYSTEM
HISTORY taking :

AGE: gastroenteritis is more common during weaning period

Thalassemia 6 months
glycogen storage disorders with hepatosplenomegaly, G6PD
deficiency in infants
ALL 2-10 years of age
Hodgkins lymphoma 15-34 years and above 50 years (bimodal)
Cystic fibrosis newborns
Wilsons disease after 5 years of age.

GENDER: Wilsons diseases , idiopathic hypertrophic pyloric stenosis

and reyes syndrome are common in boys
Hematocolpos and ovarian cysts are common in girls.

PLACES: Thalassemia in Mediterranean areas,china,india and Malaysia.

HISTORY OF PRESENTING ILLNESS:

ABDOMINAL SYMPTOMS:

IN UPPER ALIMENTARY TRACT PATHOLOGY the child presents

with:
Abdominal pain
loss of appetite
vomiting
dysphagia
flatulence
hematemesis
melena

IN LOWER ALIMENTARY TRACt PATHOLOGY The child presents

with
Vomiting
Nausea
Abdominal pain-colicky type in obstructions of the intestines
Crampy pain seen in crohns disease.
Abdominal distention- gi obstruction, paralytic ileus and hypokalemia in
diarrhea.
Constipation
URINARY SYMPTOMS: the colour of the urine gives a clue to the type
of disorder causing jaundice.
Bladder history like polyuria, oliguria, anuria must be noted.
FLUID RETENTION: collection of fluid may begin in the abdomen or
other parts of the body.
Note the mode of onset and progression.

CAUSES OF FLUID RETENTION BASED ON AREA OF ONSET:

Area of onset Organ involved
Face Renal causes
Abdomen Hepatic causes
Pedal edema Cardiac causes
Generalised edema (anasarca) Nutritional causes

EXTRAABDOMINAL MANIFESTATIONS OF
GASTROINTESTINAL DISEASES:
FEATURES DISEASES
Joint pain IBD such as
pain in the eye (uveitis, episcleritis) Chron’s disease
Skin rashes( erythema nodosum) Ulcerative colitis
Night blindness (eyes- bitot’s Cholestasis, malabsorption
spots) syndrome
Altered sensorium, jaundice Liver cell failure

Some associated features to be noted are:

H/o Skin changes: paddy field dermatosis
Flaky paint dermatosis. They indicate malnutrition states.
H/o itching or purpura with jaundice indicates liver failure.
H/o perianal excoriation is seen in acrodermatitis enteropathica.
H/o upper abdominal discomfort with dyspnea palpitation or chest pain
usually indicates CCF.
H/o loss of appetite in viral hepatitis and liver cell failure.
H/o of loss of weight is seen in malabsorptive disorders.
H/o altered behaviour in Wilson’s disease.
H/o altered sensorium and altered sleep rhythm in hepatic
encephalopathy.
H/o early morning convulsions or dizziness may indicate hypoglycaemia.
H/o joint pain and swelling may be due to arthritis in IBD.
H/o rashes (Henoch- schonlein purpura)
H/o of passing worms in stool in worm infestation.
H/o pica associated with iron deficiency anemia.
H/o symptoms of fat soluble vitamin deficiencies in liver disorders and
fat malabsorption.

Past history:
 A) Jaundice- indicates presence of chronic liver disease.
- Associated features like pruritis, high colored urine, staining of
stools

B) GI bleeds- portal hypertension

C) Passing worms in stools
D) Tuberculosis
E) Blood transfusion or needle prick- alerts to look for hepatitis B
infection.
F) Contact with a jaundiced patient- alerts to look for Hepatitis A
infection.
G) Sepsis- umbilical/intra abdominal sepsis predispose to infection
and fibrosis of biliary tract.
H) Previous illness/ surgery.

Treatment history:

1. History of hospitalisation
2. History of hepatotoxic drugs administered
• Antibiotics-erythromycin estolate causes cholestasis, jaundice and
hepatic dysfunction
• Antiepileptic drugs-phenytoin, valproic acid
• Antitubercular drugs-isonicotinylhydrazine (lNH)
• Antipyretic drugs-paracetamol is hepatotoxic.
• Sulphonamides
• Anaesthetic agents-halothane
• Antimetabolites--6-mercaptopurine, methotrexate
• Carbon tetrachloride
3. History of blood transfusion
4. History of any native treatment with drugs, toxins

Antenatal History
.
• Intrauterine infections-history of fever with rash (TORCH), or painful
retroauriculolymphadenopathy, may be suggestive of intrauterine
infections in the mother. TORCH and syphilis present with
hepatosplenomegaly in the baby.
• History of drug intake
a)Diabetes in the mother is associated
with small left colon syndrome, hyperbilirubinaemia and renal vein
thrombosis in the newborn. b)Antihypertensives such as propranolol
cause hyperbilirubinaemia;c) angiotensin-converting enzyme (ACE)
inhibitors are associated with renal dysplasia. Jaundice in the mother may
be due to hepatitis virus infection. The baby is likely to contract the
infection from the mother, which predisposes to neonatal hepatitis.

Neonatal History

• Low birth weight-congenital rubella syndrome

is associated with low birth weight and hepatosplenomegaly.
• Jaundice or kemicterus in the newborn period indicates the possibility of
liver disorders such as
neonatal hepatitis and EHBA.
• Diarrhoea/dehydration in the neonatal period may indicate the presence
of malabsorption disorders and cystic fibrosis.
• Septicaemia, intra-abdominal sepsis and umbilical sepsis are associated
with infection in the portal vein, which predispose to development of
cirrhosis or portal hypertension at a later age.
• Procedures such as umbilical cord catheterisation in neonatal period
may predispose to hepatic
damage or infection.

Developmental History
Hepatosplenomegaly with mental
retardation may be seen in storage disorders such as
mucopolysaccharidosis and glycogen storage
disorders.
Diet history:

 Malnutrition disorders such as kwashiorkor may be associated

with anasarca.
 Chronic liver disorders are associated with loss of appetite.
 Vitamin D deficiency is associated with potbelly due to hypotonia
of abdominal muscles.
Family History

• Consanguineous marriage.
• Jaundice-recent history of jaundice (hepatitis A) in the family can
identify the source of infection.
• H/o chronic liver diseases in other family members-familial neonatal
hepatitis, Byler's disease (familial progressive intrahepatic cholestasis),
Wilson's disease, etc.
EXAMINATION OF per ABDOMEN case

Head to toe examination findings to be observed in an abdominal case :

PARAMETERS FINDINGS & ASSOCIATED

CONDITIONS
Nutritional status Growth failure and failure to thrive
– In storage disorders, chronic
diarrhoeal disorders, malabsorptive
disorders.
Consciousness Altered sensorium in hepatic failure,
renal failure.
Mental retardation in storage
disorders - Mucopolysaccharidosis
Colour Jaundice – liver disorders
Pallor- Worm infestation & occult
blood loss
Hydration Dehydration – Acute GE , Vomiting
Eyes KF ring in wilsons disease
Uveitis&Episcleritis (IBD)
Mouth Aphthous ulcers (IBD)
Chest Gynaecomastia – Liver failure
Hands Flapping tremors – Liver failure,
renal failure
Fingers and toes Clubbing (IBD)
Nails White in liver failure
Legs Pedal edema in liver failure
Dilated vessels Spider angioma in liver failure
Lymph nodes Lymphadenopathy – Leukaemia,
lymphoma, septicaemia
Hair Loss of hair – Liver failure
Bones & Joints Tenderness over mid point of
sternum in leukaemia and
lymphoma
Arthritis (IBD)
Skin Erythema nodosum (IBD)
Vital signs Fever – Viral hepatitis. Abdominal
TB, Leptospirosis, leukaemia,
 lymphoma.

9 abdominal regions. These are created by the arbitrary division of the

abdomen by 4 imaginary lines:
1. Two verical lines from the mid clavicle on each side.
2. Two horizontal lines – One at the level of L1 vertebra ( transpyloric
line) and the other at the level of tubercles of iliac crest (interiliac
line).

INSPECTION

Stand on the right side of the child to be examined,The child should lie
flat on the back on a firm bed with the hip flexed. Infants are to be
examined on the mother’s lap.

Examine the following –

1. Shape of the abdomen
2. Flanks
3. Umbilicus
4. Movements of abdomen
5. Veins on the abdominal wall
6. Visible gastric or intestinal peristaltic movements
7. Skin over the abdomen
8. Swelling
9. Hernial sites (inguinal,femoral,umbilical,epigastric and surgical
incisional sites)
10.External genitalia

SHAPE
1. Varies with age
2. Protruberant / Potbellly – Seen upto 5 years, Hypotonia of
anterior abdominal wall muscles (rickets), lumbar lordosis.
 3. Scaphoid – Congenital diaphragmatic hernia and severe
malnutrition

4. Congenital absence of anterior abdominal wall muscles – seen in

prune belly syndrome.
5.Causes of uniformly abdominal distension (5F) – Fluid, Flatus,
Foetus ( pregnancy), Fat (Obesity), faeces ( intestinal obstruction)

6.Causes of localized abdominal disyension – localized ascites, large

bowel obstruction, Cyst, Tumours, distended bladder,
hepatosplenomegaly.

7)fullness of flanks – seen in ascites

UMBILICUS
i) Position – Normal – Midway between the xiphisternum and
pubic symphysis.
Dispaced down – Mass in the upper quadrant
Displaced above – Mass in the lower quadrant

ii) Appearance –
 Inverted – Normal umbilicus, obesity
 Everted – Umbilical hernia, Ascites
 Vertical slit – Ovarian or pelvic tumour
 Transverse/horizontal slit/ smiling – Ascites, ant.
abdominal wall oedema
 Protrusion of mass with positive cough impulse –
umbilical hernia ( Normally seen in some children and
may close spontaneously by 2 years. Associated with
Down’s, Cretinism, hurlers syndrome, hunters
syndrome.
 Red mass – Umbilical granuloma

iii) Discharge – Umbilical area gets dry aftr the cord falls by 7-10
days of life.
 Serous - Infection
 Blood – Granuloma
 Greenish discharge – Patent vitello intestinal duct (
which connects the intestine to the umbilicus ) is
associated with discharge of the bile.
 Pus – Infection
  Urine – Patent urachus ( A remnant of omphalo-
mesentric duct)
 Faeces – Patent vitello intestinal duct

MOVEMENTS
 Normally all the quadrants of the abdomen move equally with
respiration.
 In peritonitis, there is restriction or absence of abdominal
movements.
 Also note if only a part is moving than other parts, like in hernia.
 Normally, the abdomen rises with each inspiration due to
contraction of diaphragm. This is followed by fall during
expiration. This process is reversed in diaphragmatic paralysis.
Paradoxidcal movements are seen in such children.

VISIBLE PULSATIONS

 Visible gastric or intestinal pulsations - obstruction of the gut.

Pulsations moving left to right – Pyloric obstruction
Instestinal pulsations ( step ladder pattern) – Intestinal
obstruction in the distal part
Rt to Lt movement – Transverse colon obstruction
Expansile – Pulsations of aneurysms

SKIN OVER THE ABDOMEN

look for any changes like-

 Stretched skin,Shiny skin
 Scars of previous surgery, ascetic tap, peritoneal dialysis,etc.
 Sinuses
 Striae – purple striae are seen in cushing’s syndrome

VEINS ON THE ABDOMINAL WALL

.
Veins are visible if there is increased flow in the anterior abdominal wall
vessels.
The conditions associated with visible dilated veins over the abdomen
include
 Portal hypertension
 Constrictive pericarditis
  Superior vena cava (SVC) obstruction
 Inferior vena cava (IVC) obstruction

If the veins are seen, the following should be noted:

 Dilated/tortuous
 Position of veins in the abdominal wall-anterior/lateral/back

SWELLING

The examiner should look for any swelling on the abdomen and note the
following features:
 Site, size and shape of the swelling.
 Any increase in size after coughing (cough impulse) or straining.
 Persistent/not persistent.
 Movements of the swelling-
 Pulsatile/non pulsatile-aneurysm or swelling in front of the aorta
are pulsatile.
 Appearance on lying down-a reducible hernia appears on standing
but disappears on lying down.

EXAMINATION OF HERNIAL ORIFICES

The clinician should examine the orifice for swelling, cough impulse,
reducibility and compressibility. Hernia in the anterior abdominal wall is
the commonest form of hernia.

The common sites of hernia are

 Inguinal hernia-This can be indirect or direct.
 Indirect hernia is due to herniation into the processus
vaginalis.
 Direct hernia is due to herniation through a weak
transversalis fascia.
 Femoral hernia-.
 Umbilical hernia-
 Exomphalos is due to failure of all or a part of the midgut to
return to coelom during the growth of the foetus.
 Epigastric hernia is seen through a defect in the linea alba. .
 Incisional site.

Examination of Posterior Abdominal Wall

Examine the posterior abdominal wall for the presence of dilated vessels.
look for fullness in the renal angles.
PALPATION

 The child should lie supine on a bed with hip joints

flexed.
 The child should take deep breaths.
 stand on the right side ,the head of the child should be
turned towards the left side.

Start with superficial palpation. This is followed by deep palpation. start

the palpation from the left iliac fossa and proceed in an anticlockwise
direction ending in the suprapubic region unless tenderness is present at
any site. the intra-abdominal structures are examined in the following
order:
1. Left kidney
2. Spleen
3. Right kidney
4. Liver
5. Urinary bladder
6. Aorta and para-aortic glands
Finally, the hernial sites and the external genitalia should be examined.

SUPERFICIAL PALPATION

The examiner should note the following points during superficial

palpation.
 Local temperature.
 Feel of the abdomen-normal abdomen is soft. The abdomen will be
tense if there is collection of excessive fluid in the peritoneal
cavity.
 Tenderness- may be local or diffuse. local tenderness may point
towards the possible organ involved.
 Guarding and rigidity- Guarding and rigidity are seen in conditions
causing peritoneal inflammation or irritation.
 Divarication of recti.-the recti muscles of anterior abdominal wall
join in the midline.

DCDdndition
DIRECTION OF BLOOD FLOW IN DILATED VEINS

Away from umbilicus - Portal hypertension

From below upwards - SVC Obstruction
From above downwards - IVC Obstruction
DEEP PALPATION

Deep palpation is done to look for any organ enlargement.

Conventional Method.
The radial side of the index finger is placed parallel to the border of the
organ to be palpated and the organ is palpated by the tip of the fingers.
This helps to detect any palpable mass and define its site.

Dipping Method.
It is used to palpate abdominal organs in children with tense ascites.
The examiner should place the hand flat on the abdomen and make a
quick dipping movement so that the fluid is displaced suddenly. The
sudden displacement of fluid gives a tapping sensation over the surface of
the organ (liver/spleen) similar to a patellar tap. This helps to detect and
map the outline of any enlarged
abdominal organ.

Rebound Tenderness (Blumberg's Sign).

The examiner presses the abdomen firmly with the palm of the hand and
then suddenly releases the pressure by moving away the hand. In
peritoneal inflammation, this manoeuvre results in severe pain. For
instance, in patients with appendicitis, there is rebound tenderness in the
right ilic fossa.

EXAMINATION OF ABDOMINAL MASS

 Site,,size,Shape
 Margin/Border,Surface
 Skin over the mass,Plane
 Consistency,Tenderness
 Mobility,Pulsations
 Reducibility,Compressibility
 Transillumination,Pitting

PALPATION OF SPECIFIC ORGANS

LIVER

Liver size is measured below the right costal margin in midclavicular line
by palpation. Liver span refers to the distance between the upper and the
lower borders. The lower border is defined by palpation. The upper
border is defined by tidal percussion.
 A)
 The examiner should place the palm of the hand over the abdomen
lateral to the rectus abdominis muscle with the fingers pointing
towards the right subcostal region.
 The child is then asked to take deep breaths. The index and middle
fingers of the examiner should be used to palpate the enlarged
liver.
 The enlarged liver will touch the fingers at the height of
inspiration.
 If the liver is not felt, move the hand upwards towards the right
subcostal margin till it becomes palpable.

B)
 The examiner should place the hand over the abdomen with the
fingers parallel to the right subcostal region (parallel to the border
of liver).
 The palpation should be started from the right iliac fossa.
 The radial border of the index finger should be used to palpate the
enlarged liver. With the hand in place as described, the examiner
should ask the child to take a deep breath and the enlarged liver
will be felt by the fingers.
 If it is not felt, he should keep moving the hand upwards till it
becomes palpable. However, the examiner should be careful not to
start palpation too close to the right costal margin.

SPLEEN

A palpable spleen is always abnormal. It has been observed that the

spleen should be about three times its normal size to be palpable
clinically. The direction of enlargement is towards the right iliac fossa.
The size is measured in centimetres from the left costal margin towards
the right iliac fossa.

The palpation of spleen is usually done with the palm of the right hand
with the fingers pointing towards the left subcostal margin. The left hand
is kept posterolaterally over the left lower rib cage to support it from
below. Palpation should start from the right iliac fossa and move towards
the left hypochondrium. The examiner should ask the child to take deep
breaths during this procedure. An enlarged spleen can usually be palpated
by the tip of the fingers during
inspiration.

KIDNEY
Kidney swellings are ballotable and hence bimanually palpated. One hand
of the examiner is placed posteriorly below the lower ribcage and the
other hand is placed anteriorly in the lumbar region.

The direction of percussion should be from above downwards. The

examiner should observe the general note of the abdomen. It is normally
resonant.
 Resonant-normally present
 Dull-presence of fluid
 Hyper-resonant-presence of pneumoperitoneum
 Dull in the pubic area-bladder distension

TIDAL PERCUSSSION

 This method helps to differentiate liver dullness from the dullness

of pleural effusion.
 The examiner begins the percussion from the right infraclavicular
region and proceeds downwards.
 Once the liver dullness is reached, the examiner keeps his hand at
the same site and ask the patient to take a deep breath.
 With the patient holding his breath, the percussion is done at the
same site again. If the site becomes resonant, it is inferred that the
dullness was due to liver.

FLUID THRILL

 This method helps to detect free fluid in the abdomen.

 Ascites can be demonstrated clinically by eliciting for fluid thrill.
 The patient is asked to lie in supine position. One hand of the
examiner is placed on the flank of the abdomen.
 The nurse/attendant is asked to place the ulnar side of his/her hand
lightly on the middle of the patient's abdomen.
 It is ensured that the hand on the middle of the abdomen is held
lightly because firm pressure can prevent transmission of the thrill.
 The examiner then gently taps the other side of the abdomen and
feels the sensation by the other hand placed on the flank.
 If free fluid is present in the abdomen, a fluid thrill is appreciated
on the opposite side of the tapping hand.

LIVER SPAN
 .
 The examiner begins the percussion from the second intercostal
space in the right midclavicular line and proceeds downwards.
 The intercostal space in which dullness starts is noted.
 The length between this point and the lower border of the liver
along the midclavicular line is measured to give the liver span.
 The liver span varies with age.
 In the presence of right-sided pleural effusion or empyema, there
can be a false impression of hepatomegaly. This can be confirmed
by tidal percussion.

SHIFTING DULLNESS

 Is to detect free fluid in abdomen.

 it can be demonstrated only if about 1000 mL of fluid is present
in the peritoneal cavity in older children and adults.
 In younger children, it can be positive even with a lower amount of
fluid.
 First, the child is percussed for bladder dullness.
 The abdomen is then percussed from the midline to the lateral
side.
 Normally flanks are resonant. In the presence of ascitic fluid, there
is dullness in flanks.
 Once the dullness is noted, the pleximeter finger is fixed on the
abdomen.
 The patient is then asked to turn laterally to the opposite side.
 After about a minute, the same area is percussed again.
 If shifting free fluid is present, the previously dull area becomes
resonant. Additionally, the area on the opposite side that was
resonant previously becomes dull.

PUDDLE SIGN

 This method can clinically detect even 50 mL of fluid in the

peritoneal cavity.
 The patient is put in knee-elbow position for 5minutes and the fluid
is allowed to accumulate in the umbilical area.
 With the patient still in the same position, the examiner percusses
near the umbilicus and in the surrounding dependent.
part of the abdomen.

AUSCULTATION

BOWEL SOUNDS
  The bowel sounds are best heard in right iliac fossa ,because of
the turbulence created due to the ileocaecal valve.

 The normal bowel sounds are metallic in nature with a tinkling

quality while the abnormal bowel sounds are high pitched and
loud. Also check the frequency

OTHER ABNORMAL BOWEL SOUNDS

1. Bruit over the liver-it is caused by turbulence of blood flow and is

seen in
 aortic aneurysm
 haemangioma liver and
 coeliac artery stenosis.

2. Friction rub-this may be found in

 hepatic area (in perihepatitis) and
 splenic area (in perisplenitis).

3. Venous hum-this is heard over the collaterals due to portosystemic

shunts between the patent umbilical vein and portal vein.

4.Cruveilhier-Bawugarten syndrome- this is characterised by a loud

venous hum due to increased blood flow through the recanalised
umbilical vein.

AUSCULTO-PERCUSSION

This is a combination of auscultation and percussion. It is used to detect

minimal ascites.

MEASUREMENT OF ABDOMEN

 Abdominal girth- this should be measured at the umbilical level

using a measuring tape. It is important to assess the progress of
ascites.
 Spinoumbilical measurement- this is the distance between the
umbilicus and the anteriorsuperior iliac spine. It is measured
bilaterally and compared. In normal children, the measurements on
both the sides are equal. In unilateral masses, the distance is more
on the affected side.
EXAMINATION OF EXTERNAL GENITALIA

RECTAL EXAMINATION
Acute gastroenteritis case sheet

Name : ABC
Age : 3 years
Sex : Male
Address :
Informant : Mother (reliable)

Chief complaints :
1. Loose stools – since 3 days
2. Decreased urination- since 2 days
3. Excessive crying- since 1 day
4.
History of present illness:
Three year old male child came with history of loose stools since 3 days,
acute in onset; 7-8 episodes per day. Stools were watery in consistency,
yellow in Color, large volume. Not associated with blood or mucous.
Child has history of decrease frequency and amount of urine passed per
day for 2 days. Urine is dark yellow in color. No h/o blood in urine.
Child also has history excessive crying and irritability since 1 days.
Associated with excessive thirst.

History of consumption of food from local restaurant present 4 days back.

No h/o vomiting, pain abdomen, abdominal distension.
No h/o fever
No h/o cough, cold, ear ache or ear discharge.
No h/o consumption of any medications.
No history of lethargy/decreased activity.
No h/o abnormal movements/seizures.
No h/o refusal of feeds.

Past history: No history of similar complaints in the past.

Any hospitalization/any treatment taken before coming
Family history: Similar complaints in the sibling- subsided with oral
medications.
Birth history:
Immunisation history: rotavirus vaccination
Developmental history:
Dietary history:
Socioeconomic history:
Source of drinking and cooking water: borewell
Adequate waste disposal.

Summary:
Three year old male child who is second in order to a non consanguineous
marriage came with complaints of loose stools since 3 days, decreased
urination since 2 day and excessive cry since 1 day, following
consumption of food from a local restaurant. Similar complaints were
present in the sibling, which subsided with oral medications. Child has no
significant past or birth history, achieved all appropriate milestones,is
immunised as per age, is consuming a diet deficient in calories and hails
from a lower middle class as per modified Kuppuswamy scale .
From the above history, I would like to make a diagnosis of acute
gastroenteritis with severe dehydration, most probably secondary to food
poisoning.

General examination:
Child is crying and sitting on the mother’s lap.
Vitals:
Temp: 98 degrees Fahrenheit
Pulse rate: 76 bpm
Respiratory rate: 24 cpm
CFT : < 3 seconds
BP:90/60mmHg
Pallor: present
No icterus, cyanosis, clubbing, lymphadenopathy, edema.
Head to toe examination/ signs of dehydration:
Head: normal
Eyes: sunken, tears
Oral cavity: dry ,thirst
Skin turgor: goes back slowly
Ears: normal
Extremities: normal
Peripheral pulses: felt
Genitalia: normal

Anthropometry :
Systemic examination:
P/A:
CVS:
CNS:
RS:
Diagnosis: Acute gastroenteritis with some dehydration, secondary to
food poisoning.
 VIVA QUESTIONS:

1) Define Diarrhea
Passage of three or more liquid or watery stools within 24 hours.
It involves change in frequency and change in consistency ie
liquid or watery.
2) Characteristics of stool in different conditions

Disease Characteristics of stool

Lactose intolerance Soundy, soupy consistency, local redness over the anal
area.
Fat malabsorption Frequent, frothy, foul smelling, floats in water
Inflammatory bowel Recurrent blood and mucous
disease
Dysentery Blood stained stools
Cholera Rice water stools

3) Classification of diarrhoea
Type Duration Aetiology
Acute 3-7 days Infective
Chronic More than 2 weeks ,insidious cause Non infective
Simple persistent More than 2 weeks ,starts actively Infective
Persistent protracted More than 2 weeks with malabsorption
diarrhoea

4) Organisms causing diarrhoea

Type of organism Organisms
Virus  Rotavirus
 Norwalk virus
 Astrovirus
 Calcivirus
 Coronavirus
Bacteria  Shigella
 Ecoli
 Salmonella
 Campylobacter jejuni
 Shigella
Parasites  Giardia lamblia
 Entamoeba histolytica
 Trichuris trichura
 5) What is the composition of ORS?

Sodium 75 mmol/L
Glucose 75mmol/L
Chloride 65mmol/L
Potassium 20mmol/L
Citrate 10 mmol/L
Total: 245 mmol/L

6) Treatment of diarrhoea
A. Correct dehydration
Features No dehydration Some dehydration Severe dehydration
Sensorium Alert Irritable Lethargic
Thirst Not thirsty, drinks Thirsty, drinks eagerly Drinks poorly
normally
Skin turgor Normal Goes back slowly Goes back very slowly
Eyes Normal, tears Sunken, tears absent Very sunken, tears
present absent
Oral mucosa Moist Dry Very dry
Pulse Normal Normal, maybe Weak, thready
increased
Treatment Plan A Plan B Plan C
plan

Plan A
1. Fluid therapy
2. Continue feeding
3. Zinc supplements
4. Identification of danger signs
Plan B
1. ORS to be given -75ml/kg over 4 hours
2. Continue feeding
3. Identification of danger signs
Plan C
1. IV fluid RL or NS
2. Less than 1 year : 30ml/kg over 1 hour
70ml/kg over 5 hours
>1 year /Older child: 30ml/kg over 30 mins
70ml/kg over 2 ½ hours
3. ORS
 Per abdomen Model Case sheet

Chronic liver disease with or without portal hypertension.

Informant : mother
Name : xyz
Age : x yrs
Residing at :
Admitted with complains of: abdominal pain since 3 months
Yellowish discoloration of the skin and since 1 month
History of abdominal distention since 1 month.
Fever since 4 days.
Blood in stool since 2 days
Blood in vomitus since 1 day

History of presenting illness: X yrs of age, boy/girl , first order by birth

was admitted with history of abdominal pain since 3 months on and
off,insidious in onset,right upper quadrant (hepatic etiology or gall
bladder), dull aching type( recurrent colicky pain in cholecystitits and
cholelithiasis), non radiating in nature(cholecystitis and cholelithiasis
pain will radiate to back right scapula, arm and neck.Pancreatic pain will
radiate towards back.) No diurnal variation( nocturnal pain in sleep
associated with organic lesion).no aggravating and relieving factor(
cholecystitis and gastritis pain will aggravate with food)
Yellowish discoloration of skin and eyes since one month. History of
dark colored urine present since one month. History of anorexia since
one month. No history of itching( in obstructive jaundice,itching is
present). No history of drug ingestion( anti Tb drugs, valproic acid,). No
history of blood transfusion or previous injections( source of infective
hepatitis).No history of contact with jaundice patient.
History of abdominal distention since 1month:Insidious in onset
,gradually increase in size, non progressive in nature and not associated
with periorbital oedema.
History of fever since 4days,moderate to high grade,intermittent type ,not
associated with chills and rigor,no diurnal variation and child is not active
between fever episodes
History of blood in stools since 2 days: black tarry stools( upper GI bleed
i.e dark colored stools),foul smelling, 2 episodes in a day ,no history of
iron intake and no history of loose stools(dysentery).no history of
constipation(anal fissure). No history of colored food intake( grapes and
chocolates,beetroots ).no history of any other bleeding manifestation.
History of blood in vomitus since 1day: non projectile,contains food
particles,non bilious,1 episode,no history drug ingestion (
aspirin,NSAIDS,steroids),no history of ingestion of colored food
syrup,no history of epistaxis,no history of epigastric pain(gastric ulcer).no
history of giddiness( if present indicates heavy blood loss.)
No history of altered sensorium, seizures, involuntary moments(hepatic
encephalopathy).
No history of decreased urine output (hepatorenal syndrome or
leptospirosis)
History of etiology: No history of trauma or surgery
No history of umblical vein catherization(portal vein thrombosis)
No history of drug intake.
No history of recurrent respiratory tract infection(cystic fibrosis or alpha
1 antitrypsin deficiency).
No history of rash ,arthritis,nephritis ,thyroiditis( extrahepatic
manifestations of autoimmune hepatitis)

PAST HISTORY : no significant past history.

No history of blood transfusion.

FAMILY HISTORY : no history of jaundice,hepatitis Bor wilson’s

disease in other sibling l neuropsychiatric illness.

BIRTH HISTORY : Child born by normal vaginal delivery,full term,

cried immediately after birth.
Institutional delivery. Birthweight was 2.75kg.no history of NICU
admission( a. In neonatal seizure caused by hypoglycemia is due to
galactosemia and tyrosinemia . b. Neonatal jaundice is due to alpha 1
antitrypsin deficiency,tyrosinemia or neimann-pick disease )
No history of delayed passage of meconium( in cystic fibrosis).
No history of umblical venous catheterization.

DEVELOPMENTAL HISTORY: appropriate for age(developmental

delay possible in any chronic illness)

IMMUNIZATION HISTORY: appropriately immunised for age (NIS)(

specially ask if previously immunised with hep A and hep B vaccine.

DIETARY HISTORY: Diet deficit in 400kcal and 4g of

protein(specifically ask for copper rich food like
liver,shellfish,nuts,chocolates for wilsons disease.

SOCIOECONOMIC HISTORY: lower middle class according to

modified kuppuswamy classification
Specifically ask about using tap water, boiled or not boiled and personal
hygiene.

SUMMARY: X yr old child born to a non consanguineous marriage

couple, first order by birth, admitted with complain of pain abdomen sin 3
months,yellowish discoloration of skin and eye since 1 month,abdominal
distention since 1month,fever since 4 days,blood in stools since 2days
and blood in vomitus since 1 day with no significant past or family
history or birth history and attained all the milestones appropriate for
age,ammunised appropriate for age and belonging to socioeconomic class
of lower middle class. With above summary I would like to conclude that
the patient has some chronic liver pathology.

GENERAL EXAMINATION: child is alert and well oriented to time

place and person.(note if patient is unconscious calculate GCS score)
1) vitals

2) anthropometry: height ,weight (above 5 yrs) head circumference

,chest circumference mid arm circumference( 1-5yrs).

3)head to toe examination:

head - normal
Face - hepatic facies-sunken eyes, hollowed temporal fossa,pinched up
nose with malar prominence,muddy complexion of skin and icteric tinge
of conjunctiva.
Eyes - icterus present (cataract in galactosemia, K-f ring in wilsons
disease, features of vit A deficiency
Oral cavity - normal(bleeding manifestation, aphthous ulcer in IBD),
halitosis present
Chest - normal(evidence of rickets,spider naevi)
Gynecomastia present
Abdomen - distension present, dilated vein present( evidence of
ascites,caput medusa)
Extremities - normal
Skin: loss of body hair, dry skin.spider naevi present,striae presentor
alopecia .
Mention SMR in the older children ,check for testicular atrophy and see
for involuntary movements.

SYSTEMIC EXAMINATION:
Per abdomen examination

Upper GI : gums -normal(look for any bleeding)

Teeth : normal (check for hygiene and caries)
Tongue : dry and under surface of the tongue is yellow.
Oral mucosa : normal (look for any bleeding)
Tonsils : normal

Inspection: abdomen distention present, all parts of the abdomen move

equally on respiration but restriction of the movement due to ascites,
shiny skin over the abdomen, pink striae present, umbilicus is
transversely stretched, visible veins on the abdomen. no visible pulsations
or peristalsis. hernial orifices are normal.

Palpation : soft, tenderness present over the right hypochondrial region,

hepatomegaly present with ascites (liver span x cms [acc to age] and y
cms below the right costal margin).
liver is firm is consistency and sharp edges are felt. Splenomegaly
present (portal hypertension)[measurement of spleen to be done].No
palapable mass.

Percussion : shifting dullness present.

No fluid thrill
No puddle sign

Auscultation : bowel sounds present.

Other system examination:

CNS: WNL
[(assess concentration ,memory ,speech and handwriting)
there is dysarthria in wilsons disease.
Look for flapping tremors.

Ataxia (vit E deficiency due to malabsorption.) diminished sensation

and reflex are also possible with vit E deficiency Deep tendon reflex are
exaggerated in initial stages of hepatic encephalopathy.

Extrapyramidal manifestation in wilsons disease(like dysarthria,

athetosis, dystonia, myoclonus etc)
CVS:S1 S2 present ,no murmur (cardiomegaly due hyperdynamic
circulation in long standing cases.)

RS: bilateral normal vesicular breath sounds heard .no added sounds( in
the cases with ascites ,look for pleural effusion)

DIAGNOSIS:
Case of chronic liver disease with portal hypertension probably due to
chronic hepatitis without features suggestive of hepatic encephalopathy
which is not compensated and with no coagulopathy .
Nephrotic Syndrome Model Case Sheet

Name :
Age : birth -3months: congenital NS
3months-1year: infantile NS
2-8yrs: childhood NS
Puberty: adult NS

Sex : male: female 2:1

Address :
Informant :

Chief Complaints:-
H/o swelling of face and around the eyes
H/o swelling of the lower limbs
H/o generalized swelling ( abdomen, scrotum)

History of presenting illness:-

The __ year old M/f child was brought to the hospital with C/o swelling
in the face and eyes since 7 days. Insiduous in onset, progressive,
increased in the morning time and on lying down and decreased during
the day in upright position.
C/o swelling in the lower limbs since 7 days which started from the feet
and progressed upto the thigh relieved on elevating the limb.
C/o swelling of the abdomen insidious in onset.
C/o swelling of the scrotum in males.

H/o blood in urine .

H/o elevated BP (if previously checked).
H/o breathlessness(distended abdomen).
No H/o fever, cough, cold.
No H/o vomiting, loose stools.
No H/o impairment of higher mental fucntions.
No H/o orthopnea, chest pain, PND, palpitation (CCF)
No H/o jaundice hematemesis, melena, altered sensorium (hepatic failure)
No H/o loss of appetite &weight, skin changes (nutritional edema)

Complications :

Edema: loss of protein (h/o swelling)

Anemia : loss of transferrin(h/o generalized weakness, pica, paleness of
the body)
Hypothyroidism : loss of thyroid binding globulin. (h/o easy fatiguability,
dry skin, loss of interest, weight gain, delayed development).
Hypocalcemia : due to loss of vitamin D binding globulin.
Infections: strep.pneumonia and other gram negative organisms. (h/o
cough, cold, treatment with steroids)
Thromboembolism: renal vein, peripheral vein, cerebral vein
thrombosis(h/o immobilization, hypovolemia, infection, diuretics)
Renal failure: acute and chronic: ( h/o hypovolemia and diuresis)
Convulsions: h/o hypertension, hypocalcemia, hyponatremia, renal
failure.
Encephalopathy: h/o head ache, vomiting, convulsions, altered sensorium.
Pericardial effusion and hydrothorax due to fluid retenbtion.
Postural hypotension due to hypovolemia.
Accelerated atherosclertosis.
Zn & cu deficiency due to loss of metal binding protiens.
Complications due to drugs:
Steroids: cushingoid facies , cataract and glaucoma, short stature, peptic
ulcer, GI bleeding, suppression of HPA axis, diabetes and
hyperlipidaemia, nephrocalcinosis.
Cyclophosphamide : haemorrhagic cystitis, bone marrow depression,
alopecia.
Furosemide : hypokalemia, hyponatremia , hyperuricaemia, tinnitus and
deafness.

Past History:

h/o similar complaints in the past.

Family history: congenital NS, HSP, hereditary nephritis can cause

secondary NS.

Antenatal history
Birth History

Postnatal history exclusive breast feeding and initiation of

complementary feeds.

Diet history:

Socioeconomic history:low socioeconomic class, unhygienic condition,

open air defecation, source of water (various infection).

Summary: A _ year old M/F child was brought to the hospital with C/O
swelling in the face and limbs since 7 days, with h/o passage of blood in
urine and has no significiant family/birth history.The child consumes a
diet(veg/nonveg) deficit in proteins and calories,has been immunized
upto date and belongs to lower socioeconomic status with inadequate
personal hygiene.I would like to evaluate the child further for nephrotic
syndrome.
NEPHROTIC SYNDROME: DISCUSSION
Nephrotic syndrome is a clinical manifestation of glomerular disease
associated with heavy(nephrotic range)proteinuria .
Nephrotic range proteinuria defined as :
Proteinuria >3.5g/24hrs OR
Protein excretion of >40mg/m2/hr OR
Proteinuria 1gm/m2/day OR
Urine protein: Creatinine ratio >2.
The triad of clinical findings:
HYPOALBUMINEMIA(<2.5g/dl)

EDEMA

HYPERLIPIDEMIA (CHOLESTEROL>200mg/dl)

CAUSES:
IDIOPATHIC NEPHROTIC SECONDARY CAUSES OF NEPROTIC
SYNDROME SYNDROME
Minimal change disease Infections(Endocarditis,hepatitis
B,C,HIV-1,infectious
mononucleosis,malaria
Focal segmental Drugs
glomerulosclerosis
Membranous nephropathy Vasculitis syndromes
Glomerulonephritis associated Associated with malignant
with nephrotic diseases(lymphoma,leukemia,solid
syndrome:Membranoproliferative tumors)
Glomerulonephritis,mesenteric
glomerulonephritis,igA
nephropathy

MOST COMMON CAUSE

NEPHRITIC SYNDROME NEPHROTIC SYNDROME
CHILDREN:Post streptococcal Children:Minimal change disease
glomerulo nephritis Adults:FSGS
ADULTS: igA Overall:FSGS
Overall:igA
EDEMA is the M/C presenting symptom
Two possible hypothesis:
UNDERFILL HYPOTHESIS:proteinuria causes fall in plasma protein and
decrease in intravascular oncotic pressure which leads to leakage of
plasma water into the interstitium,generating edema.
Due to increased intravascular volume,there is increased secretion of
aldosterone,results increased sodium and water retention by the
tubules
So overall most common cause of edema in nephritic syndrome is
sodium and water retention.

OVERFILL HYPOTHESIS

Primary sodium retention ,with subsequent volume expansion and

leakage of excess fluid into the interstiuim.

IDIOPATHIC NEPHROTIC SYNDROME: It is 90% of nephrosis in

childhood.Single disorder with varying histologic features

PATHOLOGY:1)Minimal change disease 2)Focal segmental

glomerulosclerosis(10%) 3)Mesangial proliferative group(5%)

Histology of minimal change disease

INVESTIGATION FINDING
Light microscopy Normal
Electron microscopy Normal and no electron-dense
material,uniform and diffuse
effacement of foot processes
Immunofluorescence No ig or complement deposits
FEATURES OF NEPHROTIC SYNDROME

FEATURE CAUSE
Hypoalbuminemia Proteinuria
Hyperlipidemia Hypoproteinemia stimulates
generalized protein synthesis in liver
lipoprotein.First LDL and cholesterol
increases then triglycerides and
VLDL.
Lipid catabolism diminished due to
 reduced level of lipoprotein lipase.
Microcytic hypochromic anemia Loss of transferrin
Susceptibilty to infection a)Due to urine loss of igG( and
increased catabolism
b)Steroid/immunosuppressive
drug,defective cell mediated
immunity
c)Malnutrition
IMMUNIZATION WITH
PNEUMOCOCAL AND VARICELLA
VACCINES IS REQUIRED.

Hypocalcemia Due to vitD deficiency secondary to

urinary loss of cholecalciferol
binding proteins.
Hypothyroidism Loss of thyroid binding globulin
Hypercoagulability a)Urinary loss of AT-
III(Antithrombin-III); b)Reduced
levels/activity of protein C and
S;c)Hyperfibrinogenemia due to
increased synthesis; d)Impaired
fibrinolysis&Increased platelet
aggregability

NOTE:ALL PROTEIN DECREASED EXCEPT FIBRINOGEN WHICH IS

INCREASED.

CLINICAL FEATURES:

1. EDEMA first noticed around the eyes followed by anasarca.

2. Hydrothorax and hydrocoele may be present
3. With increasing edema urine output may fall.
DIAGNOSIS:

 Urine analysis:Proteinuria of 3+ or 4+ or> 40mg/m2/hr or Spot

urine protein/creatinine ratio >2.
 Serum Albumin 2.5gm%
 Serum cholesterol >200mg,Normal c3 and c4 levels.
 INVESTIGATIONS :
 Investigations for Diagnosis :
Urine Examination – Macroscopy and microscopy, proteins,
protein-creatinine ratio.
Blood Examination – Serum proteins, lipid profile, serum
complement levels, serum protein electrophoresis.
Investigations for Etiological factors :
HbsAg
ANA
Antistreptolysin-O
Mantoux test
Coombs test
Investigations for Complications :
Blood count, Hb%
Total and differential count
PBS
Blood urea and creatinine
S. calcium
Xray chest
USG abdomen
Renal biopsy
COMPLICATIONS:
1. Edema
2. Infections:M/C cause of mortality :SPONTANEOUS BACTERIAL
PERITONITIS STREPTOCOCCUS PNEUMONIAE M/C organism
causing peritonitis,gram negative bacteria like E.COLI may also be
encountered.
3. Thromboembolic complication:RENAL VEIN
THROMBOSIS,pulmonary embolus,saggital sinus thrombosis.
4. ACUTE RENAL FAILURE
5. STEROID TOXICITY.
6. IMPORTANT TERMINOLOGIES:
COMPLETE REMISSION <1+ ofprotein on urine dipstick for
3 consecutive days
STEROID RESISTANCE Failure to achieve complete
remission after 8weeks of
corticosteroid therapy.
RELAPSE 3 + protein on urine dipstick for 3
consecutive days.
FREQUENT RELAPSE Two or more relapses within
 6months of initial response, or four
or more relapses in any 12 month
period
INFREQUENT RELAPSE One relapse within 6months of
initial response,or one to three
relapses in any 12-month period
STEROID DEPENDENCE Two consecutive relapses during
cortico steroid therapy,or within 14
days of ceasing therapy.
LATE NON RESPONDERS Persistent proteinuria during 4 or
more weeks of corticosteroids
following one or more remission.

TREATMENT OF FIRST EPISODE ,INFREQUENT RELAPSE,FREQUENT

RELAPSE OF NEPHROTIC SYNDROME:

FIRST EPISODE OF NEPHROTIC SYNDROME

DAILY SINGLE ORAL PREDNISOLONE 2mg/kg to be given

for 4-6weeks followed by alternate day single dose @ 1.5mg/kg
for 2-5 month

FREQUENT STEROID STEROID -

INFREQUENT
RELAPSE RELAPSE DEPENDENCE RESISTANT

Two or Two consecutive

One relapse relapses during
more relapses
within 6mths of corticosteroid
within 6mths of
initial response,or therapy or within 14
initial response
one to three days of ceasing
or four or more
relapses in any therapy
relases in any
12mth period
12month
period
 Daily prednisolone
until the child has NO remission
Single-daily dose of Daily prednisolone
prednisolone @ been in remission following 8
until the child has for atleast
2mg/kg until the been in remission for weeks of
child has been in 3days,followed by treatment.
atleast alternate day
complete remission 3days,followed by
for atleast 3 days prednisolone for
alternate day atleast 3 months
followed bt alternate prednisolone for
day prednisolone for atleast 3 months
atleast 4 weeks
If patient
develops steroid
dependent
adverse effects

Corticosteroid sparing agents -alkylating

agents(cyclophosphamide,chlorambucil),levamisole,calcineurin
inhibitor(cyclosporin,tacrolimus),mycophenolate mofetil,rituximab

STEROID RESISTANT NEPHROTIC SYNDROME IN CHILDREN:SRNS

1. The guidelines has recommended Minimum of 8weeks treatment

with corticosteroids to define steroid resistance (in contrast with
IAP-4weeks)
2. The following are required to evaluate the child with SRNS:
a)diagnostic kidney biopsy.
b)Evaluation of kidney function by GFR.
c)quantitation of urine protein excretion.
3. Following treatment should be followed:

NO REMISSION FOLLOWING 8WEEKS TREATMENT WITH

CORTICOSTEROIDS

CALCINEURIN INHIBITORS LIKE CYCLOSPORINE,TACROLIMUS for 6months

Plus
RAS BLOCKADE BY ACE INHIBITORS LIKE ENALAPRIL(0.3-
0.6mg/kg/day.,FOSINOPRIL

Partial or complete remission No remission by 6 months

achieved
Continue inhibitor for 12 calcineurin months

MYCOPHENOLATE HIGH DOSE

MOFETIL CORTICOSTEROIDS

FREQUENT RELAPSE AND STEROID DEPENDENCE:

LONG TERM ALTERNATE DAY PREDNISOLONE:Firstly ,treat the relapse
[i.e prednisolone is given at a dose of 2mg/kg/day until protein is
negative/trace for three consecutive days,and then on alternate days
at a dose of 1.5mg/kg for 4 weeks.Thus,the treatment of relapse
usually lasts for 5-6 weeks ]
1) Small dose of prednisolone is given alternate day for9- 18months
2) If infections precipitate relapse,administer daily small dose of
prednisolone for 5-7days starting at the onset of infections.
3) Patients with repeated relapses ,while on longterm therapy should
be considered for long term treatment with a steroid sparing
agent.
4) Indications for steroid sparing agents:
a) prednisolone threshold(for maintaining remission)higher than
0.5-0.7mg/kg on alternate days
b) features of steroid toxicity(growth failure,hypertension abd
cataract.)

AGENT DOSE DURATI ADVERSE EFFECTS

ON
1)prednisolone Maintain on .3 9- Cushinoid body
to.7mg/kg on 18mont habitus,hypertension,s
alternate days hs hort
stature,cataract,hirsuti
sm.
2)a)Levamisole, 2-2.5mg/kg on 1-2yrs Leukopenia,rash,flu-
alternate days. like symptoms
b)Cyclophosphamid 2-2.5mg/kg/day 12weeks Leukopenis,alopecia,g
e onadal toxicity,nail
discoloration,(hemorr
hagic cystitis;nausea
 and vomiting).
3a)Mycophenolate 20-25mg/kg/day 1-3yrs Gatrointestinal
mofeti discomfort ,diarrhea
,leukopenia.

b)cyclosporine(CyA) CyA:4- 12- Acute and chronic

or 5mg/kg/day 36mts nephrotoxicity,elevate
c)Tacrolimus TaC:0.1-0.2 d transaminases(both
mg/kg/day agents),hirsutism,gum
hyperplasia,hypertensi
on or
hyperlipidemia,hyperg
lycemia.
4)rituximab 375mg/m2 IV 2-3 Infusion reactions
once a week doses (fever,rash,bronchosp
asm),hypogammaglob
ulinemia,neutropenia.

AGENTS FOR MANAGEMENT OF STEROID RESISTANT NEPHROTIC

SYNDROME.

AGENT DOSE DURATION EFFICAC ADVERSE

Y EFFECTS
CALCINEURIN Acute and
INHIBITORS chronic
a)cyclosporine(CsA) 4-5mg/kg/day 12-36mths 50-80% nephrotoxicity,g
b)Tacrolimus(Tac) um
.1-.2mg/kg/day 12-36mths 70-85% hyperplasia,hyp
ertension,high
cholesterol,elev
ated
trasaminase
CYCLOPHOSPHAMIDE
a)oral Leukopenia,alop
b)Intravenous 2-2.5mg/kg/day 12weeks 40-50% ecia,nausea
500-750mg/m2 6weeks 20-25% ,vomiting,gonad
al
toxicity,hemorrh
agic cystitis.
HIGH DOSE
CORTICOSTEROIDS
WITH
CYCLOPHOSPHAMIDE
a)Methylprednisolone
20-30mg/kg IV ‘pulses on 30-50% Hypertension,hy
alternate pokalemia,hype
daysX6;once rglycemia,steroi
weeklyX8;fort d
nightlyX4. psychosis,syste
mic infections
b)prednisolone
c)cyclophosphamide. Tapering doses* 18months Side effects of
2-2.5mg/kg/day** 12weeks prolonged
steroid therapy
and and
cyclophosphami
de therapy
*prednisolone 1.5mg/kg on alternate days X 4weeks;
1.25mg/kgX4weeks;1mg/kgX4months; 0.5-0.75mg/kg X 12-18months
**cyclophosphamide is administered during 3-15 weeks.

DIETARY MANAGEMENT AND MANAGEMRNT OF SYMPTOMS:

1)Adequate protein intake (2-3g/kg/day) is recommended.
2)During daily adminstration of prednisolone,dietary salt should be
restricted to decrease the tendency to hypertension.2meq/kg/day-the
usual amount of salt n cooking is allowed but salty snacks should be
temporarily withheld.
2)Fat intake should be curtailed(as administration of prednisolone may
lead to excessive weight gain
3)in non minimal lesion,steroid resistant nephrotic syndrome with heavy
proteinuria,the dietary protein is restricted to 1.5-2g/kg/day(as
continued heavy proteinuria increases renal damage)
4)water intake limited to replacement of insensible loss plus urine
output minus a planned weight loss.
5) Diuretics if edema severe especially massive ascites impending
respiratory movements.Furosemide is used(1-3mg/kg in 1-2 divided
doses)the dose may be increased to 4-6mg/kg.occassionally Iv
boluses(1-2mg/kg)admistration or its continuous infusion(4-10mg/kg
over 24hrs) may be necessary .
6)Intravenous administration of 25% human albumin .5g/bodywt over
1-2hr with monitoring of pulse and BP;followed by IVfurosemide i1-
2mg/kg is given towards the end of infusionsand is often necessary
when fluid restriction and parenteral diuretics are not effective.
Proton pump inibitors to be added.

CONGENITAL NEPHROTIC SYNDROME:

1)Presents in the first 3 months of life with anasarca,hypoalbuminemia

and oligura.Etiology is heterogenous

2)The ‘finnish’form :autosomal recessive ,mutations in the gene

encoding nephrin(NPHS1).Renal histology: microcystic dilation of
proximal tubules is seen after a few months of life, ultrastructral
abnormalties of the glomerular basement membrane are present at
birth.

4)Elevated levels of AFP in maternal serum and amniotic fluid.

5)The clinical course of the disease is complicated by failure to

thrive,recurrent infection,hypothyroidism and progression to renal
failure by 2-3yrs.

6)Patients with DENY DRASH syndrome show mutation in

WT1gene,congenital nephrotic syndrome,male pseudo hermaphroditism
and high risk of bilateral wilms tumor.

7)other causes include:infections(congenital

syphilis,CMV,toxoplasmosis) and mutation PLCE1 or NPHs2 genes

8)Therapy for patients with congenital nephrotic syndrome:supportive

treatment with appropriate nutrition,control of edema,thyroxine
supplements and reduction of proteinuria through ACE inhibitors and or
indomethacin..
ACUTE GLOMERULONEPHRITIS:
Abrupt onset of hematuria,oliguria,edema and hypertension.
M/C cause : following streptococcal infection.

ETILOGY:1)Post infectious:
streptococci,staphaococci,pneumococci,meningococci,treponema
pallidum,toxoplasma,Hep B and C 2)Systemic vasculitis: henosch-
schonlein purpura,microscopic polyarteritis,wegeners granulomatosis.
3)others:MPGN,IgA nephropathy,SLE.

POST STREPTOCOCCAL GLOMERULONEPHRTIS: Acute GN

following infection by group A beta hemolytic streptococci,preceeding
throat or skin infection(1-4weeks back).
Nepritogenic strains:type4 and 12 causing pharyngitis,type 49 causing
pyoderma.

PATHOLOGY:a)on light microscopy:ischemic enlarged

glomeruli,narrowed capillary loops-glomeruli appear blood
less,mesangial proliferation with neutrophil infiltration
b)immunofluorescence : granular deposits of !gG and c3 along capillary
walls.c) Electron microscopy: Deposits on subepethelial side of GBM.

CLINICAL PRESENTATION:1)school aged

children(uncommon<3yrs) 2)more common in boys, 3)Rapid onset
,puffiness around eyes and pedal edema 4)cola colored urine( brief
hematuria:hematuria doesn’t persist beyond 1-2 weeks) 5)oliguria
6)hypertension in half the patients.
Atypical presentation:convulsions,LVF,Pulmonary edema.

INVESTIGATIONS: 1)RFT: increased b.urea and creat 2)urine

analysis: proteinuria 1-2+ with RBC s ,red cell and granular casts 3)serum
complement C3 4)titres of antistreptolysin increased 5)anti DNAse b
6)serum electrolyte:Hyponatremia,hyperkalemia 7)CBC with ESR:
normocytic anemia,raised ESR 8)chest xray:prominent vascular markings
s/o hypervolemia.

MANAGEMENT:1) DIET:restricted fluid and salt intake, protein rich

diet 2) DIURETICS:Furosemide(1-3mg/kg),IV furosemide-incase of PE
3)for HTN: amlodipine,nifedipine and diuretics,in hypertensive
emergencies-IV nitroprusside or labetalol.3)for LVF:Iv furosemide 4)
Dialysis required in severe renal failure ,prolonged oligoanuria,life
threatening electrolyte disturbance.

RENAL BIOPSY INDICATIONS:

1)in mixed features of glomerulonephritis and nephrotic
syndrome.2)absence of serological evidence of streptococcal infection
along with presence of systemic features.3) high B.urea levels 4) oliguria
,HTN persisting for 7days 5)gross hematuria persisting for 3-4 weeks
6)persistent proteinuria beyond 6months.

VARIANTS:

1)RPGN:acute nephritic illness with rapid loss of renal function over

days to weeks .CHEIF FORMS: immune complex RPGN,pauci immune
RPGN,anti-GBM RPGM.HISTOPATHOGY:presence of cresents
involving 50% or more glomeruli.
Rx:IV and oral corticosteroids,IV cyclophosphamide fowled by
maintenance immunosuppression, plasmapheresis in case of pauci
immune and anti-GBM.

2)Henosch schnolein purpura: mild renal involvement-microscopic

hematuria and mild proteinuria,serum IgA increased.Renal biopsy shows
mesangial proliferation with mesangial deposition of IgA.
Rx: Many recover without any specific treatment. Corticosteroids,Iv
cyclophosphamide followed ny maintenance immunosuppression
inclusion steroids and azathioprine.

3)IgA nephropathy:CLINICAL PICTURE: recurrent episodes of gross

hematuria following URTI,each episodes lasts for 2-5days.IgA deposits
in glomeruli.
Rx:patients with hematuria and non ephrotic hematuria-ACE
inhibitors,patients with nephrotic range proteinuria:corticosteroids and
alkylating agents.

4)LUPUS NEPHRITIS: asymptomatic proteinuria or hematuria,cute

nephritic syndrome and nephrotic syndrome are most common.
IMMUNOFLUORESCENCE: shows mesangial and capillary wall
deposition of IgE and C3 ,c1q and IgA.
Antinuclear and double stranded DNA auto antibodies are present.
Rx:corticosteroids,cytotoxic agents ,calcineurin inhibitors and
monoclonal antibodies.
Cardiovascular system
CARDIOLOGY HISTORY TAKING

Gestational and Natal history

1)Infections: a)Maternal rubella infection: in 1st trimester – Cardiac defects and
multiple anomalies
b)CMV,Herpes,Coxsakie virus: Myocarditis

2)Medications,alcohol and smoking.

a)Amphetamines:ASD,VSD,PDA
b)Anticonvulsants:phenytoin: Aortic stenosis,coarctation of aorta,Pulmonary
stenosis
c)Lithium: Ebsteins anomaly
d)Valproic acid:ASD,VSD
e)Alcoholic intake:VSD,PDA,ASD,TOF [Fetal alcohol syndrome].

3)Maternal conditions:
Infant of diabetic mother: cardiomyopathy ,TGA.

4)Birth weight: a)small for gestational age babies-Look for rubella syndrome and fetal
alcohol syndrome.
b)Infants with high birth weight:seen in diabetic mothers,have
high incidence of cardiac anomalies.

POST NATAL HISTORY:

Ask for weight gain,development and feeding pattern.
 weight gain and development:delayed in infants and children with CCF
 -Poor feeding of recent onset? :points to early sign of CCF.Poor feeding due to
dyspnea and fatigue

Ask for cyanosis,cyanotic spells and squatting.

Ask if baby turns blue :
a)onset?(at birth or several days after birth)
b)Severity of cyanosis :seen in TGA,Tricuspid atresia.
c)Permanent cyanosis (tricuspid atresia,pulmonary atresia),paroxysmal
cyanosis(tet spells in TOF kids)
d)parts of the body that were cyanotic-fingers,toes,lips?(differential cyanosis in
PDA).
e)If cyanosis becomes worse after feeding?
->Evanescent acrocyanosis is normal in neonates.

CONDITIONS:
a)Cyanosis at birth: Transposition of great arteries(TGA),pulmonary
atresia,Hypoplastic left heart syndrome(HLHS).
b)Cyanosis appearing at first week:tricuspid atresia ,ebsteins anomaly,Total
anamolous pulmonary venous circulation(TAPVC).
c)Cyanosis after 3 months:Tetralogy of fallot ,tricuspid atresia.
d)cyanosis at later age:eisenmenger syndrome.
e)Cyanosis:a) increased on crying-cardiac cyanosis, b)decreased on crying –
respiratory cyanosis
f)Cyanosis-increases during crying,feeding,cyanotic congenital heart disease.

Cyanotic congenital heart disease Acyanotic congenital heart disease

a)Tetralogy of fallot Acyanotic with left to right shunt:
a)ASD
b)VSD
c)PDA
b)Transposition of great arteries Acyanotic without shunting
a)pulmonary stenosis
b)Aortic stenosis
c)Coarctation of aorta.
c)Tricuspid atresia
d)Total anamolous pulmonary venous
connection.(TAPVC)

Ask for cyanotic spell

a)Time of appearance: like is it usually in morning,precipitated by cold or
intercurrent infections-associated with severe cyanosis ending in fits and
fainting,or is it after excessive crying?(these usually are seen in obstructive
pulmonary CHD with decreased pulmonary circulation-TOF,TGA with
pulmonary stenosis)
b)Duration of the spell
c)Frequency of the spell
d)Note if infant was breathing fast and deep during the spell(true cyanotic spell) or
was holding his/her breath(breathholding spell)

Ask whether the child squats when tired or has a favourite body position when
tired-ex:when help upright(such as knee chest position).---history of squatting
suggests cyanotic heart disease TOF
PHYSIOLOGY :a)squatting increases peripheral resistance by muscular
compression over the arteries in lower limbs-causing increased peripheral
resistance which decreased the L-R shunt.
b)Squatting pools venous blood in lower limbs causing decreased right ventricular
venous return thus causing decreased R-L shunt.
In a nutshell,both these mechanisms act by decreased R-L shunt.

Cyanosis only in lower limbs-PDA(I.e, differential cyanosis due to reversal of

shunt)
Upper extremity remains pink because brachiocephalic trunk,left common carotid
and left subclavian trunk is given off proximal to PDA.

Ellicit history of tachypnea,dyspnea and puffy eyelids:these are signs of CHF

a)Left sided heart failure-tachypnea with or without dyspnea.
b)Tachypnea-worsens with feeding---leading to poor feeding and poor weight
gain.
c)wheezing or persistent cough at night-early signs of CCF.
d)Puffy eyelids and sacral edema-sue to systemic venous congestion.

NOTE: SIGNS OF CONGESTIVE HEART FAILURE.

Left sided failure Failure of either side Right sided failure

Tachypnea Cardiac enlargement Hepatomegaly
Tachycardia Gallop rhythm(S3) Facial edema
Cough Peripheral cyanosis Jugular venous
engorgement
Wheezing Small volume pulse Pedal edema
Rales in chest Lack of weight gain.
Ask for frequency of respiratory infections:
CHDs with a large L-R shunt and increased pulmonary blood flow predispose to
LRTI.

Exercise intolerance
Decreased in large L-R shunt lesions,cyanotic defects,valvular stenosis.
What to ask:
a)Does the child keep up with other children?
b)How much distance can the child walk or run?
c)How much flight of stairs can the child climb without fatigue?
With infants:H/o feeding pattern?

Chest pain:Cardiac causes of chest pain rare in infants and adolescents.

First rule out non cardiac causes like-costochondritis,trauma to chest wall or
muscle strain and respiratory disease with
cough(bronchiolitis,asthma,pneumonia).
A)Chest pain of cardiac origin is not a sharp pain,more like deep,heavy pressure
or the feeling of choking –triggered by exercise.
b)Pain worsening with breathing:pericarditis(Viral,rhemautic).
c)Dull heavy sensation due to enlarged heart:RHD(rheumatic heart
disease),cardiomyopathy and pericardial effusion.
d)pancarditis: viral,rheumatic,cardiomyopathy.
e)other conditions:kawasakis,severe AS,severe PS,anamolous origin of left
coronary artery,rupture of sinus of valsalva,pericardial effusion.

Syncope:transient loss of consciousness and muscle tone due to inadequate

cerebral perfusion—Most common symptom being dizziness
a)Exertional syncope:ventricular arrhythmia.
b)provoked by exercise,accompanied by chest pain-cardiac cause of syncope.
c)syncope while sitting down-arrythmias or seizure disorder
d)Syncope while standing for a long time-vasovagal syncope without any
underlying cardiac disease-most common in children.
e)syncopal duration </= 1min:suggests vasovagal syncope,hyperventilation
syncope,syncope related to orthostatic mechanism.
f)Longer duration syncope-convulsive disorder,migraine or arrythmia.

Palpitations-Subjective feeling of rapid heart beats

Causes:Supraventricular tachycardia,single premature beats.

Neurological symptoms:
a)History of stroke?: suggests thromboembolism secondary to cyanotic CHD with
polycythemia or infective endocarditis.
b)History of headache?: may be due to cerebral hypoxia with cyanotic heart
disease,severe polycythemia or brain abcess.

Family history:
Hereditary disease:
a)Marfans syndrome: Aortic regurgitation and mitral regurgitation.
b)long QT syndrome:sudden death related to ventricular arrhythmia.

NOTE:some cardiac syndromes associated with cardiac defects

DISORDER/SYNDROME COMMON CARDIAC

DEFECTS
 a)Trisomy 21(Down Endocardial cushion
syndrome) defects,VSD
b)Trisomy 12(Patau VSD,PDA,dextrocardia
syndrome)
C)Trisomy 18(Edward VSD,PDA,PS
syndrome)
d)Turner syndrome(XO) Coarctation of
aorta,AS,VSD
e)Kartagener syndrome Dextrocardia with situs
inversus,transposition of
great vessels.

PHYSICAL EXAMINATION:

1)GROWTH PATTERN:
a)cyanotic patients have disturbances in both height and weight..
b)Acyanotic patients,those with alrge L-R shunt ,have more problems with weight
gain when compared with linear growth.The degree of growth impairment is
propotional to size of shunt.

INSPECTION:
1)General appearance and nutritional state: note if child is in distress,wellnourished or
undernourished,and happy or cranky.Obesity should be
noted(dyslipidemia,hypertension,hyperinsulinemia,coronary artery disease)
2)Chromosomal syndrome:
DISORDER CV Major features
S abnormalities:freque
ncy and types
1)CHARGE TOF,truncus Coloboma,heart defects,choanal
association arteriosus,aortic arch atresia,growth/mental
anomalies retardation,genitourinary anomalies,ear
anamolies,genital hypoplasia.
2)Down Endocardial cushion Hypotonia,flat facies,slanted palpebral
syndrome(tri defect,VSD fissure,simian crease,mental deficiency.
somy 21)
3)Ehler- ASD,aneurysms of Hyperextensive joints,hyperelasticity,fragility
danlos aorta,carotids,intracr and bruisability of skin,poor wound healing.
syndrome. anial
Autosomal aneurysm,mitral
domninant valve prolapse.
4)Friedreich’ Hypertrophic Late onset ataxia,skeletal deformities
s ataxia cardiomyopathy
Autosomal
recessive(AR
)
5)Glycogen cardiomyopathy Large tongue and flabby
storage muscle,cardiomegaly,LVH,short PR interval
disease II
(Pompe’s
disease)
(AR)
6)Infant of VSH,TGA ,COA Macrosomia,hypoglycemia,hypocalcemia,pol
diabetic ycythemia,hyper bilirubinemia.
mother
7)Turner’s COA,bicuspid aortic Short female:broad chest with widely spaced
syndrome(X valve,AS,hypertensio nipples,congenital lymphedema,with residual
O,45) n,aortic dissection puffiness over the dorsa of fingers and toes.
8)VACTERL VSD Vertebral anamolies,Anal atresia,Congenital
syndrome heart defects,Tracheosphageal fistula,Renal
dysplasia,limb anomalies(radial dysplasia)
3)COLOUR:
a)cyanosis:
central cyanosis(arterial desaturation)-tongue,lips,conjunctiva

peripheral cyanosis(normal arterial saturation)-nail beds:CHF-peripheral flow is

sluggish,losing more oxygen to peripheral cyanosis.

b)Pallor: in infants with Vasoconstriction with CHF or circulatory shock or severely

anemic patients.

c)prolonged physiological jaundice: newborns with severe CHF and those with
congenital hypothyroidism.Note:PDA,pulmonary stenosis common in newborns with
congenital hypothyroidism.

4)CLUBBING:Long standing arterial desaturations(>6months)(all cyanotic

congenital heart diseases)-clubbing of fingers and toe nails,earliest noticed in
thumb.Also rule out clubbing associated with lung diseases,cirrhosis of liver,subacute
bacterial endocarditis.

5)RESPIRATORY RATE,DYSPNEA,AND RETRACTIONS:

Resting rate of >60cpm is abnormal at any age.
a)Tachypnea with tachycardia:earliest sign of left sided heart failure.
b)Dyspnea and retractions:sign of severe degree of left sided heart failure or
significant lung pathology.

6)SWEAT ON FOREHEAD:
a)Infants with CHF :cold sweat on forehead.
(MECHANISM:heightened sympathetic activity as a compensatory mechanism for
decreased cardiac output)

7)ACANTHOSIS NIGRANS:
Dark skin pigmentation of skin creases most commonly seen on neck,axilla,groin,belt
line:in obese chidren ,Type II DM.

8)INSPECTION OF CHEST:
a)Precordial bulge,with or without actively visible cardiac activity-> chronic cardiac
enlargement
b)Pectus excavatum(undue depression of sternum)causes cardiac embarrassment,or
causes pulmonary systolic murmer,or a lerge cardiac silhouette on Xray PA view.
c)Harrisons groove-a line of depression in the bottom of ribcage along the attachment
of diaphragm:indicates poor lung compliance of long duration—
seen in large L-R shunts

PALPATION:

1)PERIPHERAL PULSES:
Normal pulse rate varies with patients age and status.
Tachycardia:excitement,fever,CHF,arrythmia
Bradycardia: heart block,digitalis toxicity.
Irregularity:arrhythmias(sinus arrhythmia is normal)

Technique:
a)The right and left arm,arm and leg should be compared.
b) Every patient should have palpable dorsalis pedis pulse or tibialis posterior pulse or
both .If good pedal pulse-rules out coarctation of aorta(COA),confirm by checking
both upper and lower limb bp(normally-UL bp is >LL bp,in coarctation of aorta its
vice versa)
c)Weak leg pulses,strong arm pulses:COA
d)Right brachial pulse stronger than left brachial pulse:COA near the origin of left
subclavian artery,
d)weak right brachial pulse than left:abeerant right subclavian artery arising distal to
the coarctation.
e)bounding pulses:seenin aortic run offs-PDA,AR,large systemic AV fistula,
f)weak,thread pulses :cardiac failure,circulatory shock,leg of patients with COA.
g)Pulsus paradoxus:exaggeration of normal reduction of SBP during
inspiration(>10mmhg):cardiac tamponade secondary to pericardial
effusion,constrictive pericarditis.

APICAL IMPULSE:
1)0-7 yrs:Apical impulse is in the fourth intercostal space just to the left of the
midclavicular line.

2)After 7 yrs:It is at the fifth intercostal space in the mid clavicular line.
=> Any displacement of apical impulse laterally or downwards suggests cardiac
enlargement.

3)Point of maximal impulse:Determines if the right ventricle(RV) or the left

ventricle(LV) is dominant.
RV dominance:Impulse is maximal at the lower left sternal border or over the
xiphoid process.
LV dominance:Impulse maximal at the apex.

4)If impulse is diffuse and slow rising-heave,often associated with volume overload.

5)if impulse is well localized and sharp rising,its called a tap-often associated with
pressure over load.

6)Hyperactive precordium: seen in large L-R shunts (PDA,VSD) or heart disease with
severe valvular regurgitation(AR,MR)

7)Thrills:Thrills are vibratory sensations that represent palpable manifestations of

loud,harsh murmers.Better felt with palm of the hand.
a)Thrills in upper left sternal border-originate from pulmonary valve or pulmonary
artery-present in pulmonary stenosis.
b)Thrills in upper right sternal borders(aortic origin)seen in aortic stenosis.
c)Thrills in suprasternal notch: AS,PS,PDA or COA.
d)Thrills in the intercostal spaces are found in older children with severe COA.

BLOOD PRESSURE MEASUREMENT

1)BP cuff width should be 40%-50% of the circumference of the extremity with the
cuff long enough to encircle the extremities completely or nearly completely.
2)NHBPEP-recommends korotkoff phase 5 as the diastolic pressure.
3)Two or more readings should be averaged.
4)Child should be in sitting position with the arm at the heart level.
5)Gold standard is an intra-arterial BP.
6)Systolic pressure in the thigh or the calf is 5-10mmhg higher than that of arm,except
in newborns(arm and calf pressures are the same)

AUSCULTATION.
The entire precordium as well the sides and back of the chest should be
explored with sthethescope.
1)Heart rate and regularity:ECG to confirm if any doubt.
2)Heart sounds:intensity and quality.
3)Systolic and diastolic sounds:
ex :a)An ejection click in early systole:aortic or pulmonary valve stenosis
b)A mid diastolic click:Mitral valve prolapse.
4)Heart murmers:evaluate in terms of intensity,timing(systole or
diastole),location,transmission, and quality.

Heart sounds
1)First Heart sound: associated with closure of mitral and tricuspid valves.Best heart
at the apex or left lower sternal border.
a)abnormal wide splitting of S1:Right bundle branch block(RBBB),ebsteins anomaly.

2)Second heart sound:in upper left sternal border

Splitting of S2:Two components of s2 should be audible in the upper left sternal
border-the first is the A2,the second is the P2.
a)Normal splitting of the s2:The degree of splitting of s2 varies with
respiration,increasing with inspiration and decreasing or becoming single with
expiration.

b)ABNORMAL SPLITTING:
1) Widely split and Fixed S2:
*volume overload(ASD,PAPVR)
*Pressure overload(PS)
*Electrical delay(RBBB)
*Early aortic closure(MR)

2)Narrow split s2
*Pulmonary hypertension.
*AS

3)Single S2
*pulmonary hypertension
*One semilunar valve(pulmonary atresia,aortic atresia,persistent truncus arteriosus)
*P2 not audible(TGA,TOF,Severe PS)
*Severe AS

4)paradoxically split s2
*severe As
*LBBB,WPW syndrome(type B)

ABNORMAL INTENSITY OF P2
1)increased P2:pulmonary hypertension
2)Decreased P2:Severe Ps,TOF.

THIRD HEART SOUND:S3-low frequency sound in early diastole,related to rapid

filling of the ventricle,best heard at the apex or lower sternal border.
1)Commonly heard in normal children and young adults.
2)A loud S3-abnormal,audible in conditions with dialted ventricles and decreased
ventricular compliance.(large shunt-VSD or CHF)

FOURTH HEART SOUND or ATRIAL SOUND:S4,low frequency sound of late

diastole(presystole)-rare in infants and children.
*always pathological,seen in conditions with decreased ventricular compliance or
CHF.

GALLOP RHYTHM:It is a rapid triple rhythm,resulting from combination of a loud

s3,with or without an S4 and tachycardia.
*commonly seen in CHF.

EXTRACARDIAC SOUNDS
1)Pericardial friction rub:grating,to and fro sound produced by friction of the heart
against the pericardium-indicates pericarditis. Note:large accumulation of the
fluid(pericardial effusion)may result in disappearance of the rub.
2)pericardial knock:adventitious sound associated with chronic pericarditis.

HEART MURMERS.:
Must be analysed in terms of intensity(grade 1-6),timing(systolic or
diastolic),location,transmission,and quality(musical,vibratory,blowing and so on)

Intensity of the murmer is customarily graded from 1to 6

Grade 1: barely audible.
Grade 2: Soft,but easily audible.
Grade 3:Moderately loud but not accompanied by a thrill.
Grade 4: Louder and associated with a thrill.
Grade 5:Audible with the stethoscope barely on the chest.
Grade 6: Audible with stethoscope off the chest.

CLASSIFICATION OF HEART MURMERS:

!)Systolic murmers:
a)according to the time of onset-*Ejection type ,
*Regurgitant type
b)According to time of onset and termination –
*Midsystolic(ejection)-coincides with turbulent flow through semilunar valves-
AS,PS,pregnany,fever,anemia
*Holosystolic.:VSD,MR,TR
*Early systolic:VSD,MR,TR,may occur in neonates with large VSD,children on adult
with small VSD.
*Late systolic:itral valve prolapse.

Location of systolic murmers:

a)upper left sternal border(pulmonary valve area)
b)Upper right sternal border(aortic valve area)
c)Lower left sternal border.
4)apex.
PICTURE:

DIASTOLIC MURMERS:
1)Early diastolic decresendo murmers(or protodiastolic):Occurs early in
diastole,immediately after S2-caused by incompetence of the aortic or pulmonary
valve- a)AR murmers(high pitched,best haerd with the diaphragm of the stethescop at
the third left intercostal space,radiates to the apex. B)Pulmonary regurgitation
mumers(medium pitched,best heard third left intercostal space,radiates along left
sternal border).
2)Mid diastolic murmers:

ATRIAL SEPTAL DEFECT

ASD is a acyanotic CHD characterized by defect in the interatrial septum causing a

left to right flow between the atria.

Severity depends on:

a)Size of the defect b)size of the shunt c)associated anomalies.

Course of the disease may vary from asymptomatic to right sided overload,pulmonary
arterial hypertension , even atria arrhythmias.

ASD constitutes 8-10% congenital heart defects.

ETIOLOGY:Actual etiology is unknown.

Some factors are :1)Genetic factor 2)environmental factors including antenatal use
of teratogenic drugs,congenital infection.

Genetics: majority of cases are sporadic ,some homebox gene defects have been found
to explain some of well known cases of ASD,such as NKX2 chromosome 5,which has
an autosomal dominant inheritance and AV conduction defect.

Other genetic syndrome with skeletal abnormalities HOLT-ORAM syndrome—

mutations in the transcription factor TBX5
, essential in development of both the heart and upper limbs.

ASD can be seen in Noonan syndrome.

HEMODYNAMICS:
Desaturated blood enters the right atrium from the vena cava at a volume of
3L/min/m2 and mixed with additional 3L of fully saturated blood shunting left to
right across the ASD.

Results in
 Increase in oxygen saturation in the right atrium.
 Six litres of blood flows through the tricuspid valve and causes a mid-diastolic flow
rumble.
  Oxygen saturation may be slightly higher in the right ventricle because of incomplete
mixing at the atrial level.
 The full 6L flow across the right ventricular outflow tract and causes a systolic
ejection flow murmer.
 6L returns to the left atrium,with 3L shunting left to right across the defect and 3L
crossing the mitral valve to be ejected by the left ventricle into the asending aorta.

LEFT TO RIGHT SHUNT

Increased pulmonary blood flow( shear stress/circumferential stretch)

Endothelial dysfunction and vascular remodeling—Smooth muscle cell

proliferation,increase in extracellular matrix,intravascular thrombosis

Increase in pulmonary vasculature resistance

Inverted shunt: right to left

Cyanosis (eisengmenger syndrome}

e)

TYPES:

Ostium secundum(75-85%)
Ostium Primum (10-15%)
Sinus venosus (5-10%)
Coronary sinus septal defect

Ostium secundum
Most common type.
Defect in the region of fossa ovalis
Single or multiple
May be associated with partial anomalous venous return most commonly of right
upper pulmonary vein.

Ostium primum.
Situated in the lower portion of the atrial septum and overlies the mitral and tricuspid
valves
Often associated with clefts in the anterior mitral and septal tricuspid valve leaflets
and small VSD
Sinus venosus.
Least common type
Situated in the upper part of atrial septum in close relation to the entry of superior
vena cava
Abnormal fusion between embryologic sinus venosus and atrium.

According to size
1) in younger children: small defect : <3mm, moderate defect : 3-8 mm , large defect:
>8 mm
2) in older children: 1)small defect: <6mm , moderate defect : 6-12mm , large defect :
>12mm
Associations: 1)secundum ASD: pulmonic stenosis, mitral valve prolapse,total
anomalous pulmonary venous connection.
2)Primum ASD: cleft mitral valve.

Signs and symptoms.

Vary with size of the defect.

Small defect :asymptomatic and is usually diagnosed during a routine health

check up.

Large defect: symptomatic and patients usually present with.

 Failure to thrive
 Easy fatigability
 Increased perspiration
 Recurrent pulmonary infections
 Platypnea
 Orthodeoxia

On Examination
General examination:
Appearance: usually normal
Heart rate:Normal
Respiratory rate :normal
Weight and height :may be less than 10th centile.

Precordium
1)inspection: slight prominent precordium
2)palpation:Apex beat may be shifted to the left.
P2 many be palpable’
Left parasternal heave may be present
3)Auscultation
 S1 is normal
 S2 is widely split and fixed
 Ejection systolic murmer:medium pitched,soft , grade 1-3 and best heard at left 2nd
and 3rd ICS
 A diasolic flow rumble across tricuspid valve region.

4)INVESTIGATIONS:
Routine tests : CBC, septic screening, s.electrolye, S. creatinine, blood grouping,
coagulation profile,etc should be done before management.

Diagnostic investigations:
Xray, ECG, Echocardiography, sometimes cardiac catherization.

Xray findings:
Cardiomegaly, RA enlargement, RV enlargement,full pulmonary conus, increased
pulmonary vascular markings,plethoric lung fields.

ECG:Enlarged P waves—right atrial hypertrophy

rsR pattern and tall R wave –RBBB and RVH

ECHOCARDIOGRAM:
Primary diagnostic imaging modality
Provides exact location ,size of asd, measurement of septal rims,confirmation of the
shunt,abnormal motion of ventricular septum, associated lesions identified.
NOTE:
 Asd <3mmm in size diagnosed before 3months of age—spontaneous closure in 100%
of patients at 1.5yrs of age
 3-8mm—80% of patients show spontaneous closure before 1.5 yrs
 An Asd >8mm rarely closes spontaneously.
 Most children remain active and asymptomatic,can rarely lead to Congestive heart
failure.
 If untreated,pulmonary hypertension and subsequent CCF develop during or after 3rd
decade and reversal of shunt may occur.
 Atrial arrhythmias may occur
 Infective endocarditis doesn’t occur in patients with isolated ASD
 Cerebravascular accidents—rare complication.

MANAGEMENT:
 Patients with small shunts and normal RV size are generally asymptomatic and
require no therapy but need longtime foloow up for spontaneous closure
 Moderate to large shunts and/or symptomatic ASD are mananged by

1)medical therapy:
a)Diuretics—mechanism: Relieve ventricular overload,peripheral and pulmonary
congestion.
b)Digoxin—Mechanism: Helps to strengthen the heart muscle,enabling it to pump
more efficiently
c)Afterload reducers: Enalapril,captopril
d)Atrial arrhythmias: Appropriate antiarrythmic drugs
e)Atrial fibrillation:Anti arrhythmic drugs+anticoagulants.
f)irreversible PAH:dobutamine,CCB,diuretics,prostacyclinr,sildenafil or oxygen
therapy
g)Treatment of other complications like: pulmonary infections,thrombo-embolic
events or heart failure should be treated accordingly.
 2)Interventional therapy: ASD closure devices are used.

Safe,cost effective than surgery,fewer complications,shortened hospitalization.

Disadvantage and complications:residual leak,device misalignment etc.
Regular followups after device closure.

3)surgical management Gold standard form of treatment of ASD

Procedure:simple suture or patch closure
Timing:2-4 years
Advantages:can be performed in any type of ASD,excellent late outcome.
Disadvantages and complications:costly,pain and residual scars,pericardial
effusion, residual shunt etc.

Early post operative follow-up and annual clinical followup are necessary.

VENTRICULAR SEPTAL DEFECT

2nd most common Congenital heart disease(32%)

Pathophysiology
 Depends on : a) size of vsd b)status of pulmonary vascular bed
 Small communications (less than 0.5cm) VSD is restrictive and rt ventricular pressure
is normal—does not cause significant hemodynamic derangement.
 Moderately restrictive VSD with a moderate shunt.Pulmonary blood flow(Qp) to
systemic blood flow(Qs) =1.5-2.5:1,and this poses hemodynamic burden on LV.
 Large non restrictive VSDs (more than 1.0cm) Rt and left ventricular pressure are
equalized,here Qp:qs is >2:1.
 Large VSD s at birth ,pulmonary vascular resistance (PVR)remain higher than normal
and left to right shunt may initially be limited.Later on there is involution of media
of small pulmonary arterioles,PVR decreases---large Lt to right shunt ensues.
 In some infants large VSDs,pulmonary arterial thickness nevr decreases—pulmonary
obstructive disease develops,shunt becomes bidirectional,signs of heart failure
abate and patient becomes cyanotic(Eisenmenger syndrome.

Anatomical classification
1)MEMBRANOUS SEPTUM:Paramembranous/perimembranous defect.
2)MUSCULAR SEPTUM:Inlet,trabecular,central,apical,marginal defect
3)OUTLET SEPTUM deficient
4)SEPTAL DEFICIENCY:AV septal defect(AV canal).

ETIOLOGY:usually congenital but can be acquired.Acquired VSD may result from

post surgical residual leak,trauma or myocardial infarction.

CLINICAL FEATURES:
1)Race:No particular racial predeliction.
2)SEX: No particular sex preference.
3)Age: infants-In postnatal period diagnosis may not be picked up.But CCF during
first 6months is frequent,Xray and ECG are normal.
Children-After first year variable clinical picture emerges,small VSD—
asymptomatic,Large VSD--- symptomatic.

COMMON SYMPTOMS OF LARGE VSD.

 Palpitations.
  Breathing difficulty
 Dyspnoea on exertion
 Feeding difficulty
 Poor growth
 Frequent chest infections.

PHYSICAL FINDINGS:
 Wide pulse pressure
 Hyperkinetic precordium with systolic thrill in the left sternal border
 S1 and s2 are masked by a pansystolic murmer at left sternal border
 Max intensity of the murmer is best heard at 3 rd,4th and 5th left intercostal space
 Left 2nd intercostalspace—widely split and accentuated P2

INVESTIGATIONS
 ECHOCARDIOGRAPHY—two dimensional and Doppler colour flow
 CHEST RADIOGRAPHY- a)normal or b)Biventricular hypertrophy or c)pulmonary
plethora.
 ANGIOGRAPHY-Cardiac catherization and angiography.

ECG
 Small restrictive VSD –Normal ECG
 Medium sized VSD—Lt atrial overload—broad notched P wave
Signs of LV volume overload—deep Q and tall R waves with tall
T waves in lead V5 and V6
Atrial fibrillation.
 Large VSD: Rt ventricular hypertrophy—right axis deviation
Biventricular hypertrophy—P waves notched or peaked.

COMPLICATIONS:
 Congestive cardiac failure
 Infective endocarditis on rt ventricular side
 Aortic insufficiency
 Complete heart block
 Delayed growth and development in infancy.
 Pulmonary hypertension.
TREATMENT:
 Small VSD—hemodynamically insignificant,all close spontaneously by 6-8 yrs of
life,muscular close sooner than membranous. No intervention required
 Moderate VSD-without evidence of ccf/pulmonary hypertension can be followed
until spontaneous closure occurs
 Large VSD:Usually require surgery ,they develop CCF and failure to thrive by age of
3-6months
 Conservative treatment: Treat ccf and infections ,prevent the developmet of
pulmonary vascular disease .Drugs used: a)Digoxin—To increase the velocity and
force of contraction of the heart.b)Furosemide—reduces extra load on pulmonary
system by removing edema and lowering BP
 Prevention and treatment of infective endocarditis.

Indications for surgery

 VSD at any age where clinical symptoms and failure to thrive cannot be controlled
medically.
 Infants between 6-12 months of age with large defects associated with pulmonary
hypertension.
  >24 months with qp:qs >2

NOTE: surgical correction has to be been done before irreversible damage to

pulmonary vasculature occurs.

INTERVENTIONAL THERAPY :
a)PA banding: palliative treatment in those patients who are unable to withstand an
open heart procedure.
b)percutaneous device closure—muscular VSDs can typically be closed
percutaneously.

OPERATIVE PROCEDURE
1)Patch closure by RV approach.

Preoperatively—prophylactic antibiotics are often required to prevent infective

endocarditis.
Postoperative follow ups are required. Dysrythmia to be looked for.

PATENT DUCTUS ARTERIOSUS

 Communication between the pulmonary artery and the aorta.Allows deoxygenated
blood to bypass the lungs and enter the aorta.
 If ductus remains patent beyond 3months of life In full-term infants and beyond 1yr
in premature infants,it is termed persistent PDA.
 After birth the duct closes functionally in 12 to 18hrs and anatomically in 2-3weeks.
 Location –distal to left subclavian
 F:M =2:1
Etiology: prematurity,maternal rubella syndrome

Hemodynamics:
 Small PDA: asymptomatic throughout life.Accidental detection by ECHO for murmer
 Moderate PDA: compensate well throughout childhood and may remain completely
asymptomatic in early adulthood but eventually present wih exercise intolerance
and symptoms related to left ventricular failure,usually starting in third decade
 Moderate to large:
Blood from aorta ---enters pulmonary artery

Additional blood circulates to the lungs

Recirculates through left atrium then toleft ventricle.

Large volume of blood leads to very early development of pulmonary

congestion,decreased lung compliance.

Failure left ventricle (CCF)—within weeks.Failure to thrive,recurrent

pulmonary infections seen.

Pulmonary over circulation

IF PDA NOT CORRECTED

 Arteriolar medial hypertrophy,intimal proliferation,eventual
obliteration of pulmonary arterioles and capillaries.

Irreversible increase in pulmonary arterial pressure

Pulmonary vascular resistance >systemic vascular resistance.

Ductal shunting reversed and becomes right to left (Eisenmenger

syndrome)

Symptoms:
 Iritabilty,
 Poor feeding
 Failure to gain weight,excessive sweating –esp forehead sweating.
 Increased respiratory effort and hurried breathing.
 History of recurrent upper respiratory infections and hospital
admissions(pneumonia)

On examination:
 Physical underdevelopment
 Pulse: bounding peripheral pulses,wide pulse pressure
 Hyperkinetic apex,continuous thrill in 2 nd left intercostal space.
 Continuous murmer
 Accentuated first sound and narrowly or paradoxically split s2(large shunts)
 Differential cyanosis and clubbing in shunt reversal.

Diagnosis:

ECG-
normal or left axis deviation.
LA enlarged,LV hypertrophy

Chest X-ray
 Pulmonary plethora
 The main pulmonary artery segment dilated
 Cardiomegaly (LV,LA)
 Diameter of asending aorta is large to normal

Echocardiogram:gold standard test for diagnosing pda.

Treatment:
 Premature indomathacin 0.1mg/kg/dose: 12hrly,3doses
Ibuprofen is as effective as indomethacin
 All patients with PDA require surgical or catheter closure.
 Small PDA—prevention of bacterial endarteritis
 Moderate to large PDA—treat heart failure and/or prevent the development of
pulmonary vascular disease.
 Cardiac catherization or trans catheter closure.
 Surgery:left thoracotomy,thoracoscopic minimally invasive techniques.
Cyanotic congenital heart disease: Tetralogy of Falot – History
taking tips and examination clues

Name: XYZ
Age: TOF presents in early infancy
Sex: Female
 ASD is common in females
Address: ABC
Informant: mother

Chief complaints:
1. Difficulty in breathing
2. Bluish discolouration of lips

HOPI: Three year old female child comes with h/o difficulty in
breathing; present on and off; present more on exertion, relived by
squatting for a few minutes. No h/o hurried breathing, chest
indrawing, noisy breathing. No other postural variations.
Child has history of blue coloured discolouration of lips; on and off;
which occurs on excessive crying or exertion and relives on rest.
No h/o swelling of legs. (In children with CCF,RVF, blood from
SVC And IVC are not pumped to lungs effectively, results in tender
hepatomegaly, pedal and sacral edema).
No h/o decreased urine output.

Note: children with TOF, gradually develop cyanosis by 1-3 years of

age due to increasing severity of infundibular stenosis.

Past history: no h/o repeated lower respiratory tract infections in the

past.

Family history:

Antenatal history: no h/o any maternal drug intake. (Estrogen,

progesterone and amphetamines)
Birth history
Neonatal and postnatal history

Developmental history:
Down’s syndrome is a/w endocardial cushion defects, conotruncal
anomalies, VSD, ASD

Nutritional history:
Rule out nutritional causes of growth retardation

Immunisation history:

Socioeconomic history:
Summary:

General physical examination:

Child is comfortable and sitting on the bed,
Any dysmorphic features, maybe mentioned

Vitals
Anthropometry
Head to toe examination
Systemic examination

CVS:
 Inspection
 Palpation:
 Auscultation:
1. S1: normal
2. S2: usually single. Only aortic component is heard as
aorta is placed anteriorly. P2 is soft and delayed.
3. ESM of pulmonary stenosis – best heard at 2nd or
sometimes 3rd left ICS close to the sternum; grade 3.
RS
P/A
CNS
TETRALOGY OF FALOT

 Four major components

1. Obstruction of the right ventricular
outflow(pulmonary stenosis)- both at right
ventricular infundibulum or subpulmonic area and
pulmonary valve.
2. Ventricular septal defect(VSD)
 3. Dextraposition of the Aorta(overrides the
ventricular septum)
4. Right ventricular hypertrophy

 Pathophysiology:

1. Deoxygenated blood returns to the heart via SVC

and IVC to the right atrium and eventually to the
right ventricle normally.
2. Right ventricle contracts against a marked
pulmonary stenosis.
3. Hence desaturated blood is shunted across the
VSD into the left ventricle.
4. This desaturated blood then flows from the left
ventricle to the aorta.
5. This deoxygenated blood then enters systemic
circulation – hence cyanosis.

 Acyanotic or pink TOF: when the right ventricular

obstruction is mild and there is a balanced VSD shunt,
visible cyanosis is not present.

 Clinical manifestations:

1. Cyanosis
2. Dyspnoea on exertion- child assumes squatting
position for relief.
3. Tet/ blue spells
4. Murmur
  Common precipitation events of TET spells:
1. Crying
2. Defecation
3. Feeding
4. Awakening from naps
5. Fevers
6. Dehydration
7. Tachycardia (decreased filling time leads to reduced end
diastolic volume)
8. Medications (ACE inhibitors)

 Diagnosis by:
Typical history
1. X-ray
2. ECG
3. ECHO
4. Cardiac catheterisation
5. Ventriculography
6. Aortography

Complications
1. Cerebral thrombosis
2. Brain abscess
3. Bacterial endocarditis

Treatment
 Depends on severity it the RVO obstruction
 If severe, urgent medical and surgical intervention
required in neonatal period.
 An immediate increase in pulmonary blood flow by
1. PGE2
2. Surgery

Management of TET spells :

Initial

 Knee to chest position.

 High flow oxygen via mask or headbox.
 Avoid exacerbating distress.
 Morphine 0.2 mg/kg i.m.
 Continuous ECG and oxygen saturation monitoring, frequent
BP monitoring.
  Correct any underlying cause/secondary problems, which may
exacerbate episode, eg. cardiac arrhythmia, hypothermia,
hypoglycaemia.

If prolonged

 Consult paediatrician or cardiologist.

 Intravenous fluids - 10 ml/kg bolus followed by maintenance
fluids.
 Sodium bicarbonate 2-3 mmol/kg i.v. (ensure adequate
ventilation).
 Central nervous system

CNS EXAMINATION
Higher mental function
Mental status
Consciousness :-
Level of consciousness
Drowsy:- sleepy but arousable by ordinary stimulus or loud sound.
Stupor:- responds only to strong noxious stimuli.
Obtundation:- stage between drowsiness and delirium.
Delirium :- confusional state, responds incoherently.
Light coma :- child may be kept aroused as long the noxious stimuli is
applied.
Deep coma:- responds to noxious stimulus may be due to decortications
or decereberation.
Flaccid coma:- no response whatsoever might be ,total flaccidity with no
reflexes.

GLASGOW COMA SCALE

EYE OPENING(E) VERBAL MOTOR RESPONSE

4 Spontaneous 5 normal 6 normal
3 to call 4 sentences but not fully 5 localises pain
2 to pain oriented 4 withrawal to pain but not
1 none 3 only words proper localisation
2 no words only sounds 3 decortication
1 none 2 decerbration
1 none

Total score :-15

Minimum score:- 3
II)ATTENTION
Attention is the ability to focus and maintain one’s consciousness on a
particular stimulus or a task without being distracted by any other
stimulus.
Assess
Ask the patient to repeat short list of objects or numbers,inability to
repeat correctly 6 numbers or items or more indicates a probable attention
deficit.

III) ORIENTATION
Refers to the patient’s awareness of self and certain realities of the
present.
It also refers to as orientation of person, place and time.
PERSON what is your name?
How old are you?
PLACE:- where are you right now?
Which place do you live in ?
TIME:- what is today date and time?
What day of the week it is?

IV)SPEECH OR LANGUAGE
It assess the cognitive state of the child
It should be assessed in the following domains:-
SPONTANEOUS SPEECH : Deficient spontaneous speech is when there
is poverty of thought or expression or impairment of rhythm.
FLUENCY:-word outflow that is free from pauses or breaks
COMPREHENSION :- ability of a child to describe appropriate and
correct meaning to words and sentences.
Repetition :-ability to repeat single word or list of words without
errors.Difficulty of repetition results from lesion involving the arcuate
faciculus on the left side.
Naming and word finding:-is it child able to name the object correctly or common
objects of daily use ?
Reading :- is the child able to comprehend written language symbols ie A B C
Writing :- ability to use written language copying:- ask the child to copy a geometric
figure

V)LEARNING AND MEMORY

It depends on the integrity of the hippocampus and amygdaloid nucleus
Immediate recall
Narrate a small story, ask the child to repeat the same with atleast half the
details correctly.
short term memory
what did you have for breakfast?
Give a short list of the words or objects and ask he/ she to repeat after 10
-15 minutes.
long term memory
Enquire about the past with questions like when and which school are
studying in?

VI)CORTICAL OR COGNITIVE FUNCTION

Assessed by
Asking common general knowledge questions as appropriate for the age
of the child
Calculation ability – serial seven subtraction test and other simple sums.
Gnosia and agnosia (in ability to recognise the stimuli such as visual ,
auditory or olfactory).

PRAXIA AND APRAXIA: Praxis refers to carrying out an

action.Apraxia are characterized by inability to perform motor behavior.

VII) MOOD, AFFECT AND THOUGHT CONTENT

Mood refers to feeling and emotions evoked by situations , events and
other occurrences in daily life.
Affect refers to somatic or autonomic behaviours that are used to convey
a mood or emotion.
Thought content refers to fullness and organisation of the patients
thinking as reflected in conversation or behaviour.
These are assessed only in rare and special conditions.
DELIRIUM: It is a state of confusion with disordered perceptions and
decreased attention span and inappropriate response to stimuli.
BEHAVIOR
Eg: Avoidance of eye contact and self engrossed : Autistic behavior.
Self mutilating – Lesch-Nyhan syndrome.

Head to toe examination

Head –
Check for abnormal shape and size
Assymetrical shape:
1. dolichocephaly(if the AP diameter more than the width, sagittal
suture closes earlier)
2. brachycephaly(premature closure of coronal suture)
Head control, head tilt ( poor vision in one eye ,unilateral hearing loss,
torticollis)
head bobbing(respiratory failure meningeal irritation, kernicterus,
hemorrhage)

SCALP:
 scalp swelling(dermoid,histiocytosis,organised cephal
hematoma),
 see for fungal and parasitic infection of the scalp.
 Anterior frontanelle:A diamond shaped gap between frontal
and parietal bones is called the Anterior frontanelle
Method of examination:
a)Examine the child at 24hrs of age when normal separation of
sutures has taken place.
b)size of the AF(length+width)/2 and plot on normogram.Mean
size of AF is 2.1 cms
c)AF closes by 9-18 months

. NORMOGRAM FOR
PLOTTING ANTERIOR FRONTANELLE.
 early closure-Microcephaly,craniosynostosis,hyperthyroidism
 Delayed closure-hydrocephalus,rickets,hypothyroidism,downs
syndrome.
 Posterior frontanelle (lambdoid frontanelle,occipital
frontanelle): Triangular space between two parietal and
occipital bones is called posterior frontanelle.
a) Posterior frontanelle is either closed at birth or closes at 2
months.
b)Wide open posterior frontanelle: hydrocephalus and hypothyroidism.

 Wide open sutures: dwarfism,osteogeneis imperfect.

 Macrocephaly- An occipitofrontal circumference plotting >90th
percentile for that age,sex,gestational age and ethnic group.
Seen in conditions like hydrocephalus ,megencephaly((tay-
sachs disease,sturge –weber syndrome, Familial macrocephaly,
subgaleal hemorrhage.bulging AF , separating sutures
(subdural haematoma , intracranial space occupying lesions)
 Microcephaly :- Occipitofrontal circumferance <3SD of the
normal for age,sex,gestational age or ethnic group.
Causes: Genetic(symmetric IUGR baby),chromosomal
disorders(trisomy 13,18),congenital infections :TORCH
infections,teratogenic(fetal alcohol syndrome),
Postnatally
acquired(asphyxia,hemorrhage,meningitis,malnutrition,sepsis)

EYES :
Look for:
a)Hypotelorism ,b)Hypertelorism, c)lateral displacement of the inner
canthi, d)ptosis-third never palsy,myasthenia gravis,toxic myopathy-
botulism,eyelid or orbital tumor. e)Exophthalmus-
Hyperthyroidism,glaucoma,hemorrhage or metastasis. f)enophthalmus-
damage to cervical symphathetic nerve,apparent retraction in children
with chronic malnutrition.
 Telangiectasia in the bulbar conjunctiva.
  Seen in ataxia telangiectasia.
 Subconjunctival haemorrhage is associated with intra cranial
haemorrhage.
 Jaundice is seen in HIE.
 Phlyctens,choroid tubercles is seen in TB.
 Drooping of eyelids is seen in myasthenia gravis.
 Unilateral drooping is seen in third cranial nerve palsy.
 Unilateral ptosis with enopthalmus is seen in horners syndrome.
 Papilloedema in increased ICP.
 Lens dislocation is seen in homocystinuria.
 Eyes turn up without the lid closing (LMN facial palsy).
FACE-
 Butterfly rash is seen in SLE.
 Frontal bossing, sunset sign is seen in hydrocephalus.
 Expressionless face and drooling of saliva is seen in
hydrocephalus.
Asymmetry of face-Facial palsy
Myasthenia gravis –look for ptosis
*rule out UMN and LMN Lesions
Portwine stain :- sturge weber syndrome
DYSMORPHIC FACIES AND ASSOCIATED NERVOUS SYSTEM
DISORDERS
CONDITION DYSMORPHIC NERVOUS
FACIES SYSTEM
FEATURES
Hypothyroidism Coarse facies Mental retardation
Down’s syndrome Mongoloid facies Low IQ
Moebius syndrome Mask like facies B/L VI and VII nerve
palsy

EAR :
Ear discharge for ASOM – Cause for meningitis
Types of discharge:Watery discharge(CSF otorrhea.),blood
stained(neoplasma),purulent(infection).
Low set ear: down syndrome
NOSE:-
 Nasal swelling :- meningocele.
 Meningoencephalocele.
 Neurofibroma
 Craniopharyngioma
 Rhabydomyosarcoma

Head trauma:- look for

1. Fracture of the cribriform plate.
2. Shearing laceration of the olfactory bulb.
Rhinorrhea is seen in
1. Meningoencephalocele.
2. Cystic fibrosis
3. Traumatic
ORAL CAVITY
1. Cyanosis (cyanotic CHD)
 2. Pallor (leukaemia, SBE)
3. Tonsillitis
4. Peritonsillar abscess
5. Retropharyngeal abscess
6. paranasal sinuses:- sinus tenderness(sinusitis).
7. Ulcerated lesions,aphthous ulcers:- trauma,stress,allergy.
8. Recurrent herpes simplex infection:-Reactivation of herpes simplex
type1 due to fever,sunburn,trauma.
9. Angular chelitis.
10. Fissured tongue: Downs syndrome.
TONGUE:
1. Macroglossia: acromegaly, mongolism, hemangioma.
2. Microglossia:isolate, Pierre Robin syndrome.
3. Atrophy:lower motor neuron lesion.
4. Tremor: anxiety, neurosis.
5. Protrusion difficulty: trauma, paralysis.
6. Tonsil: tonsillitis.
7. Peritonsillar abcess, retropharyngeal abcesss
NECK : carotid artery-block- takayasu arteritis.
1. Torticolis: in the lateral rectus palsy
2. Neck stiffness:Meningeal irritation ,intracranial tumo ,
poliomyelitis, subarchanoid haemorrhage
3. Lymphadenopathy: Tb, anticonvulsant therapy with phenytoin.

LIMBS:
1. Koilonychias (iron deficiency anemia),
2. Edema (hepatic failure with encephalopathy),
3. Peripheral nerve thickening (hereditary neuropathy),
4. pallor (SBE,leukemia),
5. clubbing(cyanotic CHD)long limbs,long fingers -marfans
syndrome, homocystinuria)
6. Skin:pallor(vasomotor collapse,anemia, intracranial haemorrhage)
7. Icterus(kernicterus in newborn,liver failure with hepatic
encephalopathy)
NEUROCUTANEOUS MARKERS.
NEUROCUTANEOU NEUROCUTANEOU
S MARKERS S SYNDROMES
Cafe au lait Neurofibromatosis Café-au-lait
spots,axillary freckles spots:Dark brown
hypermelanotic
macules with smooth
or irregular
borders,commonly
seen in back,buttocks
and trunk.
Axillary freckling:
similar round spots in
axilla and inguinal
areas.
Telangiectasia Ataxia telangiectasia Dilated blood vessels
over sclera,venous
angiomas over the
bridge of
nose,butterfly area of
face,ante cubital
area,neck,popliteal
fossa.
Adenoma Tuberus sclerosis Adenoma
sebaceum,shagreen sebaceum(facial
patch,ash leaf macules angiofibroma):
Numerous smooth
glistening round
rubbery papules pin
head to pea size,over
butterfly area in the
face and nasolabial
folds,cheeks,nose,chin
.
Shagreen patch:These
are connective tissue
naevi.Skin colored
irregular lumpy
cobblestone-like
plaques in lumbosacral
areas which grow to
the size of a
palm,satellite papules
grow around a central
plaque with orange
peel like indentation.
Ash leaf
 macules:Hypomelanot
ic polygonal macules
grow upto 5cm over
trunk and buttock
Hemangioma Strugge-webber Manifested at
syndrome birth,port-wine stain
on the forehead, and
upper eyelid of one
side of face,or the
whole face.Color:light
pink to deep purple
and is caused by an
overabundance of
capillaries around the
ophthalmic branch of
trigeminal nerve
Tuft of hair Spiba bifida Look for sacral
dimples that are
accompanied by a
nearby tuft of hair,skin
tag or certain types of
skin discoloration.
Nevus Linea nevus sebaceous The sebaceous nevus
syndrome is usually located on
the face,scalp, or
neck.It can also be
located on the
arms,legs or trunk.It
maybe barely
noticeable at birth and
typically becomes
more pronounced with
age.

Markers of tuberculosis-lupus vulgaris, phylecten, scrofuloderma, BCG

scar, tuberculids
 Sacral dimple-spina bifida
 Salmon pink-maculopapular rash(collagen vascular disease)
 Multiple burns( syringomyleia)
 Vasomotor changes(coldness or edema on affected
parts,autonomous disturbances)
 Any obvious deformity:skeletal deformities and joint contractures
in cerebral palsy.
 Butterfly rash over cheeks(SLE )
 Erythema nodosum(TB)
ODOUR OF THE BODY
CONDITION BODY ODOUR ASSOCIATED
NEUROLOGICAL
DISORDERS
Phenylketonuria Musty odour Progressive mental
retardation
Maple syrup uribe Maple syrup Seizures,mental
disease subnormality and coma
Uremia Ammoniacal Encephalopathy
Hepatic failure Musty Encephalopathy

SPINE:
 scoliosis (progressive muscular dystrophy,poliomyelitis,cerebral
palsy,congenital wedge deformity,hemivertebra)
 Kyphosis(Congenital displacement of the ip,TB spine ,Ankylosis
spondylitis)
 Lordosis:look for any swellings,sinuses,spina
bifida,meningomyelocoele and CDH-bilateral)

BONES AND JOINTS:

1. Arthritis(collagen vascular disease,SLE ,RA)
2. Hypermobility of joints(Marfans syndrome)
3. Dactylitis(sickle cell anemia)
4. Joint effusion(haemophilia and collagen vascular disease
 CRANIAL NERVE EXAMINATION

 Examination of cranial nerves is important in localisation of brain

stem lesions as all cranial nerves except olfactory and optic
originate from brain stem.

1. CRANIAL NERVE I: OLFACTORY

 Function: carries smell sensation from olfactory receptors in nasal
mucosa.
 Purely sensory nerve.
 Testing the nerve:
i. Rule out obstruction to nostrils due to common cold or any
other cause.
ii. Each nostril is checked with other one compressed.
iii. Common substances like coffee, chocolate etc are used.
iv. Child is asked to identify the smells by keeping the
substance close to the nostrils. Each nostril is tested
v. Do not use irritants or pungent smells as it may stimulate the
trigeminal nerve and give false impression of normal test.
vi. Newborn: baby turns the face towards the smell of breast
milk.

 Lesions
i. Anosmia: absence of smell. Occurs in head injury involving
cribriform plate, Tumors( pituitary tumour, frontal lobe
glioma, olfactory groove meningioma), frontal lobe abscess
and raised ICT.

ii. Parosmia: altered smell with hallucinations and illusions of

smell- smell is distorted and unpleasant. Due to local causes
in nose or head injury.
Cranial nerve II: optic nerve
Anatomy:

Gross vision: test ability of child to a) recognise parents( smile at

parents); recognise strangers( stranger anxiety), follows object
Visual acuity: defined as the resolving power of the eye.
1) Distant vision
 Ability of child to see objects at a distance.
 Snellen chart is used.
  The largest letter subtends an angle of 5min at a distance 60
meters from the eyes. The letters in the consecutive rows sub
tend 5min at 36, 24, 18, 12, 9 and 6m from the eye respectively.

 Placed at eye level and 6m from patient.

 The chart is read from above downwards.

 Expressed as d/D where d is the distance of the child being

tested and D is the distance from which the letter should be read
by a normal child

 Each eye is tested separately with the other eye closed.

2) Near vision
 Charts used : Times new Roman numeral charts, Reduced
Snellens chart and Jaeger’s chart)
 Younger children can be tested by picture or block matching.

Color vision:
 Ability to identify basic colours(red, blue and green).
 In color vision defect, red is affected first
 Ishihara and Holmgrens wools are used to assess.

Visual field.
 Portion of the space within which objects are simultaneously
perceived while the eye is steadily fixed.
 Visual field is limited by margins of orbit, nose and cheek.
 Method of testing:
1. Confrontation method:
i. Visual field of the child is compared to examiner.
ii. The patient and examiner so 1m from each other with
eyes at the same level .
iii. Examiner closes his right eye and asks the patient to
close his left eye.
iv. Patient is asked to fix gaze at examiners eye and
brings his fingers with darting movement from
periphery to centre.
 v. The point at which the patient is able to appreciate the
moving finger is noted.
vi. The difference in examiners and patients ability gives
the approximate abnormality of the field of vision.
2. Perimetry:
i. Quantitative analysis of the visual field.
ii. Humphreys automated perimetry, Goldmann
perimeter and Bjerrum tangent screen are used.

Reflexes
Pupillary reflex :
 contraction of pupils to light
 Best tested in a dark room with patient looking at a distance to
avoid pupillary constriction due to accommodation reflex.
 Each eye is examined separately
 Direct reflex: bright line shone to one eye leading to pupillary
constriction of the same eye.
 Consensual reflex( indirect pupillary reflex): bright light is shone
in one eye and pupillary constriction is seen in the opposite eye.
The constriction of opposite eye is because of bilateral innervation
of the Edinger-Westphal nucleus.
Menace reflex
 Used to test vision in children who are very small, uncooperative or
totally bedridden.
 The finger of the examiner is suddenly brought towards the
patient’s eye.
 Normal response is blinking.
Accommodation reflex
 Contraction of pupils and convergence of eyeballs that occurs
when a person suddenly focuses on a nearby object after having
focused on a distant object.
 Presence of accommodation reflex with absence of light reflex is
seen in Argyll Robertson pupil.
Fundus
 Examined using at opthalmoscope.
 Clinician looks for optic disk(shape, color, edges, size and optic
cup), vessels, retina and macula.

Cranial nerve III, IV and VI:

  Occulomotor, Trochlear and Abducent respectively.
 All three nerves are tested together.
 Ptosis, squint and nystagmus must be looked for.
 Eye movements: controlled by extraocular muscles. All supplied
by occulomotor except for superior oblique ( 4th nerve) and lateral
rectus (6th nerve).
 The patient is asked to look in all directions without moving the
head.
 In comatose patients dolls eye manoeuvre is used.
 Eyelid movements: elevation of eye lids by levator palpebrae
superioris which is supplied by occulomotor. Lesions result in
ptosis.
 Pupils: look for size(normally 2-6 mm in diameter and 3-4 mm in
ambient light), shape, equality, symmetry.
 Paralysis of trochlear leads to restriction of downward eye
movements.
 Paralysis of abducent leads to loss of abduction of the affected eye
leading to convergent squint.

Cranial nerve V: trigeminal

Tests for motor:
 Masseter: patient is asked to clench his teeth. The contracted
muscle is palpated over the angle of the mouth. The contraction
should be equal on both sides.
 Temporalis: the suprazygomatic area is inspected for the muscle
bulk of temporalis. patient is asked to clench his teeth. The
contracted muscle is palpated. The contraction should be equal on
both sides.
 Pterygoid: in case of paralysis on one side, the jaw deviates to the
same side. Lateral and medial pterygoid are tested by asking the
patients to open the mouth against resistance.
Tests for sensory : sensations of touch, pain and temperature at checked.
 Ophthalmic division : both sides of the root of the nose, forehead
and scalp upto the vertex, cornea and conjunctiva.
 Maxillary division : cheek, upper lip, upper teeth, front of the
temple, side of the nose, skin and conjunctiva of the lower eye lid,
medial inferior quadrant of the medial inferior quadrant if the nose,
upper pharynx, roof of mouth, part of soft palate and tonsils.
 Mandibular division: lower part of fave, lower lip, the ear, the
tongue, both sides of chin and lower teeth.
Reflexes
 Corneal:
 Afferent is trigeminal and efferent is facial nerve.
 Reflex centre is pons
 Child is asked to look upwards
 Lateral margin is touched with a wisp of cotton just lateral to
the pupil.
 The patient blinks on both sides.
 Jaw jerk
 Both afferent and efferent are by the trigeminal nerve.
 Reflex centre is in pons.
 The child is asked to open the mouth partially.
 The examiner keeps the left index finger below the lower lip
in the mid line and strikes the finger with a hammer.
 Jaw jerk is seen as a minimal upward movement of the jaw.
 Nasolacrimal reflex.(not commonly done)
 Afferent Limb is trigeminal nerve
 Efferent is greater superficial petrodollars nerve
 Test is done by stimulating the nasal mucosa with a wisp of
cotton.
 Stimulation leads to reflex stimulation of tears.

SEVENTH CRANIAL NERVE/ facial nerve

Peripheral functions
On the face :- muscles of facial expression
Ear- tensor tympnai and stapedius
Taste – taste sensation in the anterior two third of the tongue
Tear- parasympathetic supply to lacrimal glands
Type of nerve:- both sensory and motor
Testing of the nerve:-
Tests Observation in normal Muscles involved s
cases
Ask the child to look Wrinkling or frowning Frontal belly of
above occipitofrontalis
Close the eye Tight closure , cannot Orbicularis oculi
be opened by using
examiners hands
Blow cheek Full blown cheek ,air Buccinators
cannot pass the full
blown cheek
Whistle Good whistle formed Orbicularis oculi
Eversion of lower lip Platysma becomes Platysma
taut
Lesion of the nerve
1. SUPRANUCLEAR PALSY (UMN lesion) – the lesion above the level
of facial nerve nuclei
It occurs due to involvement of
pyramidal tract.
2. INFRANUCLEAR PALSY (LMN lesion)-the lesion is at the level of
the facial nerve nuclei or below the level of the facial nerve nuclei.

Testing the sensory part of the nerve

The sensation in the anterior two third of the tongue is tested in two
halves separately.
The child is asked to protrude his tongue and the tongue is tested for
sweet , sour and bitter tastes separately after rinsing.
NOTE:- The taste sensation is lost in facial nerve palsy.

CRANIAL NERVE VIII/ VESTIBULOCOCHLEAR NERVE

TWO DIVISION:-1. COCHLEAR DIVISION – concerned with
hearing
2. VESTIBULAR DIVISION- concerned with sense
of movement ,position
and balance.

TEST OF THE NERVE

Cochlear division
Rinne’s test:-
i. It is done with a tuning fork of 512 Hz.
ii. The examiner strikes the tuning fork on a rubber pad and holds it
to the ear till the patient ceases to hear the vibrations- this
indicates the air conduction threshold.
iii. Immediately after the patient says he/ she cannot hear the sound
the examiner should place the base of the vibrating tuning fork on
the mastoid area and see if the patient can appreciate the vibrations
Weber test :-
i. The tuning fork is placed in the midline
ii. The examiner strikes the fork on a rubber pad and holds it against
the forehead in the midline
iii. The child is asked to indicate whether the vibrations are heard
equally in both ears or better in one ear.
iv. Lateralization of the sound occurs towards the affected ear in
conductive deafness
v. Lateralization of the sound toward the normal side in patients with
sensorineural deafness

Other sites of placing the tuning fork:-

1. Mentum
2. Upper incisors
3. nasion
VESTIBULAR DIVISION:- It is concerned with sense of movement ,
position and balance.
The tests include:-
CALORIE TEST
i. The patient is in supine position , the head is raised and kept at
30o from the horizontal.
ii. The child is asked to fix the eyes at a point.
iii. Water(at 30o and 44o ) is irrigated into the external auditory
meatus for a period of 40 seconds.
iv. There will be nystagmus in a child with normal labyrinth.
v. Cold water results in nystagmus towards the opposite side,
while warm water results in nystagmus towards the same side.
ABNORMAL RESPONSE
 No response – canal paresis
 Directional preponderance –nystagmus is more in one direction.
This occurs in brain stem lesions and posterior temporal lobe
lesions.

ROMBERG’S TEST
The patient is asked to close the eyes with feet together in standing
position.
If the patient has vestibular nerve dysfunction, he /she sways towards the
side of the lesion.
TANDEM WALKING
 The patient is asked to walk in a straight line with arms held
forward and eyes closed.
 The heel of one foot should touch the toes of the other foot in each
step.
 In patients with vestibular lesions, the child tends to fall on the side
of the lesion.

CRANIAL NERVE IX/GLOSSOPHARYNGEAL NERVE

Type of the nerve- motor ,sensory and secretory functions.
Function-
 Motor functions elevates the pharynx
 Sensory functions helps in the taste sensation over the posterior one
third of tongue.
REFLEXES
PALATAL REFLEX
The afferent limb is glossopharyngeal nerve and efferent limb is vagus
nerve.
Test of the reflex
 The posterior part of the pharynx is touched with a cotton swab.
  Results in elevation of the palate along with contraction of the
ipsilateral soft palate and deviation of uvula.
 Position of uvula is central in bilateral lesions.
 There is deviation of uvula to normal side.

PHARYNGEAL REFLEX (GAG REFLEX)

 The afferent fibres for this reflex are carried by the
glossopharyngeal nerve and efferent limb is formed by the vagus.
 Test of the reflex
 Stimulate the posterior pharyngeal wall by cotton swab
 Result –elevation and constriction of pharynx

CRANIAL NERVE X
Function
Type of the nerve- mixed nerve
TEST OF THE NERVE
Position of uvula
The patient is asked to say ‘Ah’ and the palate and uvula are checked.
Normal response :-
Equal deviation of the palate on both sides with no deviation of the uvula.
In vagus nerve palsy –the uvula deviates to opposite side due to pull by
the muscle on the normal side

Gag reflex
The afferent fibres- glossopharyngeal nerve
Efferent fibres – vagus nerve
Test of the reflex
i. Stimulation of posterior pharyngeal wall by a cotton swab
ii. Response-elevation and contraction of pharynx
Curtain sign
In unilateral paralysis,the posterior pharyngeal wall moves towards the
normal side on phonation.

Lesion of tenth nerve

Vagus nerve palsy
The clinical features are
1. Nasal twang
2. Nasal regurgitation
3. Choking
4. Dysphagia
 5. Hoarseness of voice due to vocal cord paralysis

Superior laryngeal nerve palsy

Unilateral paralysis does not cause any symptoms
Bilateral paralysis results in relaxed vocal cords and hoarseness of
voice.
Recurrent laryngeal nerve palsy –
CLINICAL FEATURES ARE:-
i. sensory loss in the larynx below the vocal cords
ii. Motor – all the intrinsic muscles of larynx are affected except
cricothyroid.
UNILATERAL RECURRENT LARYNGEAL NERVE
PARALYSIS- it is paralysis of abductor of vocal cord .the affected cord
lies in the midline.
Bilateral recurrent laryngeal nerve paralysis – vocal cord lies in the
cadaveric position.
Stridor or respiratory obstruction may be present.

CRANIAL NERVE XI /SPINAL ACCESSORY NERVE

Function -This nerve supplies the muscles of sternocleidomastoid and
trapezius muscle.
STERNOCLEIDOMASTOID MUSCLE- this helps in the movement
of the head towards the opposite side.
TRAPEZIUS MUSCLE-This helps in shrugging the shoulders
Type of the nerve-motor nerve with cranial and spinal components.
Test of the nerve in
STERNOCLEIDOMASTOIDMUSCLE-turn the chin to one side
against resistance tests the sternocleidomastoid muscle of the opposite
side
TRAPEZIUS MUSCLE- the examiner stands behind the patient and
keeps his hand on the patients shoulder on side to be tested
He then applies resistance over the shoulder and asks the patient to shrug
his shoulder.
The muscle strength is compared to that on the opposite side and any
weakness is noted.
Lesion of the nerve
XI nerve palsy results in drooping of the shoulder on the side of the
paralysis.

CRANIAL NERVE XI/HYPOGLOSSAL

Type of nerve:- motor nerve
Testing of the nerve
1. The patient is asked to put out the tongue and keep it out for
sometime.
2. Any weakness or inability to protrude the tongue is noted.
3. Look for deviation or atrophy of tongue to one side.
 4. The patient should be asked to keep his tongue inside the oral
cavity in arelaxed state and any fasciculations and fibrillations
5. The examiner should feel the muscle tone of the tongue and note
whether it is normal, flaccid or spastic.

The tone is increased in UMN palsy

The tone is decreased in LMN palsy
6. The patient is asked to move the tongue sidewards on both sides or
touch the inner side of the cheeks on both sides of the tongue.
7. Any weakness or inability to do it is noted.

I)(MOTOR SYSTEM EXAMINATION

INSPECTION PALPATION/MEASUREMENTS
Rt Lt Rt Lt
BULK UL-
FORARM
ARM
LL-
LEG
THIGH

Careful comparison of nutrition between two sides should be done on

inspection
Palpation – Actual measurement of the bulk should be done at the same
site on both sides.
 The measurement is taken at the midpoint in between the two bony
prominences.
 Midpoint between acromion process and olecranon in the arm
 Midpoint between olecranon and radial styloid process in the
forearm.
 Midpoint between ASIS and tibial tuberosity in the thigh
 Mid point between tibial tuberosity and medial malleolus.
 a difference of > 0.5 cm is considered significant

II)
INSPECTION PALPATION/MEASUREMENTS
Rt Lt Rt Lt
Tone UL
LL
6 points in examination of tone
1. INSPECTION – Atonic limbs assume a posturwe of limpness or lie
externally rotated.
2. Hypertonic muscles stand out prominently-decereberate or
decorticate posturing
3. Palpation – atonic muscles – soft, flabby on palpation,hypertonic
muscles –rigid and spastic
4. Tone can be assessed by
 raising the limb
 Letting them fall passively
 Atonic limbs fall easily
 Hypertonic limbs do not fall easily
Passive movements
UL- passive supination/formation
 Roll the arm from side to side over the bed.
 Full range of movements at all the joints.
LL- Roll the leg from side to side.
 Full range of passive movements at all the joints.
 Tone in leg muscles ( head lag), trunk( rounded back )to be
examined
 180degree flap test in infant
Power
Neck:
 flexion – sternocleidomatoid
 Extension-nuchal muscles
SHOULDER
 abduction( biceps ,triceps)
 Adduction ( supraspinatus , deltoid,serratus anterior, upper and
lower fibres of trapezius)
 Flexion (deltoid)
 Extension( lasstismus,deltoid)
 Internal rotation( pectoralis major,deltoid,lattismus dorsi, teres
major)
 External rotation (deltoid,infraspinatus,teres major)
ELBOW : Flexion ( biceps brachi)
Extension( ttriceps brachi)

WRIST:
 Flexion( flexor carpi radialis and ulanaris)
 dorsiflexion( extensor carpi radialis longus ,entensor carpi
ulnaris)

FINGER :
 Extension( extenstor digitorum)
 Flexion(flexor doigitorum profundum and superfuicialis)
 Abduction(dorsal introsseous)
 Adduction(second palmer introssei)
 THUMB :abduction (abductor pollicis brevis)
TRUNK: serratus anterior,Trapezius,rhomboid
LOWER LIMB:
HIP-
 flexion(iliopsoas)
 Extension(gluteus maximus)
 Abduction(gluteus medius and minius)
 Adduction(adductors)

KNEE-
 extension (quadriceps femoris)
 Flextion (hamstrings)

FOOT-
 dorsiflexion(tibialis anterior)
 Plantarflexion(gastrocnemius)
 Inversion( tibialis posterior)
 Eversion(peronius longus and brevis)

Muscle power
Grade 5 –normal power – against gravity and resistance
Grade 4 –against resistance
Grade 3 against gravity but not against resistance
Grade 2-movement with gravity eliminated
Grade 1 visible or palpable flickers of contraction but no movement
Grade 0 total paralysis

IV REFLEXES
REFLEXES ROOT NORMAL RESPONSES
VALVE
Abdominal reflex T7 to T12 Umbilicus moves in the direction
of the stimulated
quadrant
Cremastric reflex L1,2 Scrotum and testes pulled toward
the side of stimulation
Anal reflex S4 ,S5 Contraction of external spinchter

Bulbocavernous S3,S4 contraction of bulbocavernous

reflex
Planter reflex L5-S1 5 components
Contraction of tensor fascia lata
Contraction of adductors of thigh
and Sartorius
Flexion of the toes
Adduction of the toes
Dorsiflexion and inversion of
ankle
Extensor plantar Dorsiflexion of great toe
response Fanning out and extension of
other toes
Dorsiflexion of ankle
Flexion of hip and knee

Other methods of eliciting extensor response

Gordon:-hard squeeze of calf muscles i e tendo Achilles
Oppenhein :- firm strokes with the finger and thumb on either side of
anterior border of tibia
Chaddock :-light strokes below the lateral malleolus on the outside of the
foot.
Bing :-stroking the big toe along the lateral side
Gonda :-flexing and twisting the great toe

PRIMITIVE REFLEXES
1. Glabellar tap
2. Grasp reflex
3. Palma mental reflex

DEEP REFLEXES
1. Triceps-C7C8
2. Biceps –C5C6
3. Supinator-C5C6
4. Knee- L2L3L4
5. Ankle –S1S2

MRC GRADING OF DEEP TENDON REFLEXES

0-absent
1-diminished
2-normoactive
3-exaggerated
4-clonus

PROPRIOCEPTIVE SENSATION
Position sense
 With the patient’s eye being closed place the patients limb in a
particular position , move it away the ask him to replace it himself.
 Repeat the same on opposite side
Joint sense
 -after clearly explaining the procedure and clearly
differentiating the up and down movements ask the patient to
close the eyes
 -after fixing the joint , the digit or toe at the terminal
interphalangeal joint is moved up or down by holding the side
of the digits between the forefingers and the thumb .
 ( Adjacent toe or finger not to be touched and pulp of the
finger not to be touched)
 repeat on both the sides till at least 6 successive correct
responses are given
 Lost in posterior column deficit
Romberg’s test
 -patient stands upright with the feet together and eyes closed
with hands by his sides
 -proprioceptive or vestibular deficit – balance is impaired
only when the eyes are closed
 -cerebellar deficit-balance is impaired even when the eyes
are open.
Cortical sensation
Tactile localization
 -with the childs eye closed touch various parts of the
body on both the sides and ask the child to localize the
points.
(ability to localize and organize special relationship)
Two point discrimination –
ability to differentiate cutaneous stimulation at 2 different points
separately by a distance of atleast 2mm finger pulp of tips)
( >5cm on the back of the legs , dorsum of feet and 4cm on the
sole 2-3 cm on the palms)
Stereognosis – ability to recognize the size , shape, dimensions, texture,
form of objects by feeling the object with closed eyes.
Graphasthesia – ability to recognize letters or numbers written on the
skin with a blunt tip , when eyes are closed .usually tested on dorsum of
hands/palm/back.

Cerebellar
Cerebellar system examination
There are three areas of cerebellum
Lobe Function
Anterior lobe Tone
Posterior lobe Coordination of movements
Flocculo – nodular lobe Balance

Assessment of cerebellar functions:-

Upper limb Lower limb
Finger nose test Gait ataxia
Dysdiadochokinesia Tandem walking
Intentional tremor Heel – knee test
Dysmetria and past pointing Pendular knee jerk
Dyssynergia Rombergs test

Upper limb
1.Finger nose test

2.Dysdiadochokinesia- the inability to carry out rapidly alternating

movements
Test
Ask the patient to rapidly alternate pronation and supination
movements .

3.REBOUND PHENOMENON – the patient is unable to check the

action of agonist muscle by corresponding antagonist muscle

4.INTENTION TREMOR
Test- By finger nose test .as the fingers are nearing the target, this is
exaggerated tremor

5. DYSMETRIA / FAST POINTING:-inability to stop intended

movement at the correct place
Test
In finger nose test the fingers may overshoot the nose or strike the
nose with undue pressure because the distance is wrongly assessed by
the child.

6.DYSSYNERGIA (INCOORDINATION):-there is a difficulty in

smoothly carrying out complex movements
 7.Gait:- gait of the child should be closely observed to identify
abnormalities:-

NORMAL GAIT VARIATION IN CHILDREN:

1) Toe walking : common up to 3 years , may be due to femoral
anteversion.Children walk with kness and feet pointing
inwards(most common between 3-8 years)
2) Internal tibial torsion: knees point forwards but feet point in.
3) Metatarsus adductus : is a flexible ‘c shaped’ lateral border of the
foot.Most resolve by the age of 6years.
4) Bow legs (genu varus): are common from birth to early toddler-
hood,maximum at age 1year,often with out-toeing.Most resolve by
18months.
5) Knock knees(genu valgus) :are common and associated with in-
toeing.Most resolve by the age of 7 years.
6) Flat feet: are common.Most children have s flexible foot with a
normal arch on tiptoeing.Flat feet usually resolve by the age of
6yrs.
7) Crooked toes:Most resolve with weight bearing.

Type of gait description Seen in

SPASTIC GAIT There is Cerebral palsy.
circumduction and
lifting of the leg in
the form of an arc at
the hip. Hip is
elevated on the
affected side with
slight dragging of
the foot and
scraping of toes.

STAMPING GAIT the foot is placed on

the ground with a
thud due to loss of
sense of position. .
HIGH STEPPING GAIT high steps are taken Seen peripheral
due to foot drop to neuropathy ,
avoid tripping of Poliomyelitis,
toes. Progressive
muscular atrophy.
ANTALGIC GAIT Reduced time spent may be observed in
(caused by pain) : weight-bearing on juvenile idiopathic
the affected side. arthritis(JIA).

CIRCUMDUCTION
GAIT: Excessive hip seen with a leg length
abduction as the leg discrepancy,in unilateral
swings, spasticity (cerebral
palsy).

ATAXIC GAIT :
Instability with an seen in ataxic cerebral
alternating narrow- palsy affecting the
to-wide base. cerebellum,in cerebellar
ataxia,Fredrich’s ataxia.

TRENDELENBERG’S
GAIT: May be observed in
while weight- Legg-calve-perthes
bearing on the disease,slipped upper
ipsilateral side, the femoral
pelvis drops on the epiphysis,developmental
contralateral dysplasia of the hip,
side,rather than arthritis involving the
rising as in normal. hip,inherited
myopathies.
TOE WALKING GAIT
WITH ABSENT HEEL
CONTACT Persistent toe walking is
Habitual toe observed in spastic upper
walking is common motor neuron
in children and neurological disease(
associates with cerebral palsy).
normal tone,range
of movement
around the feet and
normal walking on
request.
‘CLUMSY GAIT’ Difficutly in motor Neurological
co-ordination(fine disabilities(Cerebral
and gross motor palsy,cerebellar
skills).the child may ataxia,LMN
present with disorders),inflammatory
frequent falls ,and arthritis or myopathies
difficulty in self -
help skills such as
dressing or feeding
 at school

Signs of meningeal irritation

1. Nuchal rigidity:-tested by placing the examiners hand under the
patients head and gently try to flex the neck.
Inference:-Undue resistance implies meningeal irritation

2. Brudzinski neck sign:- it is the flexion of both knees during the

manoeuvre to test nuchal rigidity.

3. Kernig sign:-elicited by flexing the hip and knee on one side to

90o while the patient is supine and then extending the knee further
with the hip still flexed at 90o.
4. Tripod sign:-when the child is asked to sit in bed with extending
legs, he does so by flexing the knees and supporting himself with
his hands placed far behind him in bed and neck extended.

Differential diagnosis of Ataxia

The causes of ataxia can be classified according to the type of illness as
follows
Chronic progressive ataxia
Symptoms and signs progress upto 1 year
Chronic non progressive ataxia
No symptoms and signs

Signs of increased ICT

1. macewen ‘s sign
2. obvious large head
3. Bulging tense AF
 4. separation of sutures
5. tachy cerebrale
6. slow bounding pulse
7. systolic hypertension
8. respiration- cheyne- strokes, biot’s or central hyperventilation
9. squint(esotropia)- due to stretch of 6 th nerve
10. false localizing signs
11. VI ,VII, nerve palsies,ipsilateral mydriasis(Hutchison ‘s pupils).

AREAS OF THE BRAIN

 CEREBRAL PALSY

History taking
Chief complaints and history

History of delayed milestones in detail

A) Gross Motor
B) Fine Motor
C) Personal ,Social
D) Language
E) Vision
F) Hearing

History of motor involvement

1 .Stiffness- Fisting - Scissoring

- Difficulty In Changing Diaper, Bathing, Dressing
2 .Floppiness-Slipping Through Shoulders
3 .Which Limb Is More Involved - Upper Or Lower
Upper Limb
Proximal – Combing, Distal - Mixing Food ,Taking Object From Floor
Lower Limb -Proximal- Getting Up From Sitting Position, Distal
Slipping
History of abnormal movements

• Involuntary movements,
• Myoclonic jerks,
• Chorea, Athethosis ,Dystonia ,
• Seizures ,
• Gait- toe walking scissoring

History suggestive of cranial nerve involvement

• Ability to follow objects(2 nd N)
• Eye position /movement ,dropping of eyelids (3 N)
• Sucking /chewing(5 N)
• Deviation of angle of mouth, difficulty in closing eyes/drooling of
saliva(7 N)
• Turning towards sounds(8 N)
Regurgitation of feeds (nasal twang) ( 9,10 N)
• Difficulty in neck movements(11N)
• Ability to protrude the tongue (12)

Associated features
• MR
• Abnormal behavior, communication, hyperactivity
• Convulsions
• Feeding problems- solids /liquids, time, tongue thrusting, weight
gain
• Recurrent RTI (GERD aspiration)
• Bowel and bladder control/disturbances
• Speech disturbances, Sleep disturbances
• Response to sound
• Dysmorphic facies/congenital anomalies

History to rule out metabolic disorders

Seizures/vomiting/sepsis-unusual odour --PKU/MPS
Dysmorphic Features/Delayed passage of Meconium,
Constipation, Excessive sleep, Dry Skin - Hypothyroid

Treatment history
• Details of investigations
• Physiotherapy details , Speech therapy ,Occupational therapy
• Squint surgery, Special school training
 Family history
• Age of both parents, Consanguinity, Married life
• Similar illness in the family, Miscarriages ,Neonatal deaths

Birth history
• Antenatal –all trimesters - 1st 2nd 3rd
Natal history
• Term/preterm, Nature of delivery
• BCIAB, resusitation if any
• Duration of labour , Premature/prolonged labour ,MSAF
• Birth injury and congenital malformations

Postnatal history
h/o NICU admission,Duration of NICU stay,h/o ventilation
• h/o jaundice,exchange transfusion phototherapy
• h/o convulsions
• BF/other methods

Diet history
• For solids and liquids
• When was complementary feed started
• Present diet
• Present calorie and protein intake

Summary
• Categorise CP by
Etiology
Topography
Physiology
Functional disability
Co morbidities

General physical examination

• Posture
• Dysmorphism
vitals
anthropometry
• Weight, Height/length
• Head circumference, Chest circumference
• Comment
Head to toe examination
• Head - Microcephaly, AF abnormal shape
• Face - Asymmetry, Dysmorphism, Drooling
 • Tongue - Protruding
• Eyes - Cornea –Size, Opacity, Cataract, Jaundice, Pallor, Vit A
deficiency
• Teeth - Dentition Malformation, Hygeine
• Skin - Neurocutaneous markers
• Decorticate posture
• Cortical thumb
• Contractures
• Dystonia

Neurological examination Higher mental function

1- Consiousness
2- Orientation-time,place,person(if possible)
3- Speech
4-DQ-developmental age/chronological agex100
< 20% - profound
20-35% - severe
35-50% - moderate
50-70% - mild
70 -90% - borderline
>90% - normal
• Child’s orientation and interest in the surroundings
• Watch for eye contact
• Following objects,alertness,obey simple commands

Cranial nerve examination

• 1 N - Smell
• 2N - Recognise and follow objects
- Field of vision
- Visual acuity
- Colour vision
- Fundus examination

• 3,4 ,6 N- Extra ocular muscle movements

- Ptosis
- Eye movement
- Light reflex

5 N- Sucking and swallowing movements, Chewing, Biting

Conjuntival and corneal reflex
Sensation on face
Rooting reflex in infants

7 N - Facial nerve
 - Deviation of angle of mouth
- Drooling of saliva
- Facial asymmetry
- Taste sensation if possible

8 N- Response to Sounds

9 ,10 N- Regurgitationof Feeds

- Position of uvula
- Gag reflex
- Dysphagia
11 N-Turn to sides ,Head lag
12 N- Tongue wasting ,Fascicuation, Deviation of tongue

Motor system examination

• Nutrition
• Tone
• Power
• Co ordination
• Reflexes

Sensory system
Response to pain ,Temperature

Meningeal signs
Cerebellar signs
Skull and spine
Special techniques for assessment
180 degree flip examination
• Supine position: Posture, Moro, Asymetrial tonic reflex, Rooting,
Sucking, Swallowing, Palmar , Plantar grasp, Glabellar tap
• Pull to sit
• Sitting position
• Ventral suspension- walking, stepping, placing
• Prone- parachute ,head lift
• Holding the infant under the shoulders

Final diagnosis

• History and physical examination confirming static encephalopathy

• Physiological classification- Spastic dyskinetic ,

ataxic,Atonic/hypotonic, mixed
 • Topograghic classification- Monoplegia, Paraplegia, Hemiplegia,
Triplegia, Quadriplegia, Diplegia, Double Hemiplegia

• Etiological classification- prenatal ,perinatal,post natal

• Funtional Classification

Level Function
1 Ambulatory
2 Walks without aids
3 Walks with aids
4 Need wheel chair ,assistance
5 Dependent for mobility

Notes
Cerebral palsy is defined as a :
1) Persistent but not unchanging
2) Disorder of movement, tone and posture
3) Due to non-progressive defect/lesion
4) Of immature brain ( fetal life, infancy, childhood)
( immature brain cut off take as 5 yrs –AAP)

Commonly associated with a spectrum of developmental disabilities

such as –
I. Mental retardation (60%)
II. Epilepsy (33%)
III. Visual , hearing (deafness-10%) and speech defects
IV. Strabismus(50%)
V. Cognitive dysfunction
VI. Sensory problems ,Emotional and behavioral problems

• EXCLUDING Progressive pathology and lesion of spinal cord.

• INCLUDING Non-progressive genetic d/s or cong malformation
CLASSIFICATIONS
TOPOGRAPHIC
• MONO
• HEMI
• DIPLEGIA
• QUADRI
• DOUBLE HEMIPLEGIA
• TRIPLEGIA
 PHYSIOLOGY

• SPASTIC
• EXTRAPYRAMIDAL
• ATAXIC
• MIXED
• ATONIC

• CLASS 1 – NO limitation of activity

• CLASS 2 – Slight limitation
• CLASS 3 – Moderate limitation
• CLASS 4 – No useful physical activity

Site of brain injury

• Cortical ,Sub – cortical, Periventricular ,Basal ganglia,Cerebellum
Brain stem

Pathological
• Periventricular leucomalacia –spastic diplegia
• Stroke in utero - hemiplegia
• Multifocal encephalomalacia -quadriplegia
• Cerebellar – ataxic ,Basal ganglia, thalamus, putamen - dyskinetic

Etiological
Prenatal
• I, iron def.,poor –nut.
• Infection, UTI, high fever,
• Chorioamniotis
• HTN, DM,Teratogens,
• Poor ANC,LOW SES
• Twins, Fetal vasculopathy

Perinatal
• Birth asphyxia,
• Premature / LBW, IUGR
• Hyperbilirubinemia , IVH
• Sepsis, pneumonia, meningitis,
• Develop. malformation

Postnatal
• CNS infections, Head injuries, Seizures,
• Hypoxic damage
• Hyperpyrexia damage

Early markers of CP
• SLOW head growth
• Poor head control
• Eye – roving eyes, poor hand regard, persistent squint.
• Ear – lack of auditory response
• Irritability, seizures, poor suck, poor quality of sleep.
• Extreme sensitivity to light
• Cortical thumb beyond 8 weeks
• Handedness before 2 yrs
• Paucity of limb movements
• Scissoring of lower limbs
• Toe walking
• Abnormal tone
• Persistence of primitive reflexes or failure to acquire postural
reflexes
• Stereotypic abnormal movements
Lack of alertness
Differential diagnosis

• Myopathies , Mental Retardation, Neurodegenerative Conditions

Organic Aciduria Like Glutaric Aciduria

Comprehensive Assessment

A Multidisciplinary Team Comprising Of A Neuro-Developmental

Pediatrician As The Team-Leader,
• Physiotherapist,
• Occupational Therapist,
• Clinical Psychologist,
• Speech Pathologist,
• Orthopedic Surgeon,
• Otorhinolaryngologist,
• Ophthalmologist,
• Teacher,
• Play Therapist And
• Social Worker Is Required, Preferably Under One Roof
Seizure case sheet

Name :
Age :
Sex :
Address :
Informant :

Chief complaints: H/O convulsions at ------- on ------

HOPI: the ------ year old male or female child who was apparently well ---
-- day back was bought to hospital with c/o convulsions ,who witnessed it
at ----- (time) on ----- (date)( day of seizure in case of new borns) 2
episodes each lasting for 2-5 mins, 10 min apart with no h/o regaining
consciousness in between convulsions.
The convulsions were characterised by uprolling of eyes and jerky
movements of right hand and right leg with h/o involuntary passage of
urine and stools, and frothing from the mouth. The convulsions were
followed by loss of consciousness.
No h/o fever
No h/o vomiting(raised ICP:-projectile,head banging,headache) / blurring
of vision
Refusal of feeds / irritability, excessive cry or high pitched cry-consolable
or not (meningitis)
No h/o ear ache or discharge from ear (meningitis)
No h/o lethargy/ abdominal distension / loose stool / rash over the body
/decreased food intake(septicaemia)
No h/o altered behaviour / inco-ordination of movements / sleepless at
night/ reversal of sleep wake cycle,jaundice . (encephalopathy)
No h/o stiffness of neck/painful movement of the neck (meningitis) /
agonizing pain / clenching of jaw (tetany)
No h/o any drug intake
No h/o trauma or head injury
No h/o consumption of any poisonous substance
No h/o trauma
No h/o bleeding tendencies
No h/o delayed attainment of milestones(CP).
No h/o spinal abnormalities.
Cranial nerves
No h/o altered sensation of smell
No h/o visual abnormalities
No h/o difficulty in movements of the eye/ ptosis / nystagmus/ squint.
No h/o loss of sensation over the face
No h/o facial asymmetry/ loss of taste sensation/ drooling of saliva.
No h/o hearing difficulty
No h/o difficulty in walking
No h/o regurgitation of feeds, hoarseness of voice
Motor
No involuntary movements
No h/o disturbance of gait
No h/o weakness of limbs/ limb stiffness{ variation between upper limb
and lower limb}
Sensory
h/o child withdrawing to hot water/ painful stimuli/responds to touch
Past history: No h/o similar complaints in the past.
Not a k/c/o IEM/ epilepsy / CHD/any AEDs taken:-dose and duration

Family history: h/o similar complaints(seizures) in the family members.

h/o contact TB

Birth history:
h/o preterm/ term, nature of delivery, birth wt-,cried immediately or not
h/o birth asphyxia
h/o neonatal seizures.
h/o congenital malformations,dysmorphisms.

Post-natal h/o: NICU admission/ prolonged ventilation/umbilical

catherization
Neonatal hyperbilirubinemia requiring exchange transfusion(kernicterus)

Neonatal hypoglycaemia( in SGA/ IUGR/ IDM):investigations

MRI,CT,USG abdomen)
AED’s given or not
DEVELOPMENT history: normal/ delayed
Developmental age-
Development quotient-
Socio economic history: father’s and mother’s education, occupation
Support system
Orientation to the condition

Summary: the ---- year old child was brought to the hospital with h/o
unprovoked seizures which was focal in nature with no h/s/o space
occupying lesions/ meningitis/ encephalopathy/ sepsis/ trauma/ drug
intake/ bleeding manifestation.
No h/o cranial nerve involvement with no h/s/o focal neurological deficits
with no significant family history or birth history with post-natal period
being uneventful.
The child who is developmentally and immunized upto date belongs to a
lower SES and consumes a diet deficit in calories.
I would like to evaluate the child further for causes of status epilepticus.
 DOWN’S SYNDROME

1. What is Down’s syndrome?

Down’s syndrome is a genetic condition caused by
chromosomal anomalies.

2. What are the chromosomal abnormalities seen in Down’s

syndrome?
a. Trisomy 21 ( due to dysjunction) -95%
b. Translocation – 4%
c. Mosaicism – 1%

3. What are the risk factors that lead to the birth a Down’s syndrome
child?
a. Maternal age ( 1 in 2000 at 20 years of age; 1 in 900 at 30
years of age; 1 in 100 at 40 years of age and 1 in 30 at 45
years of age)
b. Rarely radiation, maternal viral infections.

4. What is prenatal screening for Down’s syndrome?

All women, regardless of age have to undergo the following tests
as screening for Down’s syndrome:
a. Dual test done at the first trimester (11-13 weeks) which
includes PAPP-A and beta HCG levels.
b. Triple test done at 2nd trimester- includes beta HCG,
unconjugated estriol and alpha feto protein
c. Quad test : triple test plus inhibin A levels
d. USG in first trimester (11-13 weeks): shows increases
thickness of nuchal translucency
e. USG in second trimester: short humerus, short femur,
absent nasal bone, widened facial angle etc.

5. What are the confirmatory prenatal tests?

a. Chorionic villus sampling (11-13 weeks)
b. Amniocentesis (16-18 weeks)

6. What are the physical features of Down’s syndrome?

a. Brachycephaly
b. Microcephaly
c. Flattened nasal bridge
d. Upward slanting lateral palpebral fissures
e. Epicanthal fold
f. Small dysplastic ears
 g. Low set ears
h. Small mouth
i. Large protruding tongue/fissured tongue
j. High arched palate
k. Cleft palate
l. Short neck with redundant skin
m. Simian crease
n. Brachydactyly
o. Clinodactyly
p. Dermatoglyphics: ulnar loops, increased atd angle
q. Sandal gap
r. Pelvic dysplasia
s. Increased laxity of joints
t. Hypotonia

7. What are the common systemic findings associated with Down’s

syndrome?
a. Eyes: cataracts, myopia, brushfeld specks, glaucoma
b. Ear: recurrent ear infections
c. CNS: seizures, autism
d. Cvs: endocardial cushion defect, VSD, ASD, PDA or TOF.
MVP in adults.
e. Rs: repeated respiratory infections
f. GIT: duodenal atresia, anal atresia, tracheo-esophageal
fistula, hirshsprung disease
g. Atlanto axial deformity
8. What is prenatal screening in Down’s syndrome?
Screening done during pregnancy for mothers of all ages.
 a. Triple test (16 weeks POG): beta HCG levels(increased),
unconjugated estradiol(increased) and Alfa fetoprotein
levels(decreased).
b. Quad screen ( 15-20 weeks POG): above with inhibin A
levels.
If the above are positive, then the pregnancy is at high risk
ok Down’s syndrome.

9. What are the prenatal confirmatory tests in Down’s syndrome?

a. Chorionic villous sampling (10-12 weeks POG)
b. Amniocentesis (16-20weeks)

10.Diagnosis of Down’s syndrome?

a. Cytogenic tests like karyotyping and FISH(fluorescent in situ
hybridisation)
b. Molecular tests like MLPA(multiple ligation dependent
probe amplification ) and QF PCR(quantitative fluorescent
PCR)

11.Management of a child with Down’s syndrome

I. FOLLOW UP
a. Visual screening at 1 month, 6 months, 12 months of
age and annually thereafter.
b. Hearing screening annually for 1-10 years of age
c. Dental examination for 1-10 years of age
d. X-ray cervical spine for 1-10 years of age
e. Thyroid screening at birth, 1 year of age and between
11-17 years of age.
f. Screening for diabetes mellitus

II. REHABILITATION ( Training to do day to day routine

activities).

III. NUTRITION AND GROWTH: growth to be charted and

monitored on special Down’s syndrome chart.

IV. ASSOCIATED ANOMOLIES: other associate systemic

anomalies to be treated.
 PEM model case sheet

NAME
AGE
SEX
ADDRESS
INFORMANT
CHIEF COMPLAINTS:H/O not gaining weight for 6 months
h/o loose stools for 3 days
H/O PRESENTING ILLNESS:
A __ year old M/F child , first /second born to a non-consanguinous
marriage couple was brought to the hospital h/o not gaining weight since
past ___months
The child is being bottle fed and is on family pot feeding
h/o reduced intake of feeds
h/o lethargy for 1 month
h/o excessive cry 1 month
no h/o feeding difficulty (cleft lip/cleft palte/cp)
h/o loose stools 3 days, insidious onset 7-8 episodes/day soon after feeds
,watery to mucoid in consistency,copious amount,foul smelling,not blood
tinged (steatorrhea/malabsorption syndrome/infection/gastroenteritis)
h/o vomiting: insidious in onset for 2 days , 3-4 episodes/day non
projectile ,non bilious,not bod stained,not relieved on medication.
h/o abdominal distension-generalised , insidious onset gradually
progressive for 6 months(dyselectrolemia,hypotonia secondary to
malnourishment, ascites due to hypoproteinemia)
no h/o mass per abdomen/s/o hepatomegaly
no h/o fever
signs of dehydration
h/o excessive thirst
no h/o lethargy
no h/o decreased urine output
other signs of malnourishment
no h/o edema(hypoproteinemia)
h/o thinning of hair,observed since 6 months
h/o peeling of skin, ,active shedding of hair present
h/o depigmentation of skin over the lower limbs
no skin lesions
no h/o vitamin A deficiency (blurring of vision/night
blindness/dryness of eyes and ulceration of the surface of the eye)
h/o bleeding from the gums on brushing
no h/o deformity of legs /knock knee or difficulty in
walking(vitamin D deficiency
h/o infection:no h/o ear ache/ ear discharge
no h/o cold/cough/ear ache/discharge from ear
no h/o burning micturition or increased frequency of micturition
no h/o jaundice (hepatomegaly/fatty liver)
no h/o dyspnea or suck rest suck cycle ( CCF due to malnourishment/ wet
beri beri)
no h/o reduced urine output /haematuria( chronic renal failure)
h/o delayed attained of milestones when compared to the other hasn’t
started walking , disappearance of social smile,disinterested in the
surroundings( motor milestones more affected)
no h/o PICA
no h/o passing worms in stools

PAST HISTORY:
H/O repeated episodes of loose stools in the past,admitted once for the
same for 5 days
Treated with IV medication
h/o repeated episodes of cold and cough for 1 year atleast 1 episode
/month
admitted 2 times of pneumonia in the past
given IV medication for 5 days in each episode

FAMILY HISTORY;
H/O similar complaints in the siblings
No h/o tb contact

BIRTH HISTORY:

IMMUNISATION:

DEVELOPMENTAL: motor milestones attained

DIET HISTORY

SOCIO-ECONOMIC STATUS :
Economy class
Mother’s education and orientation
Personal hygiene

SUMMARY: A _ year old M/F, second born to a non consanguineously

married couple, with improper feeding methods was brought to the
hospital with c/o not gaining weight for 6 months,h/o loose stools since 3
days and vomiting and abdominal distension since 2 days. She also gives
h/o recurrent infections in the past. The child also has symptoms and
signs of malnourishment. The child who has insignificant birth history,is
immunized upto the date according to NIS and has delayed attainment of
motor milestones. h/o similar complaints was present in the sibilings.
The child belongs to lower socio economic class and a stable family with
inadequate personal hygiene.I would like to consider PEM in this child
and would like to evaluate further.
PROTEIN ENERGY MALNUTRITION

DEFINITION:A range of pathological conditions arising from co-

incident lack in varying proportions of proteins and calories occurring
most frequently in infants and young children and commonly associated
with infections

Types

Kwashiorkor Marasmus
* Apathic ,miserable * Wasting present
* Stunted in growth * Old man appearance
* Edema present * Alert
* Hepatomegaly,anemia * Have good apetite
* Hair and skin changes * Irritable
 SEVERE ACUTE MALNUTRITION

DEFINITION: Defined by presence of

1. Wt for Ht/length <3 sd
2. Severe visible wasting
3. Bipedal edema
4. MUAC:< 11 cm

THEORIES OF PATHOGENESIS OF PEM

1. Variable calorie and protein intake

Predominant protein deficiency :cause for kwashiorkor
Predominant calorie deficiency:cause for marasmus
Later this theory was disregarded as both the syndromes occur in children
consuming similar diet

2. Time bound development

By viteri in 1964 Chronic malnourishment :marasmus and they adapt
Acute malnourishment :kwashiorkor fail to adapt

3. Theory of adaptation : Gopalan in 1967

If the child adapts to malnutrition ,marasmus result and dysadaptation
leads to kwashiorkor
(Adaptation –biochemical and hormonal
Normally –anabolic hormones like insulin and insulin like growth factors
maintain near normal anabolism to prevent edema and fatty liver by
enabling synthesis of albumin and beta lipoproteins
In kwashiorkor –due to stress of malnutrition /infection the adaptation
fails

CLINICAL SIGNS OF PEM

Hair: depigmentation(lack of lustre) ,thinning of hair, flag sign, easy

pluckability

Face: depigmentation ,nasolabial dyssebacia , moon face

Eyes :pale conjunctiva, bitot’s spots, conjunctival xerosis, corneal xerosis

, keratomalacia ,pallor
Lips: angular stomatosis, chelosis

Tongue : scarlet/raw tongue, atropic papillae,B12 deficiency,oral

ulcers,oral thrush

Teeth: mottled enamel,caries,halitosis,oral hygiene

Gums: spongy, bleeding gums

Glands: thyroid and parotid enlargement

Skin: xerosis, flacky paint dermatosis,pellagrous

dermatosis,depigmentation or hyperpigmentation ,baggy pant appearance
,loose folds of skin,loose buccal pad of fat

Oedema:-peadl pitty oedema

Nails :koilonychias, hyperpigmented knuckles

Musculo skeleton: muscle wasting

Craniotabes,frontal bossing
Wide open anterior fontanelle
Knock knees/bow legs
Deformities of thorax ,Harrison sulcus , ricketic rosary

GIT: hepatomegaly

Nervous system : apathy/confusion

Motor weakness, loss of position sense, loss of ankle and knee
jerk

MANAGEMENT OF SAM

Step1 :treat /prevent hypoglycemia

 Blood sugar level <54mg/dl or 3 mmol/l
 Conscious child:50ml bolus of 10% glucose by nasogastric tube
 Unconscious /lethargic/convulsing: iv sterile 10%glucose
followed by 50ml of 10%glucose or sucrose by NG tube
 2ND hourly feeding
Step 2:treat /prevent hypothermia

 If Axillary / rectal temp :<35.5’c

  Rewarm the baby: by cloth/place under warmer/on mother’s bare
chest-kangaroo mother care
 Feed straightaway

Step3 : treat/prevent dehydration

 Continue feeding
 Iv fluids only in cases of shock
Assessment of dehydration in SAM
 Mental state
 Mouth ,tongue and tears
 Skin turgor
 Oedema and hypovolaemia can co-exist
 h/o diarrhea
 increased thirst
 recent sunken eyes
 prolonged CFT, Weak/absent radial pulse, decreased or absent
urine flow

Step4:Correct electrolyte imbalance

 potassium and magnesium supplementation for 2 weeks
Step 5: treat/prevent infection
 often associated with hypoglycemia /hypothermia
 no complication: co-trimoxazole / amoxicillin
 Severely ill:ampicillin with gentamycin/cephotaxime and can add
cefotaxime/ceftriaxone
Step6:correct micronutrient deficiencies

 Vitamin A ON DAY 1
 Multivitamin
 Folic acid ,zinc,iron after day 7 in rehabilitation phase
Step7:start cautious feeding

 Small, frequent feeds

  Oral /nasogastric feeds
 Milk based formulas
 If breast fed ,continue breast feeding
Step8 :achieve catch-up growth

 Recommend milk based formula

 Vigorous approach to feeding, very high intakes and rapid weight
gain
Step9:provide sensory stimulation and emotional support

 Tender love care

 Cheerful environment,
 Play therapy
 Physical activity as soon as child is well enough
 Mother involving in feeding,bathing,play.

Step10:prepare for followup after recovery

 Show parents or caregivers how to

1.feed frequently 2.structural play therapy

*Advice
Bring baby for regular check up
Ensure booster immunization given
Ensure vitamin A given every 6 months
Anemia Model Case Sheet

Name :
Age : (nutritional anemia, thalassemia >6m of age)
Sex : (x-linked G6PD deficiency)
Address :
Informant :

Chief Complaints:-
H/o Excessive tiredness x 1 month
H/o Loss of appetite x 1 month
H/o Paleness on the body x 15 days

History of presenting illness:-

The __ year old M/f child was brought to the hospital with C/o excessive
tiredness x 1 month Insiduous in onset, progressive, relieved with rest.
C/o increased sleepiness
C/o easy fatiguability,irritiability
H/o exertional breathlessness x 1 month, reduced with rest.
H/o loss of appetite x 1 month
H/o paleness on the body – observed by the attenders /parents since 15
days, non-progressive
H/o consuming mainly milk based diet
H/o PICA +
No H/o worm infestation
No H/o blood loss following trauma / No H/o bleeding manifestations
(haemoptysis ,hematemesis, hematochezia, malena  to R/o GI bleed)
No H/o abdominal distension, No H/o pain abdomen (worm colic / lead
poisoning / sickle cell crises)
No H/o yellowish discolouration of the skin, No H/o passing high
coloured urine  (hemolytic anemia / jaundice)
No H/o fever / hematuria (malaria / black water fever)
No H/o previous blood transfusion

No H/o bony deformity/ bony tenderness (extra medullaryhematopoiesis,

leukemia) No H/o loose stools / vomiting (malabsorption syndrome)
No H/o blood stained stools (HUS)
No H/o fever (malaria / salmonella infection in sickle cell anemia,
leukemia)
No H/o petechia / purpura (involvement of the other cell lines/ splenic
sequestration)
No H/o any chronic diseases (TB / CKD / chronic UTI )
No H/o drug intake ( NSAIDS, Salicylates,quinine,primaquine )
Complications :

CCF  H/o puffiness of face, tachypnoea ,tachycardia

H/o pedal edema
H/o exertional breathlessness / dyspnea
H/o palpitations
ARF  H/o oliguria / anuria
Developmental delay
H/s/o PEM / micronutrient deficiencies

Treatment history:

Past History:

1) h/o similar complaints in the past requiring blood transfusions

2) h/o recurrent episodes of URTI/LRTI
3) h/o recurrent episodes of gastroenteritis (to r/o pem/ anemia of
chronic illness)
4) h/o previous intestinal surgeries (megaloblastic anemia due to
malabsorption syndrome)

Family history: consanguinity (G6PD deficiency), similar complaints in

the family members.

Antenatal history: maternal intake of iron and folic acid, interval

between two pregnancies, maternal malnutrition, intrauterine TORCH
infection, multiple pregnancy (twin-twin transfusion), antepartum
hemorrhage.

Birth History: gestational age of the baby (preterm babies are more
prone), low birth weight (decreased iron stores),

Postnatal history: h/o neonatal jaundice (hereditary spherocytosis),

exclusive breast feeding and initiation of complementary feeds,

Diet history:

Socioeconomic history:low socioeconomic class, unhygienic condition,

open air defecation, source of water (various infection and infestation)
Summary: A _ year old M/F child was brought to the hospital with C/O
excessive tiredness,loss of appetite since 1 month and paleness of skin
noticed since 15 days with H/O pica and h/o consuming mainly mill
based diet. The child who has no h/o CCF,has significant past h/o
recurrent infections.The child has delayed development of motor
milestones when compared to other siblings has no significiant
family/birth history.The child consumes a diet(veg/nonveg) deficit in
proteins and calories,has been immunized upto date and belongs to lower
socioeconomic status with inadequate personal hygiene.I would like to
evaluate the child further for anaemia.

Discussion :

Normal range of Hb according to age:

AGE GROUP NORMAL RANGE (g/dl)
Cord blood 13.7-20.1
2 weeks 13-20
2 weeks – 3 months 9.5-14.5
6 months – 6yrs 10.5-14
7-12 yrs 11-16
Adult female 12-16
Adult male 14-18

Aetiology:

1) Decreased production of erythrocytes

Hypoplastic conditions: Aplastic anemia
Fanconi’s anemia
Osteopetrosis-marble bone
disease

Deficiency of specific patterns: iron deficiency anemia

Megaloblastic anemia

Impaired erythropoietin production:

Anemia in chronic diseases (CKD)
Hypothyroidism, severe protein
energy malnutrition

Marrow displacement: leukemia, neuroblastoma

Lead poisoning
Acute infection/ inflammation

2) Hemolysis: hereditary spherocytosis, sickle cell Hb disorders,

thalassaemia syndromes, iso-immune hemolytic anemia, SLE,
infectious mononucleosis, HUS, drugs, poisons (snake venom),
cardiac prosthesis,

3) Blood loss: trauma, bleeding manifestation

Morphological classification of anemia

 Type Investigation Condition
Microcytic Ferritin decreased IDA,
ferritin normal or increased Thalassemia,
Haemoglobinopathies,
sideroblastic anemia
Normocytic Reticulocyte count Bone marrow hypoplasia, red
decreased cell dysplasia
Reticulocyte count Hemorrhage/acute blood loss,
normal/increased hemolytic anemia
Macrocytic Megaloblastic Vitamin B12 deficiency
Non-megaloblastic Liver disorders, thyroid
disorders, congenital
dyserythropoietic anemia

Pathophysiology:
The clinical features in anemia are due to tissue hypoxia which occurs
due to decreased O2 carrying capacity of the blood (as a result of
decreased Hb)

Compensatory adjustments:
1) Decrease in physical activity in children to reduce the oxygen
requirement.
2) Increased 2,3 DPG combines with Hb and decreases the affinity of
Hb to oxygen
3) Tachycardia to increase the cardiac output and thus the stroke
volume to supply more oxygen
4) Expansion of blood volume by shift of fluid from tissue spaces to
intravascular compartment.
5) Redistribution of blood flow from tissues with lower oxygen
requirement, such as skin, to tissues with higher oxygen
requirements such as brain and heart.
Clinical features:
Symptoms: tiredness, lassitude, poor feeding, poor school performance,
PICA (geophagia, amylophagia, pagophagia), dyspnea on exertion,
palpitations

Signs:
1) CVS :pedal edema ,hepatomegaly,basal crepts hyperdynamic
circulation, raised JVP, hemic murmur(gallop ),
2) CNS – faintness, headache, lack of concentration, tinnitus, dizziness
3) Gastrointestinal – anorexia, hepatosplenomegaly
 Clinical features Causative conditions
Gum bleeding, bone pain or tenderness, Leukaemia
lymph node enlargement
Bleeding tendencies Blood loss anemia
Leg ulcers/dactylitis Sickle cell anaemia
Peripheral neuritis(rare) Vitamin B12 deficiency

Complications:
CCF, delayed wound healing,

Investigations:
CBC with ESR
Peripheral Smear
RDW
Reticulocyte count
Iron profile – serum iron, serum ferritin, total iron binding capacity,
transferrin
Hb electrophoresis
NESTROFT
Haemolytic anaemia:-LFT-direct and indirect,LDH
Urine routine and microscopy:-haematuria
Stool for ova and cysts
RFT
Serum B12 and folic acid levels

Treatment :
Oral iron supplementation:-2-3mg/kg-for 3 months
Parenteral iron supplementation
Transfusion in severe anemia

Iron rich diet: ragi, wheat, green leafy vegetables, jiggery, dates, raisins,
mutton, chicken, fish, egg, and liver preparations

First response is decreased irritability and increased appetite, followed by

a marrow response – reticulocytosis.
Thalassemia Case Discussion

It is an autosomal recessive haemolytic anaemia that results from

defective production of Hb due to mutation in the genes which direct the
production of Hb. Patients with thalassaemia produce abnormal Hb that
cannot transport enough oxygen to tissues.

Aetiology:
Haemoglobin is made up of four chains of amino acids : two identical
alpha -chains and two identical beta-chains.
Genetics:
Two copies of the abnormal, recessive gene are required for the beta-
thalessemia disease to occur . A person who has just one copy of the
mutated gene is termed a carrier.

Types
1. Beta thalssaemia-a mutation in the B-genes
decreases the production of B-chairs, resulting in thalassaemia.
2. Alpha thalassaemia-a mutation in the a-genes
decreases the production of a-chains, resulting
in a-thalauaemia.

Clinical Features
An infant born with B-thalassaemia initially appears normal.Children
remain asymptomatic up to 6-8 months of age in most cases.
It should be suspected in any child who presents with microcytic,
hypochromic anaemia and does not respond to treatment with iron.
Clinical features include the following:
Anaemia-irritability and fatigue
• Fever and diarrhoea (repeated infections)
• Failure to thrive
• Jaundice
• Haemolytic facies-maxillary hyperplasia, prominent parietal eminence,
frontal and occipital bossing, prominent malar bones, widely spaced eyes.
• Hepatosplenomegaly
• Delayed sexual development
Investigations

• DNA-based diagnostic studies

• Naked eye single tube red cell osmotic fragility
test (NESTR.OFT)
Haemoglobin low(~g/dL),
 hematocrit decreased.
• Peripheral smear-RBCs normal/microcytic,
hypochromic anaemia with anieocytosis and
poikilocytosis.
 Target cells and tear drop cells will
be seen.
 marked basophilic stippling and variable polychromasia.
Fragmented red cells, nuclear remnants such as Howell-Jolly
bodies and Heinz bodies may be seen. A large
number of early, intermediate and late erythroblast will be seen.
• Red cell indices-MCV/MCH/MCHC may be
normal or low.
• Mild leucocytosis and thrombocytosis may be present due to the
stimulation of the bone
marrow.
Leucocytosis with shift to left is seen during acute haemolytic
episodes.
• Reticulocyte count will be increased due to increased production
of the RBCs to compensate
for the haemolysis.
• Haemoglobin electrophoresis and high-performance liquid
chromatography (HPLC}-Hb.A,
raised, HbF may be raised.

Different types of Hb in a patient's blood are measured to

distinguish between normal individuals, carriers and people
with thalassaemia. This test should be done before blood
transfusion is given, as the formation of the HbF is suppressed by
blood transfusion. Using the electrophoresis method to test a
child's parents and establish that they are both carriers helps
confirm the diagnosis.
• Bone marrow is hypercellular with erythroid
hyperplasia.
There is increased number of stippled
erythroblasts and sideroblasts. During the aplastic aisis, the
marrow cellularity is decreased.
 • Screening for genetic counselling.
• Osmotic fragility test shows increased resistance to haemolysis
even in the presence of anaemia.
The cells in these patients are thinner and absorb
more water.
• Urinary urobilinogen-markedly increased.
• Stool examination-stools are dark in colour due
to increased stercobilinogen. Normal excretion of
stercobilinogen is 40-180 mg in 24 hours. This
may exceed to 200 mg.
• Serum iron-increased.
• Serum bilirubin level-moderately elevated.
• Radiological changes-medullary portion of the bone is widened
and the bony cortex is thinned out with a coarse trabecular
pattern in the medulla.
 X-ray of the metacarpals, ribs and vertebra shows thinning of
cortex.
 X-ray of the skull shows hair on end appearance.
 The frontal bone appears thickened, starting in the nasal region of
the frontal bone and extending symmetrically over the
parietotemporal regions but sparing the occiput. This gives the
appearance of bossing.
 Pneumatisation of the sinuses is delayed and the maxilla appears
overgrown with prominent malar eminencies. X-ray of bone
changes is seen after I year.
 X-ray of hand shows reticular pattern in metacarpals (after 4
months)
 Chest shows reticular pattern in ribs.
 Coagulation studies may be abnormal.
 Investigation for complications-glucose tolerance test, endocrine
studies and serum calcium.
MANAGEMENT:

It consists of a step-wise approach which includes

the following:
1. Confirmation of diagnosis- clinical examination and investigations
2. Correction of anaemia- Patients with thalassaemia major require
regular blood transfusions.

 Regimens:
Hypertransfusion is preferred as permits normal growth, prevents
anaemia and its complications, suppresses erythropoiesis, prevents
skeletal changes, prevents gastrointestinal iron
absorption, inhibits extramedullary haemopoiesis, thus preventing
splenomegaly and hypersplenism.

Leucocyte Filters. The leucocytes in the transfused blood give rise to non-
haemolytic febrile transfusion reactions. These are prevented by the use
of leucocyte filters.

Component Therapy. Packed RBC transfusion and neocyte transfusion

may be done. The neocytes have a longer lifespan. The infusion of the
neocytes will lead to the inaeue in the interval between two
transfusion. This also deaeues the risk for iron overload.

Amount and Rate of Transfusion. A total of 20 mIJkg of fresh blood is

transfused every 2-4 weeks. If packed cells are used, 10 mIJkg is given.
The blood should be transfused at a rate of 5-7mL/kglhour. In presence of
cardiac failure, the rate of transfusion should be decreased. The Hb
should increase by 3.5 g/dL.
Average annual blood requirement is lSG-200 mL/kg. In patients with
hypersplenism or antired cell antlbodies, the requirement is more.

3. Prevention/treatment of iron overload by chelating agents:

 Desferroxamine (DFO) given subcutaneously as continuous
infusion over a period of 8-12 hours/day for 5-6 times/week.
 Combination of DFO + Kclfer for 1-6 days/week . Advantage is that
they act at different sites.
  Deferriprone ( Keifer ) is an oral iron-chelating agent given in a
dose of 75-100 mg/kg/day in two to three divided doses.
4. Pharmacological methods
5. Curative treatment-
Splenectomy: should be postponed for at least up to th e age of 6 years
to avoid the risk of infections.
 Indications are as follows:
• transusion requirement of packed cells more
than 200 mlJkg/year
• Hypersplenism (leucopenia, thrombocytopenia)
• Reduced RBC survival (Cr51 radioisotope stud-
ies)
• Massive splenomegaly
The child should be immunised with pneumococcal vaccine,
Haemophilus influenzaevaccine and meningococcal vaccine 4-6 weeks
prior to splenectomy. Life-long penicillin prophylaxis
should be given. Prophylaxis for malaria can also
be given.

Bone Marrow Transplantation.:Bone marrow from a histocompatible

donor should be harvested and transplanted. It offers permanent cure.
Stem cell transplantation
6. Genetic counselling: Prenatal diagnosis is done by foetal DNA
analysis by blood sampling around 1 6-18 weeks of intrauterine life.

7. Treatment of complications
 NEW BORN CASE SHEET

1} HISTORY

B/O -------------------------------------------------------,Day of life , Term /

Preterm, Sex,

Gravida /Para, Weeks of gestation -------------------Date-------------------

Time-----------

NVD /LSCS, Birth Weight ----------------------LMP--------------------EDD-

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

Age of Mother----------------------------- -----------Age of Father -------------

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

Occupation of Mother & Father --------------------------------------------------

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

Address :-

(Example : B/O of sujatha,4day old term male baby born to G2P1L1A0

Mother born at 38 weeks of gestation on 4/11/2015 as at 10.40 am by
LSCS , Birth wt : 3kgs.
LMP----EDD---Age of Mother ---- Age of Father----occupation of
Mother &Father.)

C/C (if any ) :

Maternal History :

Blood group, para, living, dead

Past obstetric history :-

1st pregnancy :- Age & sex of child , mode of delivery complication

during
pregnancy and delivery.

2ndpregnancy :- Age & sex of child , mode of delivery complication

during
pregnancy and delivery
Medical History :-

DM, HTN,TB ,Hypothyroid seizures , History of Drug intake History of

any recurrent abortions, still birth.

Present Pregnancy :- LMP, EDD, Spontaneous /Induced.

1st Trimester :-

H/O Confirmation of pregnancy

Folic acid intake
Fever with Rash with are with out lymphadenopathy(Swelling once
neck)
Drug intake
Antenatal scan- NT scan
Hyperemesis
History of Recurrent abortions

IInd Trimester:-

1) Iron and folic acid intake , injection TT

2) History of DM, HTN, Preclampsia bleeding(Abruption placenta or
same placenta
Previa
3) Anemia
4) Fever
5) Anomaly scan

IIIrd Trimester

PROM (More than 24 hours )

Bleeding
UTI/Fever
History of DM, HTN, Preeclampsia, bleeding (abruption placenta or
placenta previa
Growth scan

Natal History

1) Mode of delivery NVD\LSCS (Indication ), forceps, Vacuum delivery.

2) Duration of 1stt & 2 nd stage of delivery.
3) Any H/O Premature Neptune of membranes
4)Nature of amniotic fluid :- i ) clear ii)Meconium Stained iii) Foul
Smelling
5)Cried immediately after delivery.
6)Any resuscitation done.
7) Breast feeding when was started.

Family History - Same

Immunization history - Same.

Newborn examination

Alert, active, cry colour ( Pink, Icteric\ Acrocyanosis)

Posture : Fixed attitude
Abnormal position – Ex – erb’s palsy or klumpkey palsy)

Vitals :
HR, RR, Temperature, CFT

Anthropometry :

Weight : Length: Head circumference: Chest

circumference:

Head to the Examination:-

Head
Shape
Fontanels\Sutures
Forceps Marks : if any
Caput succedaneum\Cephalhematoma

Ears:
Position: (Lowset ears/ Normal)
Ear recoil
Preauricular Tags

Eyes:
Cataract, Discharge, Slant
Hypertelorism
Icterus
Subconjunctival hemorrhage

Nose:
Patency, Shape

Oral Cavity:
Cleft lip \Palate
Predecidious teeth
Tongue tie
Ebstein pearl
Cyanosis
Facial asymmetry and Dysmorphism Ex: Down’s.

Neck:
Short neck\Webbing
Mass

Limbs :-
Polydactly, Syndactly , Single palmar crease, Saddle toe

Chest:-
Nipple, Mastitis, Neonatorum, Accessory
Nipple, Mass, Skin, Lesions
Signs of Respiratory Distress

Abdomen
Position of Umbilicus
No of Artery and Vein
Umbilical Discharge
Mass
Genitalia

Female
Labia Majora\minora\clitoris\vaginal\Discharge

Male:
Position of testes(Descended or Undescended

Spine & Back:& Anal Patency to be checked

Mass, Sinus, TuFt of hair

Hip examination :TO R\O CDH(any obvious position of limbs)

Skin:-

Erythema neonatorum
Mongolian spots
Haemangiomas
Cafe au lait spots
Neonatal pustulosis
Milia
Icterus
Pallor, Acrocyanosis
LIMB Exam
Any obvious position of limbs ex erb’s palsy

CNS:-
Alert active crying ( Strong, Weak)
Movement of all 4 limbs spontaneous
PA :-
CVS :-
RS :-

Reflexes:-
Moro Reflex: Symmetrical\Asymmetrical
Rooting & Sucking Response:
Palmar grasp
Plantar grasp
Tonic neck reflexes \ ATNR
Stepping reflex\Walking Reflex

Cranial Nerve Examination

CN 1 – Turns Head towards Breast

CN 2 – Papillary Reflex
– Flashing Light Causes Blink
– Papillary Constriction

CN3,4,6 – Doll’s Eye Maneuver

– Papillary Reflex

CN 5 – Rooting and Sucking Reflex

CN7 – Check for Facial Symmetry and Asymmetry

CNS – Responds to Sounds of Various Intensity

CN 9,10,12 – Sucking and Swallowing

CN 11 – Turning Head

Ballard scoring system

Diagnosis : 1. TERM/PRETERM
2. AGA/LGA/SGA
3. MALE /FEMALE BABY
( Mention if any other problems like NHB / Sepsis / HIE / RDS / MSF )
 PAEDIATRIC NEWBORN VIVA QUESTIONS FINAL MBBS

1. Define :

i) SGA( small for gestation age ) birth weight less than 10th
percentile for gestational age.
ii) AGA (appropriate for gestational age) birth weight between 10 th
and 90th percentile for gestational age.
iii) LGA(large for gestational age)infant birth weight above the 90 th
percentile for gestational age.
iv) VLBW (very low birth weight neonate) neonate weighting less
than 1500grams at birth irrespective of the gestational age.
v) LBW (low birth weight) neonate weighting less than 2500 grams
at birth.
vi) ELBW (extremely low birth weight neonate ) a neonate
weighting less than 1000 grams at birth.

2. What are the problem of

i) IUGR - hypoglycemia, hypocalcemia, meconium aspiration
syndrome, polycythemia (because of chronic hypoxia) and
resulting hyperbilirubinemia
ii) SGA- hypoglycemia, hypothermia.
iii) Pre-Term- necrotizing enterocolitis, RDS.

3. When do you advice DBF is N/B?

i) NVD –Direct Breast Feeding started by 1/2hr
ii) LSCS- within 2hrs.

4. What are the Problem Associated with Prelacteal Feeds ?

infection, delayed lactation, nipple confusion.

5. What are the 10 Steps in BFHI?

i) Have a written breastfeeding policy that is routinely communicated
to all health care staff
ii) Train all healthcare staff in skills necessary to implement this policy.
iii)Inform all pregnant women about the benefits and management of
breastfeeding.
iv)Help mothers initiate breastfeeding within half an hour of birth.
v)Show mothers how to maintain lactation even if they should be
separated from the infants.
vi)Give newborn infants no food or drink other than breast milk,unless
medically indicated
vii)Practice rooming in that is allow mothers and infants to remain
together 24 hours a day.
viii)Encourage breastfeeding on demand.
ix)Give no artificial teats or pacifiers(also called dummies or soothers) to
breastfeeding infants.
x)Foster the establishment of breastfeeding support groups and refer
mothers to them on discharge from the hospital or clinic.

6. Normal eye problems in newborns?

Subconjuctival haemorrhage, NLD obstruction, physiological jaundice.

7. What is Ballards Scoring System of Gestational Maturity

assessment?
A system for estimating newborn gestational age by rating physical
and neuromuscular characteristics of maturity.

8. What are the Skin Findings is Normal New born?

Neonatal pustulosis, erthyma neonatorum, acrocyanosis, milia,
Mongolian spots, sucking callosity in lips, harlequin skin, ebstein pearls,
Bohn’s nodules.

9. What is the Normal Temperature of a Normal New born?

36.7 – 37.4 degree Celsius.

10. What are the Reasons of Physiological Jaundice is a N/B

 Increased production of serum bilirubin due to degradation
immature RBC
 Decreased clearance from immature hepatic mechanism
 Reabsorption from enterohepatic circulation.

12. Why do Normal New born keep eyes closed?

Photophobia

13. Define Microcephaly?

Defined as head circumference below 2 nd standard deviation of the
mean for age, sex, height, and weight. It may be primarily due to
impaired growth of the brain or secondary because of premature fusion
of sutures. It may be associated with mental subnormality and
neuromotor disabilities

14. List the Causes of Microcephaly?

 Rubella, CMV, varicella, Zika infections.
 Exposure to drugs during pregnancy.
 Chromosomal abnormalities
 Cerebral anoxia.
 Severe malnutrition

15. List the Causes of Cataract is N/B?

 Rubella
  CMV
 Toxoplasmosis
 Lowes syndrome
 Galactosemia.

16. List the Causes of Large head is N/B?

 Hydrocephalus
 Familial macrocephaly
 Gangliosidoses.
 Achondroplasia
 Osteoporosis.

17. What is the Contraindications of Bag &Mask Ventilation?

 Meconium aspiration syndrome.
 Diaphragmatic hernia.
 Complete airway obstruction.

18. How do you Resusciate Meconium Aspirated Baby?

Refer to resuscitation chart below.

19. What are the Steps of Neonatal Resuscitation?

Refer to resuscitation chart below.

20. High Risk Pregnancy?

 Eclampsia and pre eclampsia
 Short stature.(140cm)
 Maternal anaemia
 Recurrent abortion history
 GDM
 Pregnancy below 18yrs or more than 35yrs.

21. What is the size of Anterior fontanelle How do you measure it?
 2.1 to 2.9 cm is normal size
 Measured with index and middle finger and asses the cross
diameter of diamond shaped anterior fontanelle.
22. Causes of wide open AF?
 Hypothyroidism
 Increased intracranial pressure.
 Achondroplasia.

23. Explain :
i) Rooting reflex ii) Sucking reflex iii) Moro's
reflex
Rooting Reflex – the baby opens his mouth and turns towards the side of
the stimulus when angle of the mouth is touched. It enables the baby to
instinctively root for nipple during breastfeeding, seen in infants above 34
wks gestation when the baby’s lips are stimulated- sucking is also
stimulated.
Rooting And Sucking Reflex – onset-32 weeks, fully developed by
36wks, disappears at 3-4 monhs of life

Moro’s Reflex – the flexed head is suddenly allowed to drop by about 30

degress. Positive reflex consists of rapid abduction, extension of
upperlimbs, opening of the hands, f/b slower adduction and flexion,
crying.
Onset- 28 to 32 wks, fully developed by 37wks, disappears by 3-4
months of life.

24. What is the Significance of absence of moro’s reflex?

Unilateral absence-erbs palsy,clavicular fracture
Bilareral-CNS cause –birth asphyxia, extreme prematrity.

25. What Advice would you give to a mother at discharge nursery?

 Avoid bottle feeding and pacifiers.
 Regular vaccination should be given.
 Explain the warning signs to mother like excessive unconsolable
cry, noisy breathing, yellowish discoloration of baby, refusal of
feeds.
 Mother should consume nutritious food.

26. What is Exclusive Breast Feeding?

 Breast feeding for six months exclusively without any other food
even water is not given. Vitamin drops are given orally if
prescribed.
 Advantages: it reduces newborn infections, morbidity.provides
good nutrition to the baby.

27. How do you Access the Adequacy of Breast feeding?

breast feeding is adequate if the baby is
 Feeding properly and can sleep well for 2-3hrs.
 Passes urine 6-8times in 24hrs.
 Baby is gaining weight.

28. What are the Advantages' of Breast feeding?

There are advantages to mother and baby.
 Advantages to mother: helps uterine involution, contraception,
reduces risk of breast cancer and ovarian cancer, emotional
bonding.
 Advantages to the baby: nutrional superiority, immunological
superiority, mental growth, protection against illness.
29. What is Ponderal Index?
 The index that is used to assess the degree of foetal wasting.
 Formula of poderal index PI=[weight(grams) / length in cubic
centimeter] * 100
 PI below 10th percentile is IUGR
 PI is less than 2 in symmetrical IUGR

30. What is the Normal

i) Head circumference of N/B : 33-37cm
ii) Length of N/B: 50cm
iii) Weight of N/B: 2.5-3.5kg

31. What are the Vaccine Preventable Diseases ?

 Diphteria, pertussis, tetanus.
 H.influenza
 Hepatitis B
 Measles, mumps, rubella.
 Meningitis
 Polio myelitis.
 Rubella
 Typhoid
 Rabies.
 JE, rotavirus
 There are around 25 vaccine preventable diseases.

32. What are the Immunization given to N/B?

Refer to chart given below.

33. What are the importance of Vit k Administration in N/B?

 To prevent – haemorrhagic disease of newborn.

34. Until what time will you wait for a N/B to pass
i)Urine –it should be passed within 48hrs.
ii) Stool-it should be passed within 24hrs.

35. What are the causes for Delayed Passage of Meconium in N/B?
Hypothyroidism ,anorectal malformations, meconium plug
syndrome, hirschsprungs disease, hypoganglionosis.

36. What is Erythema neonatonim?

 Also called as erythema toxicum.
 In term infants, an erythematous rash (like a flea bite) may appear
on the second day and disappear on its own by 4th day without any
treatment.

37. Differeniate between Caput Succedaneum & Cephalohematoma?

 Refer page 141 in OP Ghai.

38. Normal N/B Stool colour changes after birth, what are
the different types of Stools?

39. Ear Cartilage anamolies is Term New Born?

Microtia, cryptoia, ear tags, protruding ears.stahls ear.

40. Antenatal Diagnostic Tests?

Test conducted or FOETUS- chorionic villi sampling, amniocentasis,
US abdomen pelvis.For MOTHER- triple test,quadruple test for downs
sreening, PAPP-A to detect preeclampsia, glucose tolerance test,glucose
challenge to detect GDM.

41.What are the complications of Hypothermia in N/B?

 Poor weight gain
 Neurological depression.
 Acidosis
 Hypoglycaemia
 Oliguria

42. What is the importance of administration of steroids is lung maturity?

prevents the risk of –RDS, intraventricular haemorrhage,
NEC,reduces
occurrence of PDA.

43. What is the Importance of Iron & Folic Acid is ANC?

Benefits to
i) MOTHER: prevents anaemia, morbidity.
ii) FOETUS: prevents neural tube defects like spina bifida, cleft
palate,
promotes and development of infants. And bone formation.

44. Causes of Respiratory Distress in N/B?

HMD( hyaline membrane disease) , pulmonary hypoplasia, congenital
heart diseases, TOF ,PDA , metabolic acidosis.

45. Causes of Respiratory Distress in Pre-Term?

 RDS (respiratory distress of newborn)
 CDH (congenital diaphragmatic hernia)
 Underdeveloped lungs.

46. Causes of Cyanosis is N/B?

 CARDIAC causes: TOF , tricuspid atresia
 RESPIRATORY causes: foreignbody, cystic fibrosis.
 CNS causes : status epilepticus, GB syndrome.
  METABOLIC causes : Methemeglobinemia.

47. Causes of vomting is N/B?

 Swallowed amniotic fluids
 Aerophagy
 Erratic feeding

48. Causes of Convulsions in N/B?

 Hypoxic ischemic encephalopathy
 Intra cranial hemorrhage
 Intracranial infections
 Cerebral malformations

49. What are Mongolian Spots?

 Also called as congenital dermal melanocytosis
 Benign , flat, congenital, birth mark, irregular in shape.
 Location of spots : lower back , shoulders, buttocks.

50. What is Mastitis Neonatorum?

Characterized By Enlargement Of Breast Tissue In Full Term Infant On
3rd To 4th Day Of Life.
Cause : Ransplacentally Transferred Maternal Hormones.

51. What is the Causes of Bleeding PV in a N/B?

 Withdrawal type of vaginal bleeding is seen on 3rd and 4th day
usually common in female infants.
 Caused due to withdrawal of hormones
Which the baby was exposed in the womb.

52. what are the common anomalies at birth?

cleft lip ,cleft palate, club foot, polydactyly/syndactyly,

53. Indications' of Bag & Mask Ventilation?

 Hypercapnic respiratory failure.
 Hypoxic respiratory failure.
 Apnea
 In surgical procedure.
54. Components of APGAR Score?
Refer the diagram below .

55. What is Phototherapy?

 Treatment with Ultraviolet light used to treat jaundice.
 Converts bilirubin to harmless forms.
 UV light 460-490nm
 Baby eyes and genitals should be covered.
  Mechanism by which bilirubin is converted:
1. configurational isomerization
2. structural isomerization
3. photo oxidation.

57. What is Pro - Longed Laborer?

Total duration of labor is more than 24 hrs. it is called prolonged
labor.
The conditions for prolonged labor :
 In primi- more than 20hrs.
 In para – more than 14hrs.

58. Name Few Teratogenic drugs?

 Alcohol
 Phenytoin
 Thalidomide.
 Isotretinoin
 Methotrexate.

59. Methods of Assessing IUGR is Antenatal Period?

 Doppler flow studies.
 Ultrasound
 Foetal monitoring
 Amniocentasis
 Periodic weighting of mother

60. Define : i) Term –neonate between 37 – 42 weeks

ii) Preterm – neonate born before 37 weeks.
iii) Post term- neonate born after 42 weeks.
iv) IUGR – it is caused when the foetus fails to grow in
normal trajectory.

1. Symmetrical : the insult to foetal growth occurs early, then the size of
the head, body weight, length occurs uniformly.

2. Asymmetrical: insult to foetal growth occurs in late period. So the

brain sparing occurs, and hence the head circumference is relatively
preserved.

61.Complications of infant of diabetic mother ?

 Macrosomia(large baby),birthinjuries
 Neonatal Hypoglycaemia, Hypocalcaemia and
hypomagnesemia,polycythemia ,jaundice
 Respiratory distress.
 Neural tube defects (sacral agenesis) cardiac
anomalis(asymmetrical septal hypertrophy,TGA)
62. Define Hypoglycemia of Newborn ?

It is serum glucose concentration, Less than 40mg/dl in term

neonates.
Less than 30mg/dl in preterm neonates.

63. Define Newborn Indications for Phototherapy ?

Bilirubin level (mg/dl) hrs of birth

10 24
13 48
15 72
18 96

Pg no. 174 fig 8.51 in OP Ghai.

64. Indications Exchange Transaction ?

Double volume exchange transfusion,indication at birth in Rh isomerized
infant is:
 Cord bilirubin – more than 5mg/dl
 Cord hb- less than 10mg/dl

Refer pg.no 175 fig. 8.52

APGAR SCORING SYSTEM
NEW BALLARDS SCORING SYSTEM :
Viva X ray spotters
1) Basic information : Name
: Date
: Side ® or left side ( see the mark R)
: Part exposed

2) PA View or AP View :

Standard X – Ray Are PA View ( Taken With The Film Against The
Front Of The Patients Chest And The X – Ray Tube 2 Meters Behind The
Patient ) Cardiac Shadow Is Prominent

Ap View Sick Patients ( Can See Scapula Overlying The Lung

Fields, Vertebrae Appear Prominent )

3) Plain X-Ray / Contrast X-Ray

4) Orientation Rotation
Normally Medial Ends Of The Clavicle Should Lie Equidistant From
The Midline Of The Body Of The 4th Or 5th Thoracic Vertebra.
If The Medial End Overlaps The Body Of 4th Or 5th Thoracic Vertebra, It
Signifies Rotation.
Tilt – Clavicle Not At Same Level .

5) Penetration :

Ideal Just Able To See Veretebral Body Behind The Cardiac

Shadow.
3-4 Tracheal Rings Should Be Seen
Failure To See The Thoracic Veretral Bodies And Pedicles
Indicates Inadequate X-Ray Penetration.

Inflation :

* Inspiration Diaphragm At 8- 9th Rib Posteriorly At 6th Rib

Anteriorly

* Hyperinflation Flattening Of Diaphragm, Tubular Heart , Ribs

Spaces More Than 7, Hyperluscent Lung Fields.

* Usually Right Dome Of Diaphragm At A Higher Level Than Left

Dome
Of Diaphragm .
 Reading

Read Chest X-Ray Systematically

Heart
Mediastinum
Lung fields
Vascular markings
Diaphragm
Soft tissues
Bones
Right atrium
Rt heart border SVC
RV
IVC
Left heart border Aortic knuckle
Left pulmonary trunk
Left atrium
Left ventricle

Hila – Consists Vascular, Bronchial , Lymphoglandular Components

(N) Cardio Thoracic Ratio Is 0.5 In PA View
CT Ratio A+B< 0. 5, In New Born – 0.6
C
Lung Fields :
Upper Zone : Up To 2 nd Costal Cartilage
Middle Zone : From 2 nd To 4th Costal Cartilage
Lower Zone : From 4 th Costal Cartilage Till The Base Of The Lung.
In Neonates And Young Children Thymic Shadow Overlaps Upper
Borders Of Cardiac Shadow.
Sternal Angle - 2nd Rib

Tracheal Bifurcation Is Seen At The Upper Part Of Cardiac Vascular

Shadow .
Carinal Angle 60 - 750

60 – 75
LOBES OF THE LUNG :

Upper
Right side 3lobes Middle
Lower

Left side 2 lobes Upper

Lower
LUNG FISSURES :

* Main Fissure From 2 nd Dorsal Vertebra ( T4 Position ) , 5th

Rib At Midaxillary Line And Up To 6 th Costochondral Junction.

* Horizantal Fissure 4th Costal Cartilage , 5th Rib At Midaxillary

Line To Join Oblique Fissure .

LUNG SURFACE ANATOMY :

 1- ½ inch Above Clavicle

 6th 8th 10th Rib In Midclavicular , Mid Axillary And
Scapular Lines .
 Hilum – 4th 5th 6th Thoracic Vertebrae
 Pleura – 8th 10th 12th Ribs In Mcl .MA, Sub scapular line
 Exam X-ray

1) Diaphramatic Hernia :

a) Usually Seen In The Left Side

B) Left Dome Of Diaphragm Not Visualized
C) Bowel Loops Are Seen In The Left Lung Fields
D) Causes Respiratory Distress At Birth
E) Causes Mediastinal Shift To Right Side
F) Bag and Mask Ventilation Is Contraindicated
G) Insert Ng Tube To Decompress The Stomach
H) Needs Surgical Correction
I) Associated With Pulmonary Hypoplasia , May Need I NO At Birth.

3)Consolidation :

a) Usually Due To Pneumonia

B) Mention The Lobe Involved
C) Read About Pneumonia –> Theory Signs And Symptoms Of
Consolidation.
4) Pleural effusion :

a) Opacity seen along the Lung Margins ->Synpneumonic

Effusion .
B) Costophrenic Angle is Obliterated In Mod-Severe Effusion Whole
Thorax Is Opaque.
C) Fullness On That Particular Side Mediastinal Shift To Opposite Side
Of Effusion.
D) Can See ICD If Inserted
E) Read About Causes Of Effusion
F) Difference Between Transudate And Exudates
G) Management Of Pleural Effusion
H) (N) Fluid In Pleural Cavity 50ml
I) Fluid Level > 150ml Is Radiologically Detectable .

4) Cardiomegaly:

Check The CT Ratio , If> 0.5, New Born – 0.6(60%) Then We Call It As
Cardiomegaly.
Causes:
A) Congestive Cardiac Failure Left Side Heart Failure Due To
Congenital Heart Disease .
Acyanotic ( VSD, PDA, ASD), Cyanotic (TAPVC /TGA)
B) Myocarditis
C)Pericardial Effusion
D)Cardiomyopathy

5) Lung Abscess :

a) Cavity Filled With Fluid

Causes Necrotizing Pneumonias Caused By , Staphylococcus
Aureus K.P Pneumonia , Anaerobic Bacteria .
* Foreign Bodies
* Bronchial Cyst / Stenosis
* Rx Antibiotics , Physiotherapy , Surgical Resection

6) Hydropneumothorax :

a) Fluid level .
b) Air (black) along the lung borders above the fluid level.
Causes :
* Rupture of Pneumatoceles (Staph aureus )
* Thoracic Trauma (Penetrating Injuries )
 6) Bronchiectasis :

Tangential View
* Honey Combing Of Involved Area
* Tram Track Opacities In Cylindrical Bronchiectasis
* Air Fluid Level Cystic Bronchiectasis

Causes :
Bronchitis Post Measles ,Post Pertussis ,Post Pertussis, Cystic
Fibrosis, Pneumonities , Congenital Disorders Bronchomalacia
Bronchial Cyst , Sequestered Lung .
Rx- Postural Drainage Of Secretions Physiotherapy Surgical Resection

Clinical features :
Recurrent LRTI , Loss Of Appetite, Irritability, Poor Weight Gain ,
Clubbing, Cough With Copious Mucopurulent Expectoration,
Postural Variation Blood Tinged Sputum.

7)Miliary T.B :

Multiple lesions of size 2-5 mm organism mycobacterium

tuberculosis .
Predisposing factors
Malnutrition
Immunodeficiency HIV
Steroid , DM
Over crowding

Cat I :
( SPUTUM +Ve ) Rx : 2HRZE+4HR
Cat II : 2HRZES ,1 HRZE , 5 HRE
Relapse , Re failure ,Interrupted Rx.

DDS : Tuberculosis
: Fungal Histoplasmosis
: Viral Varicella pneumonia
: Metastatic Osteosarcoma
: Interstitial lung disease pneumoconiosis
: Hypersensitivity pneumonitis
: LCH, Pulmonary Alveolar proteinosis .
Rickets

Radiological Findings :

1) Widening Of Distal Ends Of Radius And Ulna.

2) Cupping – Saucer Like Depression (Cuplike ).
3) Fraying – Blurring Of Margins Of Metaphysis Of Distal Ends.
4) Splaying – Widening Of The Metaphysic.
5) Increased Distance Between Distal Ends Of Forearm Bones And
Metacarpal Bones.
6) Decreased Bone Densities Of Shaft Of Bones Osteopenia .
7) Green Stick Fracture.
8) Periosteal Reaction ( Lifting ) – Due To Excess Of Asteoid Lying
Under The Periosteum .
Healed Rickets :

1) Zone Of Preparatory Calcification - White Line Of Calcification –

1st Sign Of Healing.
2) Well Calcified Rachitic Metaphysis

Treatment ofrickets

6,00,000 IU vit D single dose oral or I.M

Repeat X- ray after 3 – 4 weeks, if no Response repeat 6,00,000 IU if Vit

D one Dose.

If no response to 2 nd dose Called as resistant rickets

(N) Daily requirement of Vit D 400 I.U.

* What is the active form of vit D 1,25,DHCC

* Where is it activated.

1st 25 (OH) Liver

2nd 1 (OH) Kidney

Mechanism of action: - calcium and phosphorous deposition

in bone matrix .

SCURVY X-RAY FEATURES

 Clinical joints are tender due to bleeding
 Pencil thin cortex
 Ground glass appearance
 Thinning of cortex and sharp out lined epiphyseal ends
 White lines of Frenkel , an irregular thickened line at the
metaphysis.
 Trummerfeld zone and pelken spur ( metaphysic open )
 Wimberger rings
Rx 100-200 mg of vitamin C

`
 Nutrition viva spotters
Food Values

• 1 cup – 100 ml or 100 gms

• 1 teas spoon – 5 ml or 5 gm
• 1 table spoon – 15 ml or 15 gm (3 teasspoon)
• 1 tumbler – 200 ml (2 cup)

Food groups and RDA

Cereals – Rice, Ragi, Wheat , Maize

Every 100 gms contain
Protein (gms) Energy(kcal)
Rice 7 350
Ragi 7 330
wheat 11 350
maize 11 340

1 Cereals lack lysine except rice

2 Wheat lacks lysine and threonine
3 Ragi is rich in calcium and iron
4 Cereals do not contain Vit A and c except maize –alpha carotene
5 Cereals contain 7 -11 gm% protein and 2-5% fat

Pulses (legumes)
Every 100 gms contain
Protein(gms) Energy(kcal)
Bengal gram 17 360
Black gram 24 350
Green gram 24 340
Red gram 22 340

• Rich sources of protein(upto 22 gm%)

• Lack Vit A and C
• Deficient in methionine
• Cereal –pulse combination leads to supplementary effect of
proteins

Vegetables
• Rich source of calcium , Iron, beta carotene-carrot (deficiency
causes night blindness), vitamin C and B complex

Fruits
• Source of vitamins and fibre
• Green ,yellow and orange fruits contain beta carotene
 • Amla ,citrus(lemon,orange) fruits and guava are rich in vitamin C
(deficiency causes Scurvy)
• Dates- Iron

Fats ,oils ,nuts,oil seeds

• They are the good sources of protein, vitamins and fats
Fats are the rich concentrates of energy

Egg
60 gm/6 gm protein/6gm fat/30 mg calcium/1.5 mg iron
• Also called as reference protein
• Rich in protein, vitamins and fat
• Deficient in carbohydrate and Vit C

Milk and milk products

 Good source of Protein, Calcium and vitamins
 Deficient in Iron and vitamin C

Human milk - 1.1 gmprotein / 3.4 fat / 65 k calories

Cows milk - 3.2/4.1/67
Buffalo milk – 4.3/6.5/117

Vaccines viva spotters

GENERAL INFORMATION OF VACCINES
LIVE VACCINES :BCG ,OPV ,MEASLES ,MMR ,CHICKENPOX,JE
VACCINE , HEPATITIS A VACCINE, ROTAVIRUS
INTRADERMAL VACCINES : BCG
ORAL VACCINES : OPV, ROTAVIRUS
SUBCUTANEOUS VACCINES :MMR ,MEASLES , CHICKENPOX ,
HEPATITIS A , JE
INSTRUCTIONS DURING IMMUNISATION
 Whenever multiple vaccines are to be given simultaneously they
should be given within 24 hrs
 The minimum interval between 2 doses of vaccines is usually 4
weeks
 Any number of vaccines can be given on a single day .
 Patients to be observed for allergic reaction for 15 to 20 mins after
receiving immunization
STORAGE OF VACCINES
 Among the vaccines polio is the most sensitive to heat, requiring
storage at minus 20 degrees C.
 Vaccines which must be stored in freezer compartment are :polio
and measles,MMR.BCG
 Vaccines must be stored at 2-8 C but never allowed to freeze are:
0

typhoid ,DPT , tetanus

  Vaccines sensitive to heat and light hence supplied in brown
bottles:-BCG ,measles andMMR
INDIVIDUAL VACCINES
1)Bacillus Calmette Guérin (BCG) vaccine
 Strain used :-Copenhagen (Danish 1331)
 Pasteur
 Given at birth, catch up till 5 years.
 Dose / Route: 0.1 ml; intradermal
 Site:- Left upper arm at insertion of deltoid

 Discard unused vaccine after 4 hours(if used beyond 4-6 hours

toxic shock syndrome can occur )
 Adverse reactions : Local ulceration or discharging sinus;
ipsilateral axillary/cervical lymphadenopathy; disseminated
infection, osteomyelitis or scrofuloderma (in immunodeficient
recipient)
 Contraindication in Cellular immunodeficiency:- symptomatic HIV.
 Following vaccination 4-6 wks induration develops,
6-8 wks papule develops,
8-10wks vesicle develops,
10-12 wks vesicle will break open and lead
the scar

2)Pneumococcal conjugate vaccines

 Dose, route/site:- 0.5 ml intramuscular, Anterolateral thigh
 Given Three doses at 6 ,10 &14 weeks and one booster at 18
months.
 Catch up:- At 7-11 months Two doses >4 weeks apart and one
booster at 18 mo
 1-2 years :Two doses 1 month apart
 2-5 years: one dose;
 >5 years: one dose, only if in high risk category
 Adverse reactions:- Fever, local pain, soreness, malaise
 Contraindication :-Anaphylaxis after previous dose
 Storage 2-8°C; do not freeze

3)Oral poliovirus (OPV) vaccine

 Dose, route :- live attenuated oral vaccine; Two drops
 Strain used:- sabin strain
 Schedule: at birth (zero dose); At 6, 10 and 14 weeks and two doses
of booster at 18 months and 5 yr give additional doses on NIDs
and SIAs catch up till 5 yr
  Adverse reactions :- vaccine associated paralytic poliomyelitis
 Contraindications :Inherited or acquired immunodeficiency
4)Haemophilus influenzae b vaccine
Dose, route ,site :-0.5 ml intramuscularat Anterolateral thigh
Given: At 6, 10 and 14 weeks and booster at 18 months
Catch up :-At 6-12 months: Two doses > 1 month apart with one booster
at 18 months;
Adverse reactions Fever, rash, local pain or redness
Contraindication Hypersensitivity to previous dose

5)Diphtheria toxoid, tetanus toxoid and killed whole cell pertussis (DTwP)
or acellular pertussis (DTaP) vaccine
Dose, route 0.5 ml; intramuscular
Site Anterolateral aspect of mid-thigh (avoid gluteal region: risk of sciatic
nerve injury; inadequate response)
Given at 6, 10 and 14 weeks (primary); and booster at 18 months and 5
years
Catch up <7 yr: DTP or DTWP at 0, 1 and 6 months
Catch up >7 yr: Tdap at 0 months; Td at 1 and 6 months
Adverse reactions Local pain, swelling, fever (DTwP>DTaP)
Contraindications: (i) Progressive neurological disease(administer DT or
dT instead); (ii) anaphylaxis after previous dose; (iii) encephalopathy
within 7 days of previous dose
Precautions: Previous dose associated with (i) fever >40.5°C within 48 hr;
(ii) collapse (hypotonic-hyporesponsive episode)
within 48 hr; (iii) persistent inconsolable crying for >3 hr within
48 hr; (iv) seizures within 72 hr
Storage 2-8°C;
6)Typhoid conjugate vaccine
nd
Dose/route:-5 ml intramuscular at 9 months and 2 dose after 1 year
(protection upto 10 years)

7)Typhoid vi capsular polysaccharide vaccine

Dose, route:0.5 ml, intramuscular at Anterolateral thigh
Adverse actions: Local pain, swelling, redness;
One dose at 2 yr; repeat every 3 yr till 12 years

8)Varicella vaccine
Dose, route 0.5 ml subcutaneously
Site Anterolateral thigh or upper arm
Given:Two doses at 15-18 mo and 4-6 yr; second dose may be given >3
mo after the first dose
Adverse reactions Fever, rash, local pain or redness
Contraindications Anaphylaxis after previous dose; lymphoma
immunodeficiency;

9)Rotavirus vaccine
Dose, route oral
Schedule 2 doses at 6-14 weeks >4 weeks apart; maximum age <15
weeks for the first dose and <8 months for the final dose, do not begin
schedule at >15 weeks
Adverse reactions Intussusception (rare)
Contraindication Past history of intussusception; severe
immunodeficiency
Precaution Postpone vaccination during ongoing diarrhea or moderate
illness

10)Measles vaccine
Route :0.5ml subcutaneous
Schedule At 9 months (at 6 months during outbreaks; revaccinate at 9
nd
months,)and 2 dose at 15 months
10)MMR
Route :0.5ml subcutaneous
Schedule At 9 months (at 6 months during outbreaks; revaccinate at 9
nd rd
months,)and 2 dose at 15 months and 3 dose at 5 years
Adverse reactions Fever, transient macular rash ('measles like' illness) 5-
10 days later
Contraindications (i) Immunosuppressive therapy (e.g.alkylating agents,
high dose corticosteroids); (ii) malignancy; (iii) severe immunodeficiency
(e.g. advanced HIV);(iv) untreated tuberculosis within 4-6 hrs of
reconstitution

11)Hepatitis B vaccine
Dose, route :-0.5 ml (1 ml in adults and in children receiving
hemodialysis); intramuscular
Site :-Anterolateral thigh (deltoid in adults);avoid gluteal region
Schedule:- At birth, 6 ,10 &14 week
Catch up :-Complete 3 doses series; second dose is given 4 weeks and
third dose >8 weeks after previous dose
Adverse reactions:- Local soreness; fever; fatigue
Storage:- 2-8°C; do not freeze
Contraindication :-Anaphylaxis after previous dose
*Alterative schedules :-(i) birth, 1 and 6 months ii) birth, 6 and 14 weeks
(iii) birth, 6, 10 and 14 weeks: (iv) 6, 10 and 14 weeks

12)Inactivated influenza vaccine

Dose, route :-0.5 ml > 3 years(0.25 ml <3 yr);intradermal(govt)&
intramuscular(IAP) at the Anterolateral thigh
Schedule:- IAP (Only in high-risk categories) It is given at 6-7 months ,1
month apart and every year 1 dose thereafter.
First time vaccination: Two dose 6 months
Adverse reactions:-Local pain, redness; anaphylaxis
Contraindication:- Anaphylaxis after previous dose
13)Inactivated poliovirus (IPV) vaccine
Dose, route:- 0.5 ml; intramuscular ;Strain used:- salk strain
Schedule: National Program one dose at 14 weeks.
IAP:- 3 doses of IPV at 6, 10 and 14 weeks, another booster of IPV at 15-
18 months Catch up:-IPV catch up schedule:2 doses at 2 months apart,
booster after 6 months dose
Contraindication :-immunocompromised babies Storage 2-8°C; sensitive
to light.

14)Hepatitis A vaccine
Two types:-i)Inactivated- derived from HM 175/ GBM strains
nd st
Dose/route :-2 drops(2 dose 6-18 months after the 1
dose)/Intramuscular
Adverse reactions:-local pain and swelling
ii) live attenuated vaccine:-derived from H2 strains of virus attenuated
after serial passage in human diploid cell (KMB17 cell line )
Dose/Route : single dose (WHO)
2 Doses live attenuated (IAP); 0.5 ml subcutaneous
nd st
Schedule:- 2 dose 6-18 months after the 1 dose
* Minimum age for both vaccine -12 months
IAP recommended vaccinesfor adolescents

Vaccine Schedule
Tadp/td* 10 yrs
HPV 10-12yrs

IAP recommendations for catch up immunization in adolescents

Vaccine Schedule
MMR 2 doses at 4 to 8 weeks interval
Hep B 3 doses at 0 , 1 and 6 months
Hep A 2 doses at 0 and 6 months
Typhoid 1 dose every 3 years
Varicella 2 doses at 4 to 8 weeks interval

IAP recommendations for immunization of HIV infected children

Vaccine Asymptomatic Symptomatic
BCG YES(at birth) No
DTwP/DTaP/TT/Td/TdaP Yes, as per routine schedule at 6,10,14 wks.18
months and 5 years
Polio vaccines IPV at 6,10,14 wks.12-18 months and 5 years
If indicated IPV to household contacts
If IPV is not affordable, OPV should be given.
Measles Yes at 9 months Yes,if CD4+ count >15%
MMR Yes at 15 months Yes,if CD4+ count >15%
and 5 years
Hep B Yes, at 0,1 and 6 Yes, four doses,double
months dose,check for
seroconversion and give
regular boosters
Hib Yes,as per routine schedule at 6w,10w,14w and 12 to
18 months.
Pneumococcal Vaccines( PCV-yes,as per routine schedule at 6w.10w,14w and
PCV and PPSV23) 12 to 15 months
nd
PPSV 23 – 1 dose 2 months after PCV,2 dose 5
yrs after first dose(not more than 2 doses)
Inactivated influenza Yes,as per routine schedule beginning at 6 months,
vaccine revaccination every year
Rotavirus vaccine Insufficient data to recommend
Hep A vaccine Yes Yes,check for seroconversion
boosters if needed
Varicella vaccine Yes, 2doses at 4 to Yes,if CD 4 count >/= 15% 2
12 weeks interval doses at 4 to 12 weeks apart
Vi-typhoid/Vi conjugate Yes , as per routine schedule
vaccine
HPV vaccine Yes females only as per routine schedule of 3 doses
at 0,1-2 and 6 months, starting at 10 years of age
INSTRUMENTS VIVA SPOTTERS
1.Infant feeding tube/Nasogastric tube

Description :-It is a plastic tube with a blunt tip for non traumatic
insertion, two lateral eyes for efficient aspiration and administration.
The tube is marked at 20cm from the distal end for accurate placement
into the abdomen.
The total length is 52cms .
The radiopaque line provided thriughtout the tube for xray visualization
Uses
Diagnostic uses
1. Diagnosis of trachea oesophageal fistula duodenal atresia and
choanal atresia
2. Diagnosis of tuberculosis
3. Internal bleeding in stomach and upper GI.

Therapeutic
1. Nasogastric Feeding
2. To remove gastric content in poisioning
3. Administration of drug
4. Meconium stomach wash
2.Meter dose inhaler

Description:-MDI consist of 3 major components

1. Canister(aluminium or stainless steel )
2. Metering valve:-which allows metered quantity of
the formulation to be dispensed with each actuation
3. Mouth piece :-which allows the patient to operates
the device and directs the aerosol into the patients
lung
Require considerable cooperation i.e press and breath.
After actuation the drug comes out at a pressure and a significant amt of
the drug gets deposited in the oropharynx
Uses for exacerbation and maintaince therapy.
Not possible in young children
Steps to use of Meter dose inhaler
 Step 1:-Remove the cap and shake the inhaler in vertical direction.
 Step 2 :-Breathe out gently.Put mouth piece in mouth and at start
of inspiration(slow and deep) press canister down and continue to
inhale deeply.
 Step 3:-Hold the breathe for10 sec or as long as possible, the
breathe out slowly
 Step 4:-Wait for few sec before repeating the inhalation once again.
3.SPACER

Description :-it is bottle shaped plastic device which has a mouth

piece at one end and the other end has an opening which the MDI
can be attached.
Steps to use a spacer
Step 1 remove cap and shake inhaler and insert into the spacer device
.
Step 2:place mouth piece or spacer in the mouth
Step 3 start breathing in and out gently and observe movements of
valve
Step 4 once the breathing pattern is established press canister and
continue to breathe 5-10 times (tidal breathing)
Step 5 remove the device from mouth and wait for 30 sec before
repeating once again
Advantages of spacer
Large proportion of medicine being deposited in the lung , with less
impaction in the opropharynx
Overcome the problems of poor technique and cooperation of
actuation and inspiration
Uses for young children

Disadvantages
Bulky
Relatively costly
4.Endotracheal tube

Types:-
CUFFED UNCUFFED

Children > 8 years Children < 8 years

Cuff when inflated Uncuffed ET tube are used

maintains the ET because the narrow
tube in proper subglottic area performs the
position and function of a cuff and
prevents aspiartion prevents the ET tube from
of contents from slipping .
GI tract into
Respiratory tract

Description :-
Et tube are curved tubes.
Proximal end :-15 mm adapter (connector) which fits to ventilator
or ambu bag
The curved tube contains markings in cms which facilitates the
placement of ET tube.
 The black line:- a vocal cord guide which should be placed at the
level of opening of the vocal cord so the tip of the ET tube is
positioned above the bifurcation in the trachea.
Distal end :- has murphy’s eye opening in the lateral wall, which
prevents complete blockage of ET tube in case the distal end is
impacted with secretions or blood etc.
Size :-from 2 mm to 16 mm (internal diameter)
The size of cuffed ET tube is taken to be 0.5mm less than that of
uncuffed ET tube
The size of the ET tube depends on the weight or gestational age of the
baby
Inner diameter of the Weight (gms) Gestational age ( in
tube (mm) weeks )
2.5 <1000 <28
3.0 1000-2000 28-34
3.5 2000-3000 34-38
4.0 >3000 >38

After 2 years, size of the ET tube = (age in yrs/ 4)+4

Uses :- for mechanical ventilation

1) For intermittant positive pressure ventilation
2) During resusitication
3) Direct suctioning of trachea in meconium aspiration
4) In angioneurotic edema
 Complication
1) Mechanical trauma to tongue ,teeth, palate, pharynx and larynx
2) Stimulation of posterior pharyngeal wall leading to coughing
,vomiting and vasovagal episode with resultant hypoxia,
bradycardia
3) Prolonged intubation may cause pressure necrosis of laryngeal
structures leading to persistent hoarseness.
4) Pneumothorax

5.laryngoscope:
 Description:- It is an instrument used for intubation.
It consist of two parts : blade and the handle
The handle contains the battery container which act as an energy source
for light source
The blades are of two varities :-straight and curved
Straight blade is used to depress the tongue
Curved blade is used to pushes the epiglottis to one side to visualize the
glottis
In infants the straight blade is preffered
In older children( > 8 years )curved blade is preferred
Size:-available in different numbers 0,1,2,3,4.
For preterm babies size 0
Term babies size 1
Indications
In infants prior to endotracheal intubation in:-
1. Neonatal asphyxia
2. Meconium aspiration
3. Respiratory distress syndrome
4. Trachea oesophageal fistula
5. Mechanical ventilation
In older children prior to endotracheal intubation
1. resuscitation
2. during administration of general anaesthesia
3. epiglottitis
4. kerosene poisioning

CONTRAINDICATIONS
diseases or injuries of cervical spine
moderate or marked respiratory obstruction.

6.Airway
Types :-1. Orpharyngeal
2.Nasopharyngeal
oropharyngeal airway it is a curved tubular medical device of rubber
plastic or metal placed in the oropharynx during G A or impaired level of
consciousness helps to maintain or an open airway by preventing the
tongue from obstructing the epiglottis
It is J shaped tube with a flang on the long of the J to keep the individual
from swallowing the tube.
Correct size of OPA is choosen by measuring from the first incisors to
the angle of the jaw.

Indication
In unconsicious patient when the tongue is obstructing the airway

Contraindication
Intact gag reflex
Foreign body obstructing the airway

Procedure
Airway is inserted in the person mouth upside down gently
Once he contact is made with the back of throat, the airway is rotated
180 degrees for easy insertion, securing the tongue

7.AMBU bag(artificial manual breathing unit bag)

Description:-the parts of ambu bag:-
1. Mask or mouth piece
2. Pressure gauze
3. Oxygen reservoir bag
4. Oxygen inlet
5. Compressible self reinflating
ventilation bag

Size :-based on volume they are divided into 2 types

1.preterm bag
2. Term bag

Indications
 Respiratory failure
 Failure of ventilation
 Failure of oxygenation
 Failed intubation
 Elective ventilation in the operating room
Contraindications
Incase of complete upper airway obstruction
Relatively contraindicated after paralysis and induction (due to
increased risk of aspiration)
Diaphragmatic hernia
Meconium stained liquor
Technique
1.Place the patient in sniffing position – it allows for greater occipito
atlanto axial angulation, prevents falling of tongue thus prevents
obstruction of upper airway.
2. thumb + index to maintain face seal & middle finger under
mandibular Symphysis. Ring and little finger under the angle of
mandible.

8. LUMBAR PUNCTURE NEEDLE

 It is a needle used for lumbar puncture procedure.
Size of the needle: <1 year: 1.5 in
1 year to middle childhood: 2.5 inches
Older children and adults: 3.5 inches
Position of the patient: lateral recumbent position.
Site: in the intervertebral space between L3 & L4 or L4 & L5.
Structure pierced during lumbar puncture:
 Skin
 Subcutaneous fat
 Supra spinal ligament
 Inter spinal ligament
 Ligamentum flavum
 dura mater
 Arachnoid matter
Indication:
 For diagnosis of infectious, inflammatory, and neoplastic diseases
affecting the central nervous system by analysis of CSF. (meningitis)
 Diagnosis of subarachnoid hemorrhage, hydrocephalus, benign
intracranial hypertension.
 Also helps in detect the presence of malignant cells in the CSF, as in
carcinomatous meningitis or medulloblastoma.
 Also useful in injection of medications into CSF (intrathecally) for
spinal anesthesia or chemotherapy.
Contraindications:
 Idiopathic increased intracranial pressure(ICP)
 Bleeding diathesis (coagulopathy, decreased platelet count)
 Vertebral deformities (scoliosis or kyphosis)
Adverse effects
 Headache with nausea
 Infection.
 Paresthesia
 Serious complications are rare (spinal or epidural bleeding, adhesive
arachnoiditis, trauma to spinal cord or spinal nerve roots)
 Cerebral herniation.
Bone marrow aspiration needle


 Description:-it consist of a
a) stillete
b)trocar
c)cannula
 a adjustable side guard:-it helps in adjusting the depth of penetration
of the needle which is located 2 cms from the tip.
 Types :-Vim silverman needle
 Jamshidi’s
 Indications
 diagnostic
1. red cell disorders:-megaloblastic anaemia and pure cell aplasia
2. WBC disorders :- Leukemia
3. Platelets:-Idiopathic thrombocytic purpura
4. Aplastic anaemia
5. Infections:-kala azar
6. Storage disorder:-Gauchers disease and Neimannpicks disease
7. In evaluating PUO
8. Myeloproliferative and myleodysplastic disorders
9. Any suspicion of metastasis
 Therapeutic indications
 Bone marrow transplantation
 Site :->1 year iliac crust
 <1 year :- proximal tibia ,medial to tibial tuberosity
 To prevent injuries to pelvic structure in plants
Complication :-
Bleeding and pain at the site
Bone injury with fracture of iliac crest
Subcutaneous infection
Osteomyelitis.
Tuberculin syringe

Description:-this syringe is a simple pump consisting of a plunger that

fits the tube to assist pushing liquids. It holds upto 0.3 ml to 1ml of the
medication.
It is used for subcutaneous injections.
Advantage:-it causes less pain as it has a finer grip.

Tuning fork

Description :-it is a fork shaped acoustic resonator instrument

consisting of a stem, two prongs and a foot piece.
It is used to produce a fixed tone.

Frequencies used:-128,256, 512,1024,Hz

512hz is most commonly used for Weber test and rinne test
 Peak flow meter

This device records the peak or maximal flow during a forced

expiratory manoeuvre (PEFR) measures how well air moves out of the
lungs (asthma)
It is not useful in children <5 years of age
Green zone
Yellow zone
Red zone

CNS EXAMINATION
Higher mental function
Mental status
Consciousness :-
Level of consciousness
Drowsy:- sleepy but arousable by ordinary stimulus or loud sound.
Stupor:- responds only to strong noxious stimuli.
Obtundation:- stage between drowsiness and delirium.
Delirium :- confusional state, responds incoherently.
Light coma :- child may be kept aroused as long the noxious stimuli is applied.
Deep coma:- responds to noxious stimulus may be due to decortications or
decereberation.
Flaccid coma:- no response whatsoever might be ,total flaccidity with no reflexes.

GLASGOW COMA SCALE

EYE OPENING(E) VERBAL MOTOR RESPONSE

4 Spontaneous 5 normal 6 normal
3 to call 4 sentences but not fully 5 localises pain
2 to pain oriented 4 withrawal to pain but not
1 none 3 only words proper localisation
2 no words only sounds 3 decortication
1 none 2 decerbration
1 none

Total score :-15

Minimum score:- 3

II)ATTENTION
Attention is the ability to focus and maintain one’s consciousness on a particular
stimulus or a task without being distracted by any other stimulus.
Assess
Ask the patient to repeat short list of objects or numbers,inability to repeat correctly 6
numbers or items or more indicates a probable attention deficit.
III) ORIENTATION
Refers to the patient’s awareness of self and certain realities of the present.
It also refers to as orientation of person, place and time.
PERSON what is your name?
How old are you?
PLACE:- where are you right now?
Which place do you live in ?
TIME:- what is today date and time?
What day of the week it is?
IV)SPEECH OR LANGUAGE
It assess the cognitive state of the child
It should be assessed in the following domains:-
SPONTANEOUS SPEECH : Deficient spontaneous speech is when there is poverty
of thought or expression or impairment of rhythm.
FLUENCY:-word outflow that is free from pauses or breaks
COMPREHENSION :- ability of a child to describe appropriate and correct meaning
to words and sentences.
Repetition :-ability to repeat single word or list of words without errors.Difficulty of
repetition results from lesion involving the arcuate faciculus on the left side.
Naming and word finding:-is it child able to name the object correctly or common
objects of daily use ?
Reading :- is the child able to comprehend written language symbols ie A B C
Writing :- ability to use written language copying:- ask the child to copy a geometric
figure
V)LEARNING AND MEMORY
It depends on the integrity of the hippocampus and amygdaloid nucleus
Immediate recall
Narrate a small story, ask the child to repeat the same with atleast half the details
correctly.
short term memory
what did you have for breakfast?
Give a short list of the words or objects and ask he/ she to repeat after 10 -15
minutes.
long term memory
Enquire about the past with questions like when and which school are studying in?

VI)CORTICAL OR COGNITIVE FUNCTION

Assessed by
Asking common general knowledge questions as appropriate for the age of the child
Calculation ability – serial seven subtraction test and other simple sums.
Gnosia and agnosia (in ability to recognise the stimuli such as visual , auditory or
olfactory).

PRAXIA AND APRAXIA: Praxis refers to carrying out an action.Apraxia are

characterized by inability to perform motor behavior.

VII) MOOD, AFFECT AND THOUGHT CONTENT

Mood refers to feeling and emotions evoked by situations , events and other
occurrences in daily life.
Affect refers to somatic or autonomic behaviours that are used to convey a mood or
emotion.
Thought content refers to fullness and organisation of the patients thinking as
reflected in conversation or behaviour.
These are assessed only in rare and special conditions.
DELIRIUM: It is a state of confusion with disordered perceptions and decreased
attention span and inappropriate response to stimuli.
BEHAVIOR
Eg: Avoidance of eye contact and self engrossed : Autistic behavior.
Self mutilating – Lesch-Nyhan syndrome.

Head to toe examination

Head –
Check for abnormal shape and size
Assymetrical shape:
3. dolichocephaly(if the AP diameter more than the width, sagittal suture closes
earlier)
4. brachycephaly(premature closure of coronal suture)
Head control, head tilt ( poor vision in one eye ,unilateral hearing loss, torticollis)
head bobbing(respiratory failure meningeal irritation, kernicterus, hemorrhage)

SCALP:
 scalp swelling(dermoid,histiocytosis,organised cephal hematoma),
 see for fungal and parasitic infection of the scalp.
 Anterior frontanelle:A diamond shaped gap between frontal and parietal
bones is called the Anterior frontanelle
Method of examination:
a)Examine the child at 24hrs of age when normal separation of sutures has
taken place.
b)size of the AF(length+width)/2 and plot on normogram.Mean size of AF is
2.1 cms
c)AF closes by 9-18 months

. NORMOGRAM FOR PLOTTING

ANTERIOR FRONTANELLE.
 early closure-Microcephaly,craniosynostosis,hyperthyroidism
 Delayed closure-hydrocephalus,rickets,hypothyroidism,downs syndrome.

Posterior frontanelle (lambdoid frontanelle,occipital frontanelle):

Triangular space between two parietal and occipital bones is called
posterior frontanelle.
a) Posterior frontanelle is either closed at birth or closes at 2 months.
b)Wide open posterior frontanelle: hydrocephalus and hypothyroidism.

 Wide open sutures: dwarfism,osteogeneis imperfect.

 Macrocephaly- An occipitofrontal circumference plotting >90th percentile
for that age,sex,gestational age and ethnic group. Seen in conditions like
hydrocephalus ,megencephaly((tay-sachs disease,sturge –weber
syndrome, Familial macrocephaly, subgaleal hemorrhage.bulging AF ,
separating sutures (subdural haematoma , intracranial space occupying
lesions)
 Microcephaly :- Occipitofrontal circumferance <3SD of the normal for
age,sex,gestational age or ethnic group.
Causes: Genetic(symmetric IUGR baby),chromosomal disorders(trisomy
13,18),congenital infections :TORCH infections,teratogenic(fetal alcohol
syndrome),
Postnatally acquired(asphyxia,hemorrhage,meningitis,malnutrition,sepsis)

EYES :
Look for:
a)Hypotelorism ,b)Hypertelorism, c)lateral displacement of the inner canthi, d)ptosis-
third never palsy,myasthenia gravis,toxic myopathy-botulism,eyelid or orbital tumor.
e)Exophthalmus-Hyperthyroidism,glaucoma,hemorrhage or metastasis.
f)enophthalmus-damage to cervical symphathetic nerve,apparent retraction in children
with chronic malnutrition.
 Telangiectasia in the bulbar conjunctiva.
 Seen in ataxia telangiectasia.
 Subconjunctival haemorrhage is associated with intra cranial haemorrhage.
 Jaundice is seen in HIE.
 Phlyctens,choroid tubercles is seen in TB.
 Drooping of eyelids is seen in myasthenia gravis.
 Unilateral drooping is seen in third cranial nerve palsy.
 Unilateral ptosis with enopthalmus is seen in horners syndrome.
 Papilloedema in increased ICP.
 Lens dislocation is seen in homocystinuria.
 Eyes turn up without the lid closing (LMN facial palsy).
FACE-
 Butterfly rash is seen in SLE.
  Frontal bossing, sunset sign is seen in hydrocephalus.
 Expressionless face and drooling of saliva is seen in hydrocephalus.
Asymmetry of face-Facial palsy
Myasthenia gravis –look for ptosis
*rule out UMN and LMN Lesions

Portwine stain :- sturge weber syndrome

DYSMORPHIC FACIES AND ASSOCIATED NERVOUS SYSTEM
DISORDERS
CONDITION DYSMORPHIC FACIES NERVOUS SYSTEM
FEATURES
Hypothyroidism Coarse facies Mental retardation
Down’s syndrome Mongoloid facies Low IQ
Moebius syndrome Mask like facies B/L VI and VII nerve
palsy

EAR :
Ear discharge for ASOM – Cause for meningitis
Types of discharge:Watery discharge(CSF otorrhea.),blood
stained(neoplasma),purulent(infection).
Low set ear: down syndrome
NOSE:-
 Nasal swelling :- meningocele.
  Meningoencephalocele.
 Neurofibroma
 Craniopharyngioma
 Rhabydomyosarcoma

Head trauma:- look for

3. Fracture of the cribriform plate.
4. Shearing laceration of the olfactory bulb.
Rhinorrhea is seen in
4. Meningoencephalocele.
5. Cystic fibrosis
6. Traumatic
ORAL CAVITY
11. Cyanosis (cyanotic CHD)
12. Pallor (leukaemia, SBE)
13. Tonsillitis
14. Peritonsillar abscess
15. Retropharyngeal abscess
16. paranasal sinuses:- sinus tenderness(sinusitis).
17. Ulcerated lesions,aphthous ulcers:- trauma,stress,allergy.
18. Recurrent herpes simplex infection:-Reactivation of herpes simplex type1 due
to fever,sunburn,trauma.
19. Angular chelitis.
20. Fissured tongue: Downs syndrome.
TONGUE:
8. Macroglossia: acromegaly, mongolism, hemangioma.
9. Microglossia:isolate, Pierre Robin syndrome.
10. Atrophy:lower motor neuron lesion.
11. Tremor: anxiety, neurosis.
12. Protrusion difficulty: trauma, paralysis.
13. Tonsil: tonsillitis.
14. Peritonsillar abcess, retropharyngeal abcesss
NECK : carotid artery-block- takayasu arteritis.
4. Torticolis: in the lateral rectus palsy
5. Neck stiffness:Meningeal irritation ,intracranial tumo , poliomyelitis,
subarchanoid haemorrhage
6. Lymphadenopathy: Tb, anticonvulsant therapy with phenytoin.

LIMBS:
8. Koilonychias (iron deficiency anemia),
9. Edema (hepatic failure with encephalopathy),
10. Peripheral nerve thickening (hereditary neuropathy),
11. pallor (SBE,leukemia),
12. clubbing(cyanotic CHD)long limbs,long fingers -marfans syndrome,
homocystinuria)
13. Skin:pallor(vasomotor collapse,anemia, intracranial haemorrhage)
14. Icterus(kernicterus in newborn,liver failure with hepatic encephalopathy)
NEUROCUTANEOUS MARKERS.
NEUROCUTANEOUS NEUROCUTANEOUS
MARKERS SYNDROMES
Cafe au lait spots,axillary Neurofibromatosis Café-au-lait spots:Dark
freckles brown hypermelanotic
macules with smooth or
irregular
borders,commonly seen
in back,buttocks and
trunk.
Axillary freckling:
similar round spots in
axilla and inguinal
areas.
Telangiectasia Ataxia telangiectasia Dilated blood vessels
over sclera,venous
angiomas over the
bridge of nose,butterfly
area of face,ante cubital
area,neck,popliteal
fossa.
Adenoma sebaceum,shagreen Tuberus sclerosis Adenoma
patch,ash leaf macules sebaceum(facial
angiofibroma):
Numerous smooth
glistening round
rubbery papules pin
head to pea size,over
butterfly area in the
face and nasolabial
folds,cheeks,nose,chin.
Shagreen patch:These
are connective tissue
naevi.Skin colored
irregular lumpy
cobblestone-like
plaques in lumbosacral
areas which grow to the
size of a palm,satellite
papules grow around a
central plaque with
orange peel like
indentation.
Ash leaf
macules:Hypomelanotic
polygonal macules
grow upto 5cm over
trunk and buttock
Hemangioma Strugge-webber Manifested at
syndrome birth,port-wine stain on
the forehead, and upper
eyelid of one side of
face,or the whole
face.Color:light pink to
 deep purple and is
caused by an
overabundance of
capillaries around the
ophthalmic branch of
trigeminal nerve
Tuft of hair Spiba bifida Look for sacral dimples
that are accompanied
by a nearby tuft of
hair,skin tag or certain
types of skin
discoloration.
Nevus Linea nevus sebaceous The sebaceous nevus is
syndrome usually located on the
face,scalp, or neck.It
can also be located on
the arms,legs or trunk.It
maybe barely
noticeable at birth and
typically becomes more
pronounced with age.

Markers of tuberculosis-lupus vulgaris, phylecten, scrofuloderma, BCG scar,

tuberculids
 Sacral dimple-spina bifida
 Salmon pink-maculopapular rash(collagen vascular disease)
 Multiple burns( syringomyleia)
 Vasomotor changes(coldness or edema on affected parts,autonomous
disturbances)
 Any obvious deformity:skeletal deformities and joint contractures in cerebral
palsy.
 Butterfly rash over cheeks(SLE )
 Erythema nodosum(TB)

ODOUR OF THE BODY

CONDITION BODY ODOUR ASSOCIATED
NEUROLOGICAL
DISORDERS
Phenylketonuria Musty odour Progressive mental
retardation
Maple syrup uribe disease Maple syrup Seizures,mental
subnormality and coma
Uremia Ammoniacal Encephalopathy
Hepatic failure Musty Encephalopathy

SPINE:
 scoliosis (progressive muscular dystrophy,poliomyelitis,cerebral
palsy,congenital wedge deformity,hemivertebra)
 Kyphosis(Congenital displacement of the ip,TB spine ,Ankylosis spondylitis)
 Lordosis:look for any swellings,sinuses,spina bifida,meningomyelocoele and
CDH-bilateral)
BONES AND JOINTS:
5. Arthritis(collagen vascular disease,SLE ,RA)
6. Hypermobility of joints(Marfans syndrome)
7. Dactylitis(sickle cell anemia)
8. Joint effusion(haemophilia and collagen vascular disease

CRANIAL NERVE EXAMINATION

 Examination of cranial nerves is important in localisation of brain stem lesions

as all cranial nerves except olfactory and optic originate from brain stem.

2. CRANIAL NERVE I: OLFACTORY

 Function: carries smell sensation from olfactory receptors in nasal mucosa.
 Purely sensory nerve.
 Testing the nerve:
vii. Rule out obstruction to nostrils due to common cold or any other cause.
viii. Each nostril is checked with other one compressed.
ix. Common substances like coffee, chocolate etc are used.
x. Child is asked to identify the smells by keeping the substance close to
the nostrils. Each nostril is tested
xi. Do not use irritants or pungent smells as it may stimulate the
trigeminal nerve and give false impression of normal test.
xii. Newborn: baby turns the face towards the smell of breast milk.

 Lesions
iii. Anosmia: absence of smell. Occurs in head injury involving cribriform
plate, Tumors( pituitary tumour, frontal lobe glioma, olfactory groove
meningioma), frontal lobe abscess and raised ICT.

iv. Parosmia: altered smell with hallucinations and illusions of smell-

smell is distorted and unpleasant. Due to local causes in nose or head
injury.
Cranial nerve II: optic nerve