Nandan's Paediatric Notes - 3rd Ed

NANDAN‘S PEDIATRICS NOTES 1
On this book
Welcome to my pediatric notes! If you are reading this book, it is likely that you are in your final year. This
book is intended to be a quick crash course in the basic facts that you are expected to know when you appear
for the university exams. I have added this preface section so you can make an informed decision whether to
use this book or not.
It is understood that most students are not going to become paediatricians, and MBBS graduates would only
require to handle basic and emergency conditions in the paediatric population in primary care settings. IAP
Textbook of paediatrics and Ghai are excellent and comprehensive texts for this purpose. For many, including
me, professional-level texts like these are simply too much. This book, inspired by my own lack of interest in
the subject and a strong disproval of the way we are tested throughout MBBS, is an attempt to create a ‘short-
cut’ using a loophole in our course.
In this book, you will find system-based chapters that are in (almost) question-answer format with direct
screenshots and tables from other standard books. In no way is this book intended to tell a story or build
interest in the subject! The goal is for you to be able to appear in the exams confidently while having not spent
too much time preparing.
Previous versions of this notes were print-only, but many scanned copies were being circulated. I felt this PDF
should ease the strain to your eyes, but feel free to print it if you enjoy using sticky notes and highlighters!
On what this book is not
1. Complete or comprehensive: This book is a very oversimplified view of paediatrics, and some advanced
topics have been omitted entirely. Few of them have been listed under ‘Further reading’ at the end.
2. A practical manual: You would still need to supplement your learning for practicals by studying books
meant for that, like Aruchamy.
3. My intellectual property! Unlike other authors that you would have studied throughout your MBBS
journey, I am a pseudo-author in the sense I have only compiled the information in this book and in
no way express my knowledge or experience. I do not take credit for the contents of this book.
On how this book came to be

I had fixated on Pathology as my specialty choice. Every piece of knowledge after my second year would pique
my curiosity if it would help me as a pathologist. Come final year, there stood this subject with huge textbooks
and only a fifty marks exam, and right next to medicine and surgery. The previous question-papers painfully
tested us on all possible topics from every nook and corner.
I sat down at the beginning of my final year, reviewed my options, and thought no way. I am not going to sit
skimming through IAP or Ghai before the exams. I needed to make my own notes. I started typing all the
topics that we were previously tested on and started entering concise point-wise information under those
headings from Aruchamy, Ghai, Parks and IAP. My batch found it helpful, and I hear subsequent batches did
too. I hear a ‘it was because of your book we passed’ every now and then, but truth be told, it is hard to believe this
book has made any difference in passing rates! All I am trying to do is make it simpler to get by, which you
would have anyway.
I will gladly welcome any feedback, as I have previously to bring this ‘third edition’ out. Suggestions on new
topics that you would like to see in this notes would be most helpful. Please reach out to me on Twitter/Gmail/
Facebook/Instagram, and I will get back to you as soon as I can.
Twitter /Gmail/ Facebook: nandanp0 (it is a zero in the end!), Instagram: nandanpadmanabha
-Nandan Padmanabha
24-Apr-2021

Acknowledgements
I would like to thank the friends from my batch who made this task so much easier! Aditya Narayan for the
foreword and multiple inputs throughout his preparation for his exam, Mohammed Shaheen for pushing me
to complete quickly, Aishwarya Rao for dictating numerous topics as I typed, Srinath Rajasekar for being a role
model for dedication, and Aditya Ramanathan for being a constant support and the first buyer of the printed
version of this notes.
I thank my 0’14 batchmates of KMC Mangalore for welcoming this notebook with such trust and
recommending it to juniors who found it helpful.
-Nandan Padmanabha
PGY1- Anatomic and Clinical Pathology
Beth Israel Deaconess Medical Center, Harvard Medical School
Boston, MA.
‘To bring a human life into this world is like bringing firewood to a burning house’

Foreword
Paediatrics is one of the most challenging specialities in medical education. The subject is undeniably vast, each
topic is dealt with a multi-systemic approach, and all this must be coupled with the intricate precision and
innumerable facts. This makes it a nightmare for the final year medical student. Nandan’s paediatric notes is a
humble attempt to change that.
As the kind of person who has always given his 100%, he went the extra mile to create a study resource that
can be used by every medical student, no matter where they sit on the academic spectrum. The notes are detailed
enough to pass the final exam and short enough to read multiple times. With this book, he has done the
unthinkable: to make a compass that guides you through the ocean of paediatrics overnight. This notes is the
most concise account of paediatrics covering almost all necessary domains for a final year to successfully answer
any question thrown at them in the theory exams. The information is updated with the latest guidelines and
recommendations from OP Ghai and the IAP textbook of paediatrics.
Having witnessed the feedback on these notes firsthand, I can assure you that the cheers Nandan received as
my batch stepped out of the paediatrics final exam were heartfelt and genuine. Many claim that the only reason
they passed the exam is because of this book. Even as a pediatric resident, I find myself reaching out to my
copy now and then.
I strongly recommend this book, and I assure you that this will become your go-to resource. To the dearest
final year students who want a quick and thorough revision of the subject a day before the exam: This is where
the magic happens.
-Aditya Narayan
Junior Resident, Dept. of Paediatrics
JIPMER, Pondicherry

Contents
NUTRITION ...................................................................................................................................................................... 6
GROWTH ......................................................................................................................................................................... 21
DEVELOPMENT ........................................................................................................................................................... 34
IMMUNIZATION .......................................................................................................................................................... 40
RENAL .............................................................................................................................................................................. 47
GASTRO-INTESTINAL TRACT ............................................................................................................................... 57
CARDIO-VASCULAR SYSTEM ................................................................................................................................. 63
RESPIRATORY SYSTEM ............................................................................................................................................. 69
NEUROLOGY................................................................................................................................................................. 77
NEONATOLOGY.......................................................................................................................................................... 86
HAEMATOLOGY .......................................................................................................................................................... 95
INFECTIOUS DISEASES ............................................................................................................................................ 99
MALIGNANCIES ......................................................................................................................................................... 111
Further reading................................................................................................................................................................ 115

NUTRITION

Vitamin A deficiency
WHO classification:
Primary signs: Secondary signs:
X1A Subconjunctival xerosis XN Night blindness
X1B Bitot’s spots XF Fundal changes
X2 Corneal xerosis XS corneal Scarring
X3A Corneal ulceration, 1⁄3rd of cornea Extra-ocular manifestations: follicular hyperkeratosis,
X3B Corneal ulceration, >1⁄3rd of cornea anorexia and growth retardation
Treatment: Oral vitamin A on days 0,1 and 28. Age-wise dose:

<6 mo:50,000 IU, 6-12 mo:1 lakh IU, >1 year: 2 lakh IU
National program for prevention of blindness (National Vitamin A Prophylaxis Program)
1. Sponsored by the MoHFW (GoI).
2. Children between 9 mo and 3y are given vitamin A 6-monthly.
At 9 months, 1 lakh IU is given orally along with measles vaccination.
Subsequently, 2 lakh IU every 6 months till the age of 3 years.
Vitamin A Supplementation for Sick Children- All children suffering from measles are given 1 dose. All
cases of severe malnutrition too, are given 1 additional dose of vitamin A.
Local treatment for corneal ulcers:
1. Antibiotic drops to prevent secondary infection.
2. Padding to promote healing, prevent dehydration, reduce pain and photophobia.
3. Mydriatics.
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Clinical features of hypervitaminosis A
1. Acute manifestations (aka pseudomotor cerebri)
i. Headache, irritability
ii. Vomiting and dizziness
iii. Signs of raised ICT (raised ant fontanelle and papilledema)
2. Chronic
i. Anorexia, weight loss
ii. Dry itchy skin
iii. Sparse hair/alopecia
iv. Hepatosplenomegaly, hypoplastic anemia
v. Hyperostosis
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Weaning
Definition: Accustoming the infant to gradual introduction of nourishment other than mother’s milk.
Solid food to replace breast feeding to be started at 6 months and completed by 1 year.
Why should weaning be started only after 6 months?
1. GI immune mechanisms are ready to protect against infected food only after 6 months.
2. Ability to digest and absorb protein, fat and carbohydrates increases.

3. Kidney develops the ability to excrete waste products when food with high renal solute load such as
meat is ingested.
4. The child develops the neuromuscular mechanisms required for food recognizing, accepting a spoon,
masticating and swallowing.
5. Tongue thrust pushes out anything other than liquid before 6 mo.
6. Non- breast milk food increases the satiety of the child and hence won’t accept breast milk.
7. Before 6 mo, the child might develop allergy to non- breast milk food.
Weaning food should be:

1. Culturally acceptable.
2. Adequate: providing all nutritional supplement.
3. Locally available and inexpensive.
4. Easily prepared at home.
5. Clean and hygienic.
6. Physiologically stable, suitable, easily digestible, bland and nourishing.
Principles of weaning
1. Exclusive breastfeeding till 6mo, and then weaning food.
2. First starts with liquid, then semi-solid, then solid.
3. Give only one food at a time, introduce new food every week.
Problems in weaning:
1. Inadequate quantity/quality leading to malnutrition.
2. Unhygienic feeding practices leading to enteric infections and diarrhea.
3. Personal likes and dislikes of the child.
4. Refusal of child to accept weaning food.
Contraindications of breastfeeding:
1. PKU
2. Galactosemia
3. Mother on anti-cancer drugs
4. HIV positive mother (relative contraindication, guidelines exist w.r.t viral load)

Exclusive breastfeeding
Definition: Only breast milk is given to baby. No other food or drink, not even water is given. Medicine,
mineral drops, vitamins are permitted if indicated. The child is breastfed as the child wants, day and night, at
least 8 times in 24 hours. Continued breastfeeding even if the child is sick. Exclusively breastfeed: for 6 months.
The wetness test

A baby less than 6 months of age only on breast milk and no other fluids or feeds. If the baby passes urine
more than 6 times in 24 hours, the urine is clear, colourless and of good quantity, the baby is getting all the
nutrition and fluid needed and there is no insufficiency.
How to identify that breast milk is not enough for the infant?
1. Baby has inadequate weight gain or the weight remains stationary.
2. The baby cries soon after feeding.
3. The baby has constipation.
4. The baby falls sick often.
Guidelines for positioning and attachment of the baby during breastfeeding

1. Proper positioning
i. The infant's head, neck and body should be held in a straight line.
ii. The whole of the baby's body should be supported, not just the head and neck.
iii. The baby's face should be directly in front of mother's breast (en face).
iv. The baby's body should be close to the mother's body.
2. Proper attachment
i. The chin should touch the breast.
ii. The mouth of the baby should be wide open.
iii. The baby's lower lip should be turned out.
iv. Most areola and nipple should be in baby's mouth. More areola should be visible above than below
the baby's mouth
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Difference between breast milk and cow milk:
Characteristics Breast Milk Cow milk
Digestion Easy, well absorbed Not easy, not well absorbed
Flocculation 60% whey proteins & 40% casein, forms 18% whey protein & 82% casein,
smaller precipitates and easier to digest forms larger precipitates
Fats Remain unbound Bound to casein
Gastric pH Not affected Increases
Gastric emptying Shortened Prolonged
Calories 71 kcal/100 mL 67 kcal/100 mL
Protein 1.1 g/100 mL 3.3 g/100 mL
Amino acids Adequate for brain development Inadequate for brain development
Fats 4 g/ 100 mL, PUFA high 3.6g /100 mL, more saturated FA
Lactose 7.5 g /100 mL, aids brain development 4.5 g/100 mL
Total salts Required amount Excess amount leading to ↑ load on
kidneys
Osmolality 290-300 mOsmL/kg >300

Characteristics Breast Milk Cow milk
Iron 0.05-0.1 mg/L only but bioavailability is 0.05-0.1 bioavailability <10%
49%
Ca:P ratio >2:1, protects against neonatal <2:1, predisposes to tetany
hypocalcemia
Vitamin A, C, D, E Higher Lower
Protective Immunoglobulins, leucocytes, bifidus Not present
substances factor, lactoferrin, lysozyme, antibodies
Bacterial Less likely More likely
contamination
Advantages of breast milk
I. Advantages to the baby
1. Nutritive value: breast milk contains all the nutrients that a baby needs for the first 6 months
of life for optimal growth and development.
2. Easily digestible: breast milk contains a higher proportion of whey proteins (lactalbumin and
lactoglobulin) whereas cow's milk contains more casein.
3. Kidney protection: breast milk has low sodium and mineral content.
4. Brain development: breast milk has higher taurine and cystine content.
5. Cardio-protective: the higher PUFA content in breast milk also protects the individual from
atherosclerosis later in adult life.
6. Retinal development: long-chain PUFA present in the breast milk.
7. pH of the breast milk is low. Hence, organisms do not grow in the breast milk.
8. Anti-infective factors: humoral (IgA, IgM) and cellular (macrophages)
9. No risk of milk allergy.
10. Protection from other allergies and diseases: breastfed babies have less chance of developing
hypertension, obesity, coronary artery disease.
11. Physiological adaptation: breast milk is not just species-specific but also individually tailored
to the needs of the baby. A mother who has delivered prematurely secrete milk that is easily
digested and is nutritive for her preterm baby.
12. Emotional bonding
13. Risk of over-feeding is minimal
II. Advantages for the mother
1. Birth control: lactation suppresses ovulation.
2. Maternal health: breastfeeding enhances involution of the uterus.
3. It also lowers the risk of ovarian and breast cancer in the mother.
4. Convenience: this mode of feeding is more convenient as it is not required to clean the bottle
and prepare the milk for artificial feeding several times during the day and night.
III. Economic factors
1. Reduced cost of the food, reduced healthcare cost (by prevention of illness).
2. Ecological: breast milk is easily available at an optimal temperature and there is no wastage.
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Rickets:
A lack of adequate mineralization of growing bones results in rickets and that of trabecular bone results in
osteomalacia.
RDA for Vitamin D in infants is 5 μg (200 IU)/day and children 10 μg (400 IU)/day.
Etiology: Nutritional rickets (vitamin D deficiency rickets)/Ca deficiency/ Phosphorus deficiency.

Clinical features
1. Age: unusual<3 mo., classically 6 mo-2y Radiological features
2. Early signs 1. Sites: growing bones around
i. Restlessness, sweating over head wrist and knee. Changes:
ii. Craniotables: feeling of cracking over parietal bones i. Fraying of metaphysis
iii. Rachitic rosary ii. Apparent increase in
3. General features growth plate
i. Flabby appearance iii. Splaying of metaphysis
ii. Muscle weakness and ligament laxity iv. Decrease in bone density
4. Head: 2. Ribs: Rachitic rosary is seen as
i. Anterior fontanelle remains open beyond 18 mo. beaded enlargement of
ii. Bossing of head (hot cross bun appearance) anterior metaphysis
5. Chest 3. Pelvis: coxa vera
i. Harrison’s groove over insertion of diaphragm 4. Spine: kyphosis, scoliosis
ii. Rachitic rosary
iii. Pigeon chest
iv. Fiddle shaped chest
6. Spine: kyphosis and/or scoliosis may occur.
7. Long bones: bow leg, knock knees, coxa vara, greenstick deformities.
8. Pelvis: difficulty in labour at a later stage. Vitamin D levels in serum (ng/mL)
9. Abdomen: pot belly and visceroptosis Deficient <10
10. Teeth: caries and delayed dentition Insufficient 10-20
Optimal 20-60
Lab diagnosis: High 60-90
1. Decreased 25(OH)D3<10 μg/mL. Toxic >90
2. Increased 1, 25(OH)D3 if deficient intake of Ca/phosp.
3. Blood ALP ↑
4. Ca and phosphate normal or decreased
Treatment of rickets:
1. Medical: Stosstherapy: Give 6 lac IU vit D3 oral/IM+ oral Ca supplements
Repeat next dose
No
Recovery Yes Healing line on X-Ray in 3-4 weeks
Responded?
Yes
No
Give 400 IU daily
till full recovery Vitamin D resistant rickets.
Investigate further for cause
2. Surgical: Correction of deformities after correction of rickets.

Scurvy
Clinical features: irritability, anorexia, anemia and petechiae (due to capillary fragility). Gingival swelling,
bleeding gums, generalized tenderness (due to periosteal bleed) and painful joint welling (due to hemarthrosis).
Frog-like posture due to pseudo-paralysis. Scorbutic rosary: annular tender swelling at costochondral junctions.
X-ray features: 1. Thinning of cortex (pencil-thin cortex)
2. Irregular thickened white line at metaphysis (white line of Frenkel)
3. Zone of rarefaction proximal to white zone of Frenkel (Trümmerfield zone)
4. Lateral to rarefaction- triangular spurs (Pelken spurs)
5. Epiphysis surrounded by thin white line (Wimberger ring sign)
Rx: Vitamin C 100-200 mg/day
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Malnutrition/PEM
Age independent criteria for assessment of malnutrition:
1. Weight for height
2. Rao’s index: constant between 1-5 years irrespective of gender
3. Kanawati’s index: constant between 3 months-4 y of age
4. Dugdale’s index
5. Mid-arm circumference between 1-5 years
1. Weight for height

Sensitive in acute malnutrition, not in chronic (because both height and weight decrease and remain
proportional to each other)
% weight for height= Weight of the child X100
Weight of normal child of same height
Name Method Normal/severe PEM

2. Rao & Singh’s Wt (kg)/h (cm) X100
2 0.15-0.16/<0.14
3. Kanawati’s MAC (cm)/HC (cm) 0.32-0.33/<0.25
4. Dugdale Wt (kg)/ht (cm) X100
1.6 0.88-0.97/<0.79
5. MAC >13.5 cm/<12.5 cm
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Classification of PEM
1. Wellcome trust classification 2. Udani classification for marasmus
Wt for age Edema + Edema - Grades Loss of fat

(Boston) (% of I Axilla/groin (boggy pants
expected) appearance)
60-80% of Kwashiorkor Undernutrition II Buttock
standard III Abd, chest, back
<60% of Marasmic Marasmus IV Buccal pad of fat (monkey
standard Kwashiorkor facies)

3. IAP classification 4. WHO classification
Nutritional status Wt for age (%) of
50th percentile of
Harvard standard
Normal >80
Grade 1 PEM 71-80
Grade 2 PEM 61-70
Grade 3 PEM 51-60
Grade 4 PEM <50
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Severe Acute Malnutrition definition: weight for height <3SD, MUAC <11.5 cm, bilateral pitting edema
and clinical signs of wasting.
Definition of PEM: class of clinical conditions consisting of classifiable or non-classifiable manifestation of
protein lack and energy inadequacy.
Complications of PEM: (SHIELDED)
S-Sugar deficiency
H-hypothermia
I-infection and shock
EL- Electrolyte imbalance
DE- dehydration
D- Deficiencies of iron, vitamins and other micronutrients
Others- behavior changes, Intelligence affected, motor coordination affected.
Marasmus
Marasmus is the most common type of severe PEM that occurs in preschool children and results in growth
retardation and muscle wasting without oedema.
Clinical features:
1. Age: highest incidence seen in infancy
2. General features
i. Gross wasting of muscle, poor tone.
ii. Loss of SC fat.
iii. Bony prominences are seen.
3. Skin
i. Wrinkled, dry and loose, inelastic.
ii. Folds are prominent over gluteal and inner thigh.
4. Psychological
i. Appears alert but irritable.

ii. Voracious appetite.
5. Growth: marked deficit in weight and to a lesser extent height.
6. GIT: distended abdomen.
Treatment (also given separately under treatment of PEM in detail)
1. Children respond well to oral diet rich in calories (appetite is good).
2. If severely malnourished, child needs to be admitted as there is atrophy of the intestinal epithelium
and the exocrine pancreas.
3. Food must be started in small quantities and weight monitored.
i. Diet should be affordable, acceptable, and available.
ii. Calorie requirement is 150-200 kcal/kg/day
iii. Protein requirement is 2-3 g/kg/day
iv. Improve the calorie content of the food by adding sugar or oil. Food should be isodense so
that 100 mL of food will provide 100 kcal.
4. Parenteral nutrition can be given if oral feeds are not tolerated or contraindicated.
5. Vitamin supplementation-vitamin A and folic acid supplementation.
6. Iron supplements are started after 3 months.
7. Electrolyte imbalance should be corrected if present.
8. Treatment of associated infections and worm infestations.
9. Treatment of complications.
Kwashiorkor
It is protein deficiency malnutrition and commonly occurs in children who are weaned from mother's breast
milk to a diet rich in starch and low in proteins.
Clinical features
1. Age: older children (1-4 y)
2. General features: pitting edema- ‘sine qua non’ for establishing diagnosis.
3. Muscle wasting: present but maybe masked by edema.
4. Face: moon like.
5. Skin
i. Flaky paint dermatosis.
ii. Dry inelastic mosaic appearance.
6. Hair changes
i. Flag sign: alternating dark and white hair.
ii. Thin, dry, brittle, sparse, and easily pluckable.
7. Mental changes
i. Lethargic, listless and apathic.
ii. Takes little interest in the environment and does not play with their toys.
8. GIT: impaired appetite and hepatomegaly
Treatment: Children with kwashiorkor cannot tolerate the feeds with required calories and proteins if given
all of a sudden. Hence, the feeding should be started with less calories and then gradually increased over a
period of 1-2 weeks.
Marasmic Kwashiorkor (features of both)
The child is said to have this condition when all of the following features are present
1. Weight <60% of the expected 3. Marked wasting and stunting
2. Oedema 4. Anaemia
5. Mental apathy
Differences between kwashiorkor and marasmus:
Management of PEM
Management of PEM includes the following:
1. Nutritional assessment
2. Investigations (has 4 categories)
3. Treatment (has 2 phases)

I. NUTRITIONAL ASSESSMENT
Causes of mortality in PEM:

1. Undermined immunity in
malnutrition may lead to
septicemia.
2. Diarrhea, hyponatremia,
hypokalemia, acceleration of
the wasting process may lead
to hypovolemic shock.
3. Other types of circulatory
disturbance are caused by very
low serum albumin values, by
the overloading of the wasted
heart by fluid, by high salt or
calorie intake.
4. Further dangers are
hypoglycemia and
hypothermia.
II. INVESTIGATIONS
Investigations may be done to support the diagnosis and for any associated infections and
complications.
1. Investigations to support the diagnosis of PEM
i. Serum proteins-total serum proteins, albumin and globulin. Total serum proteins and serum
albumin are decreased, and reversal of albumin globulin ratio is seen in kwashiorkor.
ii. Blood urea, serum creatinine, blood urea nitrogen. (BUN)-usually decreased in marasmus due to
decreased muscle mass. It is increased in marasmus with chronic renal failure which is associated
with decreased intake due to loss of appetite and vomiting.
2. Investigations to find out associated conditions and infections
i. Blood haemogram- Hb% decreased in anaemia
ii. Peripheral smear study
• Total WBC count-leucocytosis in pyogenic infections, leucopenia in severe sepsis
• Differential leukocyte count-lymphocytosis in tuberculosis
• Anaemia, leukopenia and thrombocytopenia in severe sepsis due to suppression of bone
marrow
iii. Erythrocyte sedimentation rate increases in infections like tuberculosis.

iv. Blood culture-should be done to rule out sepsis.
v. Liver function tests-bilirubin may be increased; AST & ALT may be decreased in kwashiorkor
vi. Stool examination
• Macroscopic: Soupy consistency in lactose intolerance, fatty stools in fat malabsorption
• Microscopic: Ova, cyst (in hookworm infestation/ giardiasis/ amoebiasis/ trichuriasis),
RBCs/pus cells in gastroenteritis, Crohn's disease.
• Biochemical examination: pH-acidic in lactose intolerance, reducing substances-positive
in lactose intolerance, stool fat content-increased in fat malabsorption. Normal fat
excretion is <5 g/day.
• Schilling test for absorption of vitamin B12 (very outdated)
3. Investigations to find out specific infections
i. Peripheral blood smear for malarial parasite.
ii. Chest X-ray for respiratory infections, tuberculosis, bronchopneumonia- may be seen in
immunodeficient children following measles or marasmus.
iii. Urine routine examination--presence of pus cells to rule out UTI. Chronic UTIs are associated
with malnutrition.
iv. Urine culture and sensitivity-for chronic UTI
v. Skin tests: Montoux and BCG test (accelerated BCG reaction may be seen in severely
malnourished children).
vi. Resting gastric juice examination for AFB.
4. Investigations to detect complications
i. Blood sugar-decreased in hypoglycaemia
ii. Serum electrolytes: hypokalemia, Sodium-may be increased or decreased. (increase due to
hyperaldosterone and decrease due to water retention- dilutional hyponatremia)
iii. Chest X-ray-heart failure, bronchopneumonia
iv. ECG-heart failure
III. TREATMENT
Grade I and II PEM: usually the children are hungry, tolerate feeds orally and can be fed orally. These
children can be managed at home by frequent feeding.
Severe (Grade Ill or Grade IV) PEM: managed in hospital. Treatment is given in two phases- stabilization
and rehabilitation.
1. Phase I: Stabilization-Resuscitation Phase: contains 2 phases- resuscitative and restorative.
Resuscitative Phase:
i. Hypoglycaemia(Rx- dextrose solution parenterally if symptomatic else oral/nasogastric tube)
ii. Hypothermia (Rx- warm room under a radiant warmer, if severe give warm humidified O2)
iii. Dehydration (Rx- ORS)
iv. Electrolyte imbalances—hypokalaemia (oral potassium chloride/modified ORS)
v. Anaemia, vitamin and micronutrient deficiencies- vitamin A deficiency, hypomagnesaemia
vi. Infections/infestations : pneumonia, diarrhoea, UTI and worm infestations (Rx antibiotics)
vii. Congestive cardiac failure (Rx-fluid restriction and diuretics)
viii. Convulsions, tremor and tetany.
Restorative phase: To restore the weight for height. This includes dietary management.
i. In the early stages, if not tolerated orally, feeding should be started with nasogastric tube.
ii. Small oral feeds should be started asap

iii. Breastfeeding should be continued.
iv. The diet should contain adequate calories, proteins, vitamins and minerals
v. To start with, F-75 diet should be given. It contains 75 kcal and 1.0 g protein in each 100 mL.
Slowly, F- 100 diet should be introduced which contains 100 kcal with 2.5-3 g protein in 100mL.
vi. Cereal-based low lactose and low osmolarity F-75 diets should be given as starter diets in persistent
diarrhoea. Osmolarity should be <350mOsm/L. Lactose content should not be more than 2-3
g/kg/day.
vii. Adequate bioavailability of micronutrients should be ensured.
viii. Maximum volume of feed/day should not >130 mL/kg/day. If edema+, < 100 mL/kg/day.
2. Phase II: Rehabilitative Phase

i. Registration in nutrition clinic.
ii. Nutritional counselling.
iii. Follow-up visits-should be organized every 3-4 weeks.
iv. Vocational therapy- so that parents can earn money used for purchasing food
v. Health education.
vi. Psychosocial stimulation should be provided to improve mental development.
vii. The diet should be advised.
viii. Nutritional supplementation-foods can be provided to the child by the health workers.
Prevention of PEM
1. Increasing literacy rate.
2. Increasing crop production and fortification of foods.
3. Increasing the purchasing capacity of the people by creating
employment opportunities.
4. Nutritional education.
5. Encouraging local food production.
6. Improving health and nutritional status of adolescent girls.
7. Providing good ANC for prevention of LBW babies.
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Balanced Diet
Balanced diet is defined as the one which contains a variety of foods in such quantities and proportions that
the need for energy, amino acids, vitamins, minerals, fats, carbohydrates and other nutrients are adequately met
for maintaining health, vitality and general well-being and also makes a small provision for extra nutrients to
withstand short duration of illness.
Q. Write balanced diet for a 6-month-old infant and a 6-year-old child.
Divide into 8:00 am breakfast, 11:00 am snacks, 1:00 pm lunch, 5:00 pm snacks and 8:00 pm dinner. See
boxed content for portion size of various foods to be included.

Davangere mix: A combination of groundnut 10g, Bengal gram 16g, jaggery paste 20g, ragi flour 40g. It
contains about 400 kcal and 14g of protein per 100g.If ragi flour is replaced by wheat flour, it is known as
Hyderabad mix.
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Protein requirement:
Age (y) Protein requirement in

g/kg body weight
<1 2
1-3 1.7
3-5 1.5
5-7 1.3
7-9 1.1
>9 0.9-1
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Calorie requirement
Holiday-segar formula for calculating daily requirement of calories
Weight in kg Requirement Bedside method for calculating calorie requirement: 1000
<10 100 kcal/kg/day kcal for 1 year. Add 100 kcal/year upto 12 years. Eg: 4
10-20 1000 kcal +50 kcal/kg/day y/o will require 1000 kcal+ (100X3)= 1300 kcal.
>20 1500 kcal + 20 kcal/kg/day

Under-5 clinics
It combines the concept of prevention, treatment, health provision, nutritional surveillance and education into
a system of comprehensive health within the resources available in the country. Aim and objective:
1. Care in illness
i. Diagnosis and treatment of illness, disorders of growth and development
ii. X-Ray and laboratory services
iii. Referral services
2. Preventive care:
i. Immunization
ii. Nutritional surveillance
iii. Health check-ups
iv. Oral rehydration
v. Family planning
vi. Health education
3. Growth monitoring: by the use of growth chart
Outer triangle
indicates health
education
Care in illness
Family planning
Growth monitoring Preventive care
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Child labour:
In 1973 International Labour Organization (ILO) passed a convention establishing 15 years as a minimum
work age for most sectors while permitting light work from age 13, provided that such work is unlikely to harm
child health, morals or safety or prejudice his/her school attendance.
Problem statement:
1. India fosters the largest number of child labour in the world
2. Child labour contributes to 20% of GNP
3. Maximum number of child labour are in J&K mainly engaged in carpet weaving industry
Causes:
1. Poverty
2. Unemployment
3. Lack of education
The Child Labour (Prohibition and Regulation) Act 1986:
Was implemented to protect children against labour, protect child labour against abuse, exploitation and health
hazards. It also regulated the condition of work where child labour is permitted

GROWTH

Definition: It denotes a net increase in the size/mass of tissue which is due to multiplication of cells and
increase in the intra-cellular substance. Hypertrophy contributes to a lesser extent to the process of growth.
Laws/principles of growth
1. Continuous orderly process.
2. Sequence of growth is same but pace can be non-uniform.
3. Growth pattern of every individual is unique but general
pattern is cephalo-caudal & distal to proximal.
4. Different tissues of the body grow at different rate
(as indicated by the graph).
Factors affecting growth:

1. Age: the rate of increase in height is more in children as compared to adults.
2. Sex: girls have a growth spurt earlier but boys end up taller.
3. Race: slow in certain races.
4. Biorhythm: growth of girls resembles their mother’s.
5. Hereditary/genetic factors: Children with chromosomal disorders like Down's and Turner's will be
short.
6. Seasonal variation: the rate of growth is high in spring and low in summer.
7. Antenatal factors: IUGR leads to short stature, fetal hormones: T4 & insulin (GH does not have a
role in-utero), glucocorticoid helps in maturation of organs like liver, lungs and GIT. Maternal factors
such as teenage pregnancy, ↑ parity, ↑ age at conception, tobacco consumption.
8. Natal factors: birth asphyxia results in diffuse brain damage. Such children manifest slow growth.
9. Nutritional factors: children with malnutrition/mineral/vitamins deficiency-growth retardation.
10. Hormonal factors: Thyroxine is required for skeletal maturation. Growth hormone (GH) facilitates
linear growth.
11. Environmental factors: infection (increases metabolic needs), Trauma to the epiphysis, Illness--if the
child suffers from condition like anemia
12. Social factors: socio economic factors (elaborate), cultural habits, education of parents, education of
child, psychological factors (lack of emotional support and insecurity)
How do you assess physical growth? It can be done by 1. Body measurement: height (length in <2y), weight,
HC, CC, UL/LL ratio, 2. Velocity of physical growth: by growth chart
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Weight:
Can be calculated for ages 2-12 by formula, expected wt(kg)= (age (y)+3) * 2.5
Weech’s formula
3-12 mo- expected weight (kg)= (Age (mo)+9) ÷ 2
1-6 y- expected weight (kg)= Age X2 + 8
7-12 y- expected weight (kg) = (Age X7 -5) ÷ 2

Age Weight gain Age Weight gain
At birth x 10 days – 3months 30 g/day
5 months 2x 3-6 months 20 g/day
1 year 3x 6-9 months 15 g/day
2 years 4x 9-12 months 12 g/day
3 years 5x 1-3 years 3 kg/ year
5 years 6x 4-12 years 2 kg/ year
7 years 7x >12 years 5-6 kg/year (0.5 kg/month)
10 years 10x
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Height/length:
For 2-12 y can be calculated by expected height (cm) = (Age (y) X 6) + 77
Age Height gain
Birth- 3 months 3.5 cm/month
3-6 months 2.0 cm/month
2-5 years 6-8 cm/year
5-12 years 5 cm/year
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Head circumference
Age Head circumference (cm) Age Growth velocity of HC
At birth 34-35 0-3 months 2 cm/month
2 months 38 3-6 months 1 cm/month
3 months 40 7-12 months 0.5 cm/month
4 months 41 1-3 years 1 cm/ 6 months
6 months 42-43 3-5 years 1 cm/year
1 year 45-46
2 years 47-48
5 years 50-51
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Upper segment: Lower Segment ratio
Age US:LS
Birth 1.7: 1
6 months 1.6: 1
1 year 1.5: 1
2 years 1.4: 1
3 years 1.3: 1
4 years 1.2: 1
7 years 1.1: 1
10 years 1 :1
18 years 0.9: 1

Growth chart/Road to health chart:
Graphical representation of a child’s physical growth, development primarily for long term follow-up of child
so that changes over time can be interpreted and progress of growth monitored.
Uses of growth chart: (Mnemonic: GEETA PD)
1. Growth monitoring which is of great value in child health care.
2. Educational tool: because of its visual character, the mother can be educated in the care of her own
child and encourage her to participate more actively in growth monitoring.
3. Evaluation: it provides a good method to evaluate the effectiveness of corrective measures and the
impact of a program or of special interventions for improving child growth and development.
4. Tool for teaching: it can also be used for teaching, for example, the importance of adequate feeding;
the deleterious effects of diarrhoea.
5. Tool for action: it helps the health worker on the type of intervention that is needed; it will help to
make referrals easier.
6. Planning and policy making: by grading malnutrition, it provides an objective basis for planning
and policy making in relation to child health care at the local and central levels.
7. Diagnostic tool: for identifying "high-risk" children. For example, malnutrition can be detected long
before signs and symptoms of it become apparent.
Growth chart by govt. of India has 4 reference curves: (refer to a to see the lines)
1. Topmost- 5th percentile of WHO When should growth chart be filled?
2. 2nd line- 80% of topmost standard 1st year-every month
3. 3rd line- 70% of topmost standard 2nd year- every 2 months
4. 4th line- 60% of topmost line Till 5 years- every 3 months
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Mid-arm circumference: It remains constant between ages 1-5 years in healthy children. The reason
for it to remain constant is replacement of body fat of infancy with muscle.
Technique: Measured with help of non-stretchable, plastic measuring tape mid-way between the olecranon
and acromion, with the non-flexed arm hanging by the side of the body, and with the crossed tape method.
(bangle method- bangle raised above elbow)
Grading and interpretation
Grade Circumference Colour in Shakir’s tape
Normal >13.5 cm Green

Borderline PEM 12.5-13.5 Yellow (r=4)
Severe PEM <12.5 Red (r=3.5)
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Anterior fontanelle:
Anatomy:
1. Diamond shaped defect in the front al and parietal bone. It is the largest fontanelle.
2. Formed by joining of frontal, sagittal and coronal sutures.
3. 2.1*2.1 cm AP and transverse diameter (measured by line joining midpoint of opposite sides).
4. Closes by 18 months.

Method of estimation:
1. Child is in upright position and not crying or straining.
2. Normal AF is slightly depressed and pulsatile.
Significance:
1. Reflects intracranial status: depressed in dehydration and elevated in raised ICT.
2. Facilitates moulding of head.
3. Monitoring of ICP by using fontanometer.
Delayed closure:
1. Rickets 5. Congenital rubella syndrome
2. Hypothyroidism (congenital) 6. Down’s syndrome
3. Prematurity 7. Hydrocephalus
4. Raised ICP
Early closure
1. Craniosynostosis
2. First degree microcephaly
Bulging fontanelle:
1. Bleeding due to whiplash or shaking abuse 5. Intracranial tumour
2. Galactosemia 6. Raised ICT
3. Hyperparathyroidism 7. Subdural hemorrhage
4. Hydrocephalus 8. Meningitis
----------------------------------------------------------------------------------------------------------
Causes: Microcephaly (HC <3SD)
1. Isolated: autosomal recessive/dominant or X-linked
2. Systemic: Trisomy 13,18,21, monosomy, syndromes such as William’s
3. Structural- neural tube defects such as encephalocele, holoprosencephaly
4. Metabolic: PKU, methylmalonic aciduria, citrullinemia, maternal DM
5. Infections: Congenital CMV, HSV, rubella, varicella, HIV, syphilis, meningitis
6. Teratogens: Alcohol, tobacco, marijuana, cocaine, radiation
7. Perinatal insult: hypoxemic ischemic encephalopathy, hypoglycemia
8. Endocrine: hypothyroidism, hypopituitarism, adrenal insufficiency
Causes: Macrocephaly (HC>2SD)

1. Megalencephaly
i. Benign familial
ii. Neurocutaneous syndromes: NF, Struge-Weber, linear subcutaneous nevus
iii. Others: Sotos, fragile X syndrome
iv. Lysosomal storage disorders: Tay-Sach’s, mucopolysaccharidoses
2. Increased CSF volume
i. Hydrocephalus (shows sunset sign)
ii. Benign enlargement of subarachnoid space
iii. Choroid plexus papilloma
3. Enlarged vascular compartment
i. AV malformation

ii. Subdural hemorrhage or interventricular hemorrhage
4. Increased bony compartment
i. Bone disorders: Achondroplasia, osteogenesis imperfecta, osteoporosis
ii. Bone marrow disorders: thalassemia major
5. Miscellaneous causes
i. IC mass lesions: cyst, abscess, tumour
ii. Increased ICP: lead poisoning, hypervitaminosis A, galactosemia
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Short stature
If the length or height of the child is <3rd centile or less than 2SD from the mean for age, then he/she is
considered to be short in stature.
Causes:
I. Proportional short stature
1. Normal variants
i. Familial
ii. Constitutional delay in growth
2. Prenatal causes:
i. IUGR
ii. Intrauterine infection
iii. Genetic disorders- downs, turner’s
3. Post-natal
i. Nutritional dwarfism/ under nutrition
ii. Chronic visceral disease: cerebral palsy, congenital heart disease, cystic fibrosis, asthma,
malabsorption, coeliac disease, CLD
iii. Endocrine disorders- GH deficiency /insensitivity, hypothyroidism, Cushing’s disease,
precocious or delayed puberty.
iv. Psychological
v. Skeletal dysplasia e.g. rickets
II. Disproportionate short stature
1. With short limb: achondroplasia, osteogenesis imperfect, deformities due to rickets
2. With short truck: mucopolysaccharidosis, spondyloepiphyseal dysplasia
Q. List causes of short stature without mental retardation
1. Constitutional delay Target height for girls:
2. Nutritional dwarfism (Mother’s + Father’s height) ÷ 2 -6.5 cm
3. GH deficiency: gain <4 cm/year Target height for boys:
4. Chronic visceral disease (Mother’s + Father’s height) ÷ 2 +6.5 cm
Feature Constitutional growth delay Familial short stature

Heigh Short Short
Height velocity Normal Normal
Family history Delayed puberty Short stature
Bone age < than chronological age Normal
Puberty Delayed Normal
Final height Normal Low but normal for target height

Stepwise investigative workup for short stature Clues to etiology of short stature
History Etiology
1. Level 1 (essential) investigations LBW SGA
• Complete hemogram with ESR Polyuria Chronic renal failute, RTA
• Bone age Chronic diarrhoea/ Malabsorption
greasy stools
• Urine analysis including microscopy, osmolality and pH
Neonatal hypoglycemia, Hypopitutarism
• Stool examination for parasites, steatorrhea & blood jaundice, micropenis
• Serum urea, creat, bicarb, pH, calcium, phosphate, Headache, vomiting, Pitutar/hypothalamic SOL
ALP, visual syptoms e.g., cranipharyngioma
fasting glucose, alb and AST,ALT Lethargy, constipation, Hypothyroidism
wt gain
2. Level 2 investigations Inadequate dietary intake Undernutrition
• Serum thyroxin, TSH Social history Psychosocial dwarfism
• Karyotype in girls (to check for Turner’s) Delayed puberty CGD
3. Level 3 invetigations in parents
• Celiac serology (anti-endomysial, anti-TTG)
• Provocative GH test
• Serum insulin-like growth factor-1, insulin-like growth factor binding protein-3 levels
• MRI brain (pitutary and hypothalamus) if low GH levels
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Failure to thrive:
It is a term given to infants and children <5 years whose rate of weight gain is sluggish. The length of the child
may or may not be affected.
Criteria for FTT
Based on attained growth: Weight < 3rd centile on growth chart or weight for height <5 th centile or weight
≤ 20% ideal weight for height.
Based on rate of growth: <20g/day 0-3mo or <15g/day 3-6mo or fall-off from previously established growth
curve that has crossed 2 major centiles over a period of time.
Causes
1. Extrinsic
i. Inadequate nutritional intake.
ii. Social and environmental deprivation or a combination of both.
2. Intrinsic
i. Defect in absorption-coeliac disease, lactose intolerance.
ii. Persistent vomiting-pyloric stenosis.
iii. Metabolic disorder-DM.
iv. Chronic disease- of heart, lung, kidneys and liver.
Clinical features
1. Looks small for age.
2. Wide eyed/ expressionless face and avoids direct eye gaze.
3. Vocalization delayed ad motor activity curtailed.
4. Inadequate response to social stimuli.
5. Marked pre-occupation with thumb sucking.
6. Shows lack of cuddling and assumes infantile posture.

Diagnosis
1. Based on proper history, growth chart and evidence of improvement in growth performance,
observation of parent-child interaction.
2. CBC, electrolyte, stool microscopy, urine analysis, liver and renal function.
Treatment:
1. Nutritional rehabilitation- dietary management, increase calorie and protein intake and give liquids
before solids.
2. Organic causes may require antibiotics.
3. Remedial measures for psychosocial causes- like change in environment.
Sequelae: growth retardation, mental retardation, social and emotional problems, delinquency.
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Hypothyroidism (congenital)/cretinism
Most common cause of mental retardation.
Can be due to thyroid injury/goiterogens (lithium amiodarone), transient causes- marked TSH receptor
blocking antibodies, and iodine excess.
Etiology:
1. Iodine deficiency- most common cause.
2. Thyroid dysgenesis.
3. Thyroid dyshormonogenesis.
4. Hypothalamic pituitary deficiency.
5. Complete genesis/partial thyroid- ectopic thyroid.
Clinical history- fever/goiter/MR
Physical examination
1. Large posterior fontanelle (>1 cm diameter)
2. Prolonged jaundice
3. Macroglossia
4. Hoarse cry
5. Goiter
6. Distended abdomen- umbilical hernia with constipation
7. Delayed milestone delayed milestones, delayed deciduous teeth
8. FTT- somnolence feeding problems
9. Dry skin, poor hair and nail growth.
10. Waddling gait
11. Characteristic oedematic features
12. In iodine deficiency cases:
i. Spastic diplegia
ii. Strabismus
iii. Deaf mutism
iv. Goiter
v. Short stature in older children

Neonatal screening: (window period for neurological intervention will elapse if done later)
At 3-5 days of birth by heel prick/earlobe prick estimating T4 and TSH. Usually TSH>50mm/L add
T4<6.5mcg/L.
Treatment: Lifelong thyroxine 10-15mcg/kg/day to bring T4 to 12-16mcg/dL asap
Monitoring:
1. Symptoms and signs 2. Height and bone age 3. Hormonal assessment
Clinical features in older children
1. Short and stocky
2. Immature U/L segment ratio
3. Markedly delayed bone age
4. Sexual development is infantile
5. Delayed puberty
6. Cretinoid puffy face
7. Myxedematous skin and subcutaneous tissue
8. Dull face with reaction time increased susceptibility to cold.
Q. Differences between clinical features of hypothyroidism in an infant and 6 mo old child
Congenital Acquired
Open posterior fontanel Growth retardation
Umbilical hernia Delayed skeletal maturation
Edematous facies Delayed dental development
Constipation Delayed puberty
Pallor Myopathy and pseudohypertrophy
Hypothermia Enlarged sell
Large tongue Pseudotumor cerebri
Rough and dry skin
Hypotonia
Large abdomen
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Enuresis
Definition: Normal and near complete evacuation of bladder at an inappropriate place and time for at least 2
times in a month in a child of age >5 years.
Types:
I. On the basis of achievement of control
1. Primary (common): the child has never been dry at night repeated at least twice a month, for 3
consecutive month. Passage of urine into clothes bed during night in a child >5y who has never
been at night.
2. Secondary: child has been dry at night for 6 months and then again starts bed wetting
II. On the basis of time of the day- nocturnal (night), diurnal (day), or both.
Causes
1. Genetic (40% incidence- with h/o 1 parent, 70%-both parents)
2. Markedly delayed bone age (more of an association)

3. Organic cause: spina bifida/ectopic bladder
4. Physiological factors:
i. Less secretion of ADH/ impaired response of kidney to ADH.
ii. Sound sleep compared to other children.
iii. Delayed micturition threshold.
iv. Sphincter control
5. Psychological factors-like anxiety.
6. Increased bladder irritability due to acute stress/traumatic condition/emotional difficulties/UTI
constipation.
7. Polyuria due to DM-I.
8. Micturition deferral: due to waiting until last minute to void urine.
Evaluation:
1. History- i. Type of enuresis, ii. time of enuresis, iii. frequency, iv. history related to organic pathology
2. Psychological history.
3. Examination to rule out organic causes.
4. Lab revaluation-urine analysis and culture, blood examination, intravenous pyelography to rule out
organic pathology.
5. A voiding diagram with frequency and volume charting urine output and fluid intake for the last 2
days with a record of daytime accidents, bladder symptoms and bowel habits for at least 7 days is
useful to
i. Detect non-monosymptomatic events or polydipsia.
ii. Information about nocturnal polyuria.
iii. Monitor compliance to instruction and response to therapy.
Management:
1. Depends on age of the child and type of enuresis.
2. General advice to be given to all enuretic children but active management is given after 6 y of age.
3. Counselling: (not helpful in functional bladder capacity)
i. Avoid caffeinated drinks like tea, coffee, soda in the evening
ii. Adequate fluid intake during the day
4. 1 line of treatment: non pharmacological:
st
i. Motivational therapy the child is reassured and provided emotional support. Benign nature of
the disease is explained, child is encouraged to assume active responsibility including changing
clothes and bedding. Child is encouraged void frequently (avoid urgency and daytime
incontinence) and have daily bowel movement. Stool softener such as polyethylene glycol
helps in constipation.
ii. Alarm therapy: With bed-wetting alarms, a special moisture sensor placed in the child's
pajamas triggers a bell or buzzer to go off at the start of urination. The alarm is designed to
awaken the child so he or she can get to the toilet and finish urinating.
5. Pharmacotherapy involves
i. Imipramine, ii. desmopressin
iii. Anticholinergic drugs like oxybutynin, tolterodine
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Trisomy 21 (Down’s syndrome)

1. Most common chromosomal disorder frequency is 1:800-1000 .
2. More common in mothers conceiving at older age .

3. Trisomy 94% translocation 5%.
Clinical features: Children suffering from Down’s syndrome have dysmorphic features also structural and
functional abnormality
I. Dysmorphic features
1. Facial features (Mongoloid facies)
i. Flat face**
ii. Short and upslanting palpebral fissure**
iii. Epicanthal folds
iv. Sort ear with abnormal ear lobes**
v. Protruding tongue
vi. Small teeth, small mouth
vii. High arched palate
viii. Small nose with flat nasal bridge
2. Other dysmorphic features
i. Skin excess posterior neck skin**
ii. Simian crease**
iii. Clinodactyly-short hand and finger marked by incurved fifth finger** (due to hypoplasia
of middle phalanges of fifth finger)
iv. Wide gap between first and second toe (it’s called sandal gap)
v. Duodenal atresia (common)
vi. Annular pancreas
II. Functional and structural abnormalities

1. Hypotonia**
2. Poor moro reflex and hyper flexibility of joints**
3. Mental retardation
4. cardiac defect VSD, PDA, ASD
5. Dysplastic pelvis**
6. Increased risk of cataract
7. Conductive hearing loss
8. Hypothyroidism
9. Increased risk for AML and ALL
10. Small genitalia
**Halls criteria: If 4 or more present, strong possibility of Down’s.
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Autism
Definition: Autism is characterized by profound deficit in interpersonal and communication skills. Autistic
spectrum of disorder is a triad of impaired social interaction, impaired communication, and impaired
imagination.
Etiology:
1. Intrauterine rubella.
2. Fragile X-syndrome.
3. Phenylketonuria.
4. Herpes simplex encephalitis

Specific symptoms
1. Onset before 3 years of age.
2. Impact social interactions, mental retardation.
3. Impaired verbal and nonverbal communication.
4. Restricted repertoire of activities and interest.
Management
1. Special education.
2. Medical management only for associated problems like severe hyperactivity, aggression & self-abuse.
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Breath holding spells

Definition: It is a reflexive event initiated by a provocative event that occur in anger, frustration or pain causing
the child to cry.
It is a conduct disorder due to some cause (being hurt or thwarted) where child holds his/her breathing in
expiration which may lead to cyanosis (with or without hypoxia, limpness and convulsions)
Types
1. Cyanotic breath holding spells- provocating event like anger or pain.
2. Pallid type of breath holding spells- due to fear or fight.
Clinical features
1. Rare before 6 months, peak at 2 years, abates by 5 years
2. Cyanotic type sequence:
Child starts crying
Crying stops at full expiration
Becomes apneic and cyanotic (raised intra-thoracic pressure→

decreased venous return →cardiac output)
May lose consciousness, become hypnotic and fall
If spell is >few sec, brief tonic-clonic seizures may occur
3. Pallid: precipitated by minor injury or fright: cyanosis is absent.

D/d- seizures, cardiac arrhythmia, brainstem malformation.
Investigations: to rule out the ddx- EEG, ECG, CT/MRI.
Management:
1. Reassurance that the apneic spells are self-limiting and do not cause any brain injury or death.

2. Counselling to parents: they should remain consistent in their behaviours, remain calm during the
event and avoid picking up of child (can reduce blood to the brain), turn to side so secretions don’t
get aspirated.
3. Child should never drive any benefit from a breath holding episode.
4. Dealing with an episode of breath holding is through purposeful neglect.
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Sexual Maturity Rating (SMR)

Sexual maturity ratings (SMRs) are widely used to assess adolescents' physical development during puberty in
five stages (from preadolescent to adult). Also known as Tanner stages, SMRs are a way of assessing the degree
of maturation of secondary sexual characteristics. Note that it starts from stage 1 and not 0., pre-pubertal is
stage 1)

DEVELOPMENT

Definition: Development refers to maturation of functions and acquisition of various skills for optimal
functioning of an individual.
Rules of Development
1. Development is a continuous process.
2. Development depends on the functional maturation of the nervous system. (no amount of practice
can make a child learn new skills in its absence).
3. The sequence of attainment of milestones is the same in all children.
4. The process of development progresses in a cephalocaudal direction.
5. Certain primitive reflexes have to be lost before relevant milestones are attained. (e.g., palmar grasp is
lost before voluntary grasp is attained)
6. The initial disorganized mass activity is gradually replaced by specific and willful actions.
Q. How do you assess development?
Goodenough draw-a-person test:

It is a psychosocial projective personality or cognitive test used to evaluate children and adolescents for a variety
of purposes. Developed by Florence Goodenough in 1926. (Not because it is a good enough test!) Ask the child
to draw a man, woman and themselves. No further instructions are given. Hence there is no influence of other
factors such as language and special needs. To assess intelligence, a quantitative scoring system analyzing 14
different aspects/ specific body parts and clothing is used. It should not be used instead of well-established
intelligence tests.

Factors affecting development (explain how the mentioned factors will affect, too)
I. Pre-natal factors
1. Genetic factors- Intelligence of parents, Chromosomal anomalies like Down ’s syndrome.
2. Maternal factors
i. Maternal nutrition
ii. Exposure to drugs and toxins
iii. Maternal diseases and infections.
II. Neonatal risk factors
1. Intrauterine growth restriction
2. Prematurity
3. Perinatal asphyxia
III. Postneonatal Factors
1. Infant and child nutrition (micronutrients and vitamins-zinc, vitamins A, B12, D, E)
2. Iron deficiency
3. Iodine deficiency (lead to congenital hypothyroidism and irreversible mental retardation)
4. Infectious diseases (diarrhea, malaria, HIV)
5. Environmental toxins (lead, arsenic, pesticides)
6. Acquired insults to brain (traumatic or infectious insults like meningitis, encephalitis, cerebral
malaria, near drowning, trauma)
7. Associated impairments
IV. Psychosocial Factors
1. Parenting (emotional warmth or rejection of child)
2. Poverty
3. Lack of stimulation Social and emotional deprivation and lack of adequate interaction.
4. Violence and abuse- has profound psychological effect on the child
5. Maternal depression
6. Institutionalization e.g., orphanages
Protective factors: breastfeeding and education to the mother.
Milestones: (also refer to the primitive reflexes table under CP topic under neurology)
Age Ventral suspension Prone Supine Pull to sit
Birth Lacks head control Head turned to 1 side, pelvis Asymmetric tonic Complete head
high up, knees drawn up reflex at rest lag
6w Momentarily hold head Lifts chin up momentarily, Asymmetric tonic Head lag ↓
in the same plane hips and knee partially reflex present
extended intermittently at rest
8w Head in same plane Head in midline, face lifted - Head lag ↓↓
45°
12 w Head well up beyond Lifts and holds chin and Asymmetric tonic No head lag
the plane shoulder off the couch for reflex absent
prolonged periods

Age Gross motor Fine motor Social Speech & language
1m Hands closed Looks at face when Small throaty noises,
talked to (face turns head to sound
regard)
2m Hands frequently Social smile Smiles and vocalizes
open, slight grasp Second month when talked to
reflex
3m Primitive grasp reflex Recognizes mother Squeals with pleasure,
Shows interest in cooing sounds
surroundings
4m Hands come together Shows massive Laughs loudly
in midline to play reaction with 4
Hand regard limbs on
Bidextrous approach excitement,
Turns head when
called
5m Sit with support from Plays with toes/feet Razzing- aah, ooh
others Takes foot to mouth
6m Prone- bears some wt in Unidextrous approach Shows likes & Monosyllables (Ma, Ba)
hands, Grasps object with dislikes, smiles at
Can sit with own ulnar aspect mirror image
support (tripod), Stranger anxiety
Bears some wt on legs Stretch arm when
when held in standing mother tries to lift
position
7m Rolls from supine to Transfers obj from 1 Resists things being
prone, hand to another taken away
Sit without support for (negativeism)
few mins, Separation anxiety
Bears full wt on legs
8m Crawls on abdomen Responds to own Combines syllables-
Sit without support name, Mama, dada
Enjoys peek-a-boo
9m Pull to stand Palmar grasp Waves bye-bye
obliterated Laughs when
Immature pincer laughed at
grasp-thumb and Object prominence
index finger
10m Creeps (abd off ground) Deliberate dropping Speaks 1 word with
of things meaning, says no
11m Sits up from supine Uses index finger to
position, pivots in sitting poke object, put cubes
position, in &out of container
Walk with support –
holding (cruising with
furniture)

Age Gross motor Fine motor Social Speech & language
12m Walks with 1 hand held, Mature pincer grasp Comes when called Speaks 1-2 words with
pivots and manipulates Throws objects on the Simple ball game meaning, tries to
things around floor Enjoys playing and imitate words
clapping
13m Walks independently Turns 2-3 pages/time 2-3 recognizable words
without support-broad
based gait
14m Walks sidewards & 2-6 recognizable words,
backwards can name a familiar
object (pencil)
15m Walks well Drink from cup, feed Feeds self Jargon speech
Creeps upstairs without help, Follow simple Can name pictures
tower of 2 cubes commands (kiss)
imitate scribble Domestic mimicry
18m Running Copy vertical stroke Tells mom about Speaks > 6 words
Creeps upwards and ↓ Tower of 3 cubes wetting Tries to sing a song
Carries things while Unzip pants Shows jealousy and
walking Train of 4 cubes affection
Dry by day
2y Walks ↑ 2feet/step Tower of 6 cubes Wears simple Simple 2-word
Jumps Turns 1 page/time garments (socks) sentences at 2y
Spontaneous scribble Enjoys simple Uses I, me, you
Can undress self stories/songs Speaks>50 words
Open door knobs Parallel play Points to 2-3 body
parts
2.5y Tower of 8 cubes Plays alone 2-3 words/sentence
3y Ride a tricycle Dress and undress self Identify 3 basic Good vocabulary
Alternate step climbing Tower 9 cubes colours (>250 words)
Stand momentarily on 1 Copy a circle Goes to toilet Asks questions
leg Forms a bridge unassisted Knows full name, age,
Comes ↓ 2 steps/time Obeys triple order sex
(go to room) Understands numbers
3.5 Narrate events
4 Stand on 1 leg Copy a ✕ , □ Matches 4 colours Tell long stories, asks
Can come↓ 1step/time Draw a man with 4 Right & left meaning of new words
Hops on 1 foot parts discrimination
4.5 Catch a ball, climb a tree Understands
opposites- right
&wrong
5 Skip with both feet Copy a △ Shows interest in Counts upto 10,
Throw accurately sports and study Can say address
Simple addition

Sight: 4 weeks- follows finger upto 90o, at 3 mo- 180o & fixes onto object and binocular vision
Hearing: Startling response at birth, 4 mo horizontal localization, 6 mo vertical localization, 10 mo oblique
localization of sounds.
Development quotient= Average age of attainment X 100

Observed age at attainment <70% needs evaluation
Causes of developmental delay: (maybe asked to divide into preventable and non-preventable)

IMMUNIZATION

National immunization schedule
Age Vaccine 2021 addition
Birth BCG, OPV (0 dose), HepB (0 dose)
6 weeks Pentavalent, OPV, IPV, Rotavirus PCV
10 weeks Pentavalent, OPV, Rotavirus PCV
14 weeks Pentavalent, OPV, IPV, Rotavirus PCV
9 months Measles, Vitamin A, JE
16-24 months DPT, OPV, Vitamin A, JE, Measles
5 years DT, Measles booster
10 years TT
16 years TT
Pregnant women 2 TT at 4 week interval
Pentavalent- DPT, Hib and HepB

Rotavirus- only in MP, Maharashtra, AP and Telangana
Japanese Encephalitis (JE)- only in south Indian states + Odisha
Optional vaccines: Typhoid, and cholera.
-------------------------------------------------------------------------------------------------------------------------------
Catch-up immunization
Visit Age <7 years Age >7 years
At evaluation BCG, OPV Tdap
DTwP/DTaP Hep B
Hep B
After 1 mo OPV dT3
DTwP/DTaP HepB
HepB
After 2 mo MMR/ Measles MMR
Typhoid Typhoid
After 6 mo DTwP/DTaP HepB
HepB
----------------------------------------------------------------------------------------------------------------------------- -----------
Hib vaccine
It is a conjugate vaccine consisting of capsular polysaccharide PRP of Hib, conjugate to carrier protein, for
protection against pneumonia, meningitis and bacteremia.
Types:
1. PRP-D: Polysaccharide conjugated to diphtheria toxoid.
2. PRP-T: with tetanus toxoid.
3. PRP-OMP: with outer meningococcal protein.
Dose: 0.5mL. IM, anterolateral thigh.

Vaccination: 6 mo.: 3 doses at 2 mo interval, booster 12 mo after 3 rd dose.
6-12 mo: 2 doses at 2 mo intervals, booster 12 mo after 2nd dose.
12-15mo: single dose, booster 12 mo later.
Indication: Splenectomy, Sickle cell anemia, HIV, malignancy, immune-deficient states.
----------------------------------------------------------------------------------------------------------------------------- -----------
DPT
It is combined vaccine containing diphtheria, pertussis and tetanus
Contents: Diptheria toxoid: 25Lf, tetanus toxoid 5-25Lf, B.Pertussis=20,000 million killed Bactria (4IU),
Al.phosphate 1.5mg, Thiomersal BP 0.01%
Age: 6-10-14 weeks. Booster at 16-24 mo and second booster at 5 years
Route: deep IM, anterolateral thigh, 0.5mL (as gluteal region might cause sciatic n. injury)
Complications (attributed to pertussis component): encephalitis/encephalopathy, prolonged convulsions,
and infantile spasms.
Contraindications:
1. Progressive neurological disease (CP, idiopathic epilepsy aren’t contraindications)
2. Uncontrolled convulsions.
3. Contraindication to 2nd dose- convulsions, encephalopathy, anaphylaxis, shock like syndrome,
hyperapnea, persistent high-pitched cry on 1st dose.
Storage: 4-8°C, should NOT be frozen.
DT vaccine:
Contains 2Lf diphtheria toxoid /dose. For immunizing children >12 years.
Dose: 2 doses at interval of 4-6 week followed by 6-12 mo after 2nd dose.
----------------------------------------------------------------------------------------------------------------------------------------
Combination vaccine
Definition: vaccines which merge several antigens in a single vaccine that act against different disease/
protect against multiple strains of infectious agents causing the same disease.
Characteristics:
1. Provide all antigen in single vaccine Advantages:
2. Shall be administered preferably oral 1. Fewer visits needed hence ↑ compliance
3. Shall be heat stable and coverage
4. Effective if administered soon after birth 2. ↓ storage space, ↓ expenditure on storage
5. Affordable and packing.
E.g.: Pentavalent vaccine

----------------------------------------------------------------------------------------------------------------------------- -----------
BCG
Protects against TB meningitis, miliary TB. Protection from PTB is only 50%.

Vaccine: Live attenuate vaccine. Copenhagen Danish 1331 strain of BCG bacillus.
Dose: 0.1mg/0.1mL contains 0.1-0.4 million bacilli. Diluted with NS.
Route: ID, tubercular syringe
Site: Right above insertion of deltoid. 26 gauge ID needle, causing a wheal of 5 mm.
Age: at birth/6 weeks (i.e., the next vaccination date) if not given at birth.
Catchup: Upto 1 year (National Schedule), upto 5 y (IAP)
Storage: Stable for 1 y at 6-8o C. Drops rapidly on reconstitution.
Phenomena after vaccination
BCG→ (2-3 weeks) →papule (red, tender, indurated) → (5 weeks) →increase slowly to 4-8mm→ (6-12weeks)
→Healing with permanent scar.
Positive to tuberculin test 12 weeks after vaccination
Complications
Local General
Abscess Enlargement of draining LN Fever
Indolent ulcer Suppurative lymphadenitis Disseminated BCG infection
Keloid Otitis media
Lupus vulgaris Osteomyelitis
Contraindications- generalized eczema, infective dermatosis, deficient immunity, hypogammaglobulinemia
BCG adenitis- enlargement of regional LN after BCG. May form sinuses. Rx-INH powder.
BCG test Significance: negative helps in excluding TB.

Can be done directly with prior MT or if MT is negative (MT=Mantoux test). Read on 3rd day. Type of reactions:
1. Classical reaction: develops after 3-6 weeks with erythema/papule formation and occasionally
ulceration. Subsides in 2-3 months leaving a small scar.
2. Accelerated BCG reaction: whole process is fast. Shows papule in a few hours and pustule on 3 rd day
and scab by 5-6 days.
3. Delayed reaction: papule takes 72 hr to appear and subsequent course takes place similar to the
classical reaction.
----------------------------------------------------------------------------------------------------------------------------- -----------
Hepatitis B
Contents: contains small envelope proteins which contain the principle envelope antigen HBsAg), it’s a
recombinant vaccine
Dose: 0.5mL<11y and 1mL>11y. Site: IM, at the insertion of deltoid. Normal: 0,1,6 months and booster at 5
years. High risk: 0,1,2 months and booster at 12 months given to infants of HB +ve mothers.
Adverse effects: Local soreness, fever, fatigue.
Contraindications: Anaphylaxis to previous dose
Storage: 6—8 oC, do not freeze.
----------------------------------------------------------------------------------------------------------------------------------------
Pneumococcal (Pneumococcus causes 12-50% of CAP, 30-50% of otitis media.)
Type: purified polysaccharide. 13-valent and 23-valent (commonly used).
Dose and site: 0.5 mL SC/IM. 3 doses 4 weeks apart in a child > 6 weeks of age. 1 booster not before 5 y

Indication: Sickle cell anemia, anatomic or functional asplenia, nephrotic syndrome, HIV infection, cochlear
implants, asplenia, chronic cardiac and liver diseases.
Side effects: hypersensitivity reaction. The vaccine is 95-99% effective.
----------------------------------------------------------------------------------------------------------------------------------------
Acellular pertussis vaccine: (Advantage: less reactogenic)

Content: Inactivated pertussis toxin combined with filamentous hemoglutinin. Sometimes additional
component such as a fimbrial antigen and preactin is also present.
Administration: with DP, also with hepB.
----------------------------------------------------------------------------------------------------------------------------------------
Measles vaccine
Edmonston-Zagreb strain live attenuated vaccine. Maternal immunity interferes with the vaccine.
Dose: 0.5 mL SC Right upper arm/anterolateral thigh
National Immunization schedule 9 mo (6 mo if there is a measles outbreak), 12-15 mo and followed by booster
at 4-6 years.
Adverse effects: Fever, macular rash (measles like rash 5-10 days later)
Contraindications: Immunosuppression, malignancy, Active TB
Storage: 2-8 oC, sensitive to heat and light. Use within 4-6 h after reconstitution
----------------------------------------------------------------------------------------------------------------------------------------
Meningococcal
0.5mL SC/IM anterolateral thigh. Single dose given in high-risk category patients >2 years.
Fever, pain are the adverse effects. 2 types-conjugate and unconjugated.
----------------------------------------------------------------------------------------------------------------------------- -----------
OPV
1 drop contains 105-106 attenuated viruses of each serotype (1 and 3). MgCl 2 is used as a stabilizing agent. Can
be stored at 4-8oC for 3-4 months and -20oC for 1 year. VVM is used to keep track of exposure to heat. 3
doeses are given at 6,10 and 14 weeks. Booster at 15-18 months and 5 years. Breastfeeding and diarrhea are not
contraindications for OPV. Dose: 2 drops.
IPV
Dose: 0.5mL IM/SC. Schedule: 2 doses at 6 and 14 weeks and booster at 15-18 months. Sensitive to light.
IPV (Salk type) OPV (Sabin type)
Killed formalized virus Live attenuated virus
Given SC or IM Oral
Induces circulating but not local (intestinal) immunity Induces humoral as well as local immunity
Prevents paralysis but not reinfection by wild polio virus Prevents intestinal reinfection
Not useful in controlling epidemics Single dose induces substantial immunity
during epidemics
More difficult to manufacture Easier
Virus content is 10,000 times more than OPV leading to Cheaper
increased cost
Does not require stringent conditions for storage and Requires to be stored at sub-zero
transportation, has longer shelf life temperature

Typhoid Vaccine
Vi capsular polysaccharide vaccine- 0.5mL SC/IM given in anterolateral thigh (deltoid in adults). Not
included in NIP, IAP recommends 1 dose at 2 years, repeat every 3 years. Catchup- 1 dose >2 years.
Adverse effect- Local pain and swelling. Contraindications: Anaphylaxis to previous dose.
Storage: Do NOT freeze.
Oral: live attenuated, S.typhi Ty21a, >6 y. dose: 1,3,5 days- 1 capsule each.
----------------------------------------------------------------------------------------------------------------------------------------
Varicella vaccine
Oka strain from HDC culture, contains 1000 plaque forming units/dose. Has 95-99% efficacy.
Not in NIP. Indications: Cardiac/Pulmonary disease, HIV of CD4>15% for age, leukemia during remission,
nephrotic syndrome, household contacts of immunocompromised.
Dose: 0.5 mL on anterolateral thigh/ upper arm. IAP recommends 2 doses at 15-18 mo and 4-6 years.
Catchup: complete 2 doses within 3 mo period.
Adverse effects: Fever (rare), local pain and tenderness.
Use within 30 mins of reconstitution.
----------------------------------------------------------------------------------------------------------------------------------------
Hepatitis A
Formalin inactivated, grown on HDC culture, Contains 720 ELISA forming units with Al(OH)2
0.5 mL IM deltoid, 2 doses >1 years given 6 months apart. 95-100% effective. Avoid in infancy.
Adverse effects: Local pain, nausea, anorexia, malaise.
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Rotavirus
Rotarix- Monovalent live attenuated vaccine containing G1P strain, 10 6 virus. 1mL lyophilized/ 1.5mL liquid.
RotaTeq RV5 is a pentavalent bovine +human strain. 3 doses given at 2,4,6 months completed by 8 mo.
Increases chances of intussusception. Dose: 2 mL oral.
Contraindications: past h/o intussusception, immunodeficiency.
Precautions: Postpone vaccination during diarrhea/ moderate illness.
Storage: 2-8oC, do not freeze.
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Cold chain:
Definition: it is a system of storage and transport of vaccine at low temperature from the manufacturer to the
actual vaccination site.
Vaccines kept in freezer compartment: polio, measles

Vaccines kept in cold compartment: DPT, TT, DT, BCG and diluents

Cold chain equipment
1. Storage
i. Electrical 2. Transportation
a. Walk-in-cooler (WIC) i. Refrigerated vaccine van
b. Walk-in-freezer (WIF) ii. Insulated vaccine van
c. Ice-lined refrigerator (ILR) iii. Cold box
d. Deep freezer iv. Vaccine carrier
e. Domestic refrigerator 3. Associated
ii. Solar i. Stabilizer
a. Solar refrigerators battery drive ii. Icepack
b. Solar direct drive iii. Generator, invertor
iii. Non-electrical
a. Cold box
b. Vaccine carrier
4. Temperature monitoring devices
i. Thermometer
ii. Electronic data logger
iii. Freeze indicator
iv. Real-time temperature monitoring device
v. Vaccine vial monitor
Regional level: walk-in. supplies 4-5 districts for 3 months

Deep freezer: 300L at district level and 140L in PHC.
Cold box (16-20 vials capacity), dry carriers (6-8 vials) and ice packs are used in peripheral centers.

RENAL

Acute post-streptococcal Glomerulonephritis
Definition:
Acute, specific, self-limiting glomerulonephritis following pharyngeal/cutaneous infection with nephritogenic
strains of group A β-hemolytic streptococci.
Pathogenesis
Microscopy:
Electron microscope shows lumpy
deposits on sub epithelial side of
capillary basement membrane.
Subepithelial electron dense
deposits are called humps when
they are large. Immunofluorescent
studies show granular deposition of
IgG and complement (C3) along
the capillary walls
Strains: Pharyngitis- M4 and 12, pyoderma-M 49

Clinical Features:
1. School age children, more commonly in boys (ages 3-12 y)
2. Rapid onset puffiness around eye (more in the morning) and pedal edema
3. Characteristically cola-coloured urine (microscopic hematuria not lasting beyond 1-2 weeks)
4. Oliguria
5. Hypertension (resolves with loss of edema)
6. Proteinuria
7. In atypical cases-
Convulsions (hypertensive encephalopathy)
Left ventricular and pulmonary edema (malignant HTN and hypervolemia)
Acute Renal failure
Nephrotic syndrome
Diagnosis/Investigations:
1. Blood- Leukocytosis (infection)
2. Hb- anemia (NCNC due to hemodilution)
3. ESR –raised
4. BUN- elevated
5. Blood creatinine- elevated
6. Urine- Oliguria, hematuria (RBC casts), Proteinuria (1+/2+)
WBC and Granular cast –indicates glomerular inflammation, and not evidence of UTI.
7. CRP-C3 level reduced
8. If oliguria continues- hyponatremia, hyperkalemia
9. Evidence of strep infection- Throat swab, ASO titer increased, Anti-DNAse B increased.

Indications for renal biopsy:
1. Onset with no evidence of preceding infections.
2. Atypical early features- renal failure, nephrotic range of proteinuria.
3. Atypical late features- Failure of normalization of RFT>4 weeks, azotemia >2 weeks.
C3 levels low beyond 6-8 weeks.
Proteinuria beyond 8 weeks
Gross hematuria >3 weeks, microscopic hematuria >24 months.
HTN > 2 months.
4. Systemic involvement (SLE or hereditary nephritis).
5. Family h/o renal disease.
Important Complications:
1. ARF
2. Pulmonary edema/CCF
3. Hypertensive encephalopathy
4. Hyperkalemia/hyponatremia
5. Over hydration may increase HTN and ppt LVF
Treatment
1. General
• Bed rest
• Daily weight chart
• Urine for quantity, protein and hematuria
2. Diet
• Intake of protein, sodium, and potassium should be restricted till the blood urea value reduces and
urine output increases.
• Restriction of fluid intake to an amount equal to insensible loses (lung/skin/feces/respiratory) and
2 hr urine output.
3. Antibiotics
Once acute GN has set in Rx penicillin has no effect on the course of the disease, but maybe given if
pyoderma or pharyngitis is present. Benzathine penicillin IM single dose-
If body wt <20kg: 0.5 million units, >20 kg: 1.2 million units.
4. Hypertension
Mild salt and water restriction
Other-atenolol (cardioselective β blocker) Others- amlodipine, nifedipine, diuretics
5. Edema/CCF/LVF
Furosemide (indicated only in pulmonary edema/CCF)-2-4 mg/kg
Nasal O2, respiratory supplement with PEEP (positive end respiratory pressure)
----------------------------------------------------------------------------------------------------------
Nephrotic syndrome
Definition
Clinical condition characterized by massive proteinuria(>3g/day), hypoalbuminemia, generalized edema and
associated hyperlipidemia.
(anasarca- when 2 or more areas involved (out of periorbital, legs and abdomen), or when interstitial edema
causes hypovolemia. Therefore, RAAS axis causes Na and H2O retention)

Values
1. Proteinuria >40mg/m2/hr, >1g/m2/day, 3+/4+ by dipstick, >3g/day
2. Hypoalbuminemia- serum albumin <2.5g%
3. Hyperlipidemia- cholesterol >250mg% (Liver’s compensation for hypoalbuminemia)
Types: 1. Minimal change disease 2. Significant glomerular lesions (almost never responds to steroids)
Investigations:
I. To confirm the diagnosis
1. CBC- anemia, leukocytosis
2. ESR- increased
3. Urine-proteinuria 3+/4+, Hematuria +/-, Hyaline and granular casts
4. Serum albumin <2.5g%

5. Serum cholesterol >250mg%
6. Serum BUN and creatinine -MCNS (minimal change NS)- Normal (otherwise increased in
hypovolemia)
II. To rule out infection
1. Blood culture
2. Mantoux test
3. X ray chest- pneumonia, TB
4. Urine culture (suspect UTI)
5. Peripheral smear- malaria
6. HbSAg- Hepatitis B
7. VDRL-syphilis
III. Additional test in case the scenario looks atypical
1. Frequent relapses
2. Resistant to steroids
• C3 level- decreases in GN while nephrotic normal
• ASO titre increased in GN
• Throat swab positive in GN
3. SLE/RA suspected- ANA, Ds DNA, RA factor
IV. Others- USG abdomen, renal Doppler, ascitic tap.
Complications:
1. Thromboembolism: of renal and cerebral veins
• Causes: Increased level of fibrinogen, factor V, VIII, platelets (like in DIC)- enhanced coagulation.
• Decreased levels of antithrombin III, Factor IX and XI- low ability to limit coagulation.
• Treat with LMW heparin, followed by oral anticoagulants.
2. Infection (decreased IgG due to low protein, and steroids)
Strep pyogenes, SBP, TB, Viral infections-chickenpox (give vaccine/ oral acyclovir) and measles,
cellulitis, pneumonia, meningitis.
3. Growth retardation: Due to protein deficiency anorexia and steroids.
4. Cardiovascular disease, hypertension.
5. Anemia
6. Hyponatremia
7. Acute renal failure and hypovolemia (Rx- discontinue diuretics, admit and give rapid infusion NS, or
5-20% albumin)
8. Hypocalcemia
9. Complications of steroid therapy:
Cushingoid features, short stature, HTN, osteoporosis, subcapsular cataract
*Mnemonic* GIT-CHA-CHA
G rowth retardation
I nfection
T hromboembolism
C VS disorders C omplication of steroid therapy
H ypertension H ypo natermia and hypocalcemia
A nemia A cute renal failure

Treatment
I. General
1. Diet
i. Salt restriction (salt is restricted to the amount used in actual cooking)
ii. Fluid restriction
iii. Maintenance of protein- normal to low protein diet
2. Complications
i. Thromboembolic episode
• Adequate fluid management
• Prevent immobilization
• Antiplatelet agent, - aspirin
• Anticoagulants- LMWH, followed by oral
ii. Infection- antibiotics, vaccination (pneumococcal and varicella)
iii. HTN- ACE inhibitors (enalapril), CCB (Nifedipine)
iv. Anemia- oral iron supplements.
v. Correct hypocalcemia and hyponatremia
3. Edema
i. Diuretics- furosemide 1-4 mg/kg/day in 22 divided doses
ii. Human albumin infusion- when albumin falls below 1.5 g%
II. Specific
1. APN regimen. Arbeitsgemeinschaft fur PadiatriShe Nephrologie regimen.)

Initial episode-prednisolone 60 mg/m2/day (or 2 mg/kg/day) for 6 weeks in 2 or 3 divided doses,
followed by 40 mg/m2/day (1.5 mg/kg/day) on alternate days for 6 weeks.
Relapse-prednisolone 60 mg/m2/day till remission, followed by 40 mg/m2/day for 3 days in a week
for 6 weeks.
2. ISKDC Regimen (International Study Group on Kidney Disease in Children)

Initial episode: prednisolone 60 mg/m 2/day (or 2mg/kg/day) in 2-3 divided doses for 4 weeks,
followed by 40 mg/m2/day (or 1.5mg/kg/day) for 3 consecutive days in a week for 4 continuous
weeks. Treatment stopped without tapering. Response seen in 2 weeks.
Relapse: same as for initial except that prednisolone is 60 mg/m 2/day till the urine has been free of
protein for 3 consecutive days.
3. Modified ISKDC Regimen- After 4 weeks of treatment, prednisolone 40 mg/m2 is given as a single
morning dose on alternate days for 4 weeks, rather than 3 consecutive days in a week.
4. If resistant to steroids (or frequent relapse/steroid dependent), immunomodulant/

immunostimulatory and cytotoxic drug is started of age> 6 years.

----------------------------------------------------------------------------------------------------------------------------- -----------
Posterior Urethral Valve:
Definition:
Congenital anomaly of the urinary tract and is an important cause of distal urinary tract obstruction.
Clinical features (boys>girls)
Ability to pass Foley’s +
1. In-utero: severe obstruction may lead to renal dysplasia (and decreased amniotic fluid leading to IUGR
and hence decreased lung development)
2. At birth: Mild to moderate impairment of renal function
3. Children: Dribbling, abnormal stream, palpable bladder, recurrent UTI
Investigations:
MCU: (micturating cysto-urethrogram)
• Dilated posterior urethra and valves at the junction with anterior urethra
• Enlarged bladder with diverticuli and trabeculations
• Vesico-urethral reflux
Treatment: Endoscopic fulguration of valves

Urinary Tract Infection
Definition: It is infection of any part of urinary tract (bladder- cystitis, kidney-pyelonephritis) with microscopy
showing cells >5-10/mm2 and >105 organisms/mL on urine culture.
(preferably single type of organism).
Organisms: E coli, klebsiella, Enterobacteriaceae, proteus and pseudomonas.
Predisposing factors:
1. Female sex, age<6 yrs
2. Voiding dysfunction
3. Vesico-urethral reflux
4. Obstructive uropathy (tumour, calculi, BPH strictures, post urethral valve)
5. Neurogenic Bladder (associated with myelomeningocele, tumour, trauma at the lumbosacral region)
6. Malnutrition
7. Immunosuppressive therapy
8. Instrumentation of the urinary tract
9. Uncircumcised penis
Presenting Complaints
Simple UTI Complicated UTI
Burning micturition High fever (>39° C)
Fever with chills and rigor Systemic toxicity
Increased frequency of micturition Persistent vomiting
Urgency and dysuria Dehydration
Hematuria uncommon Renal area tenderness
Suprapubic pain due to cystitis Raised creatinine
Sample collection:
1. Suprapubic aspiration (<2 y)
2. Urethral catheterization (<2 y)
3. Clean catch mid-stream urine for age > 2 years
Investigations:
1. ESR, CRP- raised
2. USG- Renal abnormalities
3. Urine microscopy and culture
• >10 WBC/mm3
• >105 bacteria/mL on culture (Any colony on suprapubic aspiration and >50,000/mL on
urethral catheterization)
4. Second UTI, investigations:
• USG for renal abnormality.
• Intravenous Pyelogram: to identify physiological, anatomical anomalies.
• Micturition cysto-urethrogram.
• DMSA scan (dimercaptosuccinic acid) for assessing renal morphology, structure and function.
• DTPA scan (Diethylene Triamine Pentaacetate)- Radioisotope renography, imaging of the
kidneys that uses radiolabeling technique.

Treatment:
I. Specific drug treatment
1. First attack:
• Neonates: parenteral ampicillin +Gentamicin for 7-10 days
• Infants: oral co-trimoxazole/ cephalosporin for 5-7 days
• Children: oral antibiotics for 5-7 days (Co-trimoxazole 5mg/kg/day)
Urine culture after 1 week, 1 month and then 3 consecutive months to ensure complete
clearing.
2. Recurrent attack:
Co-trimoxazole, 2mg/kg/day long term night dose
Duration of treatment depends on the interval between 2nd and 3rd episode
II. Supportive treatment:
1. Treat fever with anti-pyretics.
2. Fluid intake >2L/day –initiate water diuresis (and empty bladder frequently to prevent stasis)
3. Alkalinization of urine
4. Behavioral medication
5. Urinary analgesics and anti-spasmodic for detrusor muscle spasm
III. Surgical treatment
1. Renal or perineal abscess should be treated by percutaneous drainage
2. Vesico-urethral reflux should be corrected
3. Robotic-assisted laparoscopic ureteral implantation
4. Partial/subtotal nephrectomy is indicated in severe cases
Complications
1. Renal scarring, HTN, Renal failure
2. Pyelonephritis
3. Renal stones: urea-splitting organisms like proteus can lead to stones
4. Renal abscess (S. aureus)
5. Sepsis
----------------------------------------------------------------------------------------------------------------------------------------
Acute Renal Failure
Definition:
Denotes an acute impairment of renal function resulting in retention of nitrogenous wastes and other metabolic
derangements. Oliguria/azotemia is a prominent feature.
Causes
1. Pre-renal
• Acute gastroenteritis
• Hemorrhage, shock
• CCF
• Hypovolemia
• Perinatal asphyxia
2. Renal
• Acute tubular necrosis

• Glomerulonephritis
• Hemolytic uremic syndrome
• Interstitial Nephritis
3. Post Renal
• Calculus
• Posterior urethral valves
• Neurogenic bladder
----------------------------------------------------------------------------------------------------------------------------- -----------
Chronic Renal failure clinical features

1. Frequent passage of urine
2. Nocturia, Increased thirst
3. Anemia
4. Failure to thrive
5. Growth retardation
6. HTN
7. Bone deformities
8. Malnutrition
9. Peripheral neuropathy
10. Proximal muscle weakness

GASTRO-INTESTINAL
TRACT

Dehydration/Oral Rehydration Therapy
Oral rehydration therapy
Core management in diarrhea. Includes
• Complete oral rehydration with salt solution with composition within the WHO recommended range
• Solution made from sugar and salt (40g+4g/L)
• Food based solution- rice water (50+40g/L)
• In the presence of continued feeding, a variety of commonly available culturally acceptable fluid
irrespective of presence of glucose or without salt when former is present.
Assessment of dehydration (achar’s grading)

Condition Well/Alert Restless/irritable Lethargic/unconscious/floppy
Eyes Normal Sunken Very sunken and dry
Tears Present Absent Absent
Mouth & tongue Mist Dry Very dry
Thirst Drinks, normally Øthirsty Thirsty, eagerly drinks Poorly/ Does not drink
Skin pinch Retracts quickly Slowly Very slowly
Weight loss 2-5% 5-10% >10%
Pulse Normal Normal to decreased Weak/thready/impalpable
HR Normal Maybe increased Increased/ brady if v severe
Extremities Normal Cold Cold mottled and cyanotic
Achar’s grading No dehydration Some Severe
Plan A B C
ORS composition- NaCl-2.6, KCl-1.5, Trisodium citrate-2.9, glucose 13.5, Water 1L.
Osmolality- Na 75, K 20, Cl 65, citrate 10, glucose 75=245 mOsmL
Advantages of citrate IV rehydration solutions

• More stable product • Ringer lactate/ Hartmann solution
• Longer shelf life • Diarrhea treatment solution
• Less stool output • Normal Saline
• ↑ intestinal absorption of Na and H2O
Plan A:
1. Educate mother to continue breastfeeding & use increased amount of home available food.
2. Fluid therapy- ORS packets should be given for use at home.
Plan A After each episode of diarrhea For use at home
<24 months 20-100 mL/ loose stool 500 mL/ day
2-5 years 100-200 mL/ loose stool 1000 mL/day
>5 years As much as child wants 2000 mL/day
3. Zinc therapy- 20 mg OD for 14 days. (Probiotics optional)

4. Return to health worker if child does not get better in 3 days or has any danger signs:
i. Many episodes of watery stools, eating or drinking poorly (refusal to feed)
ii. Marked thirst, repeated vomiting, altered sensorium
iii. Fever, blood in stool, anuria

Plan B
It has 3 components
1. Rehydration therapy 2. Maintenance therapy 3. Provision of normal daily requirement
1. Rehydration therapy – give 75 mL/kg of ORS in first 4 hours. If no improvement repeat for
another 4 hours.
2. Maintenance- Begins when signs of dehydration disappears-normally within 4 hours. ORS should
be equal to diarrhea losses- approximately 10-20mL/kg body wt. given till diarrhea has stopped.
3. Provision for normal daily requirement-Breastfeed even during dehydration.
Semisolid food soon after deficit replacement
Plan C
1. Start IV fluids immediately
• While the drip is being set up give ORS if the child can drink.
• Solution used: RL+ Dextrose 5%, RL, NS
• Give 100mL/kg in the following way
Age First give 30mL/kg Then give 70 mL/kg
<12 months 1 hour 5 hours
1-5 years 30 mins 2.5 hours
• Repeat the 30 mL/kg dose if radial pulse is weak.
2. Cannot give IV
• Start rehydration with ORS using nasogastric tube at 20mL/kg/h (total 120 mL/kg)
• Reassess every 1-2 hours.
• If there is repeated vomiting or abdominal distension give fluids slower.
• If no improvement after 3 hours, try to start IV fluids as early as possible.
• When oral rehydration is possible give ORS at 5mL/kg/h
Monitoring
1. Every 15-30 mins till radial pulse and skin pinch becomes normal.
2. If no improvement, repeat plan C.
3. If improvement but still showing some signs of dehydration, start plan B and discontinue IV fluids.
4. If complete recovery, then observe child for at least 6 hours before discharge, to confirm that mother
is able to maintain the child’s hydration with ORS
Prevention
1. Diet: promote breastfeed, exclusive bf till 6 months, followed by complementary feeding.
2. Hygiene: improved water and sanitary facilities, hand wash.
3. Health education: inform about early signs and symptoms of diarrhea.
4. Immunization: rotavirus and cholera.
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Portal Hypertension
Definition: Elevation of portal venous pressure above 10-12 mmHg.

Causes:
1. Extrahepatic portal vein obstruction (EHPVO)- most common cause.
2. Cirrhosis- post viral, autoimmune hepatitis, Wilson’s disease.
3. Biliary tract disease: Biliary atresia, cystic fibrosis, choledochal cyst.

4. Post-sinusoidal: Budd-Chiari syndrome, veno-occlusive disease, CHF.
Signs of liver cell failure:

1. Jaundice, ascites
2. Spider naevi, palmar erythema
3. Clubbing, white nails
4. Flapping tremor (encephalopathy)
Complications:
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Lactose intolerance
Definition: Lactose intolerance is the development of clinical symptoms resulting from lactase deficiency
following ingestion of lactose in water in a standard dose.
Causes:
1. Primary- Autosomal recessive condition
2. Secondary-
• Acute gastroenteritis,
• PEM
• Worm infestations
• Malabsorption syndrome
• Animal milk allergy
Consequences
1. Osmotic diarrhea
2. Metabolic acidosis
3. Bacterial proliferation
4. Caloric loss

Clinical features
1. Diarrhea- watery, frothy, greenish yellow, sour smelling stool
2. Peri-anal excoriation
3. Failure to thrive
4. Abdominal distensions
5. Borborygmi flatulence
Investigations
1. Stool- pH<5.5 (acidic), reducing substance >0.5%
2. Lactose tolerance test
3. Interstitial enzyme activity by biopsy
Treatment
1. Primary: Eliminate lactose from diet
2. Secondary: Treatment of primary cause and lactose free diet if persistent diarrhea, weight loss, reducing
substance >1%
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Constipation
Definition: Delay or difficulty in defecation, present for 2 or more weeks and sufficient to cause significant
distress to the patient.
The normal stool frequency decreases from 4 or more per day during infancy to once per day at 4 yr of age. A
stool frequency of <2/week is considered abnormal for all ages.
Causes of constipation
1. Intestinal nerve/muscle disorders: Hirschsprung disease, intestinal neuronal dysplasia, pseudo-obstruction,
spinal cord abnormalities (tethered cord, myelomeningocele).
2. Anorectal: Anteriorly placed anus, anal stenosis, rectal stricture, pelvic mass (sacral teratoma).
3. Systemic disease: Hypothyroidism, celiac disease, diabetes insipidus, diabetes mellitus, hypercalcemia,
cystic fibrosis, myotonic dystrophy.
4. Developmental: Mental retardation, autism.
5. Drugs: Opiates, anticholinergic agents, phenobarbitone, vincristine, lead.
6. Associated with CP.
Management:
1. No investigations are required for diagnosis in the majority of children with functional constipation.
2. However, an X-ray abdomen may be done to document impaction in select situations.
3. Two main steps in the management are disimpaction and maintenance therapy. Disimpaction is done
by total bowel wash using polyethylene glycol (PEG) in a dose of 1.5 g/kg/ day for 3-4 days at home.
4. Behavioral training.
5. Dietary changes.
6. Medication: laxatives.
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Intussusception
It is the telescoping of a proximal segment of intestine (intussusceptum) into a distal segment (intussuscipiens).
This may be ileocolic, colocolic or ileoileal.

Clinical features:
1. Common cause of intestinal obstruction in 3 mo-6 yr.
2. Most cases occur in infants during the weaning period following introduction a new food, vaccination
or upper respiratory tract infection (leading to an enlarged payer’s patch acting as a lead point)
3. Else the lead point can be submucosal like lipoma and polyp (needs surgical resection otherwise will
lead to recurrence)
4. >2 y, inflammatory conditions like Henoch-Schonlein purpura also result in intussusception.
5. The classic triad- abdominal pain, red currant jelly stools (blood and mucus) and palpable mass.
Pathogenesis: This leads to venous congestion→ bowel edema →to arterial obstruction→ bowel ischemia→
necrosis→ perforation→ shock.
Investigations:
1. X-ray abdomen shows lack of air in right lower quadrant.
2. Ultrasound is the investigation of choice, confirms the diagnosis (target/ doughnut/ bull's eye sign).
3. Colour doppler to assess vascularity.
4. Barium enema shows a characteristic 'claw' sign (only if it involves colon)
Treatment: Early reduction with saline (under ultrasound guidance)
1. Barium contrast (both diagnostic and therapeutic)
2. Air insufflation (safer with lower recurrence rates).

CARDIO-VASCULAR
SYSTEM

Cyanotic spell (An effect of TOF)
Synonyms: Paroxysmal hyperpnea, dyspneic spell, anoxia/hypoxic spells, Guntheroth cycle
Onset: 1 month-12 y usually Peak: 6-12 mo. Typical attack usually occurs in the morning.
Natural history: Gradual ↓ in frequency with increase in age and ↓ in severity beyond 2-3 years.
Mechanism
Treatment
1. Knee chest position/squatting position
2. Humidified O2
3. Morphine 0.1mg/kg- SC for sedation
4. Correct acidosis. Obtain pH-give sod. bicarb IV
5. Propranolol- 0.1mg/kg IV during spell. Long
term-1mg/kg 4-6 hourly orally.
6. Vasopressors- methoxamine (IM/IV)
7. Correct anemia
8. Consider surgery- long term
• Blalock Taussig shunt
• Pott’s shunt
• Waterston shunt
9. Following spell: Check for neurological deficit,
short acting β-blocker, plan surgery and
administer iron.
10. Prevention: Counselling parents regarding
precipitating factors like dehydration, fever &
pain & measures to avoid them.
Alternate hypothesis of mechanism: infundibular pulmonary sub-valvular spasm due to catecholamine

release increasing right to left shunt.
Examination:
1. Cyanosis, clubbing
2. Prominent ‘a’ wave in JVP
3. Ejection systolic murmur
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Congestive cardiac failure
Definition: Inability of the heart to maintain an output at rest or stress, necessary for metabolic needs of the
body and inability to receive blood into the ventricular cavities at low pressure during diastole.
Etiology:
1. Volume or pressure overload in left to right shunts, or obstructive lesions of the left or right ventricle
2. Myocardial dysfunction due to endocardial fibroelastosis, viral myocarditis and cardiomyopathy
3. Acquired diseases such as acute or chronic RHD, myocarditis and infective endocarditis
4. Arrhythmia

5. Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA)
6. Non-cardiac causes such as severe anemia, thyrotoxicosis, systemic arteriovenous fistula
7. Renal causes: acute glomerulonephritis
8. Iatrogenic: Volume overload, cardiotoxic drugs (doxorubicin)
Clinical features
1. Symptoms
i. Poor weight gain
ii. Difficulty in feeding (suck rest suck cycle)
iii. Breathes too fast
iv. Breathes better when held against the shoulder- child equivalent of orthopnea in adults.
v. Persistent cough and wheezing
vi. Irritating, excessive perspiration and restlessness
vii. Puffiness of face, pedal edema
2. Signs Assessment of severity:
Treatment of CCF: Treatment consists of four-pronged attack for correcting inadequate output.
I. Reducing cardiac work
1. General measures
i. Restriction of activities- nursing in propped up position. Small meals.
ii. Treatment of fever, anemia and obesity
2. Specific supportive therapy
i. Oxygen administration- humidified- 40-50%
ii. Ventilator support
iii. Treat pulmonary edema with diuretic
iv. IV fluid should be given after assessing hydration status and presence of complication
such as pulmonary oedema and renal failure
v. Sedatives in restless children, after maintaining SpO2
vi. Salt restricted diet. High calorie and low Na given in older children
3. Specific drug therapy
i. Vasodilator therapy- Decreases TPR therefore reduces afterload.
• Venodilator: Nitroglycerine- in elevated ventricular filling pressure in AR
• Arteriodilators: hydralazine- 0.5-1 mg/kg/day orally in 3-4 divided doses

• Mixed vasodilators: Nitroprusside. 0.5 μg/kg/min
• Prazosin is useful in pts with pulmonary HTN
ii. ACE inhibitors. Captopril 0.1 mg/kg/dose increased gradually to 0.5-1 mg/kg/dose
iii. ARBs
iv. β -blockers
II. Augmenting myocardial activity
1. Digitalis- digoxin (Total digitalizing=0.04mg/kg, maintenance=0.01mg/kg). Dose given in
fraction ½, ¼, ¼ at 0,8 and 16 hours. Parenteral dose 1/10 of oral. 1 day drug holiday in a wk.
2. Sympathomimetic drugs: Dopamine (2-10μg/kg/min continuous IV), dobutamine
3. Phosphodiesterase inhibitors: Amrinone and milrinone
III. Improving cardiac performance by reducing heart size
1. Diuretics
2. Salt restriction
3. ACE inhibitors
IV. Treatment of underlying cause
1. Anemia by packed cells
2. Arrhythmias
3. Surgical correction or cardiac defects (PDA and VSD)
4. Myocarditis
5. Ppt factors such as fever and infection treated
6. Surgeries for cardiomyopathy
Step-wise Mx
1. Furosemide 1mg/kg dose +Amiloride/Triamterene
2. Add digoxin
3. Add ACE inhibitors and stop K sparing diuretics
4. Add isosorbide nitrate
5. Intermittent dopamine+ dobutamine (in separate IV) or dobutamine
6. Myocardial biopsy and add immunosuppression with steroids in case of active myocarditis and β-
blockers in cases without active myocarditis.
7. Cardiac transplantation
Prevention:
1. Lifestyle modification
2. Reduction of body weight
3. Early diagnosis and treatment of disorders that cause cardiac failure – like infections, thyroid
disorders, HTN, anemia, heart disorders (valvular, shunt, blocks)
4. Avoiding drugs that cause damage to heart
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NADA’s criteria for congenital heart disease: minimum 1 major + 2 minor required for diagnosis.
Major: Minor:
Any diastolic murmur Systolic murmur grade 1 or 2
Systolic murmur ≥ grade 3 Abnormal S2
Cyanosis Abnormal chest X-ray
CCF Abnormal ECG
Abnormal ECHO
Acyanotic heart diseases: ASD (Ostium primum and ostium secondum variety), VSD, PDA

TOF
1. VSD (large) 2. Pulmonic stenosis 3. Overlying dextroposed aorta 4. RV hypertrophy
Complications: infective endocarditis, hemiplegia due to paradoxical embolism
----------------------------------------------------------------------------------------------------------------------------- -----------
Complications of VSD: Complications of congenital heart diseases:
1. Recurrent chest infections 1. Pulmonary HTN
2. CCF 2. Infective endocarditis
3. Infective endocarditis 3. Growth retardation and malnutrition
4. Conduction disturbances 4. Myocardial dysfunction leading to failure
5. Eisenmenger’s phenomenon 5. Brain abscess
6. Pulmonary HTN 6. Polycythemia leading to gout, renal failure
7. Aortic/ Tricuspid regurgitation and gall stones
8. Growth retardation 7. Rhythm disorders and sudden death
9. Brain abscess 8. Cyanotic spells
10. Papilledema
11. Paroxysmal dyspnea
12. Hemiplegia
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Patent Ductus Arteriosus (PDA)
PDA occurs due to the persistence of the communication between the pulmonary artery and the descending
aorta & flow occurs both during systole and diastole as pressure gradient is +ve throughout.
Symptoms:
Small PDA: asymptomatic, poor exercise
Large PDA: Effort intolerance, palpitation, recurrent chest infection
Signs:
1. Harrison’s groove: horizontal line along the lower border of thorax corresponding to costal insertion
of diaphragm,
2. Cyanosis/clubbing of lower limbs if severe.
3. Pulse: water hammer pulse
4. Precordium: hyperdynamic apex, palpable D2, right ventricular heave
5. Auscultation: S1 accentuated and D2 loud. Gibbson’s/ Machinery/ Mill wheel murmur (continuous)
DDx:
1. Coronary AV fistula
2. Rupture of Valsalva sinus
3. Aortopulmonary window
4. Peripheral pulmonic stenosis
Treatment:
In infants, indomethacin is the drug of choice
1. Severity is graded based on the ratio of pulmonary and systemic flow (Qp:Qs)
2. Small PDA (ratio <1.5)-wait and follow-up for spontaneous closure.
3. Moderate PDA (1.5-2.5)-wait up to 2 years or until the baby weighs 10 kg.
4. PDA with symptoms such as CCF and infective endocarditis-close the PDA surgically.

Atrial septal defect
Types:
1. Fossa ovalis ASD: located in the central portion of atrial septum
2. Sinus venosus ASD: located at junction of superior vena cava and right atrium
3. Ostium primum ASD: lower part of right atrium
Clinical features
1. Soft delayed diastolic rumble.
2. ECG: right axis deviation and right ventricular hypertrophy.
3. X-ray shows mild to moderate cardiomegaly.
Treatment:
1. Small defects (<8 mm) can be observed.
2. Fossa ovalis defects with good margins can be closed percutaneously with occlusive devices. Others
require surgical closure. Closure is recommended before school entry to prevent late complications.
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Transposition of great vessels (TGA)

Definition: aorta arising from the right ventricle and pulmonary artery from the left ventricle.
TGA is classified into (a) with intact ventricular septum, and (b) with VSD. Presence of a VSD of adequate size
results in good mixing.
Clinical features: cyanotic at birth, rapid breathing, and congestive failure secondary to hypoxemia within the
first week of life. X-Ray: The cardiac silhouette can have an "egg on side" appearance. Auscultation: normal
first sound, single or normally split second sound and grade II-IV ejection systolic murmur.
Treatment: Prostaglandin E1 can help reduce cyanosis. The arterial switch operation is now established as the
treatment of choice for TGA.

RESPIRATORY
SYSTEM

Bronchial Asthma:
Definition: Bronchial asthma is a disease characterized by an increased responsiveness of the airways to various
stimuli.
Classification of asthma based on severity:

Step Symptoms Night time PEFR
symptoms
Step 1: <1 time a week; asymptomatic & ≤ 2 times a mo ≥80% predicted;
Intermittent normal PEFR b/w attacks variability <20%
Step 2: Mild >1 time a week, but <1 time a day >2 times a mo ≥80% predicted;
persistent variability 20-30%
Step 3: Moderate Daily use of β2 agonist; daily attacks > 1 time a week >60% & <80% predicted;
persistent variability >30%
Step 4: Severe Continuous, limited physical activity Frequent <60 predicted; variability
persistent >30%
Investigations
1. Spirometry: PEFR, FEV1, PVC and FEV25-75 decreased
2. Absolute eosinophil count- raised
3. Allergy test- positive
4. Chest X-Ray- Bilateral and symmetric air trapping
Treatment:
Classification Long-term prevention
Step 1: Intermittent Inhaled SABA, if needed >3times/week move to step 2
Step 2: Mild Inhaled SABA+ inhaled budesonide/fluticasone (100-200 μg) OD or sustained
persistent release theophylline
Step 3: Moderate Inhaled SABA+ inhaled budesonide/fluticasone (100-200 μg) BD and/or sustained
persistent release theophylline
Step 4: Severe Inhaled SABA +inhaled budesonide/fluticasone+ LABA + oral low dose
persistent prednisolone on alternate days
Aerosol therapy in asthma:

An aerosol is suspension of very fine particles of liquid or solid in gas
Advantages:
1. Delivery to the target tissue Limitations
2. Less dose, hence lesser side effects 1. Technique needs to be learnt
3. Rapid response 2. Cost is high
4. Self-administration possible
5. Decreases incidence of severe attack and hospitalization
Devices: MDI, Rotahalers, Spacers, Nebulizer
1. MDI: Puff synchronized (inspiration and breath is held for 10s)
2. Rotahalers: Pt has to inhale after the capsule is broken by a fin inside one of the valves
3. Spacers: MDI attached to one side and mouth to other side
4. Nebulizer: Given for 5-20 minutes.

Management of status asthmaticus:
Inhaled β2 agonists repeated every 20 min for 1 hour
O2 inhalation and oral prednisolone 1-2mg/kg
Improvement No improvement
Continue salbutamol and add

Stop O2 if the child is able to ipratropium br 250 mcg every 20
min+
maintain saturation >95% inj. hydrocortisone 10mg/kg
Prednisolone OD for 5-7 days

After 2 hours:
then stop without tapering imrovement: treat as
early responder No improvement after 2 hours
Start inj. thophylline bolus followed by

continious infusion
Magnesium 50mg/kg with dextrose over
30 mins
No improvement- Mechanical
ventilation
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Pneumonia
Definition: inflammatory process which involves the lung parenchyma.

(Clinical features, classification, and treatment are as given in the table on classification)
ARI in <2mo patients and 2mo-5 years have different classifications.
Complications of Pneumonia:
1. Pneumatocele
2. Empyema
3. Pyopneumothorax
4. Metastatic abscess.

ARI control program:
Acute lower respiratory tract infection is a leading cause of mortality in children <5years. WHO has
recommended certain clinical criteria for diagnosis of pneumonia in children at PHC for control of ALRTI by
judicious use of cotrimoxazole.

Criteria for diagnosis of pneumonia
1. Rapid respiration
2. Difficulty in respiration/chest in-drawing
Dose of cotrimoxazole:
Age Weight (kg) Tablet sulphamethoxazole 100mg+ trimethoprim 20mg
< 2mo 3-4 1 tablet twice daily
2-12 mo 6-9 2 tablets twice daily
1-5 y 10-19 3 tablets twice daily
Signs of severe disease in <2 months

1. Convulsions 5. Tachypnea
2. Abnormal sleep or difficult to wake 6. Chest indrawing
3. Stridor in calm child 7. Cyanosis
4. Not feeling well 8. Altered sensorium
----------------------------------------------------------------------------------------------------------------------------- -----------
Acute Bronchiolitis:
It is defined as the first episode of expiratory wheeze of acute onset usually in a child less than 2 years of age
who has features of viral respiratory illness like coryza, otitis media or fever, with or without indications of
respiratory distress, pneumonia or atopy.
Age: 2 mo to 2 y
Season: October to March
Sex: more common in males
Etiology: Viral: Respiratory syncytial virus, adenovirus, influenza virus, parainfluenza virus 1, 2, 3
Bacterial: Mycoplasma pneumoniae
Clinical Features:
Symptoms: Cough, dyspnea, fever, gradual development of respiratory distress, rhinorrhea, characterized by
paroxysmal wheezing cough, difficulty feeding.
Signs: Tachypnea, tachycardia, use of accessory muscles of respiration, chest retraction, respiratory distress is
out of proportion to the extent of physical sign in lungs. Expiration is prolonged, fine rales and rhonchi are
auscultated.
Investigations:
1. X-Ray: Hyperinflation and infiltrates, diaphragm pushed down, ill-defined small or hazy clustered
nodules or areas of air trapping characterized by hyperlucency and/or oligemia.
2. ABG
3. Serum electrolytes
Treatment:
1. Nursing care: humid atmosphere preferably sitting position at 30-40° angle with the head and neck
elevated
2. Oxygen: keep O2 saturation above 95%
3. IV fluids
4. Antibiotics have no role.

5. Ribavirin: shortens the course if given early in stages delivered by nebulizer 16 hours a day for 3-5
days- given in a child with co-morbidities.
6. Palivizumab- newer treatment: monoclonal antibody produced by recombinant DNA technology used
in the prevention of RSV infections.
7. Extracorporeal membrane oxygenation (ECMO)
----------------------------------------------------------------------------------------------------------------------------- -----------
Tachypnea:
Causes
Physiological: exercise. Pathological:
1. Anxiety, exertion, fever, sepsis, hypoxia (like in CO poisoning), acidosis (like in DKA), pulmonary
embolism
2. Respiratory causes such as pneumonia, pulmonary oedema, asthma, laryngeal spasm,
tracheobronchomalacia, foreign body aspiration.
3. Hysterical hyperventilation
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Croup
Peculiar brassy cough is the main presenting feature. Inspiratory stridor, hoarseness or respiratory distress is
also associated. The diseases include acute epiglottitis, laryngitis, laryngotracheobronchitis and spasmodic
laryngitis.
Epiglottitis
Includes epiglottitis and inflammatory edema of the hypopharynx. H. influenzae type B is the most common
cause.
Clinical features:
1. Starts with a minor URTI which progresses rapidly in a few hours.
2. High fever and dysphagia.
3. Breathing is noisy (but less than laryngotracheobronchitis).
4. Child sits up leaning forwards with neck extended and saliva dribbling from the mouth.
5. The accessory muscles of respiration are used.
6. Marked suprasternal and subcostal retraction of the chest.
7. As the child becomes fatigued, the stridor diminishes.

Diagnosis: Cautious (otherwise may cause reflex spasm of the larynx) direct laryngoscopy: epiglottis appears
angry red and swollen.
Treatment:
1. Hospitalization, humidified oxygen (As oxygen therapy masks cyanosis, a careful watch should be kept
for impending respiratory failure).
2. Fluids by intravenous route.
3. Antibiotics - cefotaxime or ceftriaxone 100 mg/kg/day is recommended.
4. Endotracheal intubation or tracheostomy may be indicated if condition deteriorates.
5. Sedatives should not be given
Laryngitis and Laryngotracheobronchitis (Infectious croup)

Nearly always caused by viral infections, usually parainfluenza type l
Clinical features:
1. The onset of the illness is more gradual.
2. Mild cold for a few days before the child develops a brassy cough and mild inspiratory stridor.
3. As the obstruction increases, the stridor becomes more marked and the suprasternal and sternal
recession with respiration become manifest.
4. The child becomes restless and anxious with fast breathing due to increasing hypoxemia. Eventually
cyanosis appears.
5. As the obstruction worsens, breath sounds may become inaudible and stridor may apparently decrease.
Treatment:
1. Mild cases: on ambulatory basis with symptomatic treatment for fever liquids orally.
2. Moderately severe illness: hospitalization and treatment with nebulized epinephrine (1:1000 in doses
of 0.1-0.5 mL/kg to a maximum dose of 5 mL) through nebulizer for immediate relief of symptoms.
Inhalation of budesonide 1 mg twice a day for 2 days.
3. Severe croup hospitalization in ICU, with oxygen inhalation and steroids (similar to moderate severity).
Worsening distress- short term ventilation.
----------------------------------------------------------------------------------------------------------
Wheezes (rhonchi)
Continuous prolonged musical sounds which arise in the bronchi. They may be high pitched (when a large
lumen is obstructed as in bronchitis and asthma); or low pitched (when a small lumen is obstructed as in
bronchiolitis).
Heard during expiration, but when the obstruction is severe, it may also be heard during inspiration, as occurs
in severe bronchial asthma. Rhonchi are heard in cases of
• Bronchitis
• Bronchial asthma
• Foreign body obstruction
• Bronchiolitis
• Left ventricular failure.

Stridor:
Noisy respiration produced by turbulent air flow through the narrowed air passages.
Maybe accompanied by hoarseness, brassy cough with chest indrawing and breathlessness.
Can by acute or chronic.
Etiology
1. Congenital: laryngomalacia (manifests in 1st/2nd week of life; disappears by 6mo-1 y), laryngeal web,
hemangioma, tongue and jaw abnormalities.
2. Mechanical: foreign body, enlarged tonsils.
3. Infection: laryngitis, epiglottitis, diphtheria, retropharyngeal abscess.
4. Trauma: intubation, inhalation burns.
5. Paralysis: bilateral vocal cord paralysis, central paralysis due to cerebral palsy.
6. Nutritional: tetany.
7. Allergic: laryngeal edema.
Acute stridor: Caused by inflammatory edema. Obstruction in the region of glottis. It can be either supraglottic
as in epiglottitis and infraglottic as in infectious croup.
Supraglottic stridor Infraglottic stridor
Stridor Inspiratory Expiratory
Cry Muffled Normal
Dyspnea Less More
Cough Less Deep barking cough
Investigations:
1. X-Ray
i. Soft tissue neck- AP and lateral
ii. Angiography of aberrant vessel suspected
iii. CT scan
2. Direct laryngoscopy without anesthesia.
3. General anesthesia followed by bronchoscopy, laryngoscopy and esophagoscopy.
Treatment:
1. Corticosteroids help recovery in laryngeal edema
2. Congenital laryngeal stridor doesn’t require treatment
3. Gauge feeding
4. Congenital goiter is treated with tri-iodothyronine and lugol’s iodine

NEUROLOGY

CSF findings in meningitis
Tubercular Meningitis:
Common 6-24 mo age. Maybe primary or disseminated (hematogenous/lymphatic).
Pathogenesis: Tubercle bacilli affect end arteries and form submeningeal tubercular foci. The tubercle bacilli
discharge into the subarachnoid space intermittently, proliferate and causes perivascular exudation followed
by caseation, gliosis and giant cell formation.
Clinical presentation
1. Stage of prodrome/invasion: low grade fever, loss of appetite, disturbed sleep, photophobia
2. Stage of meningitis: neck rigidity, drowsy/delirious, remittent or intermittent fever.
3. Stage of coma: loss of consciousness, altered breathing (Cheyne-Stokes or Biot type)
Diagnosis: Lumbar puncture (lab values as shown in table), CT scan (basal exudates, inflammatory
granulomas, hypodense lesions or infarcts, hydrocephalus), Serology (Bactec and PCR for tuberculosis)
D/d: purulent meningitis, partially treated purulent meningitis, brain abscess, encephalitis, typhoid
encephalopathy, brain tumour, chronic subdural hematoma, amoebic meningoencephalitis.
Treatment: ATT, steroids (dexamethasone 0.15 mg/kg/dose 6 hourly), symptomatic (raised ICT, seizures,
dyselectrolytemia)
----------------------------------------------------------------------------------------------------------------------------------------
Treatment of status epilepticus

Acute seizures: Assess and maintain airway,
History, exam and breathing, Give O2, establish IV diazepam or lorazepam;
repeat after 10 mins if
investigations to IV line, estimate blood
establish cause glucose seizure continues
IV Phenytoin or
fosphenytoin. IV
valproate IV levetiracetam IV phenobarbitone
(fophenytoin safer - need
not monitor ECG)
Effective intubation, mechanical ventilation
Midazolam infusion IV Pentobarbital coma

• If IV line is not secured rectal diazepam can be used.
• Diazepam is given at the dose of 0.1-0.3 mg/kg max 10mg.
• Phenytoin loading dose 15-20mg/kg at 0.5mg/kg/min (max 50 mg). Maintenance 5-8mg/kg/day.
Onset of action 20 min. NS should be used as phenytoin precipitates in dextrose. Check for
hypotension and arrhythmia during infusion (continuous ECG monitoring)
• Phenobarbital is the DOC in neonatal seizures, hypersensitivity to phenytoin, cardiac conduction
abnormality. Phenobarbital loading dose 10-20 mg/kg at 1-2 mg/kg/min. maintenance at 5
mg/kg/day. Check for hypotension, respiratory depression and bradycardia during infusion.
• Specific therapy: Glucose for hypoglycemia, Pyridoxine 50-100mg if deficient, IV Ca if hypocalcemia,
IM magnesium
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Neonatal Seizures
Poor myelination and incomplete dendritic arborization result in clinical manifestations that are different from
older children.
Clinical features: Neonatal seizures present in decreasing order of frequency as (i) subtle; (ii) focal clonic; (iii)
multifocal clonic; (iv) generalized tonic; and (v) myoclonic. Subtle seizures may manifest as eyelid blinking,
fluttering or buccal-lingual movement. There may be pedaling or automatic movements because of subcortical
neuronal discharges.
Causes: (important 5)
1. Hypoxic ischemic encephalopathy (HIE) (Most common cause- ~50% cases)
2. Hypocalcemia
3. Hypoglycemia
4. Meningitis
5. Polycythemia
All causes:
1. Perinatal complications: HIE, Birth injuries, intraventricular hemorrhage, SAH.
2. Perinatal infections: Meningitis, neonatal tetanus, TORCH.
3. Metabolic: hypoglycemia, hypocalcemia, hypomagnesaemia, kernicterus, pyridoxine deficiency and
IEM like PKU and homocystinuria.
4. Development of the brain: microcephaly, hydrocephalus, porencephaly, agenesis of corpus callosum.
5. Narcotic withdrawal syndrome: babies born to mothers who abuse narcotics.
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Febrile convulsions
Definition: Seizure during fever occurring between 6 mo to 5 y age in the absence of CNS infection in a
neurologically normal child.
Typical febrile seizures: Atypical febrile seizures (complex)
1. At the highest peak of fever 1. Focal in onset
2. Lasts less than 15 mins 2. Lasts>15 mins
3. Usually, single febrile episode 3. Prolonged unconsciousness
4. Generalized convulsions 4. Family history +
5. No post ictal neurological deficits
6. EEG is normal a few days after seizures

Investigations: Lumbar puncture is to be performed at the first episode to rule out meningitis. EEG and
neuroimaging have no role.
Treatment:
1. Acute:
i. When child is convulsing- Airway, breathing and circulation.
• Diazepam IV 0.2-0.3 mg/kg/dose (max 5mg)
• Maintain airway give O2
• Semi prone position
• Protect from injuries
• Maintain IV lines
ii. Not convulsing/ stopped convulsing- Treatment of fever- paracetamol, tepid sponging, look for
etiology and treat accordingly.
2. Prophylaxis:
i. Counselling for parents
ii. Drugs
• If convulsions are intermittent: for first 3 days of fever: Oral clobazam 0.75-1 mg/kg/day, and
treatment of fever.
• If convulsions are continuous: For those with definite CNS disease, family history of epilepsy.
Drug: Valproate 10-20 mg/kg/day, Phenobarbital: 3-5mg/kg/day for 1-2 years/till 5 years of age
whichever comes earlier.
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Cerebral palsy/Little’s disease

Definition:
1. Cerebral palsy is a non-progressive disorder of posture and movement often associated with epilepsy
and abnormalities of speech, vision and intellect. It results from a defect or lesion of the developing
brain.
2. Cerebral palsy (CP) is defined as a non-progressive neuromotor disorder of cerebral origin. It includes
heterogeneous clinical states of variable etiology and severity ranging from minor incapacitation to
total handicap. Most of the cases have multiple neurological deficits and variable mental handicap. The
term does not include progressive, degenerative or metabolic disorders of the nervous system.
Etiology:
1. Prenatal
i. Anoxia
ii. Toxemia of pregnancy
iii. Intrauterine infections
iv. Congenital malformation of brain
2. Natal
i. Anoxia
ii. Asphyxia
iii. Difficult labour
iv. Precipitate delivery
v. Birth trauma
3. Post-natal
i. Kernicterus
ii. Trauma

iii. Infection-meningitis and encephalitis
iv. Metabolic disturbances-hyperglycemia
v. Vascular- hemorrhage and thromboembolism
Classification
1. According to motor deficit
i. Spastic- quadri, hemi, para, di and mono plagia
ii. Athetoid
iii. Atonic
iv. Mixed
2. According to functional status
i. Class I- No practical limitation of activity
ii. Class II- Slight to moderate limitation
iii. Class III- Moderate to gross limitation
iv. Class IV-Inability to carry out any useful activity
3. According to therapeutic requirement:
i. Class I- No active treatment required
ii. Class II- Require minimal bracing and treatment
iii. Class III- Require balancing and service of CP team
iv. Class IV- Long term hospitalization and treatment
Clinical Features
1. Spastic: Reflex Typical age Typical age at
i. Quadriplegia, hemiplegia at disappearance
ii. Hyperirritable, opisthotonos appearance
Primitive reflexes
iii. Babinski’s positive beyond 2 y of age Moro Birth 2-3 months
iv. Pseudobulbar palsy- swallowing Stepping Birth 6 weeks
difficulty, drooling of saliva and Placing Birth 6 weeks
expression-less face Asymmetric tonic 1 month 3-5 months
2. Atonic neck reflex
i. Hypotonia: delayed talking Crossed extensor Few days 1 month
reflex after birth
ii. Cerebellar signs present
Symmetric tonic 2 months 6 months
3. Choreoathetoid neck reflex
i. Choreoathetosis Sucking and Birth 4 mo when
ii. Deafness dystonia rooting awake
7 mo when
Associated features asleep
1. Eye: strabismus, cataract, refractiveness Palmar grasp Birth 6 months
2. Ear: Deafness- partial/complete Plantar grasp Birth 10 months
3. Speech: Dysarthria- Aphasia, dyslalia Adductor response Birth 7 months
4. Sensory defects: astereognosis, spatial of knee jerk
Postural/maturational reflexes
disorientation Neck righting 4-6 months 24 months
5. Seizures: generalized/ focal tonic Landau 3 months 24 months
6. Intelligence: Borderline/moderate/severe Parachute 9 months Persists for life
mental retardation
7. GIT: Constipation, feeding difficulties
8. Teeth: malocclusion, caries
9. Miscellaneous: Critchely’s sign- thumb is persistently flexed across palm after 1 mo of life
Differential diagnosis
1. Neurodegenerative disorders

2. Hydrocephalus and subdural effusion
3. Brain tumours/ space occupying lesion
4. Muscle disorders
5. Ataxia telangiectasia
Early identification of Cerebral Palsy

1. Cortical thumb: thumb will be kept adducted along with fisting
2. Absence of cortical sensations stereognosis, graphesthesia
3. Extension of lower extremity +ankle spasm= equinovarus deformity
4. Kinaesthesia- paucity of movements on the affected side
5. Loss of normal movements od hands while walking or running
6. Brisk reflexes
7. Circumduction gait
8. Asymmetric parachute reflex
9. Hand preference in a child <12 mo age
10. Convulsions
11. Difficulty in manipulating affected side
12. Sit and crawl at normal age but delayed walking
Assessment:
1. Visual assessment <3 years: miniature toy test, 3-6 years: Illiterate E test, >6 years: Snellen’s chart,
cover test for strabismus
2. Hearing assessment: ABER in neonates, Behavioral Observation Audiometry (BOA) <5 months,
visual reinforcement audiometry 5mo-2y, play audiometry 2-5 y, audiometry >3 years.
3. Mental assessment: Bayley’s and Denver development screening test.
Investigations:
1. Urine for PKU 7. X-ray spine and hip
2. TORCH, VDRL 8. X-ray skull
3. EEG if seizures + 9. Myelogram
4. CT brain: atrophy porencephaly 10. Chromosomal analysis
5. MRI: Periventricular leukomalacia 11. IEM metabolism workup
6. Nerve biopsy 12. EMG
Treatment:
1. Young infant stimulation program (refer table)-early stimulation programs are useful in infants under
6 mo of age and lead to dendritic and synaptic proliferation. Lack of stimulation results in neuronal
extinction.
2. Behaviour modification
3. Treatment of comorbid condition-convulsions and reduction of spasm by drugs (Table)
4. Development activation and disability limitation Various types of stimulation for CP child
5. Early intervention-physiotherapy and positioning Type of stimulus Stimulus
programs are needed to prevent sequelae such as Visual Hold a toy
contractures Hearing Talk, sing, play music
6. Appropriate school placement. Tactile Touch the baby
7. Appropriate training for self-employment. Sensory Rub the body and scalp
8. Correction of associated defects gently
• Refractory errors-correct with proper lens Speech Talk to the baby

• Squint-corrective surgery
• Hearing loss-hearing aids
Rehabilitation
1. Parental counselling-aims to help the parents to cope with the psychosocial stress.
2. Social awareness-this aims to make the child as independent as possible.
3. Counselling for the cerebral palsied children. Some children with cerebral palsy with near normal IQ or
normal IQ may feel discriminated
A CP team consists of a paediatrician, orthopaedician and general surgeon, physical and occupational
therapist, speech therapist, psychologist, medical social worker.
Drugs used in conditions associated with cerebral palsy

Conditions Drugs used
Abnormal posture Antispasmodics, BZ (diazepam, nitrazepam), Baclofen (GABA receptor
agonist), botulinum toxin, Dantrolene sodium
Behavioural problem Tranquillizers
Constipation Laxatives
Dystonia L-dopa, carbamazepine, trihexyphenidate
Excessive salivation Atropine
Seizures Anticonvulsants
Gait No drugs (Surgery)
Hyperkinetic movements Methylphenidate
Involuntary movements Haloperidol, Tetra benzine, Sodium valproate, Benzodiazepines
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GB syndrome
Definition: Acute inflammatory polyneuropathy
Etiology: Viral: EBV, mumps and measles. Post Vaccination. Bacteria: campylobacter
Clinical features:
1. Predominant motor neuropathy.
2. Characterized by symmetric weakness of muscles, disseminated reflexes and subjective sensory
involvement.
3. Weakness more marked in proximal muscle group.
4. Tendon reflexes decreased.
5. Plantar reflexes are normal.
6. Hypotonia.
Miller-fisher variant- areflexia, ataxia, and ophthalmoplegia without significant limb weakness.
Albumino-cytological dissociation: characteristic findings in CSF, elevated protein & fewer than 10 WBCs
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Reye’s syndrome (Jamshedpur fever)
Definition: Acute self-limiting metabolic insult of diverse etiology resulting in generalized mitochondrial
dysfunction due to inhibition of fatty acid β-oxidation.
Etiology:
1. Salicylates- aspirin used for certain acute viral RTIs precipitates Reyes syndrome.

2. Varicella
3. Influenza B
4. Aflatoxin
Stages
1. Stage I- mild confusion, listlessness, apathy, anorexia, vomiting
2. Stage II- delusion, restlessness, lack of concentration, frightened stage
3. Stage III- coma, decorticate posture later becomes decerebrate, death
4. Sage IV- Flaccidity, areflexia, apnea, dilated pupil not reacting to light, severe hypotension
Investigations:
1. Serum ammonia level raised
2. Prothrombin time increased
3. Hepatic enzymes increase
4. Liver biopsy: shows fatty change and glycogen depletion but no necrosis of liver cells.
5. EEG: generalized slow waves
6. Hypoglycemia-mild
7. CSF- glucose level is low
Treatment:
1. Low protein diet
2. IV Mannitol
3. Glucose
4. Correct electrolyte imbalances
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Causes of Intellectual disability (previously called mental retardation)
I. Prenatal
1. Metabolic- PKU, homocystinuria
2. Chromosomal disorders: Downs, Klinefelter’s
3. Environment and nutrition gap: iodine deficiency
4. Development defect: microcephaly
5. Maternal factors
• Teratogenic drugs
• TORCH infection
• Radiation during pregnancy
II. Natal
1. Birth trauma
2. Hypoxemic encephalopathy
3. Intracerebral hemorrhage
III. Post-natal
1. Meningoencephalitis
2. Kernicterus
3. Hypoglycemia
4. Malnutrition
5. Child abuse
6. Autism
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Acute Flaccid Paralysis
Definition: Acute rapid onset of flaccid paralysis in any child ages<15 years for which no obvious cause is
found and paralytic illness in a person of any age in which polio is suspected.
Differential diagnosis: Polio, GBS, transverse myelitis, traumatic neuritis

AFP Surveillance aim: 1. To identify all remaining area. 2. Monitor progress towards eradication. 3. Target
supplementary immunization
WHO recommends immediate reporting and investigation of every case of AFP in a child <15 years of age
and collection of 2 stool samples for analysis in a WHO approved laboratory.
Outbreak response:
1. Immunization of all child <5 y by 1 dose OPV, residing within 5 km radius.
2. Search for cases <15y age for history of AFP in last 60 days.
3. 2 specimens at least 24 hours apart.
4. Collected within 14 days of AFP.
5. Adequate amount 8-10 g.
6. Reaching WHO lab in good condition.
7. Sent by reverse cold chain.
Indicators for effectiveness of surveillance
1. Sensitivity non-polio AFP at least 1/1 lakh children <15 years
2. Completion of survey- 2 adequate specimen from at least 60% of all AFP cases
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Sodium Valproate
Indication:
1. Drug of choice in absent seizures
2. Alternative drug for GTCS/SPS/CPS
3. DoC for myoclonic and atonic seizure
4. Alternative drug to lithium in mania and bipolar disorder
Side Effects:
1. Fulminant hepatitis
2. Neural tube defects
3. Alopecia, curling of hair
4. Nausea vomiting, tremor, ataxia

NEONATOLOGY

Problems of Small for Problems of prematurity:
Gestation Age baby 1. Birth asphyxia
1. Birth asphyxia 2. Feeding difficulties, poor weight gain
2. Feed intolerance 3. Hypothermia
3. Meconium aspiration 4. Infection- bacterial sepsis
syndrome 5. RS: RDS due to hyaline membrane disease, pul hemorrhage,
4. Hypothermia pneumothorax, Bronchopulmonary dysplasia
5. Hypoglycemia 6. Hyperbilirubinemia, anemia
6. Infection 7. Intra ventricular hemorrhage
7. Polycythemia 8. Necrotizing enterocolitis
8. Dysmorphism 9. Apneic spells
10. Metabolic acidosis
11. Retinopathy of prematurity- later
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Jaundice
Kramer’s rule:
Area of the body Level Bilirubin (mg/dL)

Head and neck 1 4-8
Upper trunk 2 5-12
Lower trunk and thighs 3 8-16
Arms and lower legs 4 11-18
Palms and soles 5 >18
Causes:
1. Unconjugated hyperbilirubinemia
i. Hemolysis: Rh or ABO incompatibility, drugs, infection, G6PD deficiency, autoimmune
hemolysis
ii. Bilirubin overproduction: Ineffective erythropoiesis, large hematoma
iii. Specific condition in neonates: physiologic jaundice, breast milk jaundice
iv. Enzyme defects: Gilbert, Criggler Najar syndrome
v. Miscellaneous: hypothyroidism, fasting
2. Conjugated hyperbilirubinemia
i. Neonatal cholestasis
ii. Infection: sepsis, acute viral hepatitis, enteric fever, malaria leptospirosis
iii. CLD
iv. Liver tumours: primary or mets
v. Enzyme defects: Dubin Johnson, Rotor syndrome
vi. Biliary: choledochal cysts, choledocholithiasis, ascariasis, sclerosing cholangitis
vii. Miscellaneous: Total parenteral nutrition, vaso-occlusive diseases, drug toxicity

Criteria for pathological jaundice in the newborn
1. Appearing in first 24-72 hours
2. Increase in level of total bilirubin more than 0.5mg/dL/hour or 5 mg/dL on first day, 10 mg/dL on
2nd day and 15 mg/dL thereafter
3. Total bilirubin >15 mg/dL
4. Direct bilirubin >20 mg/dL
Differentiate pathological and physiological jaundice

Pathological Physiological
1 Appears in 24 hours Appears >24 hours
2 >bilirubin level >0.5 mg/dL/hour Less increase
3 Total bilirubin >15 mg/dL Always <15 mg/dL
4 Does not have 2 phases Has 2 phases
5 Treatment is required Treatment is not required
6 Direct >20 mg/dL Indirect increased
7 Lasts > 3weeks Disappears by 3 weeks
Causes of pathological jaundice:

1. Hemolytic disorder- Rh or ABO incompatibility, G6PD deficiency, thalassemia, HS
2. Cephalhematoma
3. Rotor Dubin-Johnson syndrome
4. Maternal diabetes
5. Prematurity
6. Inadequate feeding (breastfeeding jaundice)
7. Polycythemia
8. Breastmilk jaundice
9. Idiopathic
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Kernicterus
Definition: Unconjugated hyperbilirubinemia in the neonatal period causing bilirubin encephalopathy and
staining necrosis of neuron in basal ganglia, hippocampus, and sub-thalamic nuclei.
This nuclear staining is called kernicterus.
Clinically 3 phases
1. Phase I: poor suck, lethargy, hypotonia, decreased sensorium
2. Phase II: fever, hypertonia progressing to opisthotonos
3. Phase III: high pitched cry, convulsions and death
Sequelae:
1. Deafness (VIII nerve nucleus affected)
2. Sparse/athetoid of CP
3. Mental retardation
4. Epilepsy
Treatment:
1. Exchange transfusion
2. Phototherapy

3. Drugs- phenobarbitone
Prevention of kernicterus:
1. Early detection of CO (surrogate for bilirubin)
2. Primary prevention: infant should be nursed 8-12 times/day for first several days. Water/dextrose
water is not recommended to the child even in case of dehydration
3. Secondary prevention: All mothers screened for ABO and Rh blood types, all infants are routinely
monitored for jaundice, bilirubin count obtained for every infant with jaundice
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Photo therapy
This coverts bilirubin into photoisomers that can bypass the conjugated system of liver and be excreted in the
bile or urine without further metabolism.
Wavelength of light used: 460-490nm. There is no benefit of prophylactic phototherapy as bilirubin has to be
present on the skin for phototherapy to be useful.
Mechanism of action:
1. Geometric Z →E photo-isomerization. Instantaneous but takes long time to get excreted, hence not
a major mechanism.
2. Structural isomerization: bilirubin →lumirubin. Irreversible and rapidly gets excreted.
3. Photo-oxidation- minor mechanism.
Indications for phototherapy:
1. Serum bilirubin>15mg% in term and >10mg% in preterm.
2. Hemolytic disease of the newborn.
3. Adjunct to exchange transfusion (given below).
Contraindications:
1. Obstructive jaundice.
2. Light sensitive porphyria.
Technique
1. Light source- 4 blue/green light florescent lamp.
2. Position of the infant: placed naked at a distance of 30-45cm below the light source.
3. Protection of infant: eye patch to protect retinal damage and diaper to protect external gonads.
4. Duration of therapy: 24-48 hours. Monitor every 2-3 hr. Check Total Serum Bilirubin (TSB) levels
every 12-24 hr. Stop if TSB falls below cut-off.
5. Feeding of infant during phototherapy: infant is removed from phototherapy for breastfeeding. 10-
20% extra fluid is given to compensate for the loss
6. Side effects: Dehydration, diarrhea, skin burns (bronze baby syndrome), retinal damage,
hyperthermia.
7. Maintain temperature 25-28 °C
Exchange transfusion: Double volume exchange transfusion (DVET) indications: cord bilirubin >5mg/dL or
cord Hb<10mg/dL. Done using pull and push technique using umbilical route.
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Birth Injuries- enumerate
1. Brain-related injuries: Hypoxic Ischemic Encephalopathy (HIE), Cerebral Palsy

2. Muscle-related or physical injuries: Erb’s Palsy, Klumpke’s Palsy, shoulder dystocia (leading to fracture
of clavicle)
3. Injuries from delivery: broken bones, lacerations, or skull fractures.
4. Birth injuries related to infections or developed through pregnancy: group B strep meningitis,
meconium aspiration syndrome (leading to pneumonia/atelectasis)
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Sequelae/complication of birth asphyxia
1. Mental disability: Developmental delay, intellectual disability
2. Physical disability: Spasticity, motor deficit
3. RS: RDS, pulmonary hemorrhage
4. CVS: heart failure, cardiac shock, myocardial necrosis, ventricular dysfunction
5. GIS: NEC, stress gastric ulcer, paralytic ileus
6. Renal oliguria, Anuria, acute tubular/cortical Necrosis Renal failure
7. Liver: increase in indirect bilirubin and decrease Clotting factors
8. Hematologic: DIC, Thrombocytopenia
9. Metabolic: Acidosis, hypoglycemia, hypocalcemia, hyponatremia, SIADH
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Cephalhematoma
Definition: sub-periosteal hemorrhage usually involving parietal and temporal bones.
Etiology: Forceps delivery, vacuum extraction, prolonged labor.
Clinical features: Appears as a soft fluctuant swelling with well-defined margin. A rim may be felt around
hematoma. If crossing a suture line, indicates underlying fracture of skull.
Clinical significance: Can cause exaggeration of physiological jaundice.
Treatment: No treatment required, resolves by itself.
Caput succedaneum Cephalhematoma

Incidence Common Uncommon
Location Subcutaneous Between skull and periosteum
Time of presentation Maximum at birth Increases till 12-24 hours after birth then stabilizes
Time course Resolves in 2-3 days 2-6 weeks to resolve
Characteristics Diffuse and crosses Distinct margins and does not cross suture lines
suture lines
Associated features None Linear skull fractures & 5-25% have
hyperbilirubinemia
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Baby Friendly Hospital Initiative
Launched in 1992 as a part of “INNOCENTI declaration” on promotion, protection and support of
breastfeeding by WHO and UNICEF.
Requirements:
Baby friendly hospitals are required to adopt the breastfeeding policy and confirm to its 10 steps for
successful breastfeeding. Ten steps for successful breastfeeding
1. Have a written breastfeeding policy that is routinely communicated to all healthcare staff (HCS)

2. Train all HCS in skills necessary to implement the policy
3. Inform all pregnant women about benefit and management of breastfeeding
4. Help mother initiate breastfeeding within half an hour
5. Show mother how to breastfeed and maintain lactation even if they should be separated from their
baby
6. Give newborn no food or drink other than breast milk unless indicated
7. Rooming-in practice
8. Encourage breastfeeding on demand
9. Give no pacifiers/soother to breastfeeding infant
10. Foster the establishment of breastfeeding support group and refer mothers to them on discharge.
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Warm Chain:
It is a strategy for prevention of hypothermia. 10 components:
Warm delivery room, warm resuscitation, immediate drying of the neonate, early skin to skin contact,
breastfeeding, postpone bathing, appropriate clothing, mother and baby together, professional alertness, warm
transportation (transportation is the weakest link of the chain).
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Features used for assessing maturity (refer to new Ballard’s scoring in Aruchamy)
1. Anatomical features
i. Weight more than 2500g
ii. Hard skull bones
iii. HC and CC difference 1.5 cm and HC>CC
iv. Pinna fully developed with good recoil
v. No lanugo
vi. Plantar creases present
vii. Scrotum fully developed and fully descended testis
viii. Labia majora covering minora (minora not exposed)
ix. Nails grown upto fingertips
2. Functional features
i. Respiratory system: good cry and good cough reflex
ii. GIT: suckling, oblique swallowing reflex good
iii. Neurological: Morrows reflex +, suckling and swallowing reflex +, pupillary light reflex +,
good muscle tone
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KMC
Kangaroo Mother Care (KMC) includes i. positioning of the baby, ii. its nutrition and iii. follow-up on
discharge.
Advantages (6): Keeps the baby warm, Stabilizes HR, RR, O2, increases milk production, decreases the
chances of respiratory infections, increases emotional bonding and makes early discharge possible.
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APGAR Score
It is a quantitative method for assessing the infantile respiratory, circulatory and neurological status.
When to do: 1 min, 5min and 10 min or during first cry/after regular respiration is established or delayed.
Apgar scores should be obtained every 5 minutes for upto 20 minutes, if the 5-minute Apgar score is less
than 7.

Sign 0 1 2
HR Absent <100/min >100/min
RR Absent Weak cry Good strong cry
Muscle Tone Limp Some flexion Active movements
Reflex irritability No response Grimace Cough or sneeze
Colour Blue/pale Body pink, extremities blue Completely pink
Score: >8 normal. 4-8-moderately asphyxiated. <4-severe distress.
Importance
1. Monitoring score to determine the efficacy of resuscitation
2. Gives overall view of condition of newborn
3. Prognostic value- if score<4 at 10 min, indicates very bad prognosis
4. If low, it indicates birth asphyxia/congenital malformations/ intrauterine infection or sepsis
Drawbacks:
1. Subjective scoring except HR
2. Ignores first time of cry
3. 1 minute score is not useful on deciding the intervention necessary for resuscitation as action should
be taken before that. Therefore, it’s not a tool for action.
4. Cannot be used in preterm baby, babies with Erb’s palsy and severely sedated baby.
5. It does not give any idea of duration and severity of asphyxia
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Neonatal Sepsis
Definition: It is systemic bacterial infection of the newborn which incorporates septicemia, pneumonia and
meningitis.
Etiology: E Coli, S aureus, Klebsiella pneumonia
Predisposing factors for early sepsis: LBW, prolonged rupture of membranes, foul smelling liquor, multiple
PVs, meconium aspiration syndrome.
Symptomatology of neonatal sepsis
General: Respiratory system:
1. Lethargy 1. Cyanosis
2. Poor cry 2. Tachypnea, RR>2SD
3. Poor weight gain/excessive weight loss 3. Chest retractions
4. Grunt
5. Apnea/gasping
CNS: Temperature
1. Not arousable, comatose 1. Hypothermia, <36oC
2. Seizures 2. Fever >38.5oC
3. High pitched cry GIT:
4. Excessive crying/irritability 1. Abdominal distension
5. Neck retraction 2. Diarrhea, vomiting
6. Bulging fontanelle 3. Feed intolerance & poor sucking
CVS Others:
1. Poor perfusion, shock 1. Sclerema
2. HR<100 or >180 2. Excessive jaundice
3. Arrhythmias 3. Bleeding
4. Systolic BP <65mmHg 4. Renal failure

Two types of onset:
Early Late
Time <3 days >3 days
Complicated pregnancy + +/-
Source Genital tract of the mother Post-natal environment
Clinical features Fulminant, multisystem Slowly progressive/ localized
Investigations
1. Blood - counts and culture. WBC >20,000, immature neutrophils >0.2%, platelets <1,00,000
2. Chest X Ray
3. Acute phase reactants- elevated
4. Sugar >180 or <45 mg/dL
Treatment:
1. Antibiotics
Empirical- 1st line Ampicillin/penicillin+gentamicin. 2 nd line- Ampicillin/doxycycline+amikacin.
2. Supportive therapy
i. Dopamine/dobutamine if perfusion is low
ii. Correction of electrolyte balance
iii. Correct hypoglycemia- 10% dextrose 2mL/kg.
iv. O2 ventilation if in respiratory distress
v. Vit K 1mg IM
3. Monitoring- is key for survival of the neonate.
Prevention of infections
1. Exclusive breastfeeding and no pre-lacteals.
2. Keeping cord dry.
3. Handwashing by care givers before and after handling the baby.
4. Hygiene of the baby (sponging and clean clothing).
5. Avoiding unnecessary IV fluids, injections, needle prick etc.
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Difference b/w fetal circulation and post-natal circulation:
1. Presence of placental circulation, which provides gas exchange for the fetus
2. Absence of gas exchange in the collapsed lungs; this results in very little flow of blood to the lungs and
thus little pulmonary venous return to left atrium;
3. Presence of ductus venosus, joining the portal vein with the inferior vena cava, providing a low
resistance bypass for umbilical venous blood to reach the inferior vena cava;
4. Widely open foramen ovale to enable oxygenated blood (through umbilical veins) to reach the left
atrium and ventricle for distribution to the coronaries and the brain; and lastly
5. Wide open ductus arteriosus to allow right ventricular blood to reach the descending aorta, since
lungs are non-functioning.
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Hemorrhagic disease of the newborn
1. Presents as systemic bleeding and ecchymosis.
2. Appearing in the first week of life, more in breastfed infants.
3. Because of routine administration of prophylactic vitamin K at birth, most cases of hemorrhagic
disease of the newborn are of late onset (after 2 weeks of life) and

4. It is associated with antibiotic therapy, cholestasis, maternal use of antagonist drugs (primidone,
warfarin) and fat malabsorption.
5. Confirmation of the diagnosis depends on a rapid therapeutic response to administration of vitamin K
IM.
6. Healthy newborns should receive vitamin K at a dose of 0.5-1.0 mg IM to prevent hemorrhagic disease.
7. Parenterally fed infants and children should receive 1 mg vitamin-K once weekly.
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Infant mortality rate:
IMR= Number of deaths of age <1 year X1000
Number of live births in the same year
Current IMR of India is 28.71/1000 live births. (2021)
Causes listed in order of occurrence
Neonatal mortality (0-4 weeks) Post neonatal mortality (1-12 months)
1. LBW and Prematurity 1. Diarrhoeal diseases
2. Birth injury & difficult labour 2. Acute respiratory infections
3. Sepsis 3. Other communicable diseases
4. Congenital anomalies 4. Malnutrition
5. Hemolytic disease of the newborn 5. Congenital anomalies
6. Conditions of the placenta and cord 6. Accidents
7. Diarrhoeal diseases
8. Acute respiratory infections
9. Tetanus
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Respiratory Distress Syndrome (RDS):
Different from respiratory distress which is simply RR>60/min with lower chest retractions, grunting and
cyanosis. While RDS is specific to surfactant deficiency as etiology for the respiratory distress.
Pathogenesis: surfactant deficiency→ hypoxemia→ pulmonary vasoconstriction→ right to left shunting
across foramen ovale→ worsening of hypoxemia→ respiratory failure.
Management: Xray shows ground-glass opacity, low lung volume and air bronchogram. Mild-moderate RDS
is treated with non-invasive ventilation (CPAP). Severe RDS requires mech ventilation. Exogenous surfactant
for mod-severe RDS.
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Meconium aspiration syndrome (MAS): aspirated meconium causes atelectasis, emphysema, possible
pneumothorax due to air-leak. Rx: good supportive care. Inhaled nitric oxide to reduce pulmonary arterial
hypertension and ventilatory support
Transient tachypnea of Newborn (TTN): Benign self-limiting condition. Diagnosis established after ruling
out other causes of respiratory distress. O2 treatment is sufficient.

HAEMATOLOGY

Iron deficiency Anemia (IDA)
Common in infants fed with cow-milk for prolonged period.
Definitions:
• Anemia: When the Hb level is <2SD below mean for child’s age and sex.
• Serum ferritin: Iron stores bound to apoferritin (which is also an acute phase reactant)
• Transferrin saturation: serum iron/TIBC X100
• Retic count: normal: 1-2% (adult), 2-6% (newborn), 0.5-2% (children)
• Anisocytosis: Variation in size
• Poikilocytosis: variation in shape
IDA clinical features

Symptoms: Signs
1. Failure to thrive 1. Angular stomatitis
2. Appear off-coloured and easily fatigued 2. Pallor
3. Suffer from frequent infection 3. Tongue papillae are atrophied, glossitis
4. PICA (predisposes to lead poisoning) 4. Koilonychias-thin concave raised edges
5. Mental performance is reduced 5. Thin brittle flat nails- platynychia
6. Attention span is decreased 6. Lustrous hair
7. Anorexia 7. In case of CCF, cardiac enlargement,
8. Irritability/weakness systolic murmur, JVP raised and
9. Fatigue splenomegaly
10. Tachycardia, breathlessness- CHF
11. Leg cramps
Lab diagnosis
1. RBC changes
i. HB, PCV, MCH, MCV, MCHC- all decreased. RDW increased
ii. Peripheral smear-
• Microcytic hypochromic RBC
• Anisocytosis
• Poikilocytosis and elliptical cells are seen
• Reticulocyte count decreased
• Thrombocytosis
2. Marrow changes: Prussian blue staining shows decreased iron stores
3. Blood iron:
i. Serum iron: low, less than 30 μg/dL
ii. TIBC increased, <350 μg/dL
iii. Transferrin saturation <15%
iv. Serum ferritin <10 ng/mL
Response to iron therapy
1. Child becomes less irritable in 24 hours and appetite improves.
2. Initial marrow response (retic count in peripheral smear) is observed within 48 hours
3. Rise in reticulocyte count occurs by 2 nd or 3rd day
4. Elevation of Hb level
Treatment of IDA
1. Treatment of underlying cause

2. Deworming change in dietary habits
3. Wearing of shoes
4. Iron therapy: oral/parenteral, or blood transfusion.
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Thalassemia
Three types:
Trait: mild anemia, shows target cells, hyperchromia and microcytosis
Intermedia: intermediate severity
Major: transfusion dependent, splenomegaly, bone deformities and hemolytic anemia.
Peripheral smear:
1. Microcytic hypochromic cells,
2. Anisocytosis (teardrop/target cells),
3. Poikilocytosis,
4. Marked basophilic stippling and various polychromasia
5. Fragmented RBCs,
6. Retic count is increased
Clinical features
1. Progressive pallor
2. Mongoloid facies, Bossing of skull and prominent frontal and parietal eminence with flattened vault,
prominent malar eminences, depressed nasal bridges and puffy eyes
3. Marked growth retardation
4. Poor feeding
5. Recurrent infections
6. Hepatomegaly
Complication of iron overload (check for overload by serum ferritin and T2 weighted MRI)
1. Growth failure
2. Hypogonadism
3. Diabetes
4. Hepatic disease- hemochromatosis
Treatment
1. Genetic counselling for trait, intermedia and major patients.
2. Intermedia patients are given hydroxyurea 15-20 mg/kg/day to increase HbF production
3. Thalassemia major: transfusion should be started early to keep Hb 9-11 g/dL. Give normal diet +
supplement folic acid and small doses of Vit C and E. (In low transfusion-target Hb 6-10,
hypertrasfusion - Hb 10-12 & supertransfusion Hb 12-14)
4. Treatment of iron overload: desferioxamine (best) 40-60 mg/kg/day infused over 8-12 hours during
the night for 5-6 days a week by mechanical pump. (Patient is warned about orange discolouration of
urine). Eye, hearing and RFT done to monitor adverse effects of desferioxamine. Desferiprone is less
effective. Dose 75mg/day, causes arthritis, neutropenia and agranulocytosis. Desferasirox- oral, dose:
30mg/kg/day, excretion through bile.
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Immune Thrombocytopenia (previously Idiopathic thrombocytopenic Purpura, ITP)
1. Most common bleeding disorder presenting in children (1-7y)
2. Autoantibody mediated consumption of platelets (directed against the platelet glycoprotein IIb /Illa
complex) and then sequestered in spleen
Clinical features
1. The child presents with sudden appearance of bruises and mucosal bleeding, epistaxis, oral oozing and
prolonged bleeds with superficial trauma.
2. H/o recent febrile illness +
3. Seasonal clustering of cases.
4. Petechiae and ecchymoses +
5. No dysmorphic features.
6. Bony anomalies or hyperpigmentation. The presence of lymphadenopathy or splenomegaly suggests
secondary causes of thrombocytopenia rather than ITP.
7. Lab value shows low platelet count, circulatory platelets are larger in size.
Treatment:
1. Platelet count >20,000/mm3: only close observation.
2. If active bleeding, IV immunoglobulin 1g/kg/day for 1-2 days, or 50-75 mg/kg of anti-D
immunoglobulin (only in Rh+ children)
3. Prednisone is given at 1-4 mg/kg/ day for 2-4 weeks and then tapered. (after ruling out the possibility
of malignancy by BM examination)
4. In refractive cases, danazol, vincristine, cyclosporine, thrombopoietin receptor-binding agents.

INFECTIOUS
DISEASES

Measles:
Measles virus is an RNA virus of paramyxoviridae family. Respiratory infection → primary viremia
→reticuloendothelial cells → secondary viremia.
Clinical features:
1. Infants are protected by transplacental antibodies, which decay by 9 months. Common in pre-school
children.
2. The prodromal phase-fever, rhinorrhea, conjunctival congestion and a dry hacking cough.
3. Koplik spots, appear opposite the lower second molars on the buccal mucosa on the second or third
day of the illness as gray or white lesions resembling grains of sand with surrounding erythema.
4. Rash, on 4th day with rise in fever, appears as faint reddish macules behind the ears. Rapidly progresses
to maculopapular and spreads to the face, the neck, chest, arms, trunk, thighs and legs in that order
over the next 2-3 days. Starts fading in the same order that it appeared and leaves branny desquamation
and brownish discoloration, which fade over 10 days.
5. Modified measles (seen in partially immune), is milder and shorter illness.
6. Hemorrhagic measles-purpuric rash and bleeding from the nose, mouth or bowel.
Measles complications:
1. Due to virus replication: croup, giant cell pneumonitis in immunocompromised
2. Due to secondary bacterial infection: common-otitis media, bronchitis, bronchopneumonia,
gastroenteritis uncommon-cancrum oris
3. Less common: transient hepatitis, myocarditis, conjunctivitis, keratitis, and corneal ulcer.
4. Post infectious rare complications: early-post measles encephalomyelitis late-SSPE, Measles inclusion
body myositis.
5. Others- GB syndrome, cerebral thrombophlebitis, retrobulbar neuritis, exacerbation of TB, measles
pneumonia in HIV+ patients.
Management:
Diagnosis is by IgM anti-measles antibodies. Supportive and comprises antipyretics, maintenance of hygiene,
ensuring adequate fluid and caloric intake and humidification. Vitamin A reduces morbidity and mortality of
measles; a single oral dose of
1 lakh IU for <1 yr and 2 lakh IU>1 yr.
Measles eradication
1. MMR vaccine
Content: 1000 CCID50 live attenuated measles virus
5000 CCID 50 live attenuated mumps virus
1000 CCID50 live attenuated rubella virus
Dose: 0.5 mL SC
Schedule: 9-10 mo with booster at 15-18 mo
Contraindications: leukemia, Lymphopenia, TB, on steroid/anti-metabolite therapy
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Mumps
RNA virus of paramyxoviridae family. Affects children of 5-15 years of age. Has high (80%) secondary
infection rate. Immunization confers life-long immunity. Transmitted through direct contact/ airborne /
fomites.

Clinical features:
1. Incubation p =18 days (2-4 weeks)
2. Fever, headache, nausea, malaise and loss of appetite
3. Salivary manifestations-
i. Pain near earlobe, difficulty in chewing within 24 hours, jaw tenderness.
ii. Parotid swelling
iii. Opening of Stenson’s duct appears red.
iv. Swelling disappears in 6-10 days
4. Extra salivary manifestation
i. Aseptic meningitis
ii. Encephalitis
iii. GBS
iv. Auditory nerve damage leading to deafness
Diagnosis is by detection of IgM through ELISA.

Treatment: Anti-pyretics, steroids for symptomatic relief
Complications
1. Orchitis 5. Nephritis
2. Epididymitis 6. Meningitis, encephalitis
3. Pancreatitis 7. SN hearing loss
4. Oophoritis
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Tetanus neonatorum
Agent: C. tetani (gram positive, motile, non-capsulated, sporing, anaerobic bacillus)
Clinical features:
1. Age 5-10 days after delivery
2. Excessive unexplained crying, refusal to feed, apathy
3. Spasm of neck muscles, mouth kept open
4. Masseter spasm- difficulty in feeding
5. Lock jaw/trismus
6. Risus Sardonicus- opisthotonos
7. Spasm of larynx and respiratory muscle characteristically included by stimuli of touch, noise or bright
light results in apnea and cyanosis
Treatment
1. General supportive measures
2. Immunization (passive toxoid)
3. Nutrition, fluid and electrolyte balance
4. Antibiotics
5. Tracheostomy and assisted ventilation
6. Control of spasm by diazepam
Prevention: Immunization with tetanus toxoid leads to induction of protective antibodies. Maternal and
neonatal tetanus can be effectively prevented by immunizing the mother during pregnancy, and ensuring
clean delivery and cord care.
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Complication of ascariasis
1. Malnutrition
2. Intussusception
3. Intestinal obstruction by round worm bolus
4. Jaundice and pancreatitis
5. Gall bladder disease
6. Peritonitis
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Diphtheria
Transmitted via air droplets from infants/ carriers. Portal of entry- respiratory system. Incubation period 2-5
days.
Clinical features
1. Constitutional symptoms-
i. Malaise, headache and loss of appetite
ii. Child looks toxic with fever
2. Local manifestations
i. Nasal diphtheria- nasal discharge and excoriation of upper lip
ii. Faucial diphtheria (most common)- redness and swelling of face. Pseudomembrane-formed by
exudate over tonsils. The membrane bleeds on being displaced
iii. Laryngotracheal diphtheria: membrane over the larynx results in brassy cough, hoarse voice.
Complications: Respiratory failure (due to occlusion of airways by membrane) is the most common
complication. Others include myocarditis, neurological-palatal paralysis, loss of accommodation and general
polyneuritis, renal-oliguria and proteinuria.
Treatment:
1. Neutralization of bacterial toxin by administration of antitoxin. Diphtheria antitoxin (IV /IM) should
be administered soon.
2. Antibiotics such as penicillin or erythromycin should be used to terminate toxin production, limit
proliferation of bacteria, to prevent spread of organism to contacts, and to prevent the development
of carriers.
3. Bed rest is advocated for 2-3 weeks.
4. Children should be monitored for airway obstruction and managed; tracheostomy may be required in
some cases. Sudden exertion should be avoided and changes in rate and rhythm of heart should be
looked for.
5. Children with palatal palsy should be fed by nasogastric feeding.
6. Generalized weakness due to polyneuritis is treated as for poliomyelitis or Guillain-Barre syndrome
Prevention and Control

1. Patient should be isolated until two successive cultures of throat and nose are negative for diphtheria
bacillus.
2. All contaminated articles from discharges should be disinfected. Household and contacts should be
observed carefully for development of active lesions. Contact’s lesion should be cultured for C.
diphtheria and given chemoprophylaxis with oral erythromycin for 7 days or single dose benzathine
penicillin.
3. Previously immunized asymptomatic patients should receive a booster dose of diphtheria toxoid.
4. Those not fully immunized should receive immunization for their age.

Malaria
Complications
1. Algid malaria 4. Black water fever 7. Pulmonary edema
2. Acidosis 5. Cerebral malaria (repeated 8. Renal failure
3. Anemia generalized convulsions) 9. Hypoglycemia
6. DIC
Treatment:
Chemoprophylaxis
Cl sensitive: Cl 5mg/kg daily; Cl resistant: Doxy 2mg/kg daily
Begins 1 week before entering endemic area (doxy is started 1-2 days before) and continued for 4 weeks after
leaving transmission area
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Pertussis
Incubation period 7-14 days. Causes serious infection in infancy and children. Secondary attack rate is 100%.
Has 3 phases (Mnemonic- CaPaCo): Catarrhal phase (similar to URTI lasting for 1-2 weeks, period of high
infectivity) → paroxysmal phase (2-6 weeks) →Convalescent phase (1-4weeks)
Complications
1. Respiratory system: bronchiectasis, pneumonia, pneumothorax, otitis media
2. CNS: Convulsions, encephalopathy, IC hemorrhage, seizure
3. Severe malnutrition due to interference of feeding.
4. Sub conjunctival hemorrhage, epistaxis, retinal bleed.
5. GI manifestations
6. Hernia and rectal prolapse
7. Flare up of TB
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Hepatitis B- extrahepatic manifestations:
1. Serum sickness like syndrome

2. Papular acrodermatitis (specific for pediatric population)
3. Essential mixed cryoglobulinemia
4. Polyarteritis nodosa
5. Membranous or membranoproliferative glomerulonephritis leading to renal failure.
6. Severe aplastic anemia
7. Pleural effusion, myocarditis, and pericarditis, peripheral neuropathy
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Pyrexia of unknown Origin
PUO is defined as an illness >3 weeks duration, documented fever>101°F(38.3°C) on multiple occasions,
lack of specific diagnosis after 1 week of admission and investigations or >3 outpatient visits.
Causes:
I. Infective
1. Bacterial
i. Local: abscess- brain, lung, liver, osteomyelitis, UTI
ii. Generalized: TB, infective endocarditis, rheumatic fever, brucellosis, enteric fever
2. Viral: infectious mononucleosis, AIDS, chronic hepatitis
3. Parasitic: malaria, kala azar, toxoplasmosis, filariasis, malaria
4. Rickettsial infection
5. Chlamydial infection
6. Fungal: histoplasmosis, candidiasis
II. Collagen disorders: SLE
III. Malignancy: Wilm’s tumour, neuroblastoma
IV. Miscellaneous- malingering and Munchausen by proxy, Kawasaki’s disease
V. Metabolic: storage disorders
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Tuberculosis:
Diagnostic algorithm for paediatric TB
Fever and/or cough >2 weeks ± loss of weight/ no wt gain ± h/o contact with suspected TB
Sputum examination
Positive Negative Antibiotics for 7-10 days
Mantoux +ve and

abnormal chest X-ray Chest X-ray and Mantoux test
ATT Mantoux –ve or Mantoux +ve

Investigate
and chest x-ray normal

Complications of primary complex of TB
1. Hematogenous spread: military TB, TB meningitis, skeletal TB
2. Local spread: adenitis, bronchopneumonia, bronchiectasis, collapse/consolidation.
Tuberculin skin test/Mantoux test

Used for the diagnosis of TB in children. (Neither 100 percent sensitive nor specific, but best available for
children). Mechanism: Infection with M. tb produces a delayed-type hypersensitivity reaction to the bacilli.
Reaction to tuberculin typically begins 5-6 hr after the injection, reaches maximal induration at 48 to 72 hr. ¼-
½ inch 26- gauge needle and tuberculin syringe are used to inject 0.1 ml of PPD intradermally into the volar
aspect of the forearm. The diameter of induration should be measured (48-72 h) in millimeters. A nonreactive
tuberculin skin test does not exclude latent or active tuberculosis.
Interpretation of Mantoux test

Size of induration Interpretation
<5mm Negative; no active disease
5-10 mm Borderline; consider positive in immunocompromised host & contact with adult
patient with sputum AFB +ve TB
≥10mm +ve, suggests disease in presence of clinical features
Causes of false +ve and false -ve Mantoux test

False +ve results
Infections due to atypical mycobacteria
BCG vaccination
Infection at the site of test
False -ve results
Infections Factors related to the tuberculin
Viral (measles, mumps, chickenpox, HIV) Improper storage (exposure to heat and light)
Bacterial (typhoid, brucellosis, typhus, pertussis, Improper dilutions
overwhelming TB) Contamination
Live virus vaccinations (measles, mumps, polio, Adsorption (partially controlled by adding Tween
varicella) 80)
Metabolic derangements
Chronic renal failure, liver failure, severe Factors related to method of administration
malnutrition Injection of too little antigen
Diseases affecting lymphoid organs Subcutaneous injection
Hodgkin’s disease, lymphoma, chronic leukemia, Delayed administration after drawing into syringe
sarcoidosis
Drugs: Corticosteroids, immunosuppressants Factors related to reading of test and recording of results
Age: Newborns Inexperienced reader
Stress: Surgery, burns, mental illness, GVHD Error in recording
MDR-TB
WHO definition: MDR strain is one that is resistant to INH and rifampicin
XDR-TB- resistance to INH, rifampicin, fluroquinolone, and any one of the following 3 injectables: amikacin,
kanamycin and capreomycin.
X-Ray finding in pulmonary TBL

1. In symptomatic-no findings

2. Hilar opacities
3. Apical consolidation
4. Calcification in healed lesion
5. Fibrosis in healed lesions
6. Cavitatory lesion
Disseminated TB- lab features: ESR raised. AFB sputum- positive. Antibody against TB +ve
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Enteric fever
Term enteric fever includes typhoid fever caused by salmonella enterica vor typhi and paratyphoid fever by S
paratyphi A, B and C. Gram -ve, non-lactose fermenting, flagellate bacteria possessing Vi polysaccharide
capsule. It’s the most common cause of fever lasting for >7 days in India.
1. Transmitted by feco-oral route.
2. Infective dose 103-106 organisms, conditions which reduce gastric acidity (use of antacids and PPI, H2
receptor blockers) reduces infective dose.
3. Incubation period: 7-14 days.
Clinical features:
1. First week of illness
• Step-ladder type of fever (stats as low-grade fever then stepwise rise to 103°-104°F by the end
of 1 week)
• Sudden onset fever with dull headache
• Predominant features in young children- malaise anorexia, nausea, poorly localized abd
discomfort, mild cough, diarrhea
• Constipation(rare)
• Coated tongue, hepatosplenomegaly, tumid abdomen
• Typhoid rash (rose spots) occurs on 6th day of illness.
2. Second and third week
• Abdomen distended and gives a tympanic note on gentle percussion
• Spleen and liver palpable
• Hales over base of lungs
In severe toxemia, child may have typhoid state in which child has muttering delirium.
Complications:
1. Oral: parotitis
2. Chest: pneumonia
3. Intestinal: bleeding/perforation in 2nd/3rd week of illness (in adults, less in children). Bleeding is seen
due to necrotic payer’s patches.
4. DIC
5. Heart- myocarditis
6. Selenic abscess and hepatitis
7. Neurological- meningitis encephalitis- delirium, coma, stupor
8. Other- alopecia, uveitis
9. Relapse may occur- higher with β-lactam treated as compared to quinolones. Carrier state- salmonella
may keep shedding in stools for up to 3 months after treatment.

Diagnosis:
1. In endemic area, typhoid should be a diagnostic probability in all fevers>7 days duration, especially
those without localizing signs.
2. Bradycardia
Lab diagnosis
1. Hematology
• Leucocyte count-normal or low with absolute eosinophilia and neutrophilic predominance
• Thrombocytopenia, anemia
• High CRP which helps to differentiate from viral fevers
2. Blood culture: gold standard. Blood is taken in 1 st week and stool in 2nd and 3rd week
3. Serology- Widal test. Diagnostic titre of >1 in 80 after 7-10 days of illness/ 4-fold increase in titre.
4. TyphiDot test: detects IgM antibodies
Treatment:
1. III gen cephalosporin-oral cefixime- 20 mg/kg/day- DOC
2. Azithromycin (10-20 mg/kg/day)- second choice
3. Amoxicillin-100mg/kg/day in 4 divided doses-14 days
4. Corticosteroid in children with altered mental state or shock
5. Supportive treatment:
i. Good nursing care nutritious diet
ii. Fluid and electrolyte balance
iii. Anti-pyretics
6. Treatment of complications- IV ceftriaxone and cefotaxime-100mg/kg/day if culture is +ve and shows
sensitivity, if resistant switch to ciprofloxacin 20mg/kg/day.
7. Treatment of carriers- Amoxicillin+ probenecid (30mg/kg/day) for 6-12 weeks. If sensitive to
fluoroquinolones, give for 28 days (better).
Prevention: The most effective and desirable method for preventing enteric fever is by improving hygiene and
sanitation. This will yield additional dividends of reduction in the burden of other water-borne illnesses as well.
Vaccination is a major preventive strategy.
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Giardiasis
Major cause of diarrhea in children and adults. Most cases are asymptomatic
Symptoms
1. Incubation period 1-2 weeks
2. Sudden onset explosive watery foul-smelling stool
3. Nausea and anorexia. Flatulence, epigastric cramps and mild fever.
4. No blood or mucus in stools
5. Abdominal distensions
6. Treatment: DOC: tinidazole 50mg/kg orally single dose
Metronidazole: 5-10 mg/kg orally every 8 hours for 7 days
albendazole- 400mg OD for 5 days

Poliomyelitis
Pathogenesis: mouth-entry. It invades local lymphoid tissue→ enters the bloodstream→ invades neurons.
Clinical Features
1. Inapparent infection (91-96%)
2. Abortive polio (4-8%) -low grade fever, sore throat, vomiting, abdominal pain, loss of appetite and
malaise. Recovery is rapid, no paralysis. Indistinguishable from other viral infections.
3. Nonparalytic aseptic meningitis (1-2%)-continuation of abortive polio with headache, neck, back and
leg stiffness several days. Recovery in 2-10 days.
4. Paralytic poliomyelitis (0.5-1 %). Two phases, minor and major, separated by symptom free interval.
The minor phase similar to abortive poliomyelitis. Major - muscle pain, spasms and the return of fever,
followed by rapid onset of flaccid paralysis complete in 72 hr.
Types of paralytic poliomyelitis:
1. Spinal paralytic poliomyelitis (80% of paralytic): lesion of LMN of the anterior horn cells of spinal cord
and affects muscles of the legs, arms and/ or trunk. Muscles are floppy and reflexes are diminished.
(no sensory involvement). Asymmetrical, legs>arms, proximal to distal (descending).
2. Bulbar polio (2% of paralytic): Cranial nerve lesion, resulting in respiratory insufficiency and difficulty
in swallowing, eating or speaking.
3. Bulbospinal polio (20% of paralytic): combination of spinal paralytic and bulbar polio.
4. Polio encephalitis is characterized by irritability, delirium and loss of consciousness; seizures may occur.
The paralysis may be of the upper motor neuron type. (usually seen in older children).
Residual Paralysis: Maximum neurological recovery takes place in the first 6 months of the illness; slow recovery
continues up to two yr. After two year, no more recovery is expected and the child is said to have post-polio
residual paralysis, which persists throughout life.
Treatment
1. In the acute stage, Mx at home. Rest, proper positioning of the affected limb and passive range of
movement at the joints. Frequent change of the posture is must. Made to lie on a firm bed and maintain
limbs in neutral position. Analgesics can also be given to relieve pain and fever.
2. After acute phase subsides, physiotherapy, ambulation and prevention of deformities. If deformities
and contractures, require orthopedic intervention.
3. Bulbospinal polio and respiratory paralysis require hospitalization.

Prevention:
1. Attaining high rates of routine immunization
2. National immunization days
3. Mopping-up of immunization
4. AFP surveillance
4-point strategy in eradication & prevention:
1. High routine immunization cover with OPV.
2. Supplementary immunization in the form of national immunization day or pulse polio program.
3. Effective surveillance system.
4. Final stage by mopping up by door-to-door immunization campaigns: mop-up immunization.
Pulse Polio Immunization (PPI):
The term "pulse" has been used to describe this sudden, simultaneous, mass administration of OPV on a single
day to all children 0-5 years of age, regardless to previous immunization. PPIs occur as two rounds about 4-6
weeks apart during low transmission season of polio, i.e. between November to February. The dose of OPV
during PPIs are extra doses which supplement, and DO NOT replace the doses received during routine
immunization services.
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Congenital Rubella syndrome:
Infection in 1st trimester is associated with 90% mortality (fetus completely spared beyond 16 weeks).
Clinical features:
1. Classical triad of congenital rubella syndrome consists of SN deafness, cataract and congenital heart
diseases (PDA, VSD, PS)
2. Other manifestations: Mental retardation, microcephaly, myocarditis, metaphysical bone lesions
3. Delayed manifestations- diabetes mellitus and renal disease.
Diagnosis: Rubella IgM in cord or neonatal blood.
Treatment: It doesn’t exist. MTP if diagnosed within 20 weeks POG
Prevention: Vaccination among children especially adolescent girls.
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Rheumatic fever and carditis:
Diagnostic criteria: 2 major or 1 major and 2 minor criteria are required in the presence of essential criteria
to diagnose acute rheumatic fever. (also note clinical features from the tables)

Investigations:
1. Acute phase reactants increase.
2. ECG showing prolonged PR interval.
Treatment:
1. Bed rest
2. Penicillin: 2.4 Million units of single dose benzathine penicillin.
3. Suppressive therapy: Aspirin or steroids.
4. Diet- salt restriction if cardiac failure has set in.
Clinical features, classification, treatment of

rheumatic carditis
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The essential package of PPTCT (Prevention of parent to child transmission)-HIV services in India are as
follows:
1. Routine offering of HIV counselling and testing to all pregnant women enrolled into antenatal care,
with an ‘opt-out’ option.
2. Ensuring involvement of spouse and other family members, and move from an “ANC-Centric” to a
“Family-Centric” approach.
3. Provision of life-long ART (TDF+3TC+EFV) to all pregnant and breast-feeding HIV infected
women, regardless of CD4 count and clinical stage of HIV progression.
4. Promotion of institutional deliveries of all HIV infected pregnant women.
5. Provision of care for associated conditions (STl/RTI, TB and other opportunistic infections).
6. Provision of nutrition, counselling and psychosocial support for HIV infected pregnant women.
7. Provision of counselling and support for initiation of exclusive breast-feeds within an hour of delivery
as the preferred option and continued for 6 months.
8. Provision of ARV prophylaxis to infants from birth up to a minimum of 6 months.
9. Integrating follow-up of HIV-exposed infants into routine healthcare services including immunization.
10. Ensuring initiation of co-trimoxazole Prophylactic Therapy (CPT) and Early Infant Diagnosis (EID)
using HIV-DNA PCR at 6 weeks of age onwards, as per the EID guidelines.
11. Strengthening community follow-up and outreach through local community networks to support HIV-
positive pregnant women and their families.

MALIGNANCIES

Neuroblastoma
• Neuroblastoma is the most common intra-abdominal and extracranial solid tumor in children.
• It is a malignant tumor of the ANS derived from neural crest.
• 90% of patients presenting before 5 yr of age (50% within 2 y).
• Etiology-not known but familial cases occur and associated with neurofibromatosis, Hirschsprung
disease, heterochromia, fetal hydantoin and fetal alcohol syndromes, and Friedreich ataxia.
Rearrangement or deletion of the 1p has been found in 80% cases.
• Neuroblastoma can undergo spontaneous regression
• Genetic markers: MYC-N amplification (defined as > to 10 copies of MYC-N)
• Diagnosis is by histopathology
• Favourable- Stage I, II and IVS, younger age-ferritin levels normal (<150ng/mL). Survival>90%.
• Unfavourable- Stage III and IV, ferritin>250, survival <20%.
Clinical features:
• Most common site-adrenal gland (30%), paravertebral retroperitoneum (28%).
• Cervical neuroblastoma can present with Horner syndrome.
• Patient may be asymptomatic with a paraspinal, intrathoracic or retroperitoneal mass found
incidentally. (Excellent prognosis).
• Febrile patient with periorbital ecchymoses known as raccoon eyes, scalp nodules, bone pain, limping
and anemia from widespread metastasis.
• Stage IVS (S = special), 5% of the cases have a small primary tumour (in infants) with metastatic disease
involving the liver, skin and bone marrow and regresses spontaneously.
• (5-15%) is the occurrence of spinal cord signs secondary to ‘dumbbell’ growth
Staging: (International neuroblastoma staging system)

Stage I Localized tumor confined to the area of origin; complete excision, with or without microscopic
residual disease; identifiable ipsilateral and contralateral lymph nodes negative microscopically.
Stage II: Localized tumor with incomplete gross excision; identifiable ipsilateral and contralateral lymph
nodes negative microscopically.
Stage IIB: Localized tumor with complete or incomplete gross excision with positive ipsilateral regional
lymph nodes; identifiable contralateral lymph nodes negative microscopically.
Stage III: Tumor infiltrating across the midline with or without regional lymph node involvement; or
unilateral tumor with contralateral regional lymph node involvement; or midline tumor with
bilateral regional lymph node involvement.
Stage IV: Tumor disseminated to distant lymph nodes, bone, bone marrow, liver or other organs (except
stage IVS).
Stage IVS: Localized primary tumor as defined for stage 1 or 2 with dissemination limited to liver, skin and/
or bone marrow (only in infants)
Treatment:
• Wait for spontaneous regression in IVS patients
• Surgery for localized neuroblastoma.
• For disseminated chemotherapy regimens widely used are OPEC (vincristine, cyclophosphamide,
cisplatin, teniposide (VM-26), CADO (vincristine, cyclophosphamide, doxorubicin) and PECADO
(vincristine, cyclophospharnide, doxorubicin, cisplatin, teniposide).

Acute Leukemia
History:
1. Anemia-pallor, tiredness, malaise.
2. Neutropenia- fever, infections at various site.
3. Thrombocytopenia- petechiae, purpura, bleeding.
4. Expanding cell mass in marrow- bone pain.
5. Raised ICT- nausea vomiting.
Examination
1. Anemia- pallor, hyperdynamic circulation feature.
2. Expanding cell mass in marrow and other organs- bony tenderness, lymphadenopathy, hepatomegaly,
splenomegaly.
3. Raised ICT- papilledema.
----------------------------------------------------------------------------------------------------------------------------- -----------
Wilm’s Tumor
1. 80% children present within 5yr (peak 2-3y) of age; M=F.
2. Develops in the foci of embryonal kidney tissue called nephrogenic cell rests.
3. Mutation in WT1 (11p13) - encodes for a transcription factor that is critical for normal development
of kidneys and gonads.
4. Genetic syndromes associated with Wilm’s

• WAGR (Wilms tumor, Aniridia, Genitourinary abnormalities like horseshoe or fused kidney and
mental Retardation), del 11p13,
• Denys Drash syndrome (renal failure, renal mesangial sclerosis, male hermaphrodism, WT1
missense mutation) and
• Beckwith-Wiedeman syndrome (hemihypertrophy, macroglossia, omphalocele, organomegaly).
Clinical Features:
1. Asymptomatic abdominal mass detected by parents or physician.
2. Features – hematuria, hypertension, abdominal pain, fever, anorexia and vomiting.
3. Tumor thrombus may extend into the IVC.
Investigations: Ultrasonography. CT/MRI- extent of the tumor
Prognostic Factors
1. Stage I: Tumor confined to kidney and completely excised.
2. Stage II: Tumor extends beyond kidney but completely excised.
3. Stage III: Tumor infiltrates renal fat; residual tumor after surgery. Lymph node involvement of
hilum, para-aortic region or beyond.
4. Stage IV: Metastasis in lung or liver, rarely bone and brain.
5. Stage V: Bilateral renal involvement at time of initial diagnosis.
(anaplastic and hyperploidy are also poor prognostic indicators)
Treatment:
Unilateral- nephrectomy (preoperative chemotherapy- using actinomycin D and vincristine maybe used).
Stage I and II- vincristine, actinomycin D and Adriamycin. Abdominal radiation is used in stage III disease.
Pulmonary radiation is used for pulmonary metastasis.

1. Further reading
.
1. Electrolyte imbalances: Ghai pg 68-85
2. Nutritive value of common foods: Ghai pg 89-91
3. Neonatal resuscitation: Ghai pg 127-133
4. Choosing initial methods of feeding: Ghai Fig 9.33 pg 156
5. Hypoglycemia in a neonate: Ghai pg 175-176.
6. New modified ballard scoring system for assessment of maturity: Aruchamy pg 749.

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NANDAN‘S PEDIATRICS NOTES 1

On how this book came to be

NANDAN‘S PEDIATRICS NOTES 2

NANDAN‘S PEDIATRICS NOTES 3

NANDAN‘S PEDIATRICS NOTES 4

GASTRO-INTESTINAL TRACT ............................................................................................................................... 57

CARDIO-VASCULAR SYSTEM ................................................................................................................................. 63

RESPIRATORY SYSTEM ............................................................................................................................................. 69

INFECTIOUS DISEASES ............................................................................................................................................ 99

MALIGNANCIES ......................................................................................................................................................... 111

Further reading................................................................................................................................................................ 115

NANDAN‘S PEDIATRICS NOTES 5

NANDAN‘S PEDIATRICS NOTES 6

Treatment: Oral vitamin A on days 0,1 and 28. Age-wise dose:

NANDAN‘S PEDIATRICS NOTES 7

Weaning food should be:

NANDAN‘S PEDIATRICS NOTES 8

The wetness test

Guidelines for positioning and attachment of the baby during breastfeeding

NANDAN‘S PEDIATRICS NOTES 9

NANDAN‘S PEDIATRICS NOTES 10

2. Surgical: Correction of deformities after correction of rickets.

NANDAN‘S PEDIATRICS NOTES 11

1. Weight for height

Name Method Normal/severe PEM

Wt for age Edema + Edema - Grades Loss of fat

NANDAN‘S PEDIATRICS NOTES 12

NANDAN‘S PEDIATRICS NOTES 13

NANDAN‘S PEDIATRICS NOTES 15

Causes of mortality in PEM:

NANDAN‘S PEDIATRICS NOTES 16

NANDAN‘S PEDIATRICS NOTES 17

2. Phase II: Rehabilitative Phase

NANDAN‘S PEDIATRICS NOTES 18

Age (y) Protein requirement in

NANDAN‘S PEDIATRICS NOTES 19

Growth monitoring Preventive care

NANDAN‘S PEDIATRICS NOTES 20

NANDAN‘S PEDIATRICS NOTES 21

Factors affecting growth:

NANDAN‘S PEDIATRICS NOTES 22

NANDAN‘S PEDIATRICS NOTES 23

Normal >13.5 cm Green

NANDAN‘S PEDIATRICS NOTES 24

Causes: Macrocephaly (HC>2SD)

NANDAN‘S PEDIATRICS NOTES 25

Feature Constitutional growth delay Familial short stature

NANDAN‘S PEDIATRICS NOTES 26

NANDAN‘S PEDIATRICS NOTES 27

NANDAN‘S PEDIATRICS NOTES 28

NANDAN‘S PEDIATRICS NOTES 29

Trisomy 21 (Down’s syndrome)

NANDAN‘S PEDIATRICS NOTES 30

II. Functional and structural abnormalities

NANDAN‘S PEDIATRICS NOTES 31

Breath holding spells

Child starts crying

Crying stops at full expiration

Becomes apneic and cyanotic (raised intra-thoracic pressure→

May lose consciousness, become hypnotic and fall

If spell is >few sec, brief tonic-clonic seizures may occur

3. Pallid: precipitated by minor injury or fright: cyanosis is absent.

NANDAN‘S PEDIATRICS NOTES 32