Paediatrics

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Contents

Paediatrics
1. Growth and Development 1

2. Nutrition and Genetics 10

3. Neonatology20

4. Paediatric Gastroenterology 30

5. Paediatric Pulmonology 35

6. Paediatric Nephrology 39

7. Paediatric Cardiology 44

8. Paediatric Endocrinology 51

9. Paediatric Neurology 55
 GROWTH AND DEVELOPMENT --------- My space ---------

Growth Development

Increase in size and mass Acquisition of new skills due to CNS maturation

Quantitative process Qualitative process

WEIGHT
• If body weight of a baby at birth is x = 3 kg.

Age ↑ in Weight Weight

5-6 months 2x 6 kg
1 year 3x 9 kg
2 years 4x 12 kg
3 years 5x 15 kg
5 years 6x 18 kg
7 years 7x 21 kg

HEIGHT / LENGTH

Age Height Rate

At birth 50 cm
1 year 75 cm 25 cm/yr
2 years 87-88 cm 12-13 cm/yr
4 years 100 cm 6-7 cm/yr

Note
• Birth weight doubles in 5 months.
• Height from birth doubles in 4 years.
• Age at which the child is half the adult length is 18-24 months (2 years).

HEAD CIRCUMFERENCE
• At birth → 34 - 35 cm.
• Growth in first 3 months → 2 cm/month → +6cm.
• In 3-6 months → 1 cm/month → +3cm.
• In 6 -12 months → 0.5 cm/month → +3cm.
• At 1 year of age → 46cm.
• At 2 years of age → 48cm (90% of adult head circumference).
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 Paediatrics

--------- My space --------- GROWTH CURVES (TISSUES)

S shaped curve

90%

2 years Age 2-3 10-12

Nervous tissue /CNS tissue Somatic tissue

Plateau

12 years (Age) 4 years 8 years

Gonadal tissues Lymphoid tissue

PUBERTY / ADOLESCENCE
• WHO defined age group → 10-19 years of age.
• Can be divided into three subgroups :
- Early Adolescent → 10-13 years.
- Middle Adolescent → 14-16 years.
- Late Adolescent → 17-19 years.
• Puberty refers to the appearance of secondary sexual characters (physiological
changes).

Sequence of Puberty in Girls

Thelarche (Enlargement of breast - 1st sign of puberty.)

Pubarche (Appearance of pubic hair)

(Growth spurt → Prior to menarche,
in SMR Tanner Stage III)

Menarche (Start of menses)

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 Growth and Development

Sequence of Puberty in Boys --------- My space ---------

Testicular Enlargment → 1st sign of puberty

Pubarche / penile growth

Growth spurt occurs in SMR Tanner Stage IV
• Axillary hair growth
• Voice changes

• 1st biochemical evidence of puberty - GnRh pulse

• Best marker of pubertal status - LH
TANNER STAGING / SEXUAL MATURUTY RATING

SMR Staging in Male

Stage Genitalia Pubic Hair

I Prepubertal growth Prepubertal growth
II ↑ Testicular volume = >4 mL Sparse pubic hair
III ↑ Penile length Coarsening & curling of pubic hair
IV Growth spurt Increased pubic hair
• Adult type penis & testis
V Adult type pubic hair
• Testicular volume : >20ml

SMR Staging in Female

Stage Breast Pubic Hair

I Prepubertal Prepubertal
II Breast bud appears Sparse pubic hair
III Growth spurt Curling, coarser pubic hair
IV - Adult type except involvement of medial thigh

V Adult breast Adult type pubic hair (present on medial thigh)

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 Paediatrics

--------- My space --------- ASSESSMENT OF GROWTH 

00:14:27

Assessment of growth can be done using two types of parameters :

Age-dependent parameters Age-independent parameters

• Weight • Weight for length
• Length • Mid upper arm circumference
• BMI • Skin fold thickness

Weight
Measured using bathroom scale.

Length / Height
• Length - Measured while lying supine (<2yrs )
- Measured with infantometer
• Height - Measured while standing (>2yrs)
- Measured with stadiometer

Mid Upper Arm Circumference (MUAC)

• It is an age-independent parameter.
• Measured at the mid point b/w acromian process and olecranon process.
• Valid for children b/w 6 months - 5 years of age.
• Shakir's tape is used to measure MUAC
- Red : 11.5cm (SAM)
- Yellow : 11.5 - 12.5 cm (Borderline SAM) Shakir's tape
- Green : > 12.5 cm (Normal)
SKIN FOLD THICKNESS
• Age-independent parameter.
• Skin thickness is measured using a Harpeden calliper.
• Areas where it is measured :
- Biceps
- Triceps - M/C
- Scapula.
• Normal measurement → > 10mm.
Harpenden Calliper
Malnourished → < 6mm.
GROWTH CHARTS
• Graphical representation of growth.
• Growth charts are broadly of two types :
- Indian : IAP
Male - Blue
- Worldwide : WHO (colour coded)
Female - Pink
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 Growth and Development

Interpretation --------- My space ---------

• -2 S.D : 3rd percentile.
• -1 S.D : 15th percentile.
• 0 S.D : 50th percentile.
• +1 S.D : 85th percentile.
• +2 S.D : 97th percentile.
• Normal : -2SD - +2SD

WHO length-for-age chart : Boys

ABNORMALITIES OF GROWTH 
00:22:00

SHORT STATURE
• Short stature is defined as height for age of a child <-2 SD for that gender.
• Short stature can be of two types :
Types

Physiological Pathological
H/A : - 2SD to -3SD H/A : <-3 SD
1. FSS : Familial short stature
2. CDGP : Constitutional delay in
growth and puberty

FSS CDGP
Final height ↓ Normal
Puberty Normal Delayed
Bone age (BA) BA = CA BA < CA

Upper Segment and Lower Segment Ratio (US : LS) Upper segment (US)
• At birth - 1.7 : 1
• 3 years - 1.3 : 1 Total height
of child
• 7 years - 1.1 : 1
Level of pubic symphysis
• 10 years - 1 : 1
• Adult - 0.9 : 1
Lower segment (LS)

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 Paediatrics

--------- My space --------- Pathological Short Stature

Two types : Types

Proportionate Disproportionate
(US : LS ratio is unchanged) (US : LS changes)
• Malnutrition
• Growth hormone deficiency
• Turner syndrome Increases Decreases

Disproportionate Pathological Short Stature

Types

↑ US : LS ↓ US : LS
(Short limb dwarfism) (Short trunk dwarfism)
• LS is smaller • Upper segment is smaller

Examples : Examples :
• Rickets • POTT's spine
• Osteogensis imperfecta • Spondyloepiphyseal dysplasia
• Achondroplasia • MPS
MACROCEPHALY
HC > +2 SD for that age

Causes
Mnemonic → 3H 2L 1S 1N
• Hydrocephalus • Leukodystrophies
• Hydrencephaly • SOTOS syndrome
• Haemorrhage • Neurocutaneous syndrome
• Lysosomal storage disorders
MICROCEPHALY
HC < -3SD for that age.

Causes
Mnemonic → GETTIN Short.
• Genetic disorders →Down's syndrome.
• Endocrine Disorders → Congenital hypothyroidism.
• TORCH infections (particulary ZIKA).
• Teratogens (alcohol, phenytoin)

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 Growth and Development

• Inborn errors of metabolism (IEM) → PKU. --------- My space ---------

• Neural Tube Defects.
• Structural abnormalities.

DEVELOPMENT 
00:31:57

• Qualitative process

Domains of Development
1. Gross motor
2. Fine motor
3. Social
4. Language
GROSS MOTOR MILESTONES
• 3 months - Neck control
• 6 Months → Sit with support (tripod).
• 8 Months → Sit without support / crawling.
• 10 Months → Creeps.
• 9 Months → Stand with support.
• 12 Months → Walk with support / stand without support.
• 15 Months → Walk without support.
• 18 Months → Run / explore drawers.
• 2 Years → Jumps / goes up & down the stairs two feet at a time.
• 3 Years →
- Able to ride a tricycle.
- Go upstairs (1 foot).
- Go downstairs (2 feet).
• 4 Years → Hops → Goes up & down stairs (one foot).
• 5 Years → Skips.
FINE MOTOR MILESTONES
• 3 months : Hand regard (hands in middle).
• 4 months : Overshooting bidextrous grasp.
• 5 months : Bidextrous grasp.
• 6 months : Unidextrous grasp (Ulnar grasp).
• 7 months : Radial grasp.
• 9 months : Immature pincer grasp.
• 12 months : Mature pincer grasp.
• 15 months : Scribbling.

Drawing Skills
• 2 years → Able to make a line.
• 3 years → Able to copy a circle.

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 Paediatrics

--------- My space --------- • 4 years → Able to draw a cross (+).

• 4½ year → Able to draw a rectangle / square.
• 5 years → Able to draw a triangle.
• 6-7 years → Able to draw a diamond.
• 9 years → Able to draw a cylinder.
• 11 years → Able to draw a cube.

Towers / Cubes
• Towers of two cubes → 15 months.
• Tower of three cubes → 18 months.
• Towers of six cubes → 2 years.
• Towers of nine cubes → 3 years.

SOCIAL MILESTONES
• 2 months → Social smile
• 3 months → Recognises mother.
• 6 months → Mirror play
• 7 months → Strangers anxiety.
• 9 months → Waves bye - bye.
• 12 months → Able to play simple ball game.
• 15 months → 2Ps :
- Points towards an object.
- Points towards pee.
• 18 months → 2Ds :
- Domestic mimicry (baby mimics actions of parents).
- Dry during day.
• 2 years → Parallel play (CHildren play by themselvees).
• 3 years → Cooperative play (baby can play with other children).
- Baby can identify his / her own name / age /gender.
• 4 years → Role play, group play.

LANGUAGE MILESTONES
• 2 months → Vocalise
• 3 months → Cooing
• 4 months → Laughing
• 6 months → Monosyllabic babbling (Ma / Ba / Da).
• 9 months → Bisyllabic babbling (Mama / Baba / Dada).
• 12 months → 1 meaningful word.
• 15 months → 4
 -6 words / Jargon speech (baby speaks certain words that hold
no meaning).
• 18 months → 8-10 word / picture naming.
• 2 years → 2 word sentences / uses pronouns.
• 4 years → Baby can recite story / poems, recognises past tense.
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 Growth and Development

• 5 years → 8-10 word sentences / asks meaning of words, recognises future tense. --------- My space ---------

OTHER MILESTONES
• Handedness → 3 yrs
- R / L differentiation → 4 yrs
• Binocular vision → 4 months

DEVELOPMENTAL ABNORMALITIES 
00:51:29

DEVELPMENTAL QUOTIENT (DQ)

DQ = Developmental age X 100

Chronological age
Eg : 
• Chronological age of child : 1 years
• Developmental age : 9 months (unable to walk with support)

DQ = 9 X 100 = 75
12
• If DQ < 70 in any domain → Developmental delay.
• If developmental delay in ≥2 domains → Global developmental delay.
RETT SYNDROME
• Mutation in MECP 2 gene on chromosome X.
• Seen only in girls.

Clinical Features
• Normal developmental till 1-2 yrs of age → Developmental regression afterwards.
• Writhing hand movements.
• Seizures

Treatment
• Trofenitide (IGF-1 analogue)

INTELLIGENCE QUOTIENT 
00:54:37

IQ = Mental age Category IQ

X 100
Chronological age
Mild 50-70

• Intellectual disabilty : IQ of less than 70 comes under. Moderate 36-50

Severe 25-35

Profound <20

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--------- My space ---------
NUTRITION AND GENETICS

WATER SOULBLE VITAMINS 

00:00:08

VITAMIN B COMPLEX

Vitamin Function Deficiency

• TCA cycle • Beri beri
B1 (Thiamine) • α ketoglutarate dehydrogenase - Wet → Cardiomyopathy
• Pyruvate dehydrogenase - Dry → Neuropathy
• FDA / FADH2 • Angular cheilosis
B2 (Riboflavin)
• Succinate dehydrogenase • Corneal neovascularization
Pellagra (3 Ds)
• NAD • Diarrhoea
B3 (Niacin)
• NADPH • Dementia
• Dermatitis
• Alopecia
• Dermatitis → Burning foot
B5 (Pantothenic acid) • CoA
syndrome.
• Enteritis
• Decarboxylation • Neonatal seizures
B6 (Pyridoxine) • Liver enzymes (ALT / AST) • ↑ ALT / AST
• Heme synthesis • Sideroblastic anemia
• Caused due to eating raw
white egg (Avidin).
B7 (Biotin) • Carboxylation reaction
• Leads to alopecia and
dermatitis.
B9 (Folate) • Megaloblastic anemia
• DNA synthesis
B12 (Cyanocobalamine) • CNS changes

Note
• In our body B6 (Co-factor)
Tryptophan (60mg) Niacin (1 mg)
Kyneurin pathway
• Pellagra is also seen in:
- Maize rich diet (rich in leucine and deficient in tryptophan).
- Hartnup disease → Autosomal recessive disorder (defect in neutral amino acid
transporter in the gut).
- Serotonin syndrome
- Drugs : Isoniazid

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 Nutrition and Genetics

--------- My space ---------

Casal's necklace

Dermatitis on
photo-exposed areas
Pellagra

VITAMIN C (ASCORBIC ACID)

• Main function : Hydroxylation of lysine
Scorbutic zone (Trummerfeld zone)
and proline in collagen.
Diffuse osteopenia
• Deficiency : Scurvy
White line of Frankle
- Bleeding gums
- Skin bleed (Petechiae)
- Bony changes
X-Ray Changes in Scurvy

FAT SOULBLE VITAMINS 

00:10:02

RICKETS
• Defective and poor mineralization (Ca2+/ PO4 deposition) of growing bones.
• M/C cause : Dietary deficiency of vitamin D and Ca2+/ PO4.

Clinical Features
• Craniotabes (ping pong skull) : 1st sign
• Knock knees → Genu valgum
• Bow legs → Genu varum
• Chest manifestations :
- Rachitic rosary → Costochondral junction size increased → Bead-like
structure.
- Harrison sulcus
- Pigeon chest

Pigeon Chest Knock Knees Knock Knees Bow Legs

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 Paediatrics

--------- My space --------- X ray Changes

• Loss of provisional zone of calcification (Earliest sign).
• Cupping
• Splaying
• Fraying

Fraying
Cupping Splaying

X-ray Findings of Rickets

Treatment
High dose (Stoss regimen) Low dose (preferred)
• 60000 IU/week for 6-10 weeks. • 3000-6000 IU/day for 12 weeks.
• Total dose = 6,00,000 IU.

Vitamin D Resistant Rickets

Low / Normal PO4 High PO4 levels

ABG CKD
ABG

Normal Acidosis

PTH Renal tubular acidosis

Increased Normal

Vitamin D Hypophosphataemic rickets

dependent (X-Linked disorder)
rickets (VDDR)

X-linked Hypophosphatemic Rickets

• Mutation in the PHEX gene present on chromosome X.
• X-linked dominant disorder.
• PHEX gene encodes for endopeptidase enzyme, which converts active FGF23 to
inactive form.
• FGF23 ↑↑ → ↓ PO4 → Rickets.

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 Nutrition and Genetics

VITAMIN A --------- My space ---------

• Functions
- Epithelial intergrity and differentiation.
- Vision
• Deficiency
- Toad-like dry skin → Phrynoderma.
- Earliest symptom → Night blindness.
- Earliest sign → Conjunctival xerosis.

X1A Conjunctival xerosis

X1B Bitot spots

X2 Corneal xerosis

X3A Corneal ulcer (keratomalacia) in < 1/3rd surface

X3B Corneal ulcer in > 1/3rd surface

VITAMIN K
• Functions : γ Carboxylation of II / VII / IX / X coagulation factors.
• Deficiency : Hemorrhagic diseases of newborns.
- Breast milk is deficient of Vit K.

VITAMIN E
• AKA Tocopherol.
• Function : Antioxidant.
• Deficiency:
- Hemolytic anemia
- Spinocerebellar ataxia

MALNUTRITION 
00:22:09

PROTEIN ENERGY MALNUTRITION

• Kwashiorkar : Loss of visceral protein compartments (More severe).
• Marasmus : Loss of somatic protein compartment (Less severe).

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 Paediatrics

--------- My space --------- Features Kwashiorkor Marasmus

Wasting Present (masked d/t edema) Present

Onset > 12 months <12 months

Deficit Protein Calorie

Appetite Decresed / Poor Present

Appearance Lethargic Irritable

Prognosis Poor Better

• Skin changes (Flaky paint
dermatitis) • No skin/ hair changes
Additional features
• Hair changes (Flag sign) • Shrunken liver
• Fatty liver

Moon-like face
Simian facies appearance

Severe loss of muscle

Fat sugar baby
appearance
Kwashiorkor Marasmus
Flaky Paint Dermatosis

Malnutrition Acute Chronic

AKA Wasting Stunting
Assesed by Weight for length Lenght for age
< -2 SD Moderate acute malnutrition Moderate chronic malnutrition.
< -3 SD Severe acute malnutrition Severe chronic malnutrition.

Note
• Weight for age (W/A) is an indicator of both acute and chronic malnutrition.
• W / A < -2 SD : Moderate underweight.
• W / A < -3 SD : Severe underweight.

SEVERE ACUTE MALNUTRITION

Defined under these criteria :
• Weight for length < -3 SD
• MUAC < 11.5 cm (6 months - 5 years)
• B/L pedal edema (Nutritional)

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 Nutrition and Genetics

Management --------- My space ---------

Complicated SAM Uncomplicated SAM

Appetite Poor/ + Good/ +

Edema + -

Medical complication + -

Management Hospital Home

Management of Complicated SAM

• Takes place in hospital for total 6-8 weeks
• Stabilisation phase
- Restore homeostasis
- Manage complications
- Lasts for first week
• Rehabilitation phase
- Rebuilding health
- Lasts 2nd to 6th-8th week

Steps Stabilization Rehabilitation

Day 1-3 Day 4-7 2nd week 6-8 week

1. Hypoglycemia 3 day

2. Hypothermia 3 day

3. Infections 7 day

4. Dehydration 3 day

5. Electrolyte imbalance

No iron Iron
6. Micronutrient deficiency

7. Cautious refeeding

8. Catch up growth

9. Love and care environment

10. Follow up

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 Paediatrics

--------- My space --------- Complication of SAM

• Hypoglycemia (RBS < 54 mg/dL)
• Hypothermia (Rectal temp < 35.5°C or Axillary temp < 35°C).
• Infection(usually gram -ve bacteria) : Ampicillin + Gentamycin → Fails → 3rd
gen cephalosporins (Cefotaxime).
• Electrolyte abnormalities
- Hypokalemia
- Hypomagnesemia
• Dehydration
• Micronutrient deficiency

Note
• Refeeding syndrome :
High calorie food in the 1st week

Release of excess insulin

↑ Intracellular K+ and PO4

Hypokalemia and Hypophosphatemia

Refeeding syndrome
- 1st week : Cautious feeding
- 2nd week : Catchup feeding
- Hallmark of refeeding syndrome : Hypophosphatemia

Discharge Criteria
• Weight for length should reach -2 SD.
• No edema for 2 weeks.
• MUAC should reach 12.5 cm.

GENETIC DISORDERS 
00:39:30

DOWN SYNDROME
• Occurs d/t Trisomy 21
• 95% cases of trisomy is due to non-dysjunction of maternal chromosome during
meiosis.
• 3-4% cases : Robertsonian translocation. (translocation of chromosome 21 with
another acrocentric chromosome).
• 1% cases : Mosaicism (2 cell lines in body).

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 Nutrition and Genetics

Clinical Features --------- My space ---------

• Upward slanting palpebral fissure • Low set ears
• Epicanthal fold • Single transverse creases
• Protruding tongue • Sandal gap is present
• Hypotonia • Redundant skin folds present over
• Flat facial profile neck.
• Microcephaly

Down Syndrome Child Single Transverse Crease Facial features in Down's sundrome

Systemic Features
• CVS : Endocardinal cushion defects (M/C)
• CNS : ↓ IQ/ID or pre-senile Alzheimer's disease (at 40 yrs).
• Hematological:
- ALL > AML (M7-FAB - M/C)
- Transient leukemia of Down's syndrome (GATA-1 mutation) → ↑ WBC.
• GIT : Duodenal atresia (M/C), Annular pancreas.

Screening

Radiological Screening
• ↑ Nuchal translucency > 3mm (most important) : First trimester.
• ↑ Nuchal thickness : Second trimester
• Absent / hypoplastic nasal bone.
• Echogenic focus in the heart Soft markers
• Short femur bone

Biochemical Markers
• First trimester (Dual test) :
- ↑ βhCG
- ↓ PAPP - A (pregnancy associated plasma protein - A)
• Second trimester (Triple test) :
- ↑ βHCG - ↓ Unconjugated estriol (U.E3)
- ↓ AFP (alpha feto protein)

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 Paediatrics

--------- My space --------- • Quad test : Triple test + ↑ Inhibin A

Note
• Combined test : Radiological + Dual test (in first trimester)
• Integrated test : Combined test + Quad test (in second trimester)

EDWARD AND PATAU SYNDROME

Edward Syndrome Patau Syndrome

Chromosome Trisomy 18 Trisomy 13
Incidence More common (2nd mc trisomy) Less common
Rocker bottom feet +ve -ve
Cleft lip and palate +ve / -ve +++ve
Holoprosencephaly -ve +ve
Horse shoe kidney +ve Polycystic kidney
Fingers Overlapping fingers Polydactyly Cleft Lip and Cleft Palate seen in
Patau Syndrome

TURNER'S AND NOONAN'S SYNDROME

• Nonnan's syndrome is also known as male Turner syndrome.
• Both syndromes have same phenotype also known as Turner's phenotype.
• Short stature d/t SHOX gene mutation.
• Physical features : Turner's phenotype (3Ws).
- Webbing of neck (Prone to CVS defects)
- Wide carrying angle (Cubitus valgus)
- Widely separated nipples + flat chest
- Short stature

Features Noonan Syndrome Turners Syndrome

• Left side of heart
- Bicuspid aortic
Right side of heart - Pulmonary
CVS defect valve.
stenosis.
- Coarctation of
aorta.
IQ Subnormal IQ Normal
Autosomal dominant
Defect XO
(PTPN II gene mutation).
Menses Menstruation + delayed puberty Primary amenorrhea
• Both male and female
Affects • Males with Noonan have Only females are affected
cryptorchidism (undesended testis).
Fertility Fertile Infertile (Streak ovaries)

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 Nutrition and Genetics

MICRODELETION SYNDROMES --------- My space ---------

• It cannot be diagnosed by karyotyping and needs fluorescent in-situ hybridization

(FISH).

Digeorge Syndrome
• AKA - Velocardiofacial syndrome or CATCH-22 syndrome.
• Clinical features (CATCH-22)
- C - Cardiac defects (Conotruncal defects, Eg : Truncus arteriosis and TOF)
- A - Abnormal facies
- T - Thymic aplasia (No CMI / Lymphopenia)
- C - Cleft lip and palate
- H - Hypocalcemia (due to absence of parathyroid gland → ↓ PTH)
- 22 - 22q11 deletion → No formation of 3rd / 4th pharyngeal pouch →
Absent thymus and parathyroid gland.

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--------- My space ---------
NEONATOLOGY

NORMAL NEWBORN PARAMETERS

• Vitals of newborn
- HR : 110-160 / min - BP : 60/40 mmHg
- RR : 40-60 / min - Capillary filling time (CFT) : <3 sec
- Temperature : 36.5° - 37.5°C
• 1st urine passes by : 24 hours of life.
• 1st stool passes by : 48 hours of life.
CLASSIFICATION OF NEONATES

Based on Birth Weight

• <2.5kg : Low birth weight (LBW)
• <1.5kg : Very low birth weight (VLBW)
• <1kg : Extremely low birth weight (ELBW)

On the Basis of Birth Weight in Relation

to Gestational Age
• Birth weight >90th centile : Large for gestational age (LGA)
• Birth weight 10-90th centile : Appropriate for gestational age (AGA)
• Birth weight <10th centile : Small for gestational age (SGA)

Small for Gestational Age

Constitutional
• Cause for SGA
IUGR (Intrauterine Growth Restriction)

Maternal Fetal

Cause Uteroplacental insufficiency Genetic

Brain is spared, the nutrition during

development is supplied majorly to brain, Brain is not spared. The brain & the
Brain sparing
leading toi brain being bigger in size trunk both are small.
compared to trunk.

AKA Asymmetric IUGR Symmetric IUGR

CONDITIONS IN NEWBORN WHERE TREATMENT IS NOT REQUIRED

1. Physiological weight loss
a. Term baby loses 10% of birth weight → Regains by day 10 of life.
b. Pre-term baby loses 15% of birth weight → Regains by day 15 of life.
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 Neonatology

2. Erythema toxicum neonatorum --------- My space ---------

a. Sterile eosinophilic pustules (no sepsis).
b. Seen on day 4-5 of life.
3. Acne neonatorum
4. Mastitis neonatorum
a. B/L breast enlargement : Occurs d/t transplacental passage of maternal
hormones.
b. Seen on day 3-4 of life.
5. Vaginal bleeding
a. Occurs d/t ↓ maternal hormones.
b. Seen on day 5.

Head Swelling
Cephalohematoma Caput Seccedaneum

Cause Sub-periosteal haemorrhage Subcutaneous edema

Spread over suture line Never crosses Easily crosses

Complication Neonatal jaundice No complication

HYPOTHERMIA 
00:11:25

• Temperature <36.5°C : Neonatal hypothermia

- Temperature measured in the axilla area & recorded by digital thermometer.
SEVERITY AND MANAGEMENT OF HYPOTHERMIA

Severity Temperature

Mild hypothermia 36-36.4°C

Moderate hypothermia 32-36°C

Severe hypothermia <32°C

Management

Mild Hypothermia
• Turn off fans + adequate clothing.
• Exclusive breast feeding (EBF).
• Skin to skin contact.

Moderate Hypothermia
Incubator
• Additional source of heat
Radiant warmer

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 Paediatrics

--------- My space --------- Severe Hypothermia

Hypoglycemia → Bolus 10% dextrose
• Check RBS
Normal → IV Fluids
• Give O2 + Inj. vitamin K
• Do rapid rewarming (32° → 34°C) → Slow rewarming.
KANGAROO MOTHER CARE (KMC)
• Prolonged skin to skin contact between mother (or any caregiver) & LBW infant
(stable).
• 3 components of KMC
- Kangaroo position / frog leg position : Baby being in direct skin to skin
contact on mother's chest.
- Kangaroo nutrition : Exclusive breast feeding.
- Kangaroo discharge : Early discharge & follow up.

BREAST FEEDING 
00:17:28

• Exclusive breast feeding : Breast milk feeding at least for 6 months.

• Breast milk deficient of Vitamin K → Inj. vitamin K given at birth
Vitamin D → Vit. D drops upto 1 year of age
DIFFERENCE BETWEEN BREAST MILK AND COW MILK
Breast Milk (Human) Cow Milk

Lactose 7g/dL 4g/dL

Fat 30 times DHA than cow milk -

Ca/PO4 2:1 (better calcium absorption) 1.5:1

COMPONENTS OF BREAST MILK

• Colostrum
- First 2 weeks of breast milk that is given to baby.
IgA
- Rich in
Proteins
- Color : Yellow
• Mature breast milk
- Rich in calories & fats.

SCORES IN NEWBORN 
00:21:08

3 important scores in neonatology are :

1. APGAR score
2. Silverman - Anderson Score (SAS) Respiratory distress
3. DOWNE score
22 Paediatrics • v1.0 • DBMCI one • 2024
 Neonatology

APGAR SCORE --------- My space ---------

Components 0 1 2

Appearance Fully cyanosed Acrocyanosis Fully pink

Pulse No pulse detected HR <100/min HR >100/min

Grimace No response Some grimace Full grimace / sneeze

Activity Limp / flaccid Some flexion Full flexion

Respiratory effort Apneic Respiratory distress Normal crying

• Maximum APGAR : 10, minimum APGAR : 0

• Higher score is preferred.
SILVERMAN ANDERSON SCORE
Components 0 1 2
No lag between Some lag between
Upper chest retractions See-saw pattern.
abdomen & chest. abdomen & chest.
Lower chest retractions None Minimal Marked
Xiphisternal retractions None Minimal Marked
Grunt None Audible with stethoscope Audible without stethoscope
Nasal flaring None Minimal Marked

• Used mostly in pre-term babies.

• Lower score is preferred.
• Minimum score : 0, maximum score : 10

DOWNE'S SCORE

Components 0 1 2
Present on room air
Cyanosis None Resolves with FiO2 >40%
(Resolves with FiO2 <40%)

Respiratory rate <60 60-80 >80

Grunt None Audible with stethoscope Audible without stethoscope

Air entry Normal Bilateral decreased air entry Absent

Retractions None Minimal Moderate / Severe

• Used for term babies.

• Minimum score = 0 ; Maximum score = 10 .
• Score > 7 : Severe respiratory distress.

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 Paediatrics

--------- My space --------- SEVERITY AND MANAGEMENT BASED ON SCORES

Score on either SAS / DOWNE Severity of Respiratory Distress Management

0-3 Mild O2 supplementation

4-6 Maximum CPAP

>7 Severe Mechanical ventilation

RESPIRATORY DISEASES IN NEONATES 

00:29:05

RESPIRATORY DISTRESS IN PRE-TERM BABIES

Respiratory Distress Syndrome

• Infants born at <34 weeks of period of gestation (POG).
• Lack of surfactant → ↑ surface tension in lungs → Alveolar collapse
• Prevention : Antenatal steroids - Betamethasone / dexamethasone.
• Treatment
- CPAP
- Exogenous surfactany (if CPAP fails) : Given by technique INSURE
(intubate, surfactant, extubate).

Apnoea of Prematurity (AOP)

• Immaturity of CNS chemoreceptors in the brain.
• This can result in ↑ CO2 levels → Prolonged apnea state → AOP
• Rx : Caffeine citrate
RESPIRATORY DISTRESS IN TERM NEWBORN

Transient Tachypnea of New Born (TTNB)

• Typically seen in babies born by cesarean section surgery.
LSCS

Lack of sympathetic stimulation

(ENAC channels not activated)

Retention of lung fluid

Tachypnea

• Rx : Supportive care.
- Usually resolves in 72 hours.

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 Neonatology

CONGENITAL DIAPHRAMATIC HERNIA (CDH) --------- My space ---------

• Herniation of abdominal contents through the diaphragm.

• The bowel loops obstruct the growth of lungs
Bowel in
→ Hypoplastic lungs → Respiratory distress at birth.
thoracic
• Clinical features cavity
- Respiratory distress at birth.
- Scaphoid abdomen (d/t bowel loops in
thoracic cavity)
• Cause of death : Lung hypoplasia X-ray CDH
• Bag & mask ventilation - Contraindicated (↑ respiratory system)
NECROTISING ENTEROCOLITIS (NEC)
• Risk factors
- Prematurity of newborn (most important)
- Formula feeds
- AEDF / REDF (Absent / reverse end diastolic flow)
- Umbilical artery catheterisation.
• Staging of NEC
Systemic Clinical Features Abdominal Signs Radiology

IA - Suspect NEC • Poor feeding Occult stool blood No signs

• Lethargy
IB - Suspect NEC • Apnea Frank blood in stools No signs

• Poor feeding
• Lethargy
IIA Tenderness +/- Pneumatosis intestinalis
• Apnea
• Thrombocytopenia
Triad of NEC
• Thrombocytopenia
IIB Tenderness + Portal venous gas
• Metabolic acidosis
• Hyponatremia

IIIA Peritonitis Ascites

Shock / mechanically ventilated
IIIB Perforation Air ↓diaphragm
• Treatment
- I / II / IIIA : IV antibiotics + NPO
- IIIB : Surgical management (laprotomy)

NEONATAL SEPSIS 
00:41:36

• M/C organism causing neonatal sepsis in India : Klebsiella

• M/C organism causing neonatal sepsis in world : Group B Streptococcus

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 Paediatrics

--------- My space --------- MANAGEMENT

• Gold standard : Blood culture & staining.
• High sensitivity NPV (Negative Predictive Value) : Sepsis screen

Components of Sepsis Screen

1. Absolute neutrophil count : <1800 / uL
2. µESR : >15 mm/hr
3. CRP : >1 mg/dL
4. IT ratio : >0.2
If any 2 out of 4 components are positive → Sepsis screen +ve

Treatment
• Supportive + IV antibiotics - Apmicillin / gentamycin
• If meningitis present : Cefotaxime given.
• Duration of antibiotics depends on
- Only sepsis screen +ve : 7 days.
- Culture positive : 14 days.
- Meningitis present : 21 days.
BIRTH ASPHYXIA / HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)
• WHO defination of birth asphyxia : Failure to initiate breathing at birth.
• Birth asphyxia → Hypoxia → ↓O2 in brain → HIE

Sarnat and Sarnat Staging of HIE

Stages Clinical Features
• Sympathetic overactivity
Stage I
• Exaggerated reflexes
• Parasympathetic overactivity
Stage II • Presence of seizures DOC for neonate : Phenobarbitol
• Lethargic
• Comatose
Stage III • Absent reflexes
• EEG : Isoelectric with burst suppression

NEONATAL JAUNDICE 
00:47:18

• 90% of cases - Physiological jaundice is unconjugated hyperbilirubinemia (d/t ↓

lifespan of RBC)
• 10% of cases - Pathological jaundice occurs usually :
- First 24 hours of life.
- Rate of ↑ bilirubin (>5 mg/dL/day)
- Can cause BIND (Bilirubin Induced Immunological Disfunction) / kernicterus.
- Involves palm & soles.

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 Neonatology

ASSESSMENT --------- My space ---------

• Total serum bilirubin (gold standard)

• Visual clinical assessment
• Kramer's rule : Jaundice progress in cephalocaudal direction.
Bilirubin levels

Face 5-7 mg/dL

Chest 7-9 mg/dL

Abdomen / thigh 9-11 mg/dL

Limbs 11-13 mg/dL

Palms / soles 13-15 mg/dL

TREATMENT
1. Phototherapy
2. DVET - Double volume exchange transfusion

Phototherapy
• Colour : Blue green light
• Wavelength : 460-490 nm
Phototherapy
• Mechanism of action : Unconjugated bilirubin Lumirubin

• Side effects Structural isomerisation

- Retinal & gonadal damage.
- Bronze baby syndrome (phototherapy done with conjugated bilirubin).

Double Volume Exchange Transfusion (DVET)

• Indication
- BIND / kernicterus
- If Rh immunised babies → Cord blood test → Cord bilirubin : >5 mg/dL, or
cord hemoglobin : <10 g/dL

Conjugated Hyperbilirubinemia
• Conjugated hyperbilrubinemia in newborn → Neonatal cholestasis (pathological
jaundice)
• M/C/C : Extrahepatic biliary atresia (EHBA)
• In USG : Absent gall bladder / abnormal gall bladder.
• Treatment
- If diagnosed <8 weeks → KASAI surgery
- If diagnosed later stages : Definitive → Liver transplant

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 Paediatrics

--------- My space --------- NEONATAL RESUCITATION 

00:57:32

Antenatal counseling
Team briefing Prebirth
Equipment check

Birth

Term gestation ? Yes Stay with mother for initial steps,

Good tone ? routine care, ongoing evaluation
Breathing or crying ?
No

Warm, dry, stimulate,

position airway, suction Initial steps of resucitationb (Mnemonic - Warm PaDS)
1 minute if needed (Mouth > Nose)

Apnea or gasping? No Labored breathing or

HR < 100 bpm ? persistent cyanosis ?
Yes Yes

PPV, pulse oximeter. Position airway, suction if needed.

Consider cardiac monitor Pulse oximeter.
Oxygen if needed
(hood : term babies ; CPAP : pre term babies)

HR < 100 bpm ? No Post-resuscitation care

Team debriefing
Yes

Ensure adequate ventilation (MRSOPA). Ventilatory corrective steps (MRSOPA)

Consider ETT or laryngeal mask. M - Mask readjustment neck
Cardiac monitor R - Reposition airway Slight extension
S - Suction (M>N)
If after PPV - adequate ventilation
O - Open the mouth
(that moves the chest) for 30 secs
P - ↑ pressure
No A - Alternate airway (ET / LMA)
HR < 60 bpm ?
Yes
ETT or laryngeal mask.
Chest compressions (2 thumb technique).
Coordinate with PPV - 100% oxygen (Ratio of
chest compression to breath = 3:1)
UVC
No
IV epinephrine/adrenaline
HR < 60 bpm ? Yes every 3-5 minutes.
If HR remains < 60 bpm,
Consider hypovolemia
Consider pneumothorax

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 Neonatology

• Epinephrine --------- My space ---------

• Concentration - 1 : 10000
IV : 0.2 ml/kg, i.e. 0.02 mg/kg
• Dose
Intratrachealy : 1 ml/kg, i.e. 0.1 mg/kg
• Resucitation is stopped only after 20 minutes after resucitation efforts.

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--------- My space ---------
PAEDIATRIC GASTROENTEROLOGY

DIARRHOEA 00:00:14

• Change in consistency and frequency of stools to > 3 times/day.

• Based on duration :
- Acute Diarrhoea : Diarrhoea of infective cause lasting < 14 days.
- Persistent Diarrhoea : Diarrhoea of infective cause lasting > 14 days.
- Chronic Diarrhoea : Diarrhoea of non-infective cause lasting for > 14 days.
• M/C cause of diarrhoea in children → Rota viral infection.
MANAGEMENT OF ACUTE DIARRHOEA
Management of diarrhoea consists of : Management of dehydration + Administration
of Zinc.

Administration of Zinc
Dose is dependent on age :
• <6months : 10 mg OD for 14 days.
• >6months : 20 mg OD for 14 days.

Management of Dehydration

Features No Dehydration Some Dehydration Severe Dehydration

General appearance Alert & active Irritable Comatose / Lethargic
Skin pinch Normal Goes back slowly Goes back very slowly
Thirst Normal Thirsty (drinks eagerly) Unable to drink
Eyes Normal Sunken Very sunken
Tongue Normal Parched and dry Very dry
Tears Normal Absent Absent

Criteria used in IMNCI :

• General appearance • Thirst
• Skin pinch • Eyes
• If 2 out of 4 criteria of some dehydration present; child is classified as having
some dehydration.
• If 2 out of 4 criteria of severe dehydration present; child is classified as having
severe dehydration.

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 Paediatric Gastroenterology

Plan A : Management of No Dehydration --------- My space ---------

• Replace ongoing stool losses with oral rehydration solution (ORS).
• ORS is given at 10 ml/kg with each loose stool.
• Composition of ORS :
- Sodium : 75 mmol / L - Citrate : 10 mmol / L
- Glucose : 75 mmol / L - Chloride : 65 mmol / L
- Potassium : 20 mmol / L - Total : 245 mmol / L
• Na and glucose present in same ratio stimulates SGLT1 [Sodium dependent
+

Glucose cotransporter 1 present in intestine].

Plan B : Management of Some Dehydration
• ORS is used to rehydrate the child.
• Dose used for rehydration: 75 mL/kg over 4 hrs. (given orally or NG tube )
Plan C : Management of Severe Dehydration
• Rehydration is done using IV fluids.
• IV fluid of choice is Ringer lactate with 5% dextrose.
• Dose for rehydration is 100 mL/kg.
• The total fluid is given as
First 30 mL/kg Remaining 70 mL/kg Total Duration
Child <1yr of age Given over 1 hr Given over 5 hrs 6 hrs
Child >1yr of age Given over 30 mins Given over 2-5 hrs 3 hrs

• Ongoing fluid losses should be replaced.

• Maintenance fluid given as per Holliday-Segar formula.
Summary of Management of Dehydration
Amount of Fluid Time Form
Plan A 5-10 mL/kg After each loose stool ORS
Plan B 75 mL/kg Over 4 hrs ORS
• Over 6 hrs in child <1 yr IV fluid (RL with 5%
Plan C 100 mL/kg
• Over 3 hrs in child >1 yr Dextrose)

• Maintenance fluid is the daily fluid requirement and is independent of

dehydration.
• Maintenance fluid choice → DNS (Normal saline with 5% Dextrose)
• Maintenance fluid is calculated by Holliday Segar formula

Weight of Child (kg) Maintenance Fluid

10 100mL/kg
50mL/kg
11 - 20
[(100 x 10) + 50 x X ] where X is > initial 10kg but <20kg
>20 20mL/kg

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 Paediatrics

--------- My space --------- IMPORTANT SURGICAL DISORDERS 00:11:40

TRACHEOESOPHAGEAL FISTULA (TEF)

• TEF is an abnormal connection between trachea and esophagus.
• It is closely associated with esophageal atresia.
• Clinical features :
- Antenatal polyhydramnios - Frothing from mouth while
- Inability to pass NG tube vomiting (non-bilious)
- Choking while feeding
• M/C subtype → Type C → Proximal esophageal atresia with distal fistula.
• Isolated esophageal atresia is Type A subtype.
• Treatment : Resection and anastomosis.
PYLORIC INFANTILE HYPERTROPHIC STENOSIS (IHPS)
• Thickening of circular pyloric muscles.
• Non-bilious vomiting in 2nd / 3rd week of life.
• Metabolic alkalosis with paradoxical aciduria is seen.
Dehydration / volume contraction (due to vomiting)
activates

RAAS

Aldosterone

Na+ and water retention

K+ and H+ excreted in urine

Paradoxical aciduria with hypokalemia

• Investigation of choice → USG
- Length of pylorus > 15 mm
• Treatment : Pyloromyotomy
HIRSCHPRUNG DISEASE
Failure of migration of neural crest cells

Absence of ganglion cells in submucosal and myenteric plexus in a part of the colon

Involved colon
Absence of peristalsis in that segment
Proximal colon
Collapse of involved segment and dilation of proximal colon Collapsed
Dilated

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 Paediatric Gastroenterology

• M/C area : Rectosigmoid area --------- My space ---------

• Delayed passage of mecomium
• Constipation
• Symptoms of obstruction
- Billious vomiting - Abdominal distention
- Abdominal pain - Perforation
• Screening → Anal manometry
• Diagnostic test → Biopsy
CELIAC DISEASE
• Gluten sensitive enteropathy → T-cell mediated hypersensitivity (Type IV).
• Gluten is present in wheat, barley, rye, etc.
• HLA DQ2 / DQ8 mutation
• Clinical features :
- Malabsorption
- Chronic diarrhea
• Diagnosis :
- Screening → Anti TTG & Anti-EMA antibodies (not involved in pathogenesis).
- Confirmation → Biopsy Villous atrophy
Crypt hyperplasia
↑ Increase in intraepithelial lymphocytes

METABOLIC LIVER DISORDERS 

00:24:08

WILSON'S DISEASE
• Autosomal recessive disorder.
• Gene mutated is ATP7B located in chromosome 13.
Impaired binding of copper with ceruloplasmin

Impaired excretion of copper in bile

Accumulation of excess copper in organs like liver,

CNS (multisystem disease) causing oxidative damage

• In 10-20 yrs, hepatic manifestation predominate

• In 30-40 yrs, neuropsychiatric manifestation predominate.
• Hepatic manifestations
- Cirrhosis
- Chronic liver disease
- Portal hypertension
- Jaundice

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 Paediatrics

--------- My space --------- • Neuropsychiatric manifestations

- Dystonia, ataxia, seizures due to Cu deposition in basal ganglia
- Psychiatric manifestations include psychosis, delirium, and excess irritability
• Hematological manifestations
- Coombs negative hemolytic anemia
• Musculoskeletal manifestations
- Arthritis
• Eye manifestations
- Kayser-Fleischer rings (Copper deposits in Descemet's membrane)
- Sunflower cataract

Investigations
• Serum ceruloplasmin levels <20 mg/dl
- Free ceruloplasmin has a short half-life
- Used as a screening test
• Gold standard : Liver biopsy showing excess of copper.

Treatment
• Drug of choice :
- Zinc (competes with copper absorbtion → Used for maintenance therapy)
α-1-ANTITRYPSIN DEFICIENCY
• Mutation in SERPINA-1 gene on chromosome 14

Defective α -1 antitrypsin folding

• α -1 antitrypsin inactivates neutrophil elastase in lungs normally.
• Unopposed action of neutrophil elastase in α1-antitrypsin deficiency results in
panacinor emphysema
• Misfolded protein accumulates in liver

Hepatic manifestations
• Hepatic manifestations including
- Neonatal cholestasis
- Chronic liver disease
- Cirrhosis

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 PAEDIATRIC PULMONOLOGY --------- My space ---------

INFECTIONS 
00:00:27

UPPER RESPIRATORY TRACT INFECTIONS

Epiglottitis
• Causative Organism
- Streptococcus (M/C)
- H. influenzae (M/C In unvaccinated
individuals)
• Clinical features : Inflamed epiglottis
- Thumb sign
- High grade fever
- Poor feeding
- Lethargy Epiglottitis
- Tripod position
- Drooling of saliva
• Treatment : 3rd generation cephalosporins

Larynotracheobronchitis (Croup)
• M/C organism causing laryngotracheobronchitis : Parainfluenza virus
• Initially prodromal symptoms like low grade fever, corzya
followed by
• Inspiratory stridor Steeple sign
• Barking / seal like cough

Treatment
• Drug of choice : Dexamethasone
• Moderate / severe croup : Nebulized epinephrine Xray in Laryngotracheobronchitis
- SpO2 < 90%
- Both expiratory and inspiratory stridor
LOWER RESPIRATORY TRACT INFECTIONS

Bronchiolitis
• M/C organism causing acute bronchiolitis is Perihilar infiltrates
respiratory synctitial virus.
Hyperinflation
• Typically seen in infants / upto 2 years.

Chest Xray - Broncholitis

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 Paediatrics

--------- My space --------- • Initially presents with viral prodome

followed by

- Respiratory distress)
- Wheezing
- Crepitations
Management
• Mainly supportive (hydration)
• Ribavarin is indicated in
- Immunocompromised patients
- Patients with severe cardiorespiratory illness
• Prevention in high risk group is done using monoclonal antibody - Palivizumab
IMNCI MANAGEMENT OF RESPIRATORY ILLNESS

Category Clinical features Management

• No features of pneumonia
No pneumonia • Soothing measures
or severe pneumonia
only cough and cold • Salbutamol if wheeze present
• Fever, cough, cold, wheezing (+/-)
One or both of :
• Fast breathing defined as :
- RR > 60 in child < 2 months of age • Oral Amoxicillin x 5 days
Pneumonia
- RR > 50 in child 2 months - 1 year of age • Follow up after 2 days
- RR > 40 in child > 1 year of age
• Chest indrawing
Any of the following danger signs :
• Stridor in a calm child • Give first dose of parenteral
Severe pneumonia or • SpO2 < 90% antibiotic (IV ampicillin / IM
Very severe disease • High grade fever gentamicin)
• Poor feeding / lethargy • Refer to a higher centre
• Seizure

CYSTIC FIBROSIS 
00:12:50

• Mode of inheritance : Autosomal recessive

• Due to mutation in CFTR (Cystic Fibrosis Transmembrane Regulator) gene on
chromosome 7
- Most common type of mutation is δF 508 (deletion of phenylalanine at 508
amino acid position)

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 Paediatric Pulmonology

PATHOPHYSIOLOGY --------- My space ---------

• Function of CFTR : Chloride conductance channel.

• In respiratory tract / pancreas, CFTR aids in movement of chloride from cells to
lumen.
Movement of chloride causes
Cells
CFTR movement of sodium into lumen
Na+Cl– H2O

Lumen Movement of water into lumen

Secretion becomes watery

• In cystic fibrosis, this movement of chloride, sodium and water in impaired

resulting in

Thick secretions
• In sweat glands, CFTR gene aids in absorption of chloride into the cell

Cells Na+Cl– In cystic fibrosis, chloride reabsorption

is impaired in sweat glands
Na+Cl–
Excess chloride remains in cells
Lumen
Increased sweat chloride
CLINICAL FEATURES
• Recurrent episodes of lower respiratory tract infections → Bronchiectasis.
- M/C organism : Staphylococcus aureus, Pseudomonas
• Exocrine pancreatic insufficiency

Fat malabsorption

Fat in stools
(Steatorrhea)

• Congenital absence of vas deferens → Leads to azoospermia.

• Thick secretions in intestine leading to :
- Delayed meconium passage
- Delayed intestinal obstruction syndrome (DIOS).

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 Paediatrics

--------- My space --------- DIAGNOSTIC CRITERIA

Screening for cystic fibrosis is done if :
• Clinical features of cystic fibrosis
or
• Family history of cystic fibrosis
or
• Positive newborn screening test

Positive for CF if,

• Increased sweat chloride (>60meq/L on 2 or more occasions)

or
• Abnormal nasal potential difference
or
• 2 or more known mutations of cystic fibrosis

TREATMENT
• Chest physiotherapy.
• Pancreatic enzyme replacement

Newer Drugs
• Lumecaftor
- Chaperone protein.
- ↑Expression of CFTR protein
• Ivacaftor
- ↑Chloride conductance through CFTR channel

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 PAEDIATRIC NEPHROLOGY --------- My space ---------

CONGENITAL ANAMOLIES OF KIDNEY & URINARY TRACT  00:00:10

ARPKD vs ADPKD
ARPKD - Autosomal Recessive Polycystic Kidney Disease.
ADPKD - Autosomal Dominant Polcystic kidney Disease.

ARPKD ADPKD
Presentation Infancy • 30-40 years of age
Inheritance Autosomal recessive • Autosomal dominant
• PKD 1 on Ch 16
Mutation PKHD 1 (Fibrocystin) on Chr 6p
• PKD 2 on Ch 4
• Kidney, liver and cerebrum
Site of Cysts Kidney, liver
(Berry aneurysm)

BILATERAL RENAL AGENESIS

No urine formation

↓ in amniotic fluid (oligohydramnios)

Compression of fetus within amniotic sac

Potter sequence

Facial abnormalities Pulmonary hypoplasia Limb abnormalities

such as CTEV
• Small nose Post birth
• Receeding chin
Persistant pulmonary hypertension

HORSESHOE KIDNEY
• Fusion of lower pole of kidney at midline.
• Associated with Turner's syndrome (XO) / Edward's syndrome (Trisomy 18).
• ↑ risk (4x) of Wilm's tumor.
• Leads to : Stasis of urine → recurrent UTI.

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 Paediatrics

--------- My space --------- RENAL DISEASES 

00:06:02

Renal diseases

Diseases affecting glomerulus Diseases affecting tubules

Nephritic syndrome Nephrotic syndrome

NEPHRITIC SYNDROME (GLOMERULONEPHRITIS - GN)

• M/C cause in children : Post streptococcal glomerulonephritis (PSGN).
• Mechanism of action :
Streptococcal infection
(Group A hemolytic β streptococcus)

Antigen-Ab complex formed (immune

complex) - Type III hypersensitivity reaction

Deposited in glomerulus

Complement activation

Inflammation of glomerulus.

Clinical Features Cause

Hematuria (hallmark of GN) Presence of RBC cast and dysmorphic RBCs
Non nephrotic range proteinuria
Proteinuria
(urine dipstick 1+/2+)
Hypertension ↑ BP

• Typically at first d/t streptococcal infection :

- Sore throat → 2-3 weeks later → PSGN. Hematuria
- Skin infection → 4-6 weeks later → PSGN. (cola coloured urine)
• Investigations for PSGN :
- C3 levels - low
- ↑ASO titres
- In most cases, biopsy is not necessary.
(If biposy is done → Subepithelial humps - formed by immune complexes
can be seen).

IgA Nephropathy
• M/C cause of recurrent hematuria.
• Biopsy : Mesangial IgA depositis.
• Treatment : ACE inhibitors.
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 Paediatric Nephrology

NEPHROTIC SYNDROME --------- My space ---------

• Characterized by triad of :
Nephrotic range proteinuria

Hypoalbuminemia Edema
(<3gm/dl)

• Nephrotic range proteinuria :

- Loss of >40mg/m2/hr in urine.
Urine protein
- ratio > 2.
Urine creatinine
- Urine dipstick : 3+/4+.

Features Minimal Change Disease Non-Minimal Change Disease

Occurrence Accounts for >90% cases <10% cases

Light microscopy No changes FSGS, Membranous nephropathy, MPGN.

Loss of foot process

Electron microscopy Changes seen
(podocytes)

Age 1 - 10 years <1 year & >10 years

Hypertension Absent Present

Prognosis Good Poor

Treatment of Nephrotic Syndrome

• 1st episode
(12 weeks duration): Daily Steroids (Prednisolone) : 2mg/kg × 6 weeks.

Alternate day steroids (Predinsolone) : 1.5mg/kg × 6 weeks.

Note
• Terminology :
- Remission → 3 or more consecutive days of nil / trace proteinuria as
per dipstick.
- Relapse → After remission, 3 or more days of 3+/4+ proteinuria.
• Relapse treatment : Daily steroids (2mg/kg) only till remission.

Alternate day steroids × 4 weeks.

• FRNS - Frequently Relapsing Nephrotic Syndrome : ≥3 or more relapses in first
6 months or ≥4 or more relapses in any 12 months.
Paediatrics • v1.0 • DBMCI one • 2024 41
 Paediatrics

--------- My space --------- • SDNS - Steroid Dependant Nephrotic Syndrome : Two or more consecutive
relapses on alternate day steroids or within 2 weeks of stopping steroids.
• FRNS / SDNS treatment :
Low dose alternate daily steroids (0.5 mg/kg - 0.8 mg/kg)
for 1-2 years.

Relapse

Use steroid sparing agents

• Levamisole (FRNS)
• Mycophenolate mofetil (SDNS)

Relapse

Cyclophosphamide
• SRNS - Steroid Resistance Nephrotic Syndrome : No remission despite daily
steroids for 6 weeks.
Cyclosporin A
- Treatment : DOC - Calcineurin inhibitors
Tacrolimus

TUBULAR DISORDERS 
00:21:30

Disorders Inheritance Defect Location Features

• Hyponatremia
• Hypochloridemia
Barter syndrome Na+-K+-2Cl- Thick ascending • Hypokalemia
AR
(Loop diuretics) cotransporter loop • Metabolic alkalosis
• ↓ Calcium in body
• Urine - Hypercalciuria
• Hyponatremia
• Hypochloridemia
Gittelman syndrome Na+-Cl- Distal convoluted
AR • Hypokalemia
(Thiazide diuretics) cotransporter tubule
• Metabolic alkalosis
• Hypomagnesemia
• Hypertension
Gain of function Pseudo
• Hypokalemia
Liddle syndrome AD mutation in Collecting Duct Hyperaldosternism
• Metabolic alkalosis
ENaC channel
• Aldosterone ↓

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 Paediatric Nephrology

INFECTIVE DISORDERS 
00:25:01 --------- My space ---------

URINARY TRACT INFECTION (UTI) IN CHILDREN

• M/C cause : E. coli
• Gold standard investigation : Urine culture & sensitivity.

Management

Oral Antibiotics IV Antibiotics

Age >6-12 months <6 months

• Complicated
- High grade fever
- Persistent vomiting
Severity Uncomplicated
- Poor feeding/ Lethargic
- Loin pain
• Pyelonephritis

Duration 7-10 days 14 days

• Fluoroquinolones
Drugs 3rd generation cephalosporins
• Amoxicilin

Follow Up Imaging

< 1 year 1-5 years > 5 years

1. USG-KUB USG-KUB & DMSA USG
After 3-4 weeks Abormal Abormal
2. MCUG (To r/o VUR) MCUG MCUG/DMSA
After 3-4 months
3. DMSA (To rule out
scarring)

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--------- My space ---------
PAEDIATRIC CARDIOLOGY

FETAL CIRCULATION 
00:00:11

• 4 chambered structure of heart appears by 6-7 weeks POG.

• Source of oxygenation : Placenta.
• Lungs are bypassed.

Ductus venosus
SVC

Umbilical
P
vein IVC
L LA
A RA Foramen ovale
C (Bypassing the liver) (structure helps in
E bypassing the lungs)
N
T
A
RV LV

Pulmonary artery Aorta

Ductus arteriosus
Circulation pathway

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 Paediatric Cardiology

--------- My space ---------

Placenta

Umbilical vein
Ductus venosus

Inferior vena cava (IVC)

(Oxygenated blood)
Drains into

Right atrium (RA)

Major volume of blood Minor volume of blood

Via foramen ovale

Left atrium (LA) Right ventricle (RV)

Goes into Goes into

Left ventricle (LV) Pulmonary artery

Via ductus arteriosus

Aorta

Body

Umbilical artery

Placenta

Closure of Structures

Structural (anatomical)
Structure Functional closure Remnant
closure
UV: Ligamentum teres
Umbilical veins and artery Immediately at birth 5-10 days
UA: Medial umbilical ligament

Ductus venosus Immediately at birth 5-7 days Ligamentum venosum

Foramen ovale (most

Soon after birth 3 months Fossa ovalis
delayed anatomical closure)
Ductus arteriosus (most
10-12 hrs 21 days Ligamentum arteriosum
delayed functional closure)

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 Paediatrics

--------- My space --------- CONGENITAL HEART DISEASE 

00:07:34

Congenital heart disease

Acyanotic congenital heart disease Cyanotic congenital heart disease

ACYANOTIC CONGENITAL HEART DISEASE

RA LA

RV LV

Pulmonary Aorta
artery
Ventricular Septal Defect

RA LA
RA LA

RV LV
RV LV

Pulmonary Aorta
artery
Pulmonary Aorta
artery
Atrial Septal Defect Patent Ductus Arteriosusz

• All 3 conditions have : L → R shunt → Increased pulmonary blood flow.

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 Paediatric Cardiology

Complications --------- My space ---------

• Increased risk of recurrent LRTI / infective endocarditis
• Heart failure / pulmonary congestion
• Late complication : Eisenmenger syndrome

↑PA pressure

↑RV pressure (RVP) & ↑RA pressure (RAP)

RAP / RVP > LVP (LV pressure) / LAP (LA pressure)

Reversal of Shunt

Cyanosis

Lesion Characteristic Feature

ASD 2nd Heart sound : Wide fixed split

• 2nd Heart sound : Wide variable split

VSD
• Shunt murmur : Loud pansystolic murmur (apex)

PDA Continous loud machinery like murmur

CYANOTIC CONGENITAL HEART DISEASE

Cyanotic Congenital Heart Diseases
(CCHD)

Decreased pulmonary blood flow (PBF) Increased pulmonary blood flow (PBF)

• Tetralogy of Fallot • Transposition of great arteries (TGA)

• Ebstein's anomaly • Truncus arteriosus
• Tricuspid atresia • Total Anomalous Pulmonary Venous
Connection (TAPVC)
Tetralogy of Fallot
4 components :
1. Subpulmonic stenosis (SS)
Causes
2. RVH (Right Ventricular Hypertrophy)
Causes
3. VSD (Ventricular Septal Defect) -
Large, causes R→L shunt → Cyanosis
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 Paediatrics

--------- My space --------- 4. Overriding aorta

Aorta

PA

RA Pulm
trunk LA
RV LV
1. SS 4 Overriding aorta
2. RVH
3. VSD

4 Components of TOF

• Severity of cyanosis ∝ Pulmonary stenosis

• Timing of onset of cyanosis ∝ Pulmonary stenosis

Clinical Features
• Cyanosis : Clubbing
• Cyanosis → Polycythemia : Predisposes to thromboembolic events
• Brain abscess

Tet spells
Worsening of pulmonary stenosis (crying) ↑Right-to-left shunt
Causes
Increased cyanosis
Causes
Leads to vicious cycle
Hypoxia

• Can lead to death of child.

• Treatment :
- ↑ SVR by α-agonist and β-blockers → ↓ right to left shunt → ↓ Cyanosis
- Give oxygen
- Morphine for infundibular spasm

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 Paediatric Cardiology

CHEST X-RAY & CYANOTIC CONGENITAL HEART DISEASE --------- My space ---------

• Boot shaped heart : Tetralogy of fallot • Egg on string appearance : TGA

"Egg on String" appearance

Boot-shaped Heart

• Figure of 8 or snowman • Box shaped heart : Ebstein anomaly

appearance : TAPVC

Snowman Appearance Box Shaped Heart

ACUTE RHEUMATIC FEVER 

00:23:32

• Mechanism : molecular mimicry.

• Pharyngitis / Sorethroat d/t Group A Streptococci → 2-3 weeks later → Acute
Rheumatic Fever.
• Antibodies formed against group A streptococci cross react with normal human
tissues such as cardiac tissue and joints.

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 Paediatrics

--------- My space --------- MODIFIED JONES CRITERIA

• For diagnosis of acute rheumatic fever.
• Diagnosis of acute rheumatic fever
- Essential criteria + 2 major + 1 minor (OR) essential criteria + 1 major + 2
minor criteria.
• Essential criteria (evidence of streptococcal infection).
- Increased ASO titers or,
- Throat culture sensitivity
High Risk Population Low Risk Population
Incidence of acute rheumatic fever > 1/1000
population

• Major criteria • Major criteria

- Polyarthritis / polyarthralgia / monoarthritis - Joint involvement (polyarthritis)
- Carditis - Carditis
- Subcutaneous Nodules - Subcutaneous Nodules
- Erythema marginates - Erythema marginatum
- Sydenham's chorea / St. Vitus dance - Sydenham's chorea

• Minor criteria • Minor criteria

- Monoarthalgia - Polyarthralgia / Monoarthalgia
- ESR > 30 mm/hr + CRP > 3 mg/dl - ESR > 60 mm/hr + CRP > 3 mg/dl
- Fever > 38° C - Fever > 38.5° C
- Prolonged PR interval - Prolonged PR interval

• Repeated episodes of acute rheumatic fever causes rheumatic heart disease.

TREATMENT

Secondary Prophylaxis
• Oral / IV Penicillin
• If allergic to penicillin, erythromycin can be given.
• Duration of Secondary Prophylaxis :
- ARF with carditis : 10 yrs or 25 yrs of age whichever is later.
- ARF without carditis : 5 yrs or 18 yrs of age whichever is later.

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 PAEDIATRIC ENDOCRINOLOGY --------- My space ---------

DISORDERS OF PUBERTY 
00:00:12

DELAYED PUBERTY

Definition
• In males
- Absence of secondary sexual characteristics beyond 14 years of age.
• In females
- Absence of secondary sexual characteristics by 13 years of age.
- Absence of menarche by 16 years of age.
• Hypothalamo-Pituitary Gonadal Axis
Hypothalamus
(-) (+) GnRH
Feedback inhibition Pituitary
(+) FSH / LH
(-) Gonads

Testosterone
and estrogen

Types of Delayed puberty

Central Puberty Peripheral Puberty
Affected site Hypothalamus or pituitary Testis or ovaries
LH / FSH ↓ ↑

A.K.A Hypogonadotrophic hypogonadism Hypergonadotrophic hypogonadism

Trauma
Examples Kallman syndrome
Mumps (Orchitis)

Kallman Syndrome
• Mutation : KAL-1 gene (Ch X).
• Failure of migratio of GnRH neurons.
• Anosmia + Delayed puberty.

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 Paediatrics

--------- My space --------- PRECOCIOUS PUBERTY

Definition
• Appearance of secondary sexual characteristics before
- 9 years of age in males.
- 8 years of age in females

Causes

Gonadotrophin Dependent Gonadotrophin Independent

Central precocious puberty Peripheral precocious puberty
↑ testosterone / estrogen
No effect on LH / FSH
↑ LH / FSH

Mc-Cune Albright syndrome

• D/t gain of function mutation in GNAS1 gene which encodes for α subunit of
Gs protein - Stimulatory G protein.
• Triad of Clinical Features
Precocious puberty / Endocrine excess

Polyostotic fibrous dysplasia Patchy cutaneous hyperpigmentation with

ragged borders (Coast of Maine)

• MC location of fracture:
- Base of skull
Coast of
- Femur : Shepherd's crook deformity. maine

THYROID DISORDERS 
00:07:52

CONGENITAL HYPOTHYROIDISM
• M/C cause of preventable intellectual disability.
• Screening : TSH based screening on
- Cord blood
- Dried blood spot from heel prick

Clinical Features
Seen in 2nd to 3rd week.
• Coarse facies. • Hyopotonia
• Poor feeding and lethargy. • Umbilical hernia.
• Hypothermia. • Protruding tongue.
• Prolonged jaundice
52 Paediatrics • v1.0 • DBMCI one • 2024
 Paediatric Endocrinology

Treatment --------- My space ---------

Lifelong thyroxine.

DISORDERS OF ADRENAL GLAND 

00:10:20

ADRENAL GLAND

Adrenal gland

Cortex Medulla
consists of synthesis
Three areas / zones (outside to inside) • Epinephrine
Mnemonic : GFR • Norepinephrine
• Zona glomerulosa - mineralocorticoids
• Zona fasciculata - glucocorticoids
• Zona reticularis - sex steroids

STEROIDAL SYNTHESIS

Cholesterol

Pregnenolone 17-hydroxylase
17-Hydroxypregnenolone 17, 20 lyase DHEA
3βOHSD 3βOHSD 3βOHSD
17-hydroxylase 17, 20 lyase
Progesterone 17-Hydroxyrogesterone Androstenedione
21-hydroxylase 21-hydroxylase
Deoxycorticosterone Testosterone
11-Deoxycortisol
11-β hydroxylase 11-β hydroxylase
Corticosterone
Cortisol
Aldosterone
Glomerulosa Fasciculata Reticularis

CONGENITAL ADRENAL HYPERPLASIA

21-Hydroxylase deficiency
• Most common deficient enzyme
• Leads to excess production of steroids
• Lack of glucocorticoids → Hypoglycemia
• Lack of mineralocorticoids → Hypotension & salt wasting
- ↓ Aldosterone → Hyperkalemia

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 Paediatrics

--------- My space --------- • Excess of testosterone → Virilization of females

• ↓ glucocorticoids → ↑ ACTH → hyperplasia.
• Screening : 17-OH progesterone.
CAH

Hypotension Hypertension

Virilisation (+) Virilisation (-) Virilisation (+) Virilisation (-)

21 hydroxylase deficiency 3βOHSD deficiency 11-β hydroxylase deficiency 17 hydroxylase deficiency

54 Paediatrics • v1.0 • DBMCI one • 2024

 PAEDIATRIC NEUROLOGY --------- My space ---------

CONGENITAL CNS MALFORMATIONS 

00:00:12

NEURAL TUBE DEFECTS

• M/C congenital CNS malformation.
• Cause : Failure of closure of neuropore.

Risk Factors
1. Maternal folic acid deficiency.
2. Maternal intake of anti-epileptic drugs / alcohol.
3. Maternal DM / Obesity

Types
Neural tube defects (NTDs)

Cranial NTD Caudal NTD

(failure of closure of anterior neuropore) (failure of closure of posterior neuropore)

Anencephaly Encephalocoele Spina bifida cystica Spina bifida occulta

(M/C)
Anencephaly
• Rudimentary / no brain.
• No cranium.
• No skull.

Encephalocele
• Portion of brain tissue comes out through a defect.
• M/C location : Occiput. Anencephaly

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 Paediatrics

--------- My space --------- Spina Bifida

Spina Bifida Cystica

Spina Bifida Occulta
Meningocele Myelomeningocele

Protrusion of
Defect in vertebral spine. Protrusion of meninges.
Meninges + neural tissues.
Deficits present : Severity
depends on the area involved.
• Sacral area : B  owel-bladder
No neural deficit No neural deficit. dysfunction.
• Lumbar : Bowel-bladder
dysfunction, limb
deficits.
Sometimes a tuft of hair /
Transillumination test is posi- Transillumination test is
dimple is present over the
tive. positive.
defect.

Diagnosis Antenatal Diagnosis

USG Markers

Earliest defect that can

Most sensitive Most specific
be detected is anencephaly
(by 10 weeks)
α-FP Acetylcholinesterase
Prevention
• Use of periconceptional folic acid.
- ↓ the risk by 50%
- To be started 1 month prior to conception.
- Dose : 400 μg (0.4 mg).
- If previously affected or high risk : ↑ dose by 10 times (4 mg).

SEIZURES IN CHILDHOOD 
00:08:27

• M/C cause of seizure in 6 months - 5 years → Febrile seizure.

• M/C cause of seizure in neonates → Hypoxic Ischemic Encephalopathy (HIE).

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 Paediatric Neurology

FEBRILE SEIZURES --------- My space ---------

• Seizures which occurs with significant fever (> 100.40 F) without any evidence
of CNS infections / metabolic abnormality.
• There should be no history of any prior afebrile seizure / trauma.

Types

Simple Febrile Seizure Complex Febrile Seizure

Generalised tonic clonic seizures Focal seizures
It lasts for < 15 mins It lasts for > 15 mins
Recurrence within 24 hrs of
No recurrence
1st episode of seizures

Risk Factors for Recurrence of Febrile Seizures

• Complex febrile seizure.
• 1st seizure episode occured at < 12 months age.
• Low Na+ at the time of seizure.
• Low temperature at the time of seizure.
• Family history.

Intermittent Prophylaxis
• Clobazam given for 3 days, when the child has fever.
• Intermittent prophylaxis is indicated if :
- Recurrent episodes (> 3 episodes in 6 months / ≥ 4 episodes in 12 months).
- 1st episode occurs at < 12 month age.
- Excessive parental anxiety.

Risk Factors for Epilepsy

• Complex febrile seizure
• Underlying neurodevelopmental defects.
• Family history of epilepsy.
STATUS EPILEPTICUS
• Seizure activity for > 30 mins or 2 or more seizures without regaining
consciousness in between.
• Time checkpoints for seizures
- T1 : 5 min → called impending status epilepticus and warrants treatment.
- T2 : 30 min → adverse neurological outcome.

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 Paediatrics

--------- My space --------- Management

Airway, breathing and circulation

IV Benzodiazepines (DOC)
• Lorazepam
• Midazolam
If not controlled
IV Phenytoin
If not controlled
IV Valproate / Leviteracetam / Phenobarbitone
If not controlled
General anesthesia & intubation

Refractory Status Epilepticus

When status epilepticus does not resolve with benzodiazepine and another
anticonvulsant drug.

Super - Refractory Status Epilepticus

Seizures persisting despite 24 hr of general anesthesia.
EPILEPSY DISORDERS

Age Group Clinical Features EEG DOC

Episodes of blank staring and lip 3Hz spike wave
Absence seizure 5 - 8 yrs Valproate
smacking complex
Juvenile Myoclonic Epilepsy Adolescent Myoclonic jerks (precipitated by lack of 4-6Hz polyspike
Valproate
(JME) females sleep and alcohol) & drop attacks wave complex
Infants • Develomental regression ACTH or
West syndrome Hypsarrhythmia
(< 1yr) • Infantile spasm (salam spells) steroids
Lennox Gastaut Syndrome • Developmental regression 2-3Hz spike
2-8 yrs. Valproate
(LGS) • Difficult to control seizures wave complex
Dravet syndrome (Severe • Febrile seizures → Febrile seizures at
• Valproate
myoclonic epilepsy of Infancy lower temperature → Afebrile seizures
• Stiripentol
infancy) → Seizures of multiple types

• Triad of West syndrome

- Developmental regression
- Infantile spasms
- Hypsarrhythmia

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 Paediatric Neurology

CNS INFECTIONS 
00:23:38 --------- My space ---------

MENINGITIS
• M/C cause : Bacteria > Virus
- In neonates : E.coli
- In older children : Streptococcus pneumoniae

Clinical Features
• High grade fever
• Headache
• Meningeal signs:
- Nuchal rigidity
- Kernig's sign
- Brudzinski sign

CSF Findings

Component Bacterial Meningitis Viral Meningitis TB meningitis

Sugar ↓↓ Normal ↓↓ / ↓
Protein ↑↑↑ Normal / ↑ ↑↑↑

Cells Predominnatly PMNL Lymphocytic predominance Lymphocytic predominance

Colour Turbid Clear Cobweb coagulum

Treatment
• 3rd generation cephalosporin +/- Vancomycin (if MRSA +).
• Duration of treatment :
- For neonates → 21 days.
- For older children → 14 days.
• Dexamethasone : Reduces the inflammation thereby decreasing neurological
sequelae (like SNHL).

Tubercular Meningitis
Stage Sensorium GCS score
I - Prodromal Stage (2-4 wks) (fever,
Normal 15
poor appetite etc)
II - Focal neurological deficits, seizures,
Lethargy 11-14
meningeal signs +
III - Comatose & stupor Coma <10
• CECT Head Shows :
- Basal exudates.
- Hydrocephalus.

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 Paediatrics

--------- My space --------- • Treatment : ATT for

- 2 months (intensive phase)
- 10 months (continuation phase)
- Along with Dexamethasone for 4 weeks (decreases long term sequelae)

NEUROMUSCULAR DISORDERS 
00:30:07

SPINAL MUSCULAR ATROPHY (SMA)

• Disease of anterior horn cells - LMN palsy.
• Inheritance: Autosomal recessive.
• Normally,
- SMN-1 (90-95%) produce functional protein.
- SMN-2 (5-10%) produce dysfunctional protein.
• Defect in SMN-1 gene (on chr-5) → ↑ expression of SMN-2 & production of
dysfunctional proteins
• Disease severity ∝ 1
Copy no. of SMN-2 gene
• Types :
- 0 : Most severe
- I : MC (non sitters - affects children < 6months of age)
- II
- III
- IV : Least severe ; presents in adulthood

Clinical Features - SMA Type I

• ↓ Tone.
• Deep tendon reflexes (DTR) : Absent.
• Tongue: fasciculation +.
• Frog leg posture
• Sparing of extraocular muscles.
• Sparing of IQ.

Treatment
• Classical Gene Therapy (Onasemnogene)
• Anti-Sense Oligonucleotide (ASO) based exon skipping therapy - Increase SMN2
protein expression
- Nusinersen (intrathecal)
- Risdiplam (oral)
DUCHENNE MUSCULAR DYSTROPHY (DMD)
• Type of proximal myopathy.
• X-linked recessive inheritance
• Defect in dystrophin protein.
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 Paediatric Neurology

Clinical Features --------- My space ---------

• Proximal muscle weakness → Hip girdle weakness.
• Waddling gait
• Gower's sign: The child supports himself with his upper limbs inorder to get up.
• Calf pseudohypertrophy : due to fibrofatty replacement.
• Age of onset: < 5 years.
• Death occurs by 15-25 years due to cardiorespiratory compromise.

Note
• Gower's sign is also seen in
- Juvenile Dermatomyositis.
- Steroid toxicity

Becker's Muscular Dystrophy (BMD)

• Less severe form of DMD.
DMD BMD
Onset Childhood Adulthood
IQ Decreased Normal
Survival Dies at 15-25 yr Dies at 35-40 yr

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