Paediatrics MCQ points

1
 Use this document as a guide to your final MBBS examinations, especially the
MCQs.
 Notes are deliberately written in short form.
 This is not a substitute for the recommended textbooks.
 Use this as a guide for rapid revision before the exams.
 These are personal notes created for the final MBBS examinations in 2022.
Therefore, if the facts are outdated, please refer to the latest available evidence
in practice.
 I’d like to give full credit to the respective authors.
 Good luck everyone!

2
General

Condition Epidemiology
Pyloric stenosis First born male child (2-8 wk)
Intussusception 3 m-2 years-males
Bronchiolitis First year
Viral episodic wheeze Male child ˂ 5 years
HSP Male 3-10 years, winter
Kawasaki Boys <5 years
Nephrotic Xn Male (2-6 years)
Congenital nephrotic Xn First 3 months
Constitutional delay Male children
ALL Male children
Congenital hypothyroidism Girls
Anterior fontanelle closure Boys
Idiopathic CTEV Boys
Perthes disease Boys
Hirschsprung disease Boys

 DF causes more haemorrhagic manifestations than DHF.

 Many patients infected with dengue virus remain asymptomatic (90%)
 Platelet count dropping below 100,000/mm3 is the most useful and
the earliest indicator that the patient is probably entering the
critical phase (leaking phase).
 In DF and other viral infections as fever subsides the patient's
general condition improves, but in DHF it may get worse.
 Following measles infection children develop a secondary Immunodeficiency.

 Autosomal dominant inheritance

Hereditary spherocytosis (75% of them, but AR pattern is also possible)
Achondroplasia
Osteogenesis imperfecta
Ehlers Danlos Xn
Marfan Xn
Familial hypercholesterolemia
Huntington disease
Myotonic dystrophy
Neurofibramatosis, Tuberous sclerosis
Noonan Xn
Osteosclerosis & otosclerosis
Familial hemiplegic migraine
Primary microcephaly
Hirschsprung 20%
All bilateral & 20% unilaterla retinoblastoma

3
 Autosomal recessive inheritance
Congenital adrenal hyperplasia
SMA
Congenital muscular dystrophy
CF
SCD
Friedreich ataxia
Fanconi anemia
Galactosemia
GSD
Hurler Xn
Oculocutaneous albinism
Phenylketonuria
Tay-Sachs disease
Thalassemia
Werdich-Hoffman disease(SMA1)
Vitamin D dependant rickets Type 1
Leukocyte adhesion deficiency-I (LAD)
Congenital lactase deficiency
Primary microcephaly

 X-linked recessive inheritance

Colour blindness (Red-green)
Duchenne & Becker muscular dystrophy
Fragile X Xn
G6PD deficiency
Haemophilia A,B
Hunter Xn (Mucopolysaccharidosis II)
Alport syndrome
X-linked ichthyosis
X-linked agammaglobulinemia
Congenital adrenal hypoplasia
Congenital TBG deficiency

 X-linked dominant inheritance

Hypophosphatemic /Vitamin D resistant rickets
Rett Xn
Incontinentia pigmenti

 Human genome contains 20,000 genes

 Iry microcephaly-could be AR /AD

4
 Chromosome breakage or DNA repair disorders
Ataxia telangiectasia
Xeroderma pigmentosae
Fanconi’s anaemia
Bloom syndrome

 In early neonatal sepsis-usually fetus gets congenital pneumonia due to

aspiration of amniotic fluid; but in congenital viral inf and early onset listeria
infection fetus gets the organism from the infected placenta.
 Those with intermittent asthma with moderate to severe exacerbations triggered
by viral infections may benefit from long term leukotriene receptor antagonists.

 Renal histology is less important than the response to corticosteroid therapy.

 Ante-natal corticosteroids reduce the risk of RDS, Bronchopulmunary dysplasia
and Intraventricular haemorrhage, neonatal mortality, PDA, NEC

5
 Chromosomal anomalies-10% in spermatozoa and 25% mature oocytes

 All TORCH infections can cause microcephaly and deafness.

 Maternal varicella during pregnancy is also associated with the subsequent

development of herpes zoster during infancy

 Mucocutaneous manifestations of Mycoplasma infection can present as

erythema nodosum, erythema multiforme, cutaneous leukocytoclastic vasculitis,
Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), Fuchs
syndrome, and very rarely subcorneal pustular dermatosis.

 Vesicular rash- VZV, HSV, Herpes zoster, hand foot mouth disease

 Petechial rash- DHF, meningococcemia, HSP

 Urticarial- scabies, insect bites, CLM due to hookworm, strongyloides.

 Adverse effects of IVIG therapy

1. Aseptic meningitis
2. Haemolytic anemia 5-10 days of infusion
3. Bloodborne infections

 Cleft lip-common in males; commonly on left, The environmental causes are

drugs (phenytoin, valproate, thalidomide), maternal alcohol and tobacco use,
dioxins, herbicides and high altitude, lip repaired at 3 m, palate repaired at 6-12m
 Down- t21:21 translocation has 100% recurrence
 Commonest genetic cause for low IQ-Down Xn

 Paed PCM OD
1. 150 mg/kg or 6 g, whichever is LESS, per 24 hour period over 48 hours
2. In children less than six years of age, 100 mg/kg or more per 24 hour period
for the preceding 72 hours or longer
3. Children with conditions that predispose to acetaminophen toxicity (eg,
fasting, liver disease) with an ingestion of 100 mg/kg or 4 g, whichever is less,
per day
4. Children who have received multiple excessive doses of acetaminophen
should be evaluated with a serum acetaminophen concentration and
aminotransferases.

6
Rabies
Immunoglobulin administration is an emergency.
If presents late can be given up to 3 months. (If vaccine not given)
Sensitivity testing done for immunoglobulin.
Given in and around all the wounds and remainder IM to the thigh.
Vaccine is given intradermal as standard gov practice- 2 doses to both deltoids (D0, D3, D7,
D30)
IM vaccine also there.

2nd G Nonsedating antihistamines- urticarial

Sedating antihistamines- allergic rhinitis

Palatal petechiae like lesions- Rubella & EBV

In easles ribavirin given only if immunocompromised.

GAS causes- MP rash, urticarial rash, diffuse erythroderma, vesicular/bullous, erythema

nodosum
Mycoplasma can cause- MP rash, urticarial rash, erythema multiforme, erythema nodosum

Erythema marhinatum- doesn’t involve the face

Palms & soles

Involved –HFM disease, scabies, typhus
Spared- scarlet fever,

Flexural area
Involved- candida nappy rash, atopic dermatitis, intertrigo
Spared- irritant dermatitis,

Bullous impetigo by strept only cause AGN. But IIry strep infection in scabies cause
both AGN and rheumatic fever.

HSP rash is initially urticarial.

7
 X-Ray appearances

 Total anomalous pulmonary venous disease-Snowman appearance/ Figure of 8

appearance
 Transposition of great arteries-Egg on a side or egg on a string

Vitamin A deficiency- NCB CCK

Night blindness→ Conjunctival xerosis→ Bitot’s spots→ Corneal xerosis→ Corneal
ulcer→ Keratomalacia

8
9
The area MOH will investigate all reported serious cases of AEFI, whereas the
Epidemiology Unit will investigate all deaths linked to immunization. Reporting should be
done immediately to MOH of the patient’s residential area on suspicion of AEFI using
the Notification form for AEFI. Deaths should be notified directly to the Epidemiology
Unit

10
11
Seizures mostly febrile and risk depends on age, with much lower risk in infants under
the age of 4 months

12
CTEV associations-Spina bifida, Arthrogryposis multiplex congenital

Causes of strawberry tongue

Features suggestive of NAI

 Bucket handle/ corner/ metaphyseal fracture. Caused by shaking.
 Proximal humeral #
 Scapular spinous process #
 Rib fractures- caused by tight grip.
 If multiple fractures or fractures of different ages suspect.
 Skull fractures
 Spiral/oblique fracture- twisting
 Cauliflower ear due to repeated slapping.
 Tramline contusion (whipping)
 All kinds of haemorrhages (Ex-subconjunctival)

13
 Rubella & roseola infantum are a/w occipital lymphadenopathy.
 Hypoglycemia- 50 in children and 45 in neonates (If symptomatic 45, if
asymptomatic 18, 36 if on 2 occasions in an asymptomatic baby with a r/f)
 If there’s a delay for
o Urine culture- kept in the refrigerator
o CSF- kept at room temp

14
Neonatalogy
 Transient tachypnoea of newborns settles in 24 hours
 Surfactant deficient lung disease starts within 4 hours settles within 36 hours
 Meconium aspiration Xn settles in 72 hours
 Meconium aspiration risk is higher in IUGR.

NTD occurs between 3rd to 4th week.

Gut malrotation occurs between 7th to 12th week.

Neonatal cold stress 36.1 to 36.4

Neonatal hypothermia <36

Myelomeningocoele has a familial predisposition

In Anencephaly even spinal cords and pyramidal tracts are not seen.
Lissencephaly-agyria
Schizencephaly-clefts in one or both sides
Valproate and phenobarb can result in microcephaly.
Scaphicephalic kids are normal. They don’t get raised icp or hydrocephalus.
Scaphocephaly-premature closire of sagittal suture
Frontal plafiocephaly- coronal & sphenofrontal suture

SDLD
More severe in male infants
R/F- GDM, asphyxia, twins, LSCS
Protective factors- PIH, IUGR, PROM, maternal opiates, tocolytics
CXR-Reticulo-granular pattern

Surfactent can cause pneumothorax, obstruction, pulmonary haemorrhage.

MAS
In CXR over-inflation of chest is seen

TTN
High risk in GDM mothers, large preterm babies
CXR –fluid in the horizontal fissure

congenital pneumonia.
LBW infants are at risk of
CXR-ground glass appearance
ABX- Penicillin and gentamycin

PPHN R/F- GDM, birth asphyxia, MAS, septicemia, RDS, diaphragmatic hernia. Usually
seen in term babies.

CDH- posterolateral diaphragm

15
Oxygen in preterm- started with 21-30% O2 and target saturation is 90-94%
Only exception is PPHN where saturation is maintained around 100%

Surfactant administration is beneficial in

1. SDLD
2. MAS
3. Congenital pneumonia
4. Facemasks shouldn’t be used to give oxygen in neonates.

Frequent early signs of sepsis

1. Isolated tachypnoea with absent recessions
2. Feeding difficulty

Feeding practices
<28 weeks- IVF
28 to 31- orogastric or nasogastric
32 to 34- spoon feeding
>34- breastfeeding

Neonatal sepsis
 Abx of choice in EOS- penicillin with gentamycin 12 hourly in <7 days old & 8
hourly of more than 7 days old.
 If meningitis is suspected add cefotaxime instead of gentamycin
 If pustules, omphalitis are present- add flucloxacillin instead of penicillin.
 If presumed sepsis stopped after 48 hours.
 Sepsis without localisation- 5 days
 Septicemia-7 to 10 days
 Meningitis if GBS 10 to 14 days. Others 21 days.
 Indications for LP
o All suspected meningitis
o All suspected LOS
o All culture positive sepsis
o Severe EOS
o Early onset RDS with signs and symptoms of sepsis
 In traumatic lp glucose is unaltered.
 In neonatal meningitis- steroids and fluid restriction has no place

 Pyloric stenosis has is high in B & O blood groups

 Purulent eye d/ch in a newborn is due to Chlamydia commonly.

 Bronchopulmonary dysplasia (BPD)

This is the name used for infants born preterm who still have an oxygen
requirement at a postnatal age of 36 weeks.

16
 Best measure of adequacy of BF in neonates are body weight.
 In neonates weight loss of >5% is abnormal.
 Newborns shouldn’t be discharged from the hospital until the first stools and urine is
passed.
 Both auditory brainstem response and optoacoustic emission are screening tests for
hearing.
 Newboen pulse oximetry should ideally be done after d1
 Guthrie test- best performed on D5

 Maternal CMV, Hep B and HIV can be transmitted through breastmilk to the baby.

17
 Except energy protein, carb, fats, electrolytes all are higher in formula milk.
 Risk of growth failure due to reduced energy intake is higher in first 6 months.
 Preterm infants have a particularly low stores of fat and protein. Carb is
somewhat normal
 At birth brain accounts for2/3rds of basal metabolic rate. At 1 year it’s about 50%.
 After an acute illness or a surgery children may go into a catabolic state and after
this time for a catchup growth energy intake should be around 150-200 kcal/kg/d
(100 in nl)
 In small infants with a very marked growth faltering after a surgery a period of
partial parenteral nutrition is needed to achieve catchup growth.
 Death rates due to coronary artery disease is higher in low birthweight infants.
 Commonest type of intracranial haemorrhage in newborn is subdural
hemorrhage (70%), then subarachnoid (20%) → intracerebral (20%) →
intraventricular
and epidural hemorrhage ; but in preterm it’s intraventricular haemorrhage or
periventricular haemorrhage

18
  Causes of leukocoria-absent red reflex and visible white reflex
1. Cataract
2. retinal detachment
3. retinopathy of prematurity
4. intraocular infection (endophthalmitis)
5. retinal vascular abnormality (such as Coat’s Disease)
6. intraocular tumor (retinoblastoma)

 Causes for apnoea in preterm infants

o metabolic awul (hypoxia, hypoglycemia, anemia, electrolytes)
o due to some stress (heart failure, seizures, infections, aspiration due to
GORD
 For anemia of Prematurity- iron from 4 weeks, multivitamins and folic acid from 2
weeks- guidelines iron from 2 weeks
 Iron CI in sepsis and gi bleeding.

Sensorineural Conductive

Due to, Lesions in the cochlear or auditory nerve. From abnormalities in ear canal or middle ear.

Causes Genetic (majority) Eustachian tube dysfunction

Antenatal and perinatal: Downs syndrome
Congenital infections- Cleft palate
MMR,syphilis, varicella Pierre Robin sequence
Preterm Mid facial hypoplasia
HIE Wax (rarely)
Hyperbilirubinemia
Xn-Alport, pendred
Postnatal:
Meningitis/encephalitis
Head injury
Drugs(aminoglycoside, frusemide)
Neurodegenerative d/o
Hearing loss May be profound( >95dB ) Maximum of 60 dB hearing loss

Natural Hx Doesn’t improve and progress Intermittent or resolve

19
 CP SMA Muscl Neur
e o
Tone ++/ ↓↓↓ ↓↓ ↓
-
UMN signs ++ - - -
+
Other CNS ft ++ - - -
s +
EMG _ Deneravtion patte ++ -
rn
NCS - - - +

Fasciculatio - ++ - -
n
CPK - - ++ -

20
21
22
23
24
 Amniotic band Xn
1.Limbs-Abnormally short fingers or toes with absence of the end (distal) portion,
syndactyly, constriction rings and extra strands of tissue adhering to the fingers
2. Limb-body wall complex-Encephalocoele, Gastroschisis, Thoracoschisis
3. Craniofacial abnormalities- Cleft palate, microphthalmia, choanal atresia

25
26
 Capillary haemangioma is a benign lesion while a cavernous
haemangioma is something significant and needs further evaluation.
 Pg 162 and 163 illustrated

27
28
29
30
31
 Choreo-athetoid CP and sensorineural hearing loss are the only two late manifestations of bilirubin
encephalopathy.
 In Rh incompatibility HSM is present. In ABO incompatibility HSM is absent.
 HbA starts appearing in the fetus in 28 weeks and at birth HbA to HbF ratio is 1:4.
 The only contraindication to the use of phototherapy is conjugated hyperbilirubinemia, as occurs in
patients with cholestasis and hepatic disease.
 With intensive phototherapy, the TSB level should decline by 1 to 2 mg/dL (17-34 μ mol/L) within 4-6
hours.
 Phototherapy usually can be discontinued when the TSB is less than 2-3mg/dl for the age.
 Clinically jaundice progresses in cephalo-caudal direction; But clinically we can predict the level of
TSB only if the icterus is confined above the nipple line-which is <12mg/dl
 If icterus is there in palms and soles it’s >15mg/dl
 Pahological icterus is considered when TSB is >18mg/dL or a rise of >5mg/dl/day
 For exchange transfusion recommended blood groups are
1. O negative suspended in AB positive plasma
2. O negative whole blood
3. Blood that is cross-matched for the baby
 Riboflavin or Vit B2 deficiency occurs with phototherapy.
 NICE charts are available from 23 to 38 weeks.

32
33
34
35
36
37
38
 Meconium is passed within 24 hours. But can wait upto 48 hours. Delayed
39
passage of meconium(24-48hours) is a/w maternal DM, CF, Hirchsprung
disease. In preterm also it takes ~1-2 days

40
 Commonest cause of NNJ requiring exchange transfusion worldwide—G6PD
deficiency.

Benefits of KMC
(1) Better thermal protection of neonates
(2) Increasing milk production
(3) Increasing the exclusive breastfeeding rates
(4) Reducing respiratory tract and nosocomial infections
(5) Improving weight of the baby
(6) Improving emotional bonding
(7) Reducing hospital stay

41
Nephrology
 Proteus and pseudomonas UTI produce alkaline urine.
 Uric acid, cystine, and calcium oxalate stones tend to form in acidic urine, whereas struvite
(magnesium ammonium phosphate) and calcium phosphate stones form in alkaline urine.
 Urine specific gravity
i) Normal 1.025-1.032
ii) CKD (2/3 of nephrons are lost) 1.010
iii) Diabetic insipidus 1.003
iv) Diabetic mellitus 1.030
v) Emesis/fever 1.040

 Renal threshold for glucose – 180mg/dl

 Transport maximum of glucose- 375mg/dl
 In hematuria glomerular involvement is suggested by
1. Dysmorphic cells
2. Rbc casts
3. Heavy proteinuria- 3/4+
4. HTN
5. Renal impairment
 In nonglomerular hematuria RBCs are uniform in shape, highly acidic and has
high Hb content.
 Benign familial hematuria- AD/AR, persistent hematuria without proteinuria or
other defects, will not progress to ESKD. But in alport it’s recurrent, a/w hearing
impairment, will progress into ESKD.
 Reasons for referral of a child with microscopic hematuria to a nephro centre
1. In a symptomatic child if the disease has a renal involvement
2. In a symptomatic if it’s a self limiting disease, treat it and followuo. Have to
refer only if there’s a recurrence.
3. In an asymptomatic if there’s associated proteinuria.
4. In an asymptomatic without proteinuria if the hematuria is persistent in a 6
month repeat urinalysis should refer. If it’s intermittent or no hematuria in
repeat tests don’t need to refer.
 Refer all cases of macroscopic hematuria unless
1. The MSU becomes positive and treated for uti
2. The MSU becomes negative, but you have a clear Dx and with treatment, the
child responds completely.

 VUR is a/w renal dysplasia

 Commonest cause for hematuria in children is infection

 RPGN can occur in any cause of acute nephritis, but uncommon when the cause
is post-streptococcal.

42
  Indications for dialysis in AKI:
Refractory hyperkalaemia
Refractory severe acidosis
Refractory hypertension
Refractory fluid overload
Uraemic symptoms
Blood urea more than 40mmol/l
Prolonged anuria or oliguria
Deteriorating level of consciousness (uremia & hyponatremia)

 PSGN can be associated with mild normochromic anemia due to haemodilution

& low grade haemolysis.

 In PSGN- anti DNAse B levels cab used to detect past skin infections.

 RPGN, B/L renal vein thrombosis & renal cortical necrosis has a poor prognosis.

 Pre-renal AKI, acute TIN, ATN, HUS has a good prognosis.

 VUR causes-Familial, Bladder pathology (Neuropathic bladder), urethral

obstruction, UTI (But temporary)

 Indications for renal biopsy in nephrotic syndrome

Steroid resistance whether primary or secondary
Onset < 6 months of age
Features of secondary causes like rash and arthropathy
Deranged renal functions not attributable to hypovolaemia
Persistent microscopic haematuria with hypertension
Macroscopic haematuria
Low compliment C3 and C4 levels

 Indications for renal biposy in nephritic syndrome

Rapidly rising creatinine
Presence of nephrotic syndrome
Clinical or immunological features suggestive of non post-streptococcal GN.
Persistent low compliment levels for more than 3 months
Moderate proteinuria for 2-3 months
Persistent hypertension or deranged renal functions for more than 2 to 4 weeks.

4 types of imaging Ix are performed in UTI

1. USS in the acute phase
Never done if responds well to Tx within 48 hours.

43
 In atypical UTI at any age.
For recurrent UTI only if ˂6m old.

2. USS after 6 weeks

If responds well to Tx done only in ˂6m old.
Never in atypical UTI.
In recurrent UTI in ˃6m old.

3. MCUG after 6 weeks

Only done in ˂6m old if there’s atypical or recurrent UTI.
Never recommended for UTI well responding to Tx within 48 hours.

4. DMSA after 4-6 months

Never done if it responds well to Tx
Upto 3 years in all atypical and recurrent UTI.
˃3 years only in recurrent UTI.

Normal SBP= 90+ (age*2)

ARPCKD is a/w hepatic fibrosis & portal HTN.

Commonest cause of obstructive uropathy in paed- PUJO; Majority of them resolve
spontaneously.

Twenty-eight weeks is considered the optimum time for performing ultrasound to detect
fetal urological anomalies

In the neonate whose hydronephrosis was diagnosed antenatally, USS should be

repeated 48 hours after birth unless there are indications for an immediate postnatal
scan such as bilateral hydronephrosis, hydronephrosis in a solitary kidney or
Oligohydramnios.
All newborns with antenatally detected hydronephrosis should be started on
antibiotic prophylaxis until vesico-ureteric reflux is excluded.

Duplex USS can be used to differentiate obstructive vs nonobstructive hydronephrosis.

Once USS detects a PUJO DTPA with MAG3 (preferred than technetium 99m) with a
diuretic or MR urography can be done.

In the evaluation of a child with a hydronephrotic kidney, diuretic renography has taken
the place of IV urography.

CKD
 Hypertension
 Growth
 Dialysis

44
  Anemia
 MBD
 Nutrition
 Acidosis
 Fluids and electrolytes

Oliguria
<0.5ml/kg/hr- children
<1ml/kg/hr- neonates

45
Oncology
 Commonest malignancies in childhood
Leukemia˃ CNS tumours˃ Lymphoma
Most common solid tumours-CNS (out of them infra-tentorial tumours)
 Commonest solid organ malignancy is CNS tumours.
 Commonest pituitary tumour in children- craniopharyngioma
 Most common malignant brain tumour in children-medulloblastoma
 Most common malignant brain tumour in adults- Glioblastoma multiforme (Gr IV
astrocytoma)
 ALL age-2 to 5 years
 Nephroblastoma
o Peak age 3 years
o 5% bilateral
o 1/3rd AD
o 2/ 3rd sporadic
o Common presentation is abdominal mass or incidental
o PUO
o Presentation with hematuria or pain is rare
o Common is direct spread
o Lymphatic spread rare
o Polycythemia
o Under 2 years -no CT or RT
o Nephrectomy can be done
o Better prognosis than neuroblastoma
 Neuroblastoma
o Most common extracranial solid organ malignancy in infancy. And
malignancy??
o Commonest is from adrenal medulla
o Rarely hereditary
o Peak age 1 to 2 years. Median age at Dx 20 months
o Commonly present as pallor, LOW, fatiguability, limping, hepatomegaly
o Mass hard, smooth and nontender
o Can cause both proptosis and enophthalmos
o PNS
o Xray calcifications
o Pancytopenia
o Definitive Dx- biopsy and genetic testing
o Localised-surgery
o CT and surgery combined
o Prognosis good if less than 1 year old, normal LDH and normal
catecholamines. In very young even spontaneous regression can happen.
Hypertension can be present in both neuro and nephroblastoma.

46
Philadelphia translocation (9:22) carries a bad prognosis in ALL; good prognosis in CML

47
 Retinoblatoma-RB gene on chromososme 13
 Down Xn-A/W leukemia, neurofibromatosis, glioma
 Translocation of chromosome 11 and 22- Ewing’s sarcoma

48
49
Neurology

 Location of focal seizure origin

 Temporal >frontal>occipital>parietal
 Frontal lobe seizures usually occur at night. Frontal lobe seizures are also known
as adversive seizues because they cause turning of head to the opposite side.
 Seizures that needs lifelong treatment
1. Juvenile absence seizures
2. Atypical absence seizures.
3. Juvenile myoclonic epilepsy
4. Progressive myoclonic epilepsy
5. Lennox-Gestaut Xn

 Absence seizures are common in girls.

 IN absence seizures PVC is avoided-phenytoin, vigabitrin, carbamazepine
 Infantile spasms could be secondary to- prematurity, HIE, PVL, congenital
infections, IEM, neuromuscular disorders
 GTC seziures last for less than 1 min; if persists beyond that it’s due to status
epilepticus or false seizure.
 Typical and atypical absence seizures, infantile spasms & atonic seizures are
universally recurrent therefore TX is started from the first episode onwards.

 Meningitis caused Lyme disease-though it’s a bacterial infection causes

leukocytic leukocytosis.
 In enterovirus meningitis glucose levels can be low.
 2/3 of CNS infections are viral in origin.

 Tension type headaches in children are usually not a/w features like N or V.
 Migraines last for 1-72 hours; relieved by sleep; commonly B/L; 90% present
w/out aura.
 DOC for status migrainous (migraine lasting more than 72 hours)- IV
prochloperazine.
 In an acute attack of migraine 5HT-1 agonists are used-sumatriptan
 In prophylactic prevention of migraine 5HT-2 antagonists are used-pizotifen

 Most common cause of choreoathetoid CP in children at present is HIE at term;

not kernicterus.

 High IQ 140, genius IQ 160

50
51
52
 Commonest cause of meningitis is viral and most are self resolving.-but treat all
meningitis as bacterial at first presentation.
Bacterial meningitis are severe than viral.
Tubercular mainly affects under 5 years.
Fungal & parasitic are in immunocompromised
Other causes: Malignancy , AI diseases
 10% of of bacterial meningitis survivors are left with long-term neurological
impairment.
 Subdural effusions as a complication of meningitis is commonly due to
H.influenze & pneumococci.
 Seizures in first 4 days of memingitis is common and doesn’t carry any climical
significance. But if they occur 4 days of illness it implies poor prognosis.

53
 Initial empirical antibiotics in meningitis
o Neonates- Ampicillin and cefotaxime(not ceftriaxone) If GBS sus-High
dose penicillin alone
o IV cefotaxime 200mg/kg/24hours
o If resistant IV vancomycin
o Listeria- IV ampicillin
o Immunocompromised- ceftazidime & gentamycin
 More than 6 weeks 0.15mg/kg 6 hourly for 48 hoursZ steroids are proven reduce
hearing loss. Not proven on long term outcome. Guidelines- use after 3months
 Highest mortality-pbeumpcoccus
 Poor progbosis on less than 6m old and in multiple seizures.
 Hib aw hearing loss.
 Most common neuro sequelae
o Hearing loss
o MR
o CP
o Recurrent seizures
 Prophylaxis
o Neisseria all contacts rifampicin 10mg/kg/dose bd for 48 hlurs
o Haemophilus- househild contacts of patients with invasive disease
20mg/kg daily for 4 days
 Meningoencephalitis is self limiting in most.
 Enteroviruses are the commonest patbogens causing meningoencephalitis.
 Mumps meningoencephalitis will cause deafness later on.
 In meningoencephalitis initially polymorphs then mononuclear cells.
 Fever is not always present on presentation of acute bacterial meningitis.
 Neck stiffness is better assessed after 3 years.
 Streptococcus and haemophilus can also cause petechial/ purpura in meningitis.
 CSF glucose concentration can be used to identify partially treated meningitis.
 Gram stain is the most rapid test that can be used to diagnose bacterial
meningitis
 Haemophilus gram negative cocco bacilli

54
55
56
Hypotonia

 In myopathies proximal muscles are affected more than the IV amistal muscles; but
in myotonia dystrophica distal muscles are affected more.
 In neuropathies distal muscles are affected more than the proximal muscles; but in
SMA proximal muscles are more affected.
 Even cerebellar d/o can cause hypotonia.
 Infections that are a/w central hypotonia- tox, CMV, rubella, herpes
 Though prader willi Xn, brain infarctions & haemirrhages are central casues of
hypotonia they cause profound loss of tone.
 Gower’s sign is a normal finding in <3 year olds.
 In SMA diaphragmatic involvement is less; commonest cause of death is respiratory
failure due to intercostal muscle involvement.
 Sepsis and severe congenital heart disease can cause a picture of central hypotonia

57
58
Gastroenterology

 75% of Hirschsprung –rectosigmoid region-short segment disease

10% -Entire colon
 Unsual in preterm
 Hirschsprung disease and duodenal atresia may be a/w Down Syndrome.
 Hirschsprung has familial tendency(AD) and common in male children.
 In Hirschprung rectosigmoid ration is <1 (1:4)
 Hirschsprung can even present as bilious vomiting
 Short segment hirschsprung- p/w constipation; long segment- p/w failure to pass
meconium
 Some pass meconium normally and later p/w chronic constipation.
 Enterocolitis- Clostridium difficile, Staph aureus, Anaerobes, Coliforms

 Some children with IBS have Coeliac disease

 Intestinal atresia is a/w polyhydramnios
 Pyloric stenosis- More common in
1.firstborn
2.boys
3. O positive and B blood groups
4. Associated with UCB
5.Macrolid use-infant and maternal use
6.Bottle feeding
Presents at 2-8 weeks
Vomiting increases in frequency and forcefulness over time
Unlike in sepsis they’re hungry active babies.
Haemetemesis can be present
Hypochloremic metabolic alkalosis, hyponatremia, hypokalemia
O/Ex-Infants are not ill looking or febrile, Mass at right upper quadrant, Left to
right visible peristalsis.
First correct fkuids for cl and hco3. Then for alkalosis.
If uss is non diagnostic do barium studies.

 Commonest congenital anomaly in esophagus is Esophageal Atresia; 90% of

them are associated with TOF. Prematurity is a risk factor.
 Usually Pyloric stenosis is an isolayed defect. But TOF & dodenal atresia are
affected with other anomalies.
 Duodenal atresia is a/w preterm and Down xn
 Trisomies are associated with omphalocoele.
 Meconium plug- small left colon syndrome, Hirschsprung disease, CF, MgSO4
tgerapy, maternal opiate use, congenital hypothyroidism.
 NEC is seen in distal ileum and proximal colon. Present in 2nd to 3rd week. This
canalso present as bilious vomiting.

59
 Risk factors for NEC-birth asphyxia, Down syndrome, congenital heart disease,
rotavirus infections, and Hirschsprung disease.
 Intestinal malrotation-nonbilious vomiting & volvulus-bilious vomiting

GER in children predisposed by cough, asthma,CF

Other R/F for pyloric stenosis

 Adenoviral infection is a/w high rates of intussusception. Steroids are given to reduce
recurrence.
 Rotaviral vaccine is a/w intussusception.
 In gi problems if less than 3years- intussusception
 >3 years- appendicitis
 Sx is done for intussusception if more than 3 days, pt unstable, signs of peritonism,
intestinal obstruction ,recurrent ones.

 Leading COD in children <5years is pneumonia, then diarrhoea

 Leading cause of malnutrition in children <5years-diarrhoea

 Almost all affected neonates with meconium ileus have cystic fibrosis
 Absence of pneumatosis on abdominal radiographs does not rule out the
diagnosis of NEC.
 Patients diagnosed with Hirschsprung enterocolitis or severe gastroenteritis may
present with pneumatosis intestinalis.
 Probiotics: Lactobacillus, Bifidobacterium, Saccharomyces, and Streptococcus
sp. Used in the treatment for treatment of infectious diarrhea, antibiotic
associated diarrhea, atopic dermatitis, necrotizing enterocolitis, Helicobacter
pylori infection, Crohn’s disease, and ulcerative colitis.

60
  Risk factors for GORD in children
o CP
o Preterm, especially if bronchopulmonary dysplasia is present
o Surgeries in lower esophagus-hiatal hernia

Red flag features of abdominal pain in children

 Pain away from umbilicus in right upper or lower quadrant
 FTT
 Nocturnal pain
 Significant vomiting
 GI blood loss
 Chronic blood loss
 Persistent fever
 Jaundice
 Arthritis
 Rash
 Family history of IBD
 Localized tenderness or mass in abdomen: organomegaly
 Perianal fistula

Red flag features of constipation

 Present at birth or first few weeks of life
 Not passing stools in first 48 hours.
 Ribbon stools
 Vomiting with abdominal distension
 Previously undiagnosed leg weakness or motor delay
 FTT
 Evidence of child maltreatment

Laxatives
1. Osmotic laxatives- lactulose and PEG
2. Stimulant laxatives- bisacodyl & senna
3. Bulk forming agents- methylcellulose
4. Stool softener- docusate
5. Lubricants- liquid paraffin, arachis oil

Both IBS & abdominal migraine has positive family history.

 Osmotic diarrhoea- osmotic gap >50, <200ml/day, acidic ph<5, anal excoriations.
 Growth failure is more common in CD than UC.

61
 Causes for watery diarrhoea
1. Enterotoxigenic ecoli
2. Bacillus cereus
3. Vibrio
4. Clostridium perf

 Causes for bloody diarrhoea

1. Campylobacter
2. Shigella
3. Yersinia
 Both types
1. Nontyphoidal salmonella
2. Clostridium difficile
3. EHEC/ STEC- shiga like toxin
4. EIEC
5. EPEC
EIEC & EPEC commonly watery

Time of presentation and organism

o <6 hours- preformed toxin of bacillus cereus or staph aureus
o 6-24 hours- bacillus cereus or clostridium perfringens
o 16-72h- norovirus, salmonella, shigella, E. coli, campylobacter etc

Giardia has been associated with iron deficiency, growth stunting, and repeated Giardia
infections correlate with a decrease in cognitive function in children in endemic areas

Infant colic - Paroxysmal, inconsolable crying or screaming often accompanied by

drawing up of the knees and passage of excessive flatus takes place several times a
day. Occurs in first few weeks of life and resolves gradually from 3-12 months of age. If
severe and persistent, may be due to cow’s milk protein allergy.

In the elderly intussusception colocolic is the commonest unlike in children.

In ISS-Right iliac fossa is empty, stepladder peristalsis; hydrostatic reduction is
contraindicated in complete obstruction; perforation and peritonitis.
Indications for sx-recurrent, persistent for >48 hours,

Causes for acute liver failure

Children <2 years
1. congenital infections (most common HSV)
2. inborn errors of metabolism
ex: galactocaemia,tyrosinaemia
3. neonatal haemochromatosis
4. hereditary fructose intolerance
5. drug induced
Children >2 years
1. sero negative hepatitis

62
2. PCM overdose
3. Wilson dx-KF rings not seen upto 7 years, renal tubular dysfunction, vit D
resistant rickets
4. AI hepatitis

63
In addition diabetes insipidus, mental retardation are risk factors.

64
Haematology

 HSP is a clinical Dx. A/w ileus, protein losing ebteropathy, nephrotic syndrome,
nephrotic syndrome, orchitis, CNS involvement-fbc and coagulation stidies are
normal, rash is symmetrical and starts as urticarial, trunk is usually spared
 Intusussceptions in HSP -70% occur in ileoileal locations, with only 30% being
ileocolic (unlike typical intussusception, which occurs most commonly at ileocolic
locations.
o Contrast enema may not diagnose it, because of the ileoileal location.
o Ultrasound is preferred imaging modality, augmented by serial examinations.
o Upper GI Series with small bowel follow-through may be necessary as well.
 In thalassemia MCV is frequently <75. But in IDA it’s occasionally <80; RDW is
usually normal in thalassemia but increased with IDA.(normal is 80-96)
 Haemorrhagic disease of the newborn- both PT & APTT are increased.
o Early-within 24 hours maternal drugs
o Classic-2 to 10 dayslack of vit K in breastmilk
o Late-usually after 2 weeks Neonatal hepatitis, biliary atresia
 Polycythemia-Packed cell volume >65%--> will cause hypocalcemia & hypoglycemia
 Neonatal polycythemia causes- full correction (80ml/kg)*2
o Placental insufficiency:
 Preeclampsia
 Primary renovascular disease
 Chronic or recurrent abruptio placenta
 Maternal cyanotic congenital heart disease
 Postdate pregnancy
 Maternal smoking
o Endocrine abnormalities
 Thyrotoxicosis
 Poorly controlled maternal DM
o Chromosomal
 Trisomy 13, 18, 21
o Hypertransfusion
 TTTS
o High altitude
 Fetal cord blood Hb is less than 3. More than 5 is significant.

 Systemic diseases a/w haemolytic anemia

o Renal diseases
o Liver diseases
o Infections- C.perf, malria
o Wilson’s

65
 Normal Hb levels
o Neonate 14
o Infant 10
o Upto 12 years 11
 Normal iron dosages
o Deficiency 6mg/kg/d
o Prematurity or LBW 2mg/kg/d
o Normal healthy kiddis 1mg/kg/d
 Homocysteine elevation in nkth. Methylmalonic acid only in b12 deficiency

66
 Aplastic anemia can cause both normocytic and macrocytic anemia.
 Iron deficiency can cause normocytic, macrocytic & microcytic.

 PNH- both intra and extrvascular, risk factor for AML, causes puo, steroids are ci
in tx

 In hereditary spherocytosis- normal or low MCV, high MCHC, high RDW.

 PK deficiency is AR, extravascular haemolysis, severity of anemia doesn’t

correlate with Hb levels, def tx is BM transplant

67
68
Transferrin IDA ↑ Thal minor and AOCD-nl
Transferrin saturation IDA ↓ Thal minor and AOCD-nl

69
70
71
 B12 deficiency causes hyporeflexia with Babinski and clonus

72
73
74
Etiology of childhood leukaemia is multifactorial;

 Down syndrome
 Fanconi anemia
 Bloom syndrome
 Ataxia - telangiectasia
 Wiskott - Aldrich syndrome
 Neurofibromatosis type 1
 Ionizing radiation
 Chemotherapy agents (Hydroxyurea, Chorambusil)
 Viruses (HTLV1,EBV,HIV)
 Immunodeficiency

75
76
Chromosomal

 Autosomal trisomies are the commonest aneuploidies that are not related to sex
chromosome d/o
 Down Xn is the commonest autosomal trisomy-commonest cause is non-dysjunction
 Klinefelter is the commonest sex chromosome aneuploidy.
 Only viable monosomy is turner (45,X)
 Turner Xn most children are of normal intelligence. But, they can have intellectual
impairment.
 Prader Willi occurs due to microdeletion
 Buccal smear can be used to diagnose Turner Xn

77
78
Cardiology

 Commonest cyanotic CHD in neonates is TGA & in children is TOF.

 DCM is the commonest myocardial disease in children.
 TGA- single and loud S2 is heard
 TGA- egg on a side appearance on CXR narrow mediastinum
 TAPVD- wide mediastinum egg on a side appearance
 Adult type co-arctation of aorta is post ductal & duct independent. Paediatric
coarctation of aorta is preductal and duct dependant.
 Essential hypertension risk in children is increased with prematurity, obesity, LBW
and family history. Commonest manifestation in infants is cardiac failure & faltering
growth. Hypertension in children can present as facial palsy.
 Prophylaxis for rheumatic fever
o Acute rheumatic fever without carditis- 5 years or until 21 years, whichever is
longer
o ARF with carditis but no residual valve lesion- 10 years or until 21 years,
whichever is longer
o ARF with residual valve lesion- life long prophylaxis
 The most common cyanotic congenital heart defects are the five Ts:
1. Tetralogy of Fallot
2. Transposition of the great arteries
3. Tricuspid atresia
4. Truncus arteriosus
5. Total anomalous pulmonary venous return
 In TOF normal o2 saturation is 80%; anything less than this indicates a spell
 Infective endocarditis complicating a VSD is rare.
 SVT in infants generally produces a heart rate >220bpm, and often 250–300bpm.
Sinus tachy has a rate <200 in infants and children. And SVT is felt as regular
palpitations.
 In sinus arrhythmia- variation upto 30/min is normal
 When managing unstable in SVT in infants (<1 year)-amiodarone is contraindicated.
 Carotid bruit is a normal finding when heard in children.
 AS is a/w MS and coarctation.

 Pulmonary stenosis associations

 Noonan Xn
 Allagille Xn
 William’s syndrome
 Congenital rubella syndrome
 TOF
 Leopard syndrome
 Rheumatic fever

 Aortic stenosis

79
  Turner Xn
 Rheumatic heart disease
 TOF associations
o CHARGE
o VACTERL
o DiGeorge anomaly
o R aortic arch
o Fetal alcohol Xn
o Fetal warfarin syndrome
o Male child is a R/F
 Intermittent chest pain in a 10 year old
o Coarctation
o Bicuspid AV causing AS

 Tuberous sclerosis is a/w cardiac rhabdomyoma.

Heart failure in children
 Volume overload is the commonest cause of HF in children-VSD, PDA, valvular
insufficiency
 In 1st week of life HF occurs due to obstructive lesions which are duct dependant.
 After 2nd week of life HF occurs due to L R shunts; in this symptoms worsen upto 3
months and the settle with the development of Eisenmenger syndrome.
 RHF causes pleural effusion while the LHF causes pulmonary edema.
 DCM is the commonest cardiomyopathy in children.

 Ductus
 Functional closure-first 15 hours
 Anatomical closure- completed in 2 to 3 weeks
 Named PDA if persists beyond 3 months.
 PDA associations
 Hypoplastic left heart syndrome
 Pulmonary atresia
 TOF
 Eisenmengers
 Preterm
 Surfactant deficiency
 Rubella
 Warfarin syndrome
 Trisomy 21 & 18
 Familial
 Renal failure

HF causes
 Presentation in infancy
First days: HLHS, Critical AS
First Month: COA
First Two Months: Left to Right shunts_ VSD, PDA, Truncus Arteriosus
80
  Presentation after infancy
Progression of structural Heart diseases
Arrhythmias
Infectious Diseases- Myocarditis
Late Onset Myopathies
Toxins
Anthracyclines
Diphtheria

 Partial AVSD- ASD type murmur with fixed splitting + MR type murmur at the apex
Sx is done at 2-5 years
 Complete AVSD- No murmurs are heard corrected at 3-6 months

Rheumatic fever
 Evidence of carditis-prolonged PR interval is not an evidence of carditis
1. Soft s1
2. S3 gallop
3. Mid-diastolic murmur
4. Congestive cardiac failure
 Evidence of endocarditis
1. MR w or w/out AR
2. Pulmonary valve involvement is rare
 Early features of rheumatic heart disease
1. Carditis
2. Arthritis-extremely painful large joint arthritis
3. Erythema marginatum-spares the face
 Late features of rheumatic carditis
1. Subcut nodules-after 6 weeks almost always heart is involved
2. Sydenhams chorea-4 to 6m
 Prevalence of Cx
Arthritis> Carditis> chorea > Erythema marginatum > Subcutaneous nodules
 Drugs in rheumatic fever
1. Oral penicillin for 10 days
After that IM benzathine penicillin 4 weekly if there’s no cardiac
involvement & 3 weekly if there’s cardiac involvement upto
5 years or 21 years whichever is longer if there was no carditis
10 years or 21 years whichever is longer if there was carditis but now
completely resolved.
Lifelong if there’s a residual cardiac defect.
2. Anti-inflammatory drugs
If there’s no carditis aspirin 100mg/kg for 3-4 days until the APR starts
dropping and then 75mg/kg for 4 weeks
If there’s carditis prednisolone 2mg/kg/day for 2-3 weeks and then taper
the dose; when starting to taper add aspirin 75mg/kg
3. Diuretics
4. ACEI

81
82
 Sinus Tachycardia Supra ventricular Tachycardia

Heart rate < 200/mt Heart rate > 220/mt

P – difficult to identify if HR >200 P – Not identifiable

P Up right in lead 1 and AVF P – Negative in lead 2, 3, and AVF

Beat to beat variation + No beat to beat variation

Gradual cessation Abrupt cessation

But all clinically innocent murmurs too need routine 2D-echo.

83
84
1.Medications used by the mother can cause an increase in congenital heart
disease. Anticonvulsants, lithium, indomethacin, nonsteroidal anti-inflammatory drugs
(NSAIDs), ibuprofen, sulfasalazine, thalidomide, trimethoprim, sulfonamide, vitamin A,
selective serotonin reuptake inhibitors (SSRIs), marijuana, alcohol, cigarette smoking,
cocaine, and exposure to organic solvents.

2. Maternal illnesses that increase the risk of congenital heart disease. Untreated
phenylketonuria (PKU), maternal pregestational diabetes, febrile illness during
the first trimester, influenza, maternal rubella, epilepsy, and maternal lupus/connective
tissue disease.

3. Maternal congenital heart disease and/or congenital heart disease in a first degree
relative. Increased incidence of heart disease in the child.

85
86
87
Endocrine
 Deficiency of 21-hydroxylase, resulting from mutations or deletions of CYP21A, is
the most common form of CAH, accounting for more than 90% of cases.
 Acquired hypothyroidism in children is a cause for both delayed puberty and
pseudoprecocious puberty.
 Normal thyroxin dose
 Infants 10-15mcg/kg/d
 Children 4mcg/kg/d
 Commonest cause of hypothyroidism is –thyroid dysgenesis > dyshormonogenesis>
iodine deficiency
 Birthweight and length are normal, but head size may be slightly increased because
of myxedema of the brain. The anterior and posterior fontanels are open widely;
observation of this sign at birth can serve as an initial clue to the early recognition of
congenital hypothyroidism.
 Approximately 10% of infants with congenital hypothyroidism have associated
congenital anomalies. Cardiac anomalies are most common, but anomalies of the
nervous system and eye have also been reported.
 Infants with congenital hypothyroidism may have associated hearing loss.
 Congenital hypothyroidism is a/w hypotonia.
 Congenital hypothyroism is a/w anemia infants can be pale

 Stress, anxiety and alcohol causes hypoglycemia.

 DKA Dx criteria
1. RBS more than 200
2. Ketonemia more than or equal to 3 or urine KB more than or equal to 2
3. HCO3 less than 15 and or venous pH less than 7.3
 Cerebral edema in DKA occurs typically 4-12 hours after treatment is initiated.
 R/F for the development f cerebral edema in DKA
1. Early insulin therapy
2. NaHCO3 treatment
3. Failure of sodium to rise during fluid resuscitation.
4. Acidosis
5. Hypocapnea
6. Duration of DKA
7. Overenthusiastic fluid administration

 Cushings Xn due to functional adrenocortical tunours is common in infants.

 Ectopic ACTH- islet cell CA of pancreas, neuroblastoma.

88
89
Respiratory

 Most common serious respiratory infection of infancy-Bronchiolitis

 Most common ch.respiratory d/o in childhood-Asthma
 Bronchiolitis-RSV Bronchiolitis obliterans-Adenovirus
 Dx of asthma in children
o FEV1/ FVC ratio <85%
o Post bronchodilator FEV1 more than 12%
 LABA-always with corticosteroids,12 hrs action,good for exercise induced
asthma
 Drug induced asthma-penicillin, aspirin, beta blocker, NSAID

 Intermittent asthma- started at step 1

 Mild persistent- step 2
 Mod and severe persistent- step 3 or 4

When exposed to an allergen Th1 response occurs in healthy people which is IgG
mediated; in atopic individuals IgE mediated Th2 response occurs.
 Allergic march
o Eczema- food allergy- rhinitis- asthma
 Rhinitis-commonest organism is rhinovirus
 For allergic rhinitis sedative antihistamines are more effective than non-sedative
ones.
 AOM & sinusitis organism
o S.pneumoniae is the commonest
o Haemophilus influenza
o Moraxella catarrhalis
o Staph and anaerobes are not common.
 Both ethmoid and maxillary sinuses are present at birth; but, only ethmoid sinus
is pneumatized. Maxillary only at 4 years. Sphenoid by 5 years. Frontal sinuses
begin development at 7 years and mature in adolescents.
 Chronic sinusitis- a/w GOR
 Pharyngitis is most commonly due to viruses. Group A beta haemolytic
streptococcus is associated; but, streptococcus pneumonia and haemophilus are
not proven yet.
 AOM- commonest organism is streptococcus pneumoniae
 GABHS has A, B & C type toxins. Therefore, one kid may develop minimum of 3
episodes of scarlet fever.
 Bacterial & viral pharyngitis can’t be distinguished ckinically.
 Retropharyngeal abscess is uncommon after 5 years.
 Risk factors for severe bronchiolitis-bronchiolitis is commoner in boys
o Prematurity
o Age<6w
o CHD

90
 o Immunodeficiency
o Malnutrition
o Parity
o Overcrowding
o Passive smoking
o Formula feeding
 Croup
o 6m- 3 years
o Org-parainfluenza, influenza, adenovirus & RSV rarely mycoplasma
o Symptoms are worse at night.
o Recurrence is common
o Fever may be present; but no signs of toxicity.
o Harsh stridor and barking cough
o Leukocytosis is uncommon & if present look for epiglottitis or bacterial
tracheitis.
o Reduced oxygen saturation is a late finding
o Xray neck AP- steeple sign
o Failure to respond to nebulised adrenaline should question the diagnosis
of croup – consider bacterial tracheitis, epiglottitis or foreign body.
o RR and the degree of sternal recession are valuable clinical indicators of
severity and response to treatment, the degree of hypoxia is the best
assessment.
o ABx not indicated unless there’s a IIry bacterial inf; humidified air not
proven.
o Tx-oral dexa or inhaled budesonide- don’t cannulate airway till is secured.
If severe give adrenaline.

 Acute epiglottitis
o 2-6 years
o Org- Haemophilus influenza. Also GABHS & staph
o Rapid sudden development of symptoms; cough is absent
o Stridor is a late feature-if present very soft
o Drooling of saliva, tripod position are typically present. Child will be upright
and not moving. Cough is minimal.
o Lateral xray & venipuncture should be avoided.
o Lateral neck xray- thumb sign but not performed
o WBC raised
o Intubation is likely to be required by gaseous inductionblood culture-start
cefuroxime
o Rifampicin prophylaxis to close contacts
o Extubate after 24 hours.
o Adrenaline and steroids are not useful.
o hypoxic cerebral damage, pulmonary oedema and other serious
Haemophilus infections are rare.

 Bacterial tracheitis AKA pseudomembranous croup

91
 o 3w to 16 years
o Staph aureus is the commonest
o No drooling; no specific positioning; but barking like cough is present and
a longer history differentiates it from epiglottitis.
o Majority needs intubation.

 Tracheomalcia-apparent only during forced expiration or cough/ while crying

Congenital laryngomalacia
● Cry is normal
● Inspiratory stridor, high pitch
● Within a few days of birth following URTI
● Starts to resolve after I yr
● Worsens – supine position, suckling, crying
● Improves in prone position
● Dx- Flexible nasopharyngolaryngoscopy- omega shaped epiglottis
● Tx- 90% of cases resolve by 2 yrs
o Tx URTI effectively
o Surgical intervention in severe respiratory distress ,feeding difficulty,
failure to thrive

Pertussis
 B.pertussis is the only cause fir epidemic
 <5 year olds and unimmunized
 3 phases- catarrhal ,paroxysmal, convalescent phases
 Cx-secondary bacterial pnemonia, AOM, pneumothorax, Encephalopathy,
convulsions, apnoea
 Dx per nasal swab for culturebefore abx
 Doc-erythromycin- aim is to prevent the spread
 Infection doesn’t confer immunity, need to complete vaccination
 Chemoprophylaxis to all vulnerable and high risk contacts.
 Vulnerable contacts- neonate, unimmunized or partially immunized less than 5
year olds, persons with chronic illness.
 High risk-t3 of pregnancy, children under 1 yr

Pneumonia
 Neonates bacteria are the commonest, neonates and children-viral, >5 years
bacterial. TB in all ages.
 In neonates staph is not a cause
 Commonest cause is streptococcus pneumonia
 Viruses are common upto 5 years.
 Tachypnea with chest in drawing is the best predicotr of pneunonia in all age
groups.
 Tachypnoea neonates 60, infants 50
 Bacterial LRTI- higher fever, tachypnoea, wheezing only in mycoplasma

92
 Viral lrti- low fever, wheezing, marked recessions, hyperinflation, collapse
 Duration of abx- usually 5 to 7 days. 10 d of severe.
 0 to 3 m- iv penicillin or penicillin and genta
 3m to 1 yr- amoxicillin, ampicilin
 1 to 5 years- amoxicillin, penicillin
 >5 years- macrolides
 staph-abrupt and severe onset, usually unilateral, even if small effusion should
be drained, pneumatocoeles are common
 Haemophilus- coryzal symptoms precedes, commonly a/w pleural effusion, doc
ampicillin
 Klebsiella- fulminant and frequently upper lobes, rare as cap, commonly hap,
cefotaxime
 Chlamydia trachomatis-crepts common, staccato cough, conjunctivitis,
erythromycin.
 Pneumatocoele- staph, streptococcus, haemophils, klebsiella, serratia, ecoli, tb
 Necrotising & parapneumonic effusion- staph aureus, streptococcus pyogenes &
pneumonia
 Atypical pneumonia- rare under 4 years
 Mycoplasma- usually >1 week, bullous myringitis, erythema nodosum &
multiforme , sickle cell anemia is Risk factor,pleural effusion rare, dx by rising
plasma titers, WBC normal.
 Legionella- prodromal viral like illness, cough, confusion ,diarrhea, lymphopenia
without marked leukocytosis, hyponatremia, urine ag highly specific,
 Unilateral hilar ln- primary tb or mycoplasma
 VZV pneumonitis- commonly complicated by staph aureus

Risk factors for asthma

 Transient early wheezing- Prematurity, Maternal smoking before or after

preegnanacy,family hx of viral wheezing in early childhood
Family hx of asthma or allergy is not a R/F
 Atopic asthma- Family hx of asthma/allergy, hx of eczema, less than 20 years
maternal age
Prematurity and Smoking are not R/F
 Non atopic wheezing- usually starts after RSV
 Surfactent deficienct lung disease
Risk increased in-preterm,GDM,multiple pregnancies,asphyxia, LSCS, cold
injury,Chorioamnionitis, Non-immune hydrops fetalis
Risk reduced in-PIH,PROM, Maternal opiates,tocolytics,Heamolytic disease of
newborn, IUGR/SGA

93
INAH prophylaxis for TB – only inah, only for 6m, only after excluding active disease
 Less than 5 year olds who are close contacts
 Plhiv who are close contacts
 Plhiv mantoux more than 5mm
 Transplant recipients
 Before anti tnf

Mantoux positivity
 >0-9 negative
 10-14 positive
 15 & more-strongly positive
 >5- Positive in immunocompromised, malnourished
 Regardless of the status of BCG vaccination >10 is considered postitive.

94
95
96
97
98
99
Fluids and electrolytes
Osmolarity of new ORS- 245mOsm/L
Wide qrs and st dep are commin to hypo and hyperkalaemia

100
101
102
High anion gap
 Salicylates ~20
 Renal failure ~25
 DKA 35-40
 Lactic acidosis more than 35
 Largest anion gaps -Lactic acidosis and DKA

Low anion gap

 Hypoalbuminemia-Nephrotic Xn, Liver cirrhosis, Haemorrhage, intestinal
obstruction, multiple myeloma

103
Renal

104
Musculoskeletal
 SOJIA has-quotidian fever (everyday there’s a fever spike with a fever free
interval-fever comes in the eve or morning)
 In JIA positive FHx is rare.
 JIA is the commonest rheumatological condition in children.
 Poor prognostic indicators in JIA
o Active disease despite tx for >6m – high plt, fever
o Early onset disease
o Rheumatoid factor positivity
o ANA positivity
 Transient synovitis 2-12 years
 Perthes disease 5-10 years
 SCFE 10-15 years
 Post streptococcal arthritis goes upto 8 weeks and poorly responds to NSAIDs.
But arthritis in rheumatic fever persists only for less than a week and responds
well to NSAIDs.
 In dermatomyositis - the erythematous facial rash involves the nasolabial fold
unlike in SLE.
 In calcipenic rickets ALP is high & PTH is also high. IN phosphopenic rickets ALP
is marginally elevated and PTH is normal.
 Commonest Cx of JIA is uveitis.
 Non-thrombocytopenic palpable purpura.

105
106
107
108
109
Nutrition
 Vitamin A supplementation- Postpartum mothers 200,000 IU & children first dose at
6 months 100,000 IU. In children given at 6 monthly intervals from 6m until 5 years
and then on grade 4 & 7.

110
 Thriposha is given from 6months if there’s growth faltering.

 All breast feeding mothers are provided with iron, calcium, vitamin c, folic acid ,
thriposha for a minimum of 6 months.

 All infants are provided with a daily dose of 12.5mg iron from 6months for atleast 2
months.

 Preterm, low birth weight, babies of anemic mothers are provided iron from 2months
for atleast a year.
 Fore milk- at beginning of a feed
● Grey and watery
● Rich in protein, lactose, vitamins, minerals and water
 Hind milk- towards an end of a feed
● Whiter than foremilk
● More fat
Low iron, vit K and vit D in breast milk
Breast milk has a smaller amount of proteins compared to cow milk
breast milk is rich in poly unsaturated fatty acids (PUFA), low in sdium; cow’s milk has
more elctrolytes

 Flaky paint dermatitis is classic of Kwashiorkor

Vitamin A deficiency
 Eye signs
 Infertility
 Metaplastic bones
 Skin changes
 Urine calculi

Eye signs NCB CCK night blindednessconjunctival xerosis bitot spots

corneal xerosis corneal ulcers  keratomalacia

 Riboflavin deficiency occurs with phototherapy

 Scurvy- hallmark feature is sub-periosteal haemorrhages & bone tenderness; in
scurvy petechiae are similar to HSP where they occur in dependent parts such as
lower limbs & buttocks
 Iodine deficiency leads to LBW babies.

111
Growth

 Fetal growth
o 20w- 500 g & 20cm
o 30w- 1500g & 40 cm
o 35w-2.5kg & 45cm
 BW doubles by 4-5 months; For a preterm doubles in 6 weeks. Trebles by 1 year.
 Term infants regain BW in 2 week; Preterm infants regain BW in 2-3 weeks.
 Avg wt gain of a term baby after 5d of birth is 10g/kg/day.
 OFC trend
1cm/month for 6 months 0.5 cm/month for next 6 months= ~10-12cm/1st year
2cm/m for 3 months? 1cm/m for 3 m , 0.5 cm/m for 3 m
OFC at birth 35cm
1 year 47 cm
Adults 52-55 cm
 For the assessment of developmental age in less than 2 y/o best is gross
motor.
 For the assessment of development standard deviations are not used.
 Aetiology of cp can go upto 2 years of age.

Reflex Appearance Disappears

Moro Birth 3 months
Rooting Birth 4 months
Palmar grasp Birth 6 months
Sucking 34 weeks 4 months
ATNR 4 weeks 4 months

 Causes of short stature

o Syndromes- down, turner, silver russel, noonan
o Klinefelter- tall stature
o Extreme ss- idiopathic or turner
o In chronic illnesses and malnutrition- ht centile is higher than weight
centile
o In endocribe diseases- wt centile is higher than height centile.
o Pseudohypoparathyroidism is a cause for short stature, but
hypoparathyroidism isn’t.
 Hypothyroidism causes disproportionate short stature.
 Height velocity is normal in both constitutional growth delay and familial short
stature.

112
Growth
 Weight for age- to classify PEM Gomez classification -1SD to +2SD is
normal in weight faultering it drops 2 major centile bands or lies below 0.4 th
centile (90, 75, 60)
 Height for age- to classify stunting Waterlow classification -1SD to +2SD is
normal (95, 90, 85)
 Weight for height- to classify wasting, MAM, SAM, overweight & obesity. -
2SD to +2SD is normal; -2SD to -3SD MAM; <-3SD SAM; >+2 overweight (90,
80, 70)

BMI
Normal 15-85th centile (-2 to +1)
Overweight 85-95th centile (+1 to +2)
Obesity >95th centile
Severe obesity >35kg/m2

In neonates after the intial wt loss in the next 2 weeks weight increases by 10g/kg/d

Genetic causes of obesity

1. Trisomy 21
2. Turner
3. Prader Willi

 In infancy adiposity increases upto 1 year; reaches a nadir at 5-6 years & increases
again throughout childhood.
 Greatest predictor of childhood obesity is  parental obesity

 Precocious puberty is comminer in girls and delayed puberty is commoner in boys.

 Central Precocious puberty
o In girls majority are idiopathic; in boys sinister- cns tumour or beta hcg
secreting liver tumour
o Causes in girls
 Primary hypothyroidism- when severe this is also a cause for isolated
premature menarche
 Hydrocephalus
 Neoplasia
 Hcg producing tumour
 Posttrauma
 Mccune albright xn is a cause for both pseudoprecocious puberty and premature
menarche.
 Premature thelarche and pubarche may have a slightly increased bone age
 Prepubertal testicular volume- 4 ml
 Prematureadrenarche is a/w obesity, but doesn’t progress.
 Central precocious puberty can be with or without consonance.
 Testicular enlargement to >4ml volume is measured using an orchidometer-the first
sign of

113
 puberty.
 Pubic hair growth-follows testicular enlargement ,usually between 10-14 years of
age.
 Height spurt-when the testicular volume is 12-15ml ,after a delay of around 18
months

 Simple obesity is a/w advanced bone age..

 Live vaccines

o High dose steroids- 1 to 3 months

o Low dose steroids-2 weeks
o Replacement steroids- continue
o IVIg- 11 months
 If temp >39.5 delay the vaccine, doesn’t have to delay if simple viral URTI

114
115
116
Compiled by: Dhanushkar Ravindran

117