Paediatrics | Master Of Medicine

Category Archives: Paediatrics

Developmental milestones in a child

  1. Draws a vertical line – 2 year
  2. Draws a circle – 3 years
  3. Become aware of his/her sex- 3 -4yrs
  4. Draw a cross or plus sign – 4years
  5. Draw a Rectangle – 4 years
  6. Draw a triangle – 5 years
  7. Draw a tilted cross/multiplication sign- 5years

Tips for memory

  1. A girl understands her sex by 3 years isn’t it a coincidence that she learns to put a circle on her forehead by that time?
  2. Cross has 4 parts and rectangle has four sides.
  3. A multiplication sign if cut in half reads like V,it is the roman letter for 5.
  4. A Triangle on removing one side reads like V, so 5 comes to your mind.

Causes of hyperbilirubinemia in paediatric age group

Unconjugated hyperbilirubinemia

1) Increased production- hemolytic anemia (Hereditary spherocytosis, G6PD deficiency)
ineffective erythropoesis (Thalassemia, Pernicious anemia)
2) Reduced hepatic intake from bilirubin-albumin complex – drug induced
3) Impaired hepatic conjugation
a) Physiological – functionally immature liver
b) Breast milk jaundice - pregnendiol and FFA in breast milk interferes conjugation (in susceptible)
c) Genetic deficiency of UDPG transferase – Crigler-Najjar, Gilberts
d) Hepatocellular dysfunction- Viral or drug induced Hepatitis, Cirrhosis
e) Hypothyroidism
f) Cephalhematoma

Conjugated Hyperbilirubinemia

1) Impaired secretion of conjugated bilirubin into bile – Dubin-Johnson, Rotor’s
2) Impaired bile flow

a) Obstructive jaundice
b) Primary biliary cirrhosis
c) Neonatal cholestasis – extrahepatic biliary atresia/neonatal idiopathic hepatitis
Choledochal cyst,sclerosing cholangitis,Caroli’s disease
d) Metabolic- Tyrosinemia, Wolman disease, Niemann Pick, Galactosemia, Fructosemia

Appearance of Jaundice – Area of infant body to s.bilirubin levels

Head&neck — 5mg/dl
Upper trunk & proximal Upper limb — 10mg/dl
Lower trunk & thigh – 12mg/dl
Legs — 15mg/dl
Palms & sole – >15mg/dl

Causes of jaundice and time of onset

a) within 24 hours

  • Rh incompatibility (most common)
  • Concealed haemorrhage
  • Sepsis
  • Cong. Infections – CMV, Rubella, Syphillis, Toxoplasma
b) appears in 2nd to 3rd day
  • Physiological
  • Crigler najjar
  • Early onset breast milk jaundice
c) from 3rd day to 7th day
  • Bacterial sepsis
  • UTI
  • Polycythemia
  • Cong. Infections
d) after first week -All other caouses other than those mentioned above
Physiological Jaundice (unconjugated bilirubin)
  • After 24 hours
  • progressive rise in s.bilirubin- <5mg/dl per day (no sudden rise)
  • Peaks in 3-5 days, total not more than 15mg/dl
  • Clinical jaundice resolved by 1 week in term infants and 2 week in preterm
  • 2 phases – (phase 1 – lasts 5 days in term (12mg/dl) and 7 days in preterm (15mg/dl); phase 2 – gradual decline to 2mg/dl, which          lasts 2 weeks, before falling to adult values)
Breast milk Jaundice (unconjugated)
  • After 30 hrs, exclusively breast fed infants,
  • May continue way into 3rd month
  • bilirubin may reach 20mg/dl
  • Temprorary intererruption of breast feeding will dramatically bring down bilirubin levels, once within control values restart breast feed.
Crigler Najjar syndrome

Type 1

  • Inheritance –    autosomal recessive
  • LFT    –      normal
  • Liver histology  –    normal
  • Kernicterus –  yes
  • UDPG transferase – absent
  • response to  phenobarbitone-   no response
  • hemolysis –  absent

Type 2

  • inheritance – autosomal dominant
  • LFT –  normal
  • Liver histology- normal
  • Kernicterus-   rare
  • UDPG transferase- reduced
  • response to   phenobarbitone-  decreases bilirubin
  • hemolysis –   absent

Dubin Johnson Syndrome

  1. AR, conjugated hyperbilirubinemia becoz of mutation in canalicular multidrug resistance protein 2(MRP2)
  2. LFT normal; accumulation of black granular pigment in lysosomes of centrilobar hepatocytes
  3. Increased urinary coprophorphyrin but total coprophorphyrin is normal
  4. Gall bladder is not visualised on oral cholecystography

Rotor syndrome

  • AR, congenital conjugated hyperbilirubinemia. decreased biliary excreation
  • Liver is not pigmented, urine as well as total coprophorphyrin will be increased
  • Gall bladder will be visualized

This post was written by my friend Kim George, you can contact him

Wilms tumour and associated syndromes

Wilms tumour

  1. Also known as nephroblastoma.
  2. Wilms tumour is the most common primary renal tumour in children.
  3. Usually wilms tumour is a solitary,well circumscribed lesion,but 10% is bilateral or multicentric.
  4. Triphasic combination of epithelial,stromal and blastemal elements.
  5. 5% show anaplasia associated with underlying P53 mutation and unresponsive to chemotherapy.
  6. Nephrogenic cell rests- High correlation with Wilms tumour in contralateral kidney.

Syndromes associated with wilms tumour

WAGR syndrome

  1. Wilms tumour
  2. Aniridia
  3. Genital abnormalities
  4. Mental retardation

Denys Drash Syndrome

  1. Gonadal dysgenesis(Male pseudohermaphroditism)
  2. Renal abnormalities

Beckwith Weidman syndrome

  1. Organomegaly
  2. Hemihypertrophy
  3. Renal medullary cysts
  4. Hepatoblastoma
  5. Adrenal cortical tumour
  6. Rhabdomyosarcoma
  7. Pancreatic tumour

Tetrad of congenital Toxoplasmosis

Congenital toxoplasmosis is characterized by the classical tetrad described below

  1. Hydrocephalus/Microcephaly
  2. Chorioretinitis
  3. Convulsions/seizures
  4. Cerebral calcification

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