Neonatal jaundice — pathological features, phototherapy and exchange thresholds

This is pathological jaundice until proven otherwise. Red flags here:

• Onset within first 24–36 h (pathological if <24 h; early intense jaundice always concerning)
• TSB already high at 36 h (plot on hour-specific nomogram; 18 mg/dL is in treatment range for many term infants at this age)
• Neurobehavioural change (lethargy, poor feeding) — possible acute bilirubin encephalopathy
• ABO setting (mother O, baby A) → risk of haemolytic disease
• Weight loss ~6% — assess dehydration/breastfeeding jaundice contributors

Physiological jaundice (contrast): appears after 24 h, peaks day 3–4 (term), TSB usually <15 mg/dL, baby well, resolves by 1–2 weeks; due to high neonatal haematocrit, shorter RBC lifespan, immature conjugation, increased enterohepatic circulation.

Urgent evaluation:

• Plot TSB (and direct/conjugated fraction) on age-in-hours chart (Bhutani/AAP).^[1]
• Blood group + DCT/Coombs, peripheral smear, reticulocyte count, haematocrit/Hb (haemolysis)
• G6PD assay (important in India/Mediterranean/African ancestry) — do not wait if severe
• Sepsis screen if unwell; TFTs if prolonged later; urine for reducing substances if conjugated/prolonged
• Assess hydration and feeding; mother–infant blood group incompatibility

Treatment principles:

1. Intensive phototherapy immediately when at/above phototherapy threshold for age/risk — blue-green light isomerises bilirubin to excretable photoisomers; maximise skin exposure, eye protection, monitor temperature/hydration, continue feeds.^[2]
2. Intravenous immunoglobulin may be considered in immune haemolytic disease with rising TSB despite phototherapy (protocol-dependent).
3. Exchange transfusion if TSB reaches exchange threshold, rises despite intensive phototherapy, or there are signs of acute bilirubin encephalopathy (even at lower levels) — double-volume exchange with intensive phototherapy continuum.^[1]
4. Treat underlying cause (sepsis, dehydration); do not interrupt phototherapy unnecessarily.
5. Follow rebound TSB after stopping phototherapy; safety-net for re-presentation.

Complications of severe unconjugated hyperbilirubinaemia:

• Acute bilirubin encephalopathy → kernicterus (chronic: athetoid CP, upward gaze palsy, sensorineural deafness, dental enamel dysplasia)
• Prevention is the entire point of hour-specific screening and early treatment.

Conjugated hyperbilirubinaemia note (if asked): direct bilirubin elevation suggests cholestasis (biliary atresia, infection, metabolic) — phototherapy is not the primary therapy; needs urgent conjugated pathway work-up.