Neonatal jaundice - ED overview and practical approach
Neonatal jaundice is yellowing of the skin and sclera caused by raised bilirubin. It is common and usually physiological (unconjugated) but may be pathological - particularly when jaundice appears in the first 24 hours, when there are signs of illness, or when conjugated (direct) bilirubin is raised.
Early recognition, timely measurement and prompt escalation where indicated reduce the risk of bilirubin neurotoxicity (kernicterus) and identify treatable causes (haemolysis, sepsis, biliary atresia, metabolic disease). This section summarises a pragmatic ED approach consistent with NICE CG98 and ED guidance (RCEM).
Pathophysiology
- Unconjugated (indirect) bilirubin is produced by haem breakdown, circulates bound to albumin, and is conjugated in the liver for biliary excretion. Newborns have reduced conjugation capacity and increased red‑cell turnover.
- Conjugated (direct) hyperbilirubinaemia reflects impaired hepatic excretion or cholestasis and is always pathological.
Key distinctions
- Unconjugated jaundice is often physiological after 24 hours in term infants but may be pathological (haemolysis, cephalhaematoma, polycythaemia, breastmilk/breastfeeding‑related issues, infection).
- Conjugated jaundice is always abnormal - consider neonatal hepatitis, TORCH infections, metabolic disease (eg galactosaemia), alpha‑1 antitrypsin deficiency, biliary atresia or obstructive lesions.
Red flags requiring urgent action and paediatric input
- Jaundice appearing within the first 24 hours of life; this is always pathological.