Newborn Jaundice — Causes, Bilirubin Levels & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Newborn jaundice (neonatal jaundice or neonatal hyperbilirubinaemia) is a yellow discolouration of the skin and sclerae in newborns caused by accumulation of bilirubin — a yellow pigment produced during the normal breakdown of red blood cells. It affects approximately 60% of term and 80% of preterm infants in the first week of life. In most cases, physiological jaundice is a normal, self-limiting condition that resolves without treatment within 2 weeks. However, excessively high bilirubin levels can cross the blood-brain barrier in neonates, causing acute bilirubin encephalopathy and its chronic irreversible form — kernicterus — characterised by cerebral palsy, deafness, and cognitive impairment. Identifying those with pathologically elevated bilirubin requiring phototherapy or exchange transfusion is the critical clinical task in managing neonatal jaundice.

Physiological jaundice (most common): occurs because neonatal red blood cells have a shorter lifespan (70-90 days vs 120 in adults), producing excess bilirubin that the immature neonatal liver (with lower UDP-glucuronosyltransferase activity) cannot conjugate fast enough. Appears on day 2-3, peaks day 3-5, resolves by day 10-14 in term infants. Pathological causes appearing within the first 24 hours: haemolytic disease of the newborn from ABO or Rh blood group incompatibility (maternal antibodies cross the placenta and destroy fetal red blood cells), G6PD deficiency, hereditary spherocytosis, and sepsis. Breastfeeding jaundice: inadequate milk intake in the first week (insufficient feeding reduces stool frequency, increasing enterohepatic bilirubin reabsorption). Breast milk jaundice: persists beyond 2 weeks due to compounds in breast milk inhibiting bilirubin conjugation — generally benign. Conjugated hyperbilirubinaemia (direct bilirubin >20% of total) is always pathological: biliary atresia (urgent surgical referral required before 60 days of age), neonatal hepatitis, and metabolic disorders.

Yellow discolouration of the skin progressing from head downward (face, trunk, limbs, palms, and soles in increasing severity). Assessment by skin blanching in natural light — Kramer zones help estimate severity. Jaundice visible in the sclera (whites of eyes). In physiological jaundice: infant is otherwise well, feeding normally, active, with normal urine and stool colour. Warning signs requiring urgent evaluation: jaundice appearing within the first 24 hours of life (always pathological), yellow palms and soles (indicates very high bilirubin), pale or white stools (biliary atresia or cholestasis), dark urine (conjugated jaundice), poor feeding, lethargy or irritability, high-pitched cry, arching of the back (opisthotonus — acute bilirubin encephalopathy requiring emergency exchange transfusion), and jaundice persisting beyond 14 days in term infants (prolonged jaundice — requires investigation).

Jaundice visible to the naked eye in a neonate is present when serum bilirubin exceeds approximately 85-120 micromol/L (5-7 mg/dL). Transcutaneous bilirubin (TcB) measurement using a bilirubinometer provides a non-invasive estimate for screening — if elevated, confirmed with serum total bilirubin. Serum total bilirubin (TSB) and direct/conjugated bilirubin (distinguish unconjugated from conjugated jaundice). Blood group, Coombs (DAT) test, and maternal blood group (identify ABO/Rh incompatibility). FBC, blood film (spherocytes in hereditary spherocytosis, fragmented cells in haemolysis), reticulocyte count. G6PD screen. Sepsis screen (blood culture, FBC, CRP) if clinically unwell. Treatment threshold is determined by plotting TSB on age-specific nomograms (NICE Jaundice Threshold Charts — accounting for gestational age and risk factors for neurotoxicity). Prolonged jaundice beyond 14 days (term) or 21 days (preterm): split bilirubin, liver function tests, TFTs, urine culture, and metabolic screen.

Phototherapy: blue-spectrum light (wavelength 460-490 nm) converts unconjugated bilirubin in skin and superficial vessels into water-soluble photoisomers excreted in bile and urine without requiring hepatic conjugation. Intensive phototherapy uses multiple high-irradiance LED or fluorescent light sources covering maximum skin surface area. NICE guidelines define treatment thresholds based on gestational age and postnatal age (in hours) using validated threshold charts. During phototherapy: increase feed frequency (every 2-3 hours) to promote bilirubin excretion; protect eyes with eye mask; monitor TSB 4-12 hourly depending on rate of rise. Discontinue when TSB falls 50 micromol/L below threshold. Exchange transfusion is reserved for very high bilirubin levels or acute bilirubin encephalopathy — double volume exchange transfusion removes bilirubin and maternal antibodies. Haemolytic disease: IVIG may reduce need for exchange transfusion in ABO incompatibility. Biliary atresia: Kasai portoenterostomy before 60 days of age.

When bilirubin rises to dangerous concentrations and crosses the immature neonatal blood-brain barrier, severe and irreversible neurological complications occur. Acute bilirubin encephalopathy (ABE) presents in three phases: early — poor feeding, lethargy, high-pitched cry, hypotonia; intermediate — stupor, irritability, and opisthotonus (backward neck arching); advanced — deep stupor, apnoea, seizures, and coma. ABE is a medical emergency — prompt exchange transfusion can reverse early-stage injury. Kernicterus is the chronic irreversible form of bilirubin-induced brain damage following untreated ABE: characterised by the classic triad of athetoid cerebral palsy (involuntary writhing movements from basal ganglia damage), sensorineural hearing loss (auditory neuropathy from cochlear hair cell bilirubin deposition), and upward gaze palsy (midbrain damage). Cognitive impairment and dental enamel hypoplasia are additional sequelae. Conditions increasing bilirubin neurotoxicity at any given level include prematurity (more permeable blood-brain barrier), sepsis, acidosis, and hypoalbuminaemia — these infants require treatment at lower bilirubin thresholds. Kernicterus is largely preventable with universal bilirubin screening and timely phototherapy. Exchange transfusion complications include hypocalcaemia, hypoglycaemia, thrombocytopaenia, air embolism, and nosocomial infection.

Ensure adequate feeding frequency from birth — breastfeed every 2-3 hours (8-12 times per day in the first week), or formula-feed as directed, to maximise stool frequency and reduce enterohepatic bilirubin reabsorption. All newborns should be assessed for jaundice at every postnatal check in the first week. High-risk infants (gestation below 38 weeks, significant bruising, blood group incompatibility, sibling requiring phototherapy, or infant of diabetic mother) require TcB or serum bilirubin screening. Rhesus prophylaxis (anti-D immunoglobulin) prevents Rh haemolytic disease in subsequent pregnancies. G6PD testing in newborns in high-prevalence regions to avoid trigger exposures. Prolonged jaundice beyond 14 days must be investigated — biliary atresia has a narrow treatment window and urgent Kasai surgery before 60 days of life is essential for best outcomes.

Seek emergency care immediately if your newborn develops a high-pitched cry, extreme lethargy, refusal to feed, arching of the back, or eye deviation — these are signs of acute bilirubin encephalopathy requiring urgent exchange transfusion. See a doctor the same day for jaundice appearing within the first 24 hours of life, yellow colouration extending to the palms and soles, pale or white stools, dark urine, or rapidly worsening jaundice. Bring your baby in for assessment if jaundice persists beyond 14 days in a term baby or if you are worried at any point. Never assume newborn jaundice is always normal without professional assessment — the consequences of missed severe hyperbilirubinaemia (kernicterus) are irreversible.