NEONATAL CONDITIONS
Neonatal Jaundice
A practical guide for SCN clinical staff · Unconjugated hyperbilirubinaemia in the newborn - common, usually benign, occasionally dangerous
PATHOLOGICAL IF
UNDER 24 HOURS
Bilirubin production
About 75% comes from breakdown of senescent red cells: haem oxygenase converts haem to biliverdin, then biliverdin reductase makes unconjugated bilirubin. Newborns make 2-3x more per kg than adults - a high red cell mass and a short (~70-90 day) red cell lifespan.
Albumin transport
Unconjugated bilirubin is fat-soluble and water-insoluble, so it travels bound to albumin. The small unbound "free" fraction is the neurotoxic one, and it rises with acidosis, sepsis, prematurity and competing drugs.
Hepatic uptake & conjugation
Hepatocytes take up bilirubin (ligandin) and the enzyme UGT1A1 conjugates it with glucuronic acid into a water-soluble form. UGT1A1 activity is low at birth and matures over the first weeks - and is genetically variable (Gilbert, Crigler-Najjar).
Biliary excretion
Conjugated bilirubin is actively secreted into bile and delivered to the gut. A block at this step (not of production) is what produces conjugated jaundice and points to cholestasis or biliary atresia.
Enterohepatic recycling
The newborn gut is rich in β-glucuronidase and lacks the flora that convert bilirubin to urobilinogen, so conjugated bilirubin is deconjugated and reabsorbed. Poor feeding, delayed stooling and dehydration exaggerate this.
Unconjugated load rises
Increased production, immature conjugation and enhanced recycling overwhelm clearance. Haemolysis (ABO/Rh, G6PD) or reabsorption of extravasated blood (cephalhaematoma, bruising) pushes the level higher and faster.
Neurotoxicity
Free unconjugated bilirubin crosses the blood-brain barrier and deposits in the basal ganglia (globus pallidus, subthalamic nuclei) and brainstem - acute bilirubin encephalopathy, and if untreated, permanent kernicterus.
CLINICAL FINDINGS
- Cephalocaudal progression - face first, then trunk and limbs
- Best assessed in natural light with the skin blanched
- Acute encephalopathy: lethargy, poor feeding, hypotonia changing to hypertonia, retrocollis/opisthotonus, high-pitched cry
- Pallor (haemolysis), hepatosplenomegaly, bruising or cephalhaematoma
- Dark urine and pale stools suggest a conjugated (biliary) cause
INVESTIGATIONS
- Serum bilirubin (total + conjugated) plotted on an hour-specific nomogram
- Transcutaneous bilirubinometer for screening (not if <24h or on phototherapy)
- Blood group + DAT (Coombs), FBC and film, reticulocytes
- G6PD assay, LFTs and TFTs if prolonged
- Always check the conjugated fraction in prolonged jaundice - exclude biliary atresia
- Sepsis screen, metabolic and urine work-up if unwell or conjugated
COMPLICATIONS & RED FLAGS
- Jaundice in the first 24h is pathological until proven otherwise (haemolysis/sepsis)
- Kernicterus: athetoid cerebral palsy, sensorineural deafness, gaze palsy, dental dysplasia
- Conjugated jaundice is never physiological - exclude biliary atresia (Kasai works best <60 days)
- Prolonged jaundice >14 days (term) or >21 days (preterm) needs a work-up
- Do not rely on visual estimation at high levels - send a level
MANAGEMENT
Plot the level, treat to threshold with phototherapy, and act early on rapidly rising or very high bilirubin to prevent kernicterus.
Phototherapy
- Plot bilirubin against age in hours on the treatment nomogram and treat at threshold
- Intensive phototherapy: maximise skin exposure, eye protection, maintain hydration and feeds
- Recheck the level 4-6h after starting, then follow the trend
- Keep feeding - feeding plus phototherapy reduces enterohepatic recycling
Escalation / Exchange
- Exchange transfusion if at/above the exchange line or signs of encephalopathy
- IVIG for isoimmune haemolysis (Rh/ABO) with rising bilirubin despite phototherapy
- Treat the cause - sepsis, haemolysis, dehydration
- Discuss with NICU/NETS early for high or rapidly rising levels
Conjugated / Prolonged
- Split the bilirubin; if conjugated, arrange urgent work-up (exclude biliary atresia)
- Prolonged unconjugated: check TFTs, G6PD and ongoing haemolysis
- Breast-milk jaundice is a diagnosis of exclusion in a thriving baby
- Ensure feeding and weight gain are adequate
- Assess jaundice in good light with the baby blanched; never rely on the visual level alone - send a bilirubin.
- During phototherapy: eye protection, maximise skin exposure, monitor temperature and hydration, and support feeding.
- Watch for encephalopathy - lethargy, poor feeding, abnormal tone or a high-pitched cry - and escalate immediately.
- Flag jaundice <24h, dark urine or pale stools, or prolonged jaundice for medical review.
How do you use an hour-specific nomogram to decide between phototherapy and exchange?
Which features make you worry about pathological rather than physiological jaundice?
Which baby with prolonged jaundice needs a split bilirubin, and why does it matter?
What risk factors lower the threshold for kernicterus at a given bilirubin level?
Take-home message: Neonatal jaundice is usually physiological, but bilirubin must be plotted on an age-specific nomogram and treated to threshold. Jaundice under 24h, conjugated, or prolonged jaundice is pathological until proven otherwise. Phototherapy is first-line; act early on rising levels to prevent kernicterus.
For educational purposes only. Always align management to current ANZCOR/NRP guidelines and your local SCN/NICU or NETS protocols.