Conditions · Metabolism: heme, bilirubin and iron
Neonatal jaundice !
Yellow colouring of a newborn from high bilirubin; it is nearly always mild and temporary, but very high levels can damage the brain.
Updated 2026-11-01
Structures involved
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In biochemistry
- Heme breakdown and bilirubin: Step 5 · Colonic bacterial β-glucuronidases and reductases
- Heme oxygenase
- Biliverdin reductase
- UGT1A1 (bilirubin UDP-glucuronosyltransferase)
- Bilirubin
- Albumin
- Xenobiotic biotransformation: phases I, II and III
- Glucuronidation
In immunology
- Type II hypersensitivity (antibody against cells)
- ABO and Rh blood groups, hemolytic disease of the newborn
- Neonatal immunity: maternal IgG and breast-milk IgA
- Passive immunization: immunoglobulins and antitoxins
- Direct and indirect Coombs test
In embryology
In the clinical exam
- Pallor, cyanosis and jaundice
- Pediatric history: perinatal, growth, development and vaccines
- Jaundice: prehepatic, hepatic and posthepatic
In physiology
- Blood groups, transfusion and transfusion reactions
- The red cell life cycle and the spleen
- Rh incompatibility
- Bile and the enterohepatic circulation
- Newborn physiology and fetal maturation
Why it happens
- Fetal hydrops: immune and nonimmune
- Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon
What it is
Hyperbilirubinemia of the newborn, usually unconjugated; it may be physiological or pathological (hemolysis, infection, cholestasis).
Who gets it
About 60 % of term newborns and over 80 % of preterm infants have it. In Colombia it is one of the most frequent causes of neonatal readmission; blood-group incompatibility and G6PD deficiency are important causes of severe cases.
Causes
- Physiological: more short-lived red cells, immature UGT1A1 and more enterohepatic circulation
- From insufficient breastfeeding (first week) and from breast milk (after the first week)
- Hemolysis: ABO or Rh incompatibility, G6PD deficiency, spherocytosis
- Cholestasis (conjugated bilirubin): biliary atresia, infections, hypothyroidism
Risk factors
- Prematurity
- Breastfeeding with poor intake and weight loss
- A sibling who needed phototherapy
- Cephalohematoma or bruising
- Mother blood group O or Rh negative
Pathophysiology
The newborn makes more bilirubin (larger red-cell mass, red cells living about 80–90 days) and conjugates less (immature UGT1A1). The nearly bacteria-free gut and mucosal β-glucuronidase return bilirubin to the blood. Excess free bilirubin crosses the blood–brain barrier and damages the basal ganglia and auditory nuclei.
Classification
- Physiological: appears after 24 hours, peaks at 3–5 days
- Pathological: within 24 hours, rises fast, lasts over 2 weeks or is conjugated
Symptoms and signs
- Yellow colour that spreads from the face to the trunk and legs
- Yellow sclerae
- Drowsiness and weak sucking when high
Diagnosis
- Clinical
- Visual assessment in good light before discharge and at early follow-up; visual estimation alone is not reliable.
- Tests
- Transcutaneous or total serum bilirubin, read against hours of life and risk factors on a nomogram; direct bilirubin; blood group and direct Coombs; blood count with reticulocytes; G6PD.
- Imaging
- Biliary ultrasound if jaundice is conjugated; brain MRI if kernicterus is suspected.
Treatment
- Conservative
- Breastfeeding support and frequent feeding to increase stool clearance
- Procedure
- Blue-light phototherapy when bilirubin exceeds the threshold for its age in hours
- Acute
- Exchange transfusion for very high levels or signs of encephalopathy
- Medical
- Intravenous immunoglobulin in immune hemolysis not responding to phototherapy
- Surgical
- Early portoenterostomy (Kasai) if biliary atresia is present
Complications
- Acute bilirubin encephalopathy
- Kernicterus: cerebral palsy, deafness, gaze abnormalities and dental enamel defects
Prognosis
Excellent in physiological jaundice; kernicterus is preventable with timely detection and treatment.
Prevention
- Measuring bilirubin before discharge and follow-up within 48–72 hours
- Prenatal blood grouping and anti-D immunoprophylaxis
Test yourself
Think of the answer, then tap the question to see it.
Why are newborns prone to jaundice?
They make more bilirubin, have immature UGT1A1 and more enterohepatic circulation.
Which neonatal jaundice is always pathological by its timing?
Jaundice that appears in the first 24 hours of life.
What do jaundice, pale stools and dark urine suggest?
Cholestasis, such as biliary atresia, which needs urgent investigation.
How does phototherapy work?
Blue light turns bilirubin into soluble isomers that are excreted without conjugation.
Related conditions
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Newborn jaundice: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Bilirubin blood test: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Jaundice | Icterus | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026).
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