Neonatal Jaundice

Why is this topic important?

Neonatal jaundice is one of the commonest neonatal conditions encountered in clinical practice and a favourite MRCPCH examination topic.

Definition

Jaundice is the yellow discoloration of the skin and sclera caused by elevated bilirubin levels.

Visible jaundice usually occurs when bilirubin exceeds approximately 85 micromol/L.

Key MRCPCH Facts

Around 60% of term infants develop jaundice.
Around 80% of preterm infants develop jaundice.
Jaundice appearing within the first 24 hours is always pathological until proven otherwise.
Unconjugated bilirubin can cross the blood-brain barrier and cause kernicterus.
Breastfeeding should usually continue during phototherapy.

Pathophysiology

Physiological Jaundice

Occurs due to:

Increased bilirubin production
Shorter neonatal red cell lifespan
Immature hepatic conjugation
Increased enterohepatic circulation

Typically:

Appears after 24 hours
Peaks at 3–5 days
Resolves within 1–2 weeks

Pathological Jaundice

Occurs when bilirubin rises excessively or early due to an underlying disease process.

Causes

Haemolysis

ABO incompatibility
Rhesus disease
G6PD deficiency
Hereditary spherocytosis

Infection

Neonatal sepsis
TORCH infections

Metabolic Disorders

Congenital hypothyroidism
Galactosaemia

Hepatobiliary Disease

Biliary atresia
Neonatal hepatitis

Clinical Features

Typical Features

Yellow skin discoloration
Yellow sclera
Normal feeding
Normal examination

Concerning Features

Poor feeding
Lethargy
High-pitched cry
Hypotonia or hypertonia
Hepatosplenomegaly

Red Flags

Urgent assessment is required if:

Jaundice within first 24 hours
Rapidly rising bilirubin
Pale stools
Dark urine
Unwell infant
Hepatosplenomegaly
Prolonged jaundice

Investigations

Initial Investigations

Serum bilirubin
Blood group
Direct Coombs test
Full blood count
Reticulocyte count

Additional Investigations

Blood culture if sepsis suspected
Thyroid function tests
Liver function tests
G6PD screen

Management

Phototherapy

Main treatment for unconjugated hyperbilirubinaemia.

Mechanism:

Converts bilirubin into water-soluble isomers
Allows excretion without hepatic conjugation

Exchange Transfusion

Consider if:

Bilirubin reaches exchange threshold
Signs of acute bilirubin encephalopathy

Treat Underlying Cause

Examples:

Antibiotics for sepsis
Immunoglobulin in selected haemolytic disease

Complications

Acute Bilirubin Encephalopathy

Features:

Poor feeding
Lethargy
High-pitched cry
Hypertonia
Seizures

Kernicterus

Permanent bilirubin-induced neurological injury resulting in:

Cerebral palsy
Hearing impairment
Developmental delay

Common Exam Traps

Trap 1

Jaundice before 24 hours is pathological until proven otherwise.

Trap 2

Pale stools and dark urine suggest conjugated jaundice.

Trap 3

Breastfeeding should usually continue during phototherapy.

Trap 4

Visible jaundice alone should not determine treatment. Always use bilirubin levels and treatment threshold charts.

One Minute Revision

First 24 hours = pathological
Pale stools = biliary atresia until proven otherwise
Phototherapy = first-line treatment
Exchange transfusion for severe hyperbilirubinaemia
Watch for kernicterus

Suggested References

NICE Guideline: Jaundice in Newborn Babies Under 28 Days
RCPCH Guidance
BNF for Children
Nelson Textbook of Pediatrics
Illustrated Textbook of Paediatrics
Rennie & Roberton's Textbook of Neonatology

Disclaimer

These notes are intended for MRCPCH revision and educational purposes only. They do not replace local, national or institutional guidelines. Clinical decisions should always be based on current guidance, senior advice and individual patient circumstances.

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