Jaundice (newborn)

Introduction

Jaundice in newborns refers to the yellow discoloration of the skin, sclera, and mucous membranes due to elevated serum bilirubin levels. It is a common condition, affecting up to 60% of term and 80% of preterm infants in the first week of life. In most cases, it is a benign, self-limiting process, but in certain situations, it can indicate underlying pathology and pose a risk of bilirubin-induced neurologic dysfunction (BIND) and kernicterus.

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Causes and Types

1. Physiological Jaundice

• Cause: Immature liver enzymes leading to reduced bilirubin conjugation, combined with increased red blood cell breakdown.

• Timing: Appears after 24 hours of age, peaks at 3–5 days, resolves within 1–2 weeks.

• Bilirubin levels: Usually < 15 mg/dL in term infants.

2. Pathological Jaundice

Features suggesting pathological cause:

• Onset within the first 24 hours of life.

• Rapid rise in bilirubin (> 5 mg/dL per day).

• Prolonged jaundice beyond 2 weeks in term infants or 3 weeks in preterm infants.

• Conjugated hyperbilirubinemia (> 20% of total bilirubin).

Causes include:

• Hemolytic diseases:

  • ABO incompatibility.

  • Rh incompatibility.

  • G6PD deficiency.

  • Hereditary spherocytosis.

• Infections: Sepsis, TORCH infections.

• Liver disorders: Neonatal hepatitis, biliary atresia.

• Endocrine/metabolic disorders: Hypothyroidism, galactosemia.

3. Breastfeeding-Associated Jaundice

• Breastfeeding jaundice: Occurs in the first week due to poor milk intake and dehydration.

• Breast milk jaundice: Appears after the first week and may persist for several weeks; caused by substances in breast milk that inhibit bilirubin conjugation.

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Pathophysiology

Bilirubin is produced from the breakdown of hemoglobin. In newborns:

• Increased red blood cell turnover → higher bilirubin production.

• Immature hepatic UDP-glucuronyl transferase enzyme → reduced conjugation.

• Increased enterohepatic circulation → reabsorption of bilirubin.
  Unconjugated bilirubin is lipid-soluble and can cross the blood-brain barrier in high concentrations, leading to neurotoxicity.

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Clinical Features

Symptoms

• Yellow discoloration of the skin and sclera.

• Progression: Cephalocaudal (from head to toe) as bilirubin levels rise.

• Severe cases: Poor feeding, lethargy, hypotonia, high-pitched cry, seizures (signs of acute bilirubin encephalopathy).

Signs of Severe Disease

• Early onset (< 24 hours).

• Deep jaundice.

• Signs of underlying illness (fever, poor suck, hepatosplenomegaly).

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Diagnosis

Clinical Assessment

• Visual estimation can be unreliable, especially in dark-skinned infants.

• Risk factor evaluation (prematurity, blood group incompatibility, family history).

Laboratory Investigations

• Serum total and direct bilirubin levels.

• Blood group and Coombs test for hemolysis.

• Complete blood count and reticulocyte count for hemolysis assessment.

• G6PD level if deficiency suspected.

• Liver function tests for cholestasis or liver disease.

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Management

Treatment depends on the cause, bilirubin level, age in hours, and risk factors (based on bilirubin nomograms such as the Bhutani chart).

1. Phototherapy

• Indication: Unconjugated hyperbilirubinemia above treatment threshold for age and risk category.

• Mechanism: Blue light converts bilirubin into water-soluble isomers excreted in bile and urine without conjugation.

• Administration:

  • Use blue-green spectrum light (wavelength 460–490 nm).

  • Infant is undressed except for eye protection; ensure adequate hydration.

• Monitoring: Serum bilirubin every 4–24 hours depending on severity.

2. Exchange Transfusion

• Indication: Very high bilirubin levels at or above exchange thresholds or signs of acute bilirubin encephalopathy.

• Procedure: Replacement of infant’s blood with donor blood to remove bilirubin and antibodies.

• Risks: Electrolyte imbalance, infection, bleeding.

3. Intravenous Immunoglobulin (IVIG)

• Indication: Isoimmune hemolytic disease (e.g., Rh or ABO incompatibility) with rapidly rising bilirubin despite intensive phototherapy.

• Dose: 0.5–1 g/kg IV over 2 hours; may repeat in 12 hours if needed.

4. Treat Underlying Cause

• Antibiotics for infection (e.g., ampicillin + gentamicin as empiric neonatal coverage; dose based on weight and age).

• Manage hypothyroidism, metabolic disorders, or biliary obstruction as indicated.

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Medication Use

Phenobarbital

• Role: Enhances bilirubin conjugation by inducing hepatic enzymes; used in certain hemolytic disorders or prolonged jaundice.

• Dose: 3–5 mg/kg/day orally in divided doses for several days (specialist use).

Cholestyramine

• Rarely used for breast milk jaundice to interrupt enterohepatic circulation.

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Monitoring

• Close follow-up in the first week after discharge, especially for preterm infants and those with risk factors.

• Regular bilirubin checks in high-risk infants.

• Neurological monitoring for signs of bilirubin toxicity.

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Complications

• Acute bilirubin encephalopathy – reversible if treated early.

• Kernicterus – permanent brain damage with choreoathetoid cerebral palsy, hearing loss, gaze abnormalities, and intellectual disability.

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Prevention

• Early initiation and frequent breastfeeding to promote bilirubin excretion.

• Monitoring high-risk newborns (premature, hemolysis risk, poor feeding).

• Parental education on signs of worsening jaundice.