Neonatal Jaundice

Neonatal Jaundice is a topic covered in the 5-Minute Emergency Consult.

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Produced by an imbalance between rates of bilirubin production and bilirubin elimination:
  • Newborns have higher rate of bilirubin production than adults because of increased RBC mass and shorter RBC life span.
  • Newborns, especially preterm infants, have rate limitations in hepatic conjugation and biliary excretion of bilirubin, increased enterohepatic circulation, and diminished bilirubin binding to albumin- and bilirubin-binding protein.


  • In most newborns, this represents physiologic jaundice and is not pathologic:
    • Bilirubin normally increases from 1.5 mg/dL in cord blood to a mean of 6.5 mg/dL on day 3, followed by a gradual decline to levels of <1.5 mg/dL by day 10 or 12 of life.
  • Serum bilirubin may rise to levels exceeding neuroprotective defenses, causing bilirubin tissue binding in basal ganglia, hippocampus, brainstem nuclei, and cerebellum:
    • Bilirubin-induced neurologic dysfunction (BIND) caused by increasingly severe hyperbilirubinemia from mild dysfunction to acute bilirubin encephalopathy (ABE) and kernicterus.
      • ABE describes the acute manifestations of bilirubin toxicity seen in the 1st wk after birth.
      • Kernicterus: Chronic form of BIND, with significant mortality or permanent sequelae including choreoathetoid type of cerebral palsy, gaze abnormalities, hearing loss, and dental dysplasia.
    • Rate of progression of BIND depends on rate of increase of bilirubin levels, duration of hyperbilirubinemia, albumin-binding reserves, unbound bilirubin level, host susceptibility, and comorbidities.
    • Death is due to respiratory failure and progressive coma or intractable seizures.
  • Risk factors for severe hyperbilirubinemia:
    • Jaundice observed in 1st 24 hr
    • Predischarge total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) (see “Diagnosis”) in high-risk or high–intermediate-risk zone
    • Lower gestational age, 35–38 wk
    • Exclusive breastfeeding, especially if inadequate with excessive weight loss
    • Isoimmune or other hemolytic disease
    • Sibling with neonatal jaundice
    • Cephalohematoma or excessive bruising
    • Ethnicity: East Asian
  • Severe hyperbilirubinemia is associated with perinatal factors: Low birth weight, macrosomia from maternal diabetes, infection, polycythemia
  • Hyperbilirubinemia neurotoxicity risk factors:
    • Isoimmune hemolytic disease
    • G6PD deficiency
    • Asphyxia
    • Sepsis
    • Acidosis
    • Albumin <3 mg/dL
  • Postphototherapy (post-PT) bilirubin rebound to bilirubin levels of concern may occur:
    • At high risk are newborns <37 wk gestation, patients with hemolytic disease, patients treated for <72 hr.


  • Unconjugated hyperbilirubinemia:
    • Physiologic jaundice
    • Jaundice in breastfed infants:
      • Breastfeeding failure jaundice: Exaggeration of physiologic jaundice due to inadequate ingestion/production of sufficient volume of breast milk in the 1st wk of life
      • Breast milk jaundice: Begins days 3–5, peaks within 2 wk but lasts up to 8 wk; caused by increased β-glucuronidase in breast milk
      • May be exacerbated by dehydration
    • Specific hemolytic conditions:
      • Blood group isoimmunization due to ABO, Rh, and minor blood group incompatibility; ABO is most common: Rh disease is unusual (RhoGAM prevents).
      • Red cell enzyme deficiencies: G6PD deficiency
      • Red cell membrane defects: Hereditary spherocytosis and elliptocytosis
    • Sepsis: Bacterial, viral, or protozoal
    • Birth trauma:
      • Increased heme load from resolving cephalohematoma or ecchymosis
    • Polycythemia:
      • Caused by maternal–fetal transfusion
      • Fetal–fetal transfusion
      • Infants of diabetic mothers
    • Congenital hypothyroidism
    • Defective hepatic conjugation:
      • Gilbert syndrome (familial partial defect in glucuronyl transferase activity) is benign.
      • Crigler–Najjar syndrome (congenital absence of glucuronyl transferase), lifelong unconjugated hyperbilirubinemia
    • Intestinal obstruction such as ileus, functional or anatomic, increases enterohepatic circulation
  • Conjugated hyperbilirubinemia:
    • Failure of hepatic excretion of conjugated bilirubin
    • Causes include neonatal hepatitis, congenital biliary atresia, extrahepatic biliary obstruction, shock liver from neonatal asphyxia, neonatal hemosiderosis

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