Description

The 3 major categories of unconjugated hyperbilirubinemia associated with breastfeeding:

• Physiologic jaundice: occurs between 1 and 7 days of life and peaks at 3–5 days.
• Breastfeeding jaundice (BFJ): exaggerated physiologic jaundice associated with inadequate milk intake.
• Breast milk jaundice (BMJ): occurs between 1 and 12 weeks in thriving breast milk–fed infant.

Epidemiology

Risk Factors

• Jaundice in first 24 hours (pathologic)
• Predischarge elevated total serum bilirubin
• Blood type incompatibility
• Glucose-6-phosphate dehydrogenase (G6PD) deficiency
• Gestational age <36 weeks
• Previous sibling receiving phototherapy
• Cephalohematoma or significant bruising
• Exclusive breastfeeding
• Eastern Asian race

Pathophysiology

• Normal physiology: Bilirubin is a breakdown product of hemoglobin. Unconjugated bilirubin is bound to albumin, transported to the liver, and conjugated by the hepatic enzyme uridine diphosphate glucuronosyl transferase (UGT1A1). Conjugated bilirubin is transported into the small intestines via the bile ducts, where it is modified and excreted in stool. If stooling is delayed, bilirubin is deconjugated by intestinal enzymes and returned to the liver via the portal circulation (enterohepatic circulation).
• Physiologic jaundice: bilirubin levels are elevated in newborns due to several factors:
  • Increased hematocrit and red blood cell volume
  • Increased red blood cell lysis due to shorter red blood cell lifespan.
  • Impaired bilirubin excretion because of an immature hepatic UGT1A1 enzyme and increased enterohepatic circulation.
• BFJ: Lack of effective breastfeeding causes inadequate milk and calorie intake and results in decreased stooling and increased enterohepatic circulation. Infants may also be dehydrated.
• BMJ: Mechanism unclear. Hypotheses include factors found in the milk that may inhibit hepatic UGT1A1. BMJ is associated with East Asian infants who are more likely to have a UGT1A1 mutation and weight loss.