Hyperbilirubinemia
Description
Excessive serum bilirubin levels and jaundice
Result of hemolytic processes in the neonate
Can be physiologic (with jaundice the only symptom) or pathologic (resulting from an underlying disease)
Also called neonatal jaundice
Pathophysiology
As erythrocytes break down at the end of their neonatal life cycle, hemoglobin separates into globin (protein) and heme (iron) fragments.
Heme fragments form unconjugated (indirect) bilirubin, which binds with albumin for transport to liver cells to conjugate with glucuronide, forming direct bilirubin.
Fat-soluble unconjugated bilirubin not excreted in the urine or bile may possibly escape to extravascular tissue, especially fatty tissue and the brain.
May develop when:
certain factors disrupt conjugation and usurp albumin-binding sites, including drugs (such as aspirin, tranquilizers, and sulfonamides) and conditions (such as hypothermia, anoxia, hypoglycemia, and hypoalbuminemia)
decreased hepatic function results in reduced bilirubin conjugation
increased erythrocyte production or breakdown results from hemolytic disorders or Rh or ABO incompatibility
biliary obstruction or hepatitis results in blockage of normal bile flow
maternal enzymes present in breast milk inhibit the infant’s glucuronosyltransferase conjugating activity (rare).
