PATHOPHYSIOLOGY
Neonatal hyperbilirubinemia results from a predisposition to the production of bilirubin in newborn infants and their limited ability to excrete it. Infants, especially preterm infants, have higher rates of bilirubin production than adults, because they have red cells with a higher turnover and a shorter life span.13 In newborn infants, unconjugated bilirubin is not readily excreted, and the ability to conjugate bilirubin is limited. Together, these limitations lead to physiologic jaundice — that is, high serum bilirubin concentrations in the first days of life in full-term infants (and up to the first week in preterm infants and in some full-term Asian infants), followed by a decline during the next several weeks to the values commonly found in adults. The average full-term newborn infant has a peak serum bilirubin concentration of 5 to 6 mg per deciliter (86 to 103 μmol per liter). Exaggerated physiologic jaundice occurs at values above this threshold (7 to 17 mg per deciliter [104 to 291 μmol per liter]). Serum bilirubin concentrations higher than 17 mg per deciliter in full-term infants are no longer considered physiologic, and a cause of pathologic jaundice can usually be identified in such infants.14