Chapter 38 Hyperbilirubinemia
PATHOPHYSIOLOGY
Neonatal hyperbilirubinemia or physiologic jaundice, a total serum bilirubin level higher than 5 mg/dl, is due to the neonate’s predisposition for bilirubin production and limited ability to excrete it. By definition, there is no other abnormality or pathologic process present to account for the jaundice. The yellow coloration of the skin and mucous membranes is due to the deposition of unconjugated bilirubin pigment. The primary source of bilirubin is the breakdown of hemoglobin in aging or hemolyzed red blood cells (RBCs). In the neonate, RBCs have a higher turnover and a shorter life span, which enhances the higher production rate of bilirubin. The immaturity of the neonatal liver is a limiting factor in bilirubin excretion.
Unconjugated or indirect bilirubin is lipid soluble and binds to plasma albumin. The bilirubin is then taken up by the liver, where it is conjugated. Conjugated or direct bilirubin is excreted in the bile into the intestines. In the intestines, bacteria convert the conjugated bilirubin into urobilinogen. The majority of the highly soluble urobilinogen is reexcreted by the liver and is eliminated in the feces; the kidneys excrete 5% of the urobilogen. Not only do increased RBC destruction and liver immaturity promote increased bilirubin levels, but other intestinal bacteria can deconjugate bilirubin, which allows it to be reabsorbed into the circulation and further raises bilirubin levels.
INCIDENCE
1. Up to 60% of term newborns have clinical evidence of jaundice.
2. Age of onset is 2 to 3 days.
3. Severity differs among different races, with Asian and Native American infants manifesting higher bilirubin levels.
4. Infants from certain geographic areas, particularly areas around Greece, have an increased incidence of hyperbilirubinemia.
5. Birth trauma (cephalohematoma, cutaneous bruising, instrumented delivery) increases risk for hyperbilirubinemia.
