Hyperbilirubinemia type 2
Overview
Hyperbilirubinemia, also called neonatal jaundice, is the result of hemolytic processes in the neonate. It’s marked by elevated serum bilirubin levels and mild jaundice and can be physiologic (with jaundice the only symptom) or pathologic (resulting from an underlying disease). Physiologic jaundice tends to be more common and more severe in certain ethnic groups (Chinese, Japanese, Koreans, Native Americans), whose mean peak of unconjugated bilirubin is approximately twice that of the rest of the population. Physiologic jaundice is self-limiting; the prognosis for pathologic jaundice varies, depending on the cause.
Causes
❑ 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 neonate’s glucuronyl-transferase conjugating activity.
Treatment
Depending on the underlying cause, treatment may include phototherapy, exchange transfusions, albumin infusion and, possibly, drug therapy. Phototherapy is the treatment of choice for physiologic jaundice, and pathologic jaundice due to erythroblastosis fetalis (after the initial exchange transfusion). Phototherapy uses fluorescent light to decompose bilirubin in the skin by oxidation and is usually discontinued after bilirubin levels fall below 10 mg/dl and continue to decrease for 24 hours. However, phototherapy is rarely the only treatment for jaundice due to a pathologic cause. An exchange transfusion replaces the neonate’s blood with fresh blood (less than 48 hours old), removing some of the unconjugated bilirubin in serum. Possible indications for exchange transfusions include hydrops fetalis, polycythemia, erythroblastosis fetalis, marked reticulocytosis, drug toxicity, and jaundice that develops within the first 6 hours after birth. Other therapy for excessive bilirubin levels may include albumin administration (1 g/kg of 25% salt-poor albumin), which provides additional albumin for binding unconjugated bilirubin. This may be done 1 to 2 hours before exchange or as a substitute for a portion of the plasma in the transfused blood. Drug therapy, which is rare, usually consists of phenobarbital administered to the mother before delivery and to the neonate several days after delivery. This drug stimulates the hepatic glucuronide-conjugating system.