Neonatal jaundice : bilirubin and phototherapy

Abstract

Bilirubin is a product of hemoglobin breakdown. Catabolism of the heme group of haemoglobin involves the opening of the porphyrin ring, usually at the a position, and loss of the a carbon atom to yield bilirubin IX-a. In normal adults the latter is excreted in the bile primarily as a conjugate with glucuronic acid. In adults a red blood cell has an average life spa n of 120 days; in babies, the value is only 70 days. The rate of bilirubin production in the newborn is, therefore, several times that of the adult on body weight basis. This rapid turnover implies that metabolism and eventual excretion of bilirubin is more critical in babies if accumulation and subsequent damage due to its toxicity are to be avoided. A potential consequence of hyperbilirubinemia in the newborn is irreparable damage to the central nervous system due to precipitation of this substance in certain areas of the brain (kernicterus). This follows damage to the blood-brain bamerprecipitated by situations such as asphyxia in an ill premature baby . Lesser, but still hazardous complications include mild types of encephalopathy and damage to the auditory nerve.