Neonatal jaundice is a frequent problem in neonatology, but the advent of
phototherapy which has simplified its treatment, it no longer represents a major concern. Early hospital discharge of neonates has now resulted in a re-emergence of
kernicterus.
Neonatal jaundice is principally the result of a transient deficiency of
bilirubin conjugation, of a partial deficiency of hepatic
bilirubin uptake and intracellular transport and of an increased enterohepatic circulation of the pigment. The fact that
bilirubin production in the neonate is 2 or more times greater than in the adult per kilogram of bodyweight represents the mainstay of this condition. Prevention of
kernicterus in full term infants is based on the detection of neonates at risk for developing hyperbilirubinaemia, and can be accomplished with simple tests performed on umbilical cord blood such as blood type, Rh, Coombs' test and
glucose-6-phosphate dehydrogenase, in order to detect haemolytic diseases. The daily evaluation of transcutaneous
bilirubin measurement gives additional information on the rise of serum
bilirubin level, and can help to distinguish physiological from nonphysiological hyperbilirubinaemia. A significant hyperbilirubinaemia is more frequent in infants born before term, and in neonates who do not feed well and lose more than 10% of bodyweight. In preterm infants the typical clinical feature of
kernicterus is seen very rarely, and
kernicterus is now a very infrequent postmortem observation. Since it is very difficult to distinguish the effects of
bilirubin from other potentially toxic factors, it is difficult to give guidelines for the treatment of
jaundice in very low
birthweight infants other than to keep the serum
bilirubin levels to a lower level than in full term infant (e.g. 10 mg/dl lower than in full term babies). The intramuscular administration of a single dose of
Sn-mesoporphyrin (6 mumol/kg bodyweight) in healthy term or near-term infants seems to be a promising treatment modality for controlling hyperbilirubinaemia.