Neonatal Jaundice

Excerpt

Neonatal jaundice or neonatal hyperbilirubinemia results from elevated total serum bilirubin (TSB) and clinically manifests as yellowish discoloration of the skin, sclera, and mucous membrane. The term jaundice derives from the French word "jaune," which means yellow. It is the most commonly encountered medical problem in the first two weeks of life and a common cause of readmission to the hospital after birth. Approximately 60% of term and 80% of preterm newborns develop clinical jaundice in the first week after birth. In most cases, it is a mild, transient, and self-limiting condition and resolves without treatment referred to as "physiological jaundice." However, it is imperative to distinguish this from a more severe form called "pathological jaundice." Failure to identify and treat this entity may result in bilirubin encephalopathy and associated neurological sequelae.

Unconjugated hyperbilirubinemia (UHB) is the cause of clinical jaundice in most neonates, but some infants with jaundice have conjugated hyperbilirubinemia (CHB), which is always pathological and signifies an underlying medical or surgical cause. The etiology of pathological UHB and CHB is vast and varied. Preterm infants and those born with congenital enzyme deficiencies are particularly prone to the harmful effects of unconjugated bilirubin on the central nervous system. Severe hyperbilirubinemia can cause bilirubin-induced neurological dysfunction (BIND) and, if not treated adequately, may lead to acute and chronic bilirubin encephalopathy. Phototherapy and exchange transfusions are the mainstay of treatment of UHB, and a subset of patients also respond to intravenous immunoglobulin (IVIG). Treatment of CHB is more complex and depends mainly on the etiology. Despite advances in care and management of hyperbilirubinemia, it remains a significant cause of morbidity and mortality.