Neonatal Jaundice

Excerpt

Neonatal jaundice is a clinical manifestation of elevated total serum bilirubin (TSB), termed neonatal hyperbilirubinemia, which results from bilirubin that is deposited into an infant's skin. The characteristic features of neonatal jaundice include yellowish skin, sclerae, and mucous membranes. Jaundice derives from the French word jaune, meaning yellow. Neonatal jaundice is the most frequently encountered medical condition in the first 2 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. Neonatal jaundice is usually a mild, transient, and self-limiting condition known as physiologic jaundice. However, this should be distinguished from the more severe pathologic jaundice. The two types of neonatal hyperbilirubinemia are unconjugated hyperbilirubinemia (UHB) and conjugated hyperbilirubinemia (CHB).

When neonatal jaundice is clinically identified, the underlying etiology of neonatal hyperbilirubinemia must be determined. In most neonates, unconjugated hyperbilirubinemia is the cause of clinical jaundice. However, some infants have conjugated hyperbilirubinemia, which is always pathologic and signifies an underlying medical or surgical etiology. Failure to identify and treat pathologic jaundice may result in bilirubin encephalopathy and associated neurological sequelae. The causes of pathologic UHB and CHB are numerous and varied. Preterm infants and those with congenital enzyme deficiencies are particularly prone to the harmful effects of unconjugated bilirubin on the central nervous system.

Unconjugated hyperbilirubinemia is diagnosed by assessing bilirubin levels with a transcutaneous measurement device or blood samples for total serum bilirubin. Conjugated hyperbilirubinemia is typically diagnosed through laboratory studies, including serum aminotransferase, prothrombin time, urine cultures, tests for inborn errors of metabolism, and, in some cases, imaging studies. 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 mainstays of treatment of UHB, and a subset of patients also respond to intravenous immunoglobulin (IVIG). Treatment of CHB is more complex and depends on the etiology of the jaundice. Despite advances in the care and management of hyperbilirubinemia, it remains a significant cause of neonatal morbidity and mortality.