The epidemiology of neonatal jaundice

Abstract

Neonatal jaundice (NJ) is one of the most common causes for medical intervention in the newborn period. While transitory hyperbilirubinemia (HB) is present in almost all newborns, detection of jaundice requires a trained observer and good lighting. Thus, jaundice in the newborn has a reported incidence between 60% to more than 90%. Bilirubin, the molecule that causes the color of jaundice, is the end product of disassembly of heme-containing molecules, primarily hemoglobin. Therefore, conditions that increase hemolysis will increase bilirubin production and cause jaundice. Common conditions in the newborn are blood group incompatibilities and congenital hemolytic anemias. A family history of NJ increases the likelihood of jaundice in the present newborn, and is one of several examples of genetic conditions that contribute. Endocrine and metabolic conditions contribute, the most common being maternal diabetes. An increased incidence is seen in infants of Southeast Asian mothers, while African infants have a lower incidence unless they suffer from G-6-PD-deficiency. Drugs taken by the mother during pregnancy may impact on hepatic metabolism of bilirubin in the newborn, often by reducing the incidence of jaundice, and the same may happen with certain drugs given to the newborn. Birth trauma, through extravasation of blood, will increase bilirubin production and jaundice. Preterm infants have immature bilirubin metabolism and a higher incidence of jaundice. Breast-fed infants have an increased incidence of jaundice, which may also last longer. Extreme NJ, associated with risk of kernicterus spectrum syndrome, has an estimated worldwide incidence of 99/100,000 or more, thus affecting 130,000 or more infants each year and calling for increased vigilance and preparedness for rapid therapeutic intervention.