Neonatal Hyperbilirubinemia

Abstract

Neonatal jaundice is a common problem associated with the transition from fetal to neonatal life. It is caused by the accumulation of bilirubin in the skin. Bilirubin is created from biliverdin, which is the breakdown product of heme proteins. In the older child and adult, bilirubin is conjugated in the liver, excreted into the intestine, and eliminated from the body. Over 50% of newborns exhibit jaundice in the first few days of life and, in most cases, this is physiologic and due to a physiologic delay in bilirubin conjugation. In certain clinical circumstances, pathological etiologies of hyperbilirubinemia should be entertained. The mainstay of treatment for hyperbilirubinemia is phototherapy, which converts bilirubin into a water-soluble and easily excretable form. Intravenous γ-globulin (IVIG) is used as adjunctive therapy for isoimmune hemolytic disease. In severe cases, a double-volume exchange transfusion is indicated. Gestational age and postnatal age-specific guidelines guide therapy. The reason to treat jaundice is the association with neurological sequelae when bilirubin levels rise high enough to overwhelm protein binding, cross the blood–brain barrier, and cause neuronal injury.