Hyperbilirubinemia in the Newborn

Bryon J. Lauer; Nancy D. Spector

doi:10.1542/pir.32-8-341

This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.

Download PDF

Bryon J. Lauer, MD*
Nancy D. Spector, MD^†

^*Assistant Professor of Pediatrics, Drexel University College of Medicine, St. Christopher's Hospital for Children, Philadelphia, PA.
^†Professor of Pediatrics, Drexel University College of Medicine, St. Christopher's Hospital for Children, Philadelphia, PA.

Author Disclosure

Drs Lauer and Spector have disclosed no financial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.

Objectives

After completing this article, readers should be able to:

List the risk factors for severe hyperbilirubinemia.
Distinguish between physiologic jaundice and pathologic jaundice of the newborn.
Recognize the clinical manifestations of acute bilirubin encephalopathy and the permanent clinical sequelae of kernicterus.
Describe the evaluation of hyperbilirubinemia from birth through 3 months of age.
Manage neonatal hyperbilirubinemia, including referral to the neonatal intensive care unit for exchange transfusion.

Introduction

For centuries, neonatal jaundice (icterus neonatorum) has been observed in newborns. As early as 1724, Juncker, in the Conspectus Medicinae Theoreticopraticae, began distinguishing between “true jaundice” and “the icteric tinge which may be observed in infants, immediately after birth.” In 1875, Orth noticed during autopsies the presence of bilirubin in the basal ganglia of infants who had severe jaundice, which was labeled kernicterus by Schmorl in 1903. (1) In 1958, however, a nurse in the nursery of the General Hospital in Rothford, Essex, Great Britain, reported “an apparent fading away of the yellow pigmentation in the skin of the jaundiced babies when they had been a short time in sunlight.” (2)

Icterus neonatorum occurs in approximately two thirds of all newborns in the first postnatal week. Jaundice results from bilirubin deposition in the skin and mucous membranes. For most newborns, such deposition is of little consequence, but the potential remains for kernicterus from high bilirubin concentrations or lower bilirubin concentrations in preterm infants. (3) Although rare, kernicterus is a preventable cause of cerebral palsy.

Hyperbilirubinemia was treated aggressively in the 1950s to 1970s because of a high rate of Rh hemolytic disease and kernicterus. However, data from the 1980s and 1990s …