Published on 21/03/2015 by admin

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Jonathan M. Wong and Theodore X. O’Connell

General Discussion

This discussion focuses on neonatal hyperbilirubinemia in infants 35 or more weeks of gestation.

Neonatal hyperbilirubinemia is defined as a total serum bilirubin greater than 5 mg/dL. Jaundice results from the deposition of unconjugated bilirubin pigment in the skin and mucus membranes. Up to 60% of term newborns have clinical jaundice in the first week of life, yet few have significant underlying disease. However, neonatal hyperbilirubinemia can be associated with hemolytic disease, metabolic and endocrine disorders, infections, and anatomic abnormalities of the liver.

Bilirubin is the final product of heme degradation. Newborns produce bilirubin at twice the rate of adults because of relative polycythemia and increased red blood cell (RBC) turnover. Bilirubin production typically declines to adult levels within 10-14 days after birth. Neonatal hyperbilirubinemia results from a predisposition to the production in newborn infants and their limited ability to excrete it.

The term kernicterus has come to be used interchangeably with both the acute and chronic findings of bilirubin encephalopathy. Bilirubin encephalopathy describes the clinical central nervous system (CNS) findings caused by bilirubin toxicity to the basal ganglia and various brainstem nuclei. It is unclear what level of total serum bilirubin is associated with kernicterus, although most experts agree that bilirubin levels greater than 20 mg/dL in the term infant warrant concern. Early signs of kernicterus are subtle and nonspecific, but bilirubin encephalopathy may be more evident by 3 years of age and leads to developmental and motor delays, sensorineural deafness, and mild mental retardation.

Physiologic jaundice in the healthy term newborn usually peaks at 5 to 6 mg/dL on the third to fourth day of life and then declines over the first week after birth. Bilirubin elevations up to 12 mg/dL can sometimes occur. Infants with multiple risk factors may develop an exaggerated form of physiologic jaundice. Breastfed newborns may be at increased risk for exaggerated physiologic jaundice because of relative caloric deprivation and mild dehydration with resulting delayed passage of meconium in the first few days of life. Formula supplementation may be necessary, but breastfeeding should be continued to maintain breast milk production. Serum bilirubin concentrations higher than 17 mg/dL in full-term infants are no longer considered physiologic, and a cause of pathologic jaundice can usually be identified in these infants.

Breast milk jaundice occurs later in the newborn period, with the bilirubin level usually peaking between 6 and 14 days of life. Breast milk jaundice may occur in up to one third of healthy breastfed infants and is believed to be the result of substances in maternal milk which may inhibit normal bilirubin metabolism. The bilirubin level usually falls after the infant is 2 weeks old but may remain elevated for 1 to 3 months. Breastfeeding may be temporarily interrupted if the diagnosis of breast milk jaundice is in doubt or the total serum bilirubin level becomes markedly elevated.

Any jaundice beyond physiologic and breast milk jaundice is considered pathologic. Features of pathologic jaundice include the appearance of jaundice within 24 hours after birth, an increase of total serum bilirubin greater than 5 mg/dL per day, and a total serum bilirubin level higher than 17 mg/dL in a full-term newborn. Other features suggesting pathologic jaundice include prolonged jaundice, evidence of underlying illness, and elevation of the serum conjugated bilirubin to greater than 2 mg/dL or more than 20% of the total serum bilirubin concentration.

Risk factors for neonatal hyperbilirubinemia are outlined below.