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Hyperbilirubinemia is the most common condition requiring evaluation and treatment of newborns, but for the vast majority of neonates, it is a benign, transitional phenomenon of no overt clinical significance. In a few infants, however, serum bilirubin may rise to hazardous levels that pose a direct threat of brain damage. Acute bilirubin encephalopathy, an uncommon disorder,1 may ensue, frequently evolving into kernicterus, a devastating chronic disabling condition characterized by the clinical tetrad of choreoathetoid cerebral palsy, central neural hearing loss, palsy of the vertical gaze, and tooth enamel hypoplasia as the result of bilirubin-induced cell toxicity.2 Originally described in newborns . . .
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Jon F. Watchko (2006) studied this question.
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