Abstract
Although jaundice affects more than half of infants in the first week of life, only a few of them develop severe hyperbilirubinemia and are at risk of developing bilirubin encephalopathy. Neurological involvement may occur acutely (acute bilirubin encephalopathy,) which may or may not progress to a chronic form (Kernicterus), or with a constellation of sensory, motor and cognitive, subacute or chronic symptoms, depending on the presence of risk factors that increase susceptibility to neurological damage. Free bilirubin interacts with inflammatory cytokines and is responsible for neuronal and glial cell damage in the central nervous system. Despite different methods to prevent severe hyperbilirubinemia, Kernicterus cases continue to be reported, especially in developing countries, including some where this condition constitutes a public health problem.