Kernicterus is a form of severe neonatal hyperbilirubinemia resulting in neurotoxicity and brain damage. Involved areas of the brain include the nuclear region, basal ganglia, hippocampus, and cerebellum. Bilirubin-induced neurologic dysfunction (BIND) is the term for the spectrum of clinical neurologic manifestations caused by bilirubin-related neurotoxicity, with kernicterus lying on the severe end. Complications of kernicterus include brain damage, sensorineural hearing loss, cerebral palsy, and permanent gaze defects.

There are many risk factors than can lead to BINDs. Increased bilirubin production can be caused by conditions that lead to increased immune and nonimmune related hemolysis. These include blood group incompatibilities between mother and infant (Rh, ABO, and minor antigens), enzyme defects (glucose-6-phosphate dehydrogenase deficiency), abnormal RBC morphology (spherocytosis), deep bruising, and cephalohematomas. Conditions that lead to impaired bilirubin metabolism, such as Crigler-Najjar syndrome type 1, can also can cause severe hyperbilirubinemia and kernicterus.

Additional risk factors include breast-feeding, sepsis, prematurity, acidosis, hypoalbuminemia, and dehydration.

Kernicterus is largely a preventable disease with early detection of rising bilirubin levels, and appropriate treatment includes phototherapy and exchange transfusions. There are many available published guidelines for the management of hyperbilirubinemia and prevention of kernicterus.