TY - CHAP M1 - Book, Section TI - Chapter 11. Kernicterus A1 - Shapiro, Steven M. A2 - Stevenson, David K. A2 - Maisels, M. Jeffrey A2 - Watchko, Jon F. PY - 2012 T2 - Care of the Jaundiced Neonate AB - Excessive newborn hyperbilirubinemia can cause permanent brain damage, that is, chronic bilirubin encephalopathy (BE), also known as kernicterus. The effort to understand and treat neonatal hyperbilirubinemia is for the most part an effort to prevent kernicterus and bilirubin-induced neurological dysfunction (BIND), the latter referring to subtle neurodevelopmental disabilities without classical findings of kernicterus.1–4 Kernicterus is a matter of concern for pediatricians and neonatologists. Historically, kernicterus caused a significant number of cases of cerebral palsy (CP), particularly the athetoid or dystonic type. Kernicterus remains a significant problem in underdeveloped countries where bilirubin screening and treatment of excessive hyperbilirubinemia is not routinely available as highlighted in Chapter 13 Neonatal Jaundice in Low-Middle-Income Countries. The “classic” literature on kernicterus evolved during an era when Rh disease was the main cause and therapeutic options for treatment were limited. The resulting acute bilirubin encephalopathy (ABE) was dramatic, with prominent central nervous system (CNS) signs of lethargy, ophthalmoplegia and setting sun sign (impairment of upward gaze), high-pitched cry, opisthotonus, and seizures.5 Both the basal ganglia, with yellow staining (icterus) of the deep nuclei or “kernel” of the brain, and brainstem auditory pathways were recognized as being particularly vulnerable.5,6 SN - PB - The McGraw-Hill Companies CY - New York, NY Y2 - 2024/03/28 UR - accesspediatrics.mhmedical.com/content.aspx?aid=56323801 ER -