RT Book, Section
A1 Shapiro, Steven M.
A2 Stevenson, David K.
A2 Maisels, M. Jeffrey
A2 Watchko, Jon F.
SR Print(0)
ID 56323801
T1 Chapter 11. Kernicterus
T2 Care of the Jaundiced Neonate
YR 2012
FD 2012
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-176289-2
LK accesspediatrics.mhmedical.com/content.aspx?aid=56323801
RD 2024/04/16
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