ABSTRACT
Contents Introduction .............................................................................................................................768 History of Bilirubin Encephalopathy ........................................................................................768 E•ects on the Child ................................................................................................................ 770 Kernicterus Classication ........................................................................................................ 770
Classical Kernicterus ........................................................................................................... 771 Motor-Predominant Kernicterus ......................................................................................... 771 Auditory-Predominant Kernicterus ..................................................................................... 771 Subtle Kernicterus or Bilirubin-Induced Neurological Dysfunction (BIND) ...................... 771 Classication by Severity and Type of Sequelae ................................................................... 771
Life Expectancy ....................................................................................................................... 772 Treatment ................................................................................................................................ 772 Implications for the Life Care Planner ......................................................................................774 Conclusion .............................................................................................................................. 775 Case Study .............................................................................................................................. 775 Appendix: Common Kernicterus Resources for the Life Care Planner ..................................... 788 References ................................................................................................................................789
Introduction Most full-term babies in the United States are born healthy and spend their neonatal period (the rst 28 days of life) growing and developing. Some of these infants, approximately 50%–60%, develop jaundice or hyperbilirubinemia in the rst week of life (American Academy of Pediatrics, 2004). Jaundice is a yellowish discoloration in skin pigment caused by too much bilirubin (a breakdown product from red blood cell destruction) in the blood and hyperbilirubinemia in infancy may result from bilirubin toxicity (Shapiro, 2010). Hyperbilirubinemia leads to jaundice in the skin as well as the sclerae of the eyes and the nails and is commonly seen in newborns (Kramer, 1969; Wong & Hockinberry-Eaton, 2001). In most cases, infant jaundice is benign and resolves on its own. However, in some cases, jaundice requires treatment with phototherapy and ²uids, and, on occasion, with exchange blood transfusions. ’ere are a few uncommon, but signicant causes of jaundice from which an infant’s bilirubin value can rise to high and dangerous levels rapidly over a short period of time* and, if not treated promptly and appropriately, may lead to neurotoxicity resulting in irreversible brain damage known as bilirubin encephalopathy or kernicterus. ’e terms bilirubin encephalopathy and kernicterus will be used interchangeably to describe the condition that results in neurotoxicity as these terms are both used in referenced literature.
