Articles: kernicterus.
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This article describes new findings concerning the basic science of bilirubin neurotoxicity, new considerations of the definition of clinical kernicterus, and new and useful tools to diagnose kernicterus in older children, and discusses treatments for kernicterus beyond the newborn period and why proper diagnosis is important.
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In this review the historical tenets and evidence-based clinical research in support of a bilirubin exchange threshold of >20 mg/dL for the healthy term neonate are revisited. In addition, a hypothesis is ventured that recent cases of kernicterus are related in part to changes in population factors coupled with genetic predispositions that have unmasked an unappreciated potential for marked neonatal hyperbilirubinemia.
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The serum total bilirubin concentration at any point in time represents the amount of bilirubin being produced minus that being excreted. Hyperbilirubinemia develops when bilirubin production exceeds the body's capacity to excrete it, primarily by conjugation. When extreme, hyperbilirubinemia may lead to the development of free bilirubin, that form of bilirubin which may cross the blood-brain barrier and enter and damage the basal nuclei of the brain. ⋯ Hyperbilirubinemia is a condition of major importance and a source of concern to all involved in the management of the newborn. Its prevention and management should be based on the recently revised American Academy of Pediatric guidelines, with special attention paid to neonates manifesting risk factors for kernicterus. Close cooperation between the clinical laboratory and the medical team managing the newborn is an essential component in the management of a hyperbilirubinemic baby.
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Seminars in perinatology · Oct 2004
ReviewGlucose-6-phosphate dehydrogenase deficiency: a hidden risk for kernicterus.
Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, a commonly occurring enzymatic defect, is an important risk factor in the pathogenesis of severe neonatal hyperbilirubinemia. Many of the recently reported cases of kernicterus, even in countries with a low overall incidence of the G-6-PD deficiency such as the United States and Canada, have been found to be enzyme deficient. In many cases the hyperbilirubinemia may be due to acute hemolysis precipitated by exposure to an identifiable chemical trigger, or to infection. ⋯ Neonates whose families originated in areas at high risk for G-6-PD deficiency should be vigilantly observed for jaundice. Phototherapy is the mainstay of treatment, with exchange transfusion being performed in those unresponsive to phototherapy. A high degree of physician awareness is essential in the identification and follow-up of these high-risk neonates.