Virtually all infants develop hyperbilirubinemia with serum bilirubin levels of at least 1.4 mg/dL (24 μmnol/L) in the first 7 d of life. Clinically apparent jaundice develops in greater than one third of healthy newborns. In most cases, the jaundice is “physiologic” or associated with breast-feeding (1). Physiologic jaundice is generally defined as a benign increase in serum unconjugated bilirubin in newborns. Clinically apparent jaundice does not appear before 36 h of age, total serum bilirubin levels do not generally exceed 12 mg/dL (204 μmol/L), and clinical jaundice resolves within 7–10 d. Conjugated bilirubin does not exceed 2 mg/dL (34 μmol/L). Practitioners caring for newborns must recognize the clinical and laboratory features of jaundice which are “pathologic,” leading to appropriate diagnosis and management. The morbidity and mortality associated with neonatal jaundice can be attributed to the underlying disease process, as well as from the neurologic sequelae of kernicterus. These complications are largely preventable with timely diagnosis and treatment.
KeywordsToxicity Albumin Estrogen Cortisol Pyruvate
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