| Abstract: | The aim of this study is to identify clinical, etiologic, and laboratory factors that potentiate adverse outcome of hyperbilirubinemia among term and late preterm neonates in logistic regression analysis. A retrospective cohort of infants with total serum bilirubin (TSB) ? 20 mg/dL from 1995 to 2007 was surveyed. Eighteen infants had adverse outcome. Controls were 270 infants without sequelae. Risks were significantly higher in infants with six etiologies causing hyperbilirubinemia: sepsis (odds ratio [OR] = 161.7, 95% confidence interval [CI] = 11.7 to 2242.8), gastrointestinal obstruction (OR = 39.2, 95% CI = 2.7 to 567.3), Rh incompatibility (OR = 31.0, 95% CI = 5.1 to 188.9), hereditary spherocytosis (OR = 19.6, 95% CI = 1.6 to 235.5), ABO incompatibility (OR = 5.1, 95% CI = 1.3 to 19.7), and glucose-6-phosphate dehydrogenase deficiency (OR = 4.7, 95% CI = 1.3 to 16.7). Infants with acute bilirubin encephalopathy were more likely to have adverse outcome than subjects without acute bilirubin encephalopathy (OR = 281.7, 95% CI = 25.8 to 3076.7). Adverse outcome was more common in infants with a positive direct Coombs test (OR = 4.5, 95% CI = 1.3 to 15.4). Infants with hemoglobin < 10 g/dL tended to have adverse outcome more often than those with hemoglobin ? 13 g/dL (OR = 11.8, 95% CI = 3.3 to 42.9). Infants with TSB of 35 mg/dL or more (OR = 472.5, 95% CI = 47.8 to 4668.8) and of 30 to 34.9 mg/dL (OR = 9.5, 95% CI = 1.6 to 57.9) carry greater risks as compared with those with TSB of 20 to 24.9 mg/dL. In conclusion, this study quantitatively verified the potential risks for adverse outcome of neonatal hyperbilirubinemia. |
