Risk Assessment for Adverse Outcome in Term and Late Preterm Neonates with Bilirubin Values of 20 mg/dL or More

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.