Abstract 1189 Poster Session IV, Tuesday, 5/4 (poster 365)

Background Hypoxia augments the toxicity of bilirubin, but bilirubin, as an antioxidant, may decrease hypoxic injury. Methods: To explore this phenomena, we studied the 31,759 ≥ 2500g BW newborn infants in the 1959-66 CORE Project whose jaundice was not treated with exchange transfusion (or phototherapy). We analyzed the relationship of the 5 minute Apgar score and peak serum bilirubin (SB) level to 7 year neurologic outcome. Results: For babies with peak SB <20 mg/dl, there was a significantly higher incidence of suspicious and abnormal (Susp/Abn) neurologic ratings among infants with Apgar scores of ≤ 6 (n = 192) as compared to scores of 7 to 10 (20 vs 14.8%) p<0.0001. For the same Apgar categories, among infants with SB ≥ 20 mg/dl the incidence was 44.8% (n = 4) vs 18.5%, but because of the small numbers in the SB ≥ 20, in the Apgar ≤ 6 group, the difference was not significant (p=0.06). In 13,272 babies with peak SB was <5 mg/dl; in 14,855 it was between 5 and 10 mg/dl. Considering Apgar scores of ≤ 3, 4 to 6 and 7 to 10, there was a significant correlation between low scores poor neurologic outcome (see Table). The highest incidence of abnormal neurologic findings was in babies with Apgar Scores ≤ 3 and peak SB ≤ 5mg/dl. This suggests consumption of bilirubin by oxidant radicals generated during hypoxia and reperfusion. Conclusion: The degree of hypoxia at birth and severity of hyperbilirubinemia modulate both bilirubin and hypoxia related neurologic damage. The interaction is complex and includes disruption of the BB barrier, reperfusion injury and the action of bilirubin as a toxin and an antioxidant.

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