Excessive free radical production and associated cellular damage are major contributors to sequelae of extreme premature birth, eg mental retardation(MR)/CP and ROP. Bilirubin, a cellular toxin in the unbound state, is also a potent antioxidant. Low SB levels in the early neonatal period have been reported to be associated with severe ROP, suggesting that its antioxidant properties may protect against ROP. Management goals for VLBW infants at PAH include keeping SB levels below 1% of BW by intensive photoRx and if needed, Ex Tx, and maintenance of VE levels between 1 and 3 mg/dl to improve antioxidant defenses. Threshold ROP is treated with pharmacologic VE and, as needed, cryo/lazer therapy. Findings in 145≤ 800g BW infants cared for at PAH from 1981 to 91 and surviving 2 yrs are presented in the table. No relationship between low x peak SB levels and ROP or high x peak SB levels and CP was apparent. Severe CP (17/145, 12%) and blindness (6/145, 4%) in one or both eyes, was low. (Multivariate analysis with illness risk factors, serum VE levels and follow-up at ≥ 4 years is in progress. In contrast, a multivariate logistic regression analysis reported(1996 APS/SPR) among 131≤ 800g BW 18 month survivors cared for Toronto Sick Children from 1980 to 89, (15.5% with severe CP/MR, 11% blind), suggested that xbar peak SB levels below 9.4 mg/dl may be associated with blind-ness (p = 0.053) and levels above 11.7 mg/dl with CP/MR (p = 0.43). Our data suggest both ROP and CP can be minimized by the PA H protocol for management of serum bilirubin levels (bilirubin exposure) and Vitamin E nutrition.

Table 1
Full size table