Postnatal Cerebral Hyperoxia Is Associated with an Increased Risk of Severe Retinopathy of Prematurity

Background: High arterial oxygen saturation (SaO 2 ) is associated with the development of retinopathy of prematurity (ROP), but difficult to avoid. Objective: To assess the association between severe ROP and a burden of cerebral and arterial hyperoxia. Methods: We retrospectively analyzed 225 preterm infants born ≤30 weeks’ gestation. The cerebral oxygen saturation (r c SO 2 ) and SaO 2 were measured within the first 96 h after birth. We determined the burden of both cerebral and arterial hyperoxia, which was defined as the percentage of time spent at saturation thresholds exceeding 85 and 90%, respectively. Their association with severe ROP (prethreshold disease type 1) was tested using logistic regression analyses. Results: Median gestational age (GA) was 28.0 weeks (interquartile range 26.7–29.0) and mean birth weight 1,032 g (±281 SD). Eight infants developed severe ROP. Infants with severe ROP spent more time at cerebral hyperoxic levels than infants without severe ROP (medians 30 vs. 16%). Adjusted for GA, for every 10% increase in burden of cerebral hyperoxia, the OR for developing ROP was 1.50 (95% CI 1.09 – 2.06, p = 0.013). A burden of arterial hyperoxia was not associated with ROP. Infants with severe ROP experienced even less arterial hyperoxia, although not statistically significant. Conclusions: Cerebral hyperoxia may be a better early predictor of severe ROP than arterial hyperoxia. Moreover, under strict oxygen management, cerebral hyperoxia in these infants may result from cerebral immaturity rather than a high SaO 2 . Whether reducing cerebral hyperoxia is feasible and might prevent ROP needs to be further examined.