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

High arterial oxygen saturation (SaO2) is associated with the development of retinopathy of prematurity (ROP), but difficult to avoid.

To assess the association between severe ROP and a burden of cerebral and arterial hyperoxia.

We retrospectively analyzed 225 preterm infants born ≤30 weeks' gestation. The cerebral oxygen saturation (rcSO2) and SaO2 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.

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.

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 SaO2. Whether reducing cerebral hyperoxia is feasible and might prevent ROP needs to be further examined.