The role of hyperoxia in the aetiology of retinopathy of prematurity.

Oxygen in excess is toxic to living tissues and a capacity to neutralise its harmful potential is a requirement for survival. Experimental and circumstantial clinical evidence suggests that the requisite protective mechanisms are insufficiently advanced in the retinal vasculature of the premature neonate, such that babies of very low birth weight are vulnerable to even minor hyperoxia. Sustained hyperoxia produces degenerative effects on the developing endothelium with the result that the newest vessels at the retinal periphery are obliterated. Factors other than the level of inspired oxygen per se may serve to increase the risk of retinopathy by raising the rate of delivery of hyperoxygenated blood.