Oxygen toxicity in premature infants

Abstract

Oxygen causes tissue injury through the formation of reactive oxygen intermediates and peroxidation of membrane lipids. Premature infants, who have severely reduced antioxidant defenses, are particularly sensitive to the toxic effects of oxygen. Supplemental oxygen in premature infants contributes to the development of chronic lung disease (bronchopulmonary dysplasia), characterized by dysregulated inflammation and altered expression of proteases and growth factors. This can result in fibrosis, asymmetric aeration, and respiratory insufficiency. Oxygen also induces aberrant physiologic responses that can be damaging in premature infants. For example, vasoconstriction in the retina is an early response to oxygen that can lead to vasoobliteration, neovascularization, and retinal traction (retinopathy of prematurity). Increasing knowledge of the mechanisms underlying oxygen toxicity in premature infants has suggested strategies to minimize tissue injury and to optimize long-term medical outcomes. These include limiting oxygen supplementation and light exposure, the use of antiinflammatory agents or antioxidants, and the use of room air in neonatal resuscitation.