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Published on: November 20, 2015
Oxygen toxicity in premature infants
Barry Weinberger1, Debra L Laskin, Diane E Heck
1Department of Pediatrics/Neonatology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903, USA.
Insights
Oxygen harms premature infants by damaging tissues and causing lung disease (bronchopulmonary dysplasia) and eye problems (retinopathy of prematurity). Strategies to limit oxygen exposure and use antioxidants may reduce this toxicity.
Area of Science:
- Neonatal Medicine
- Pediatric Pulmonology
- Ophthalmology
Background:
- Oxygen exposure can cause tissue injury via reactive oxygen intermediates and lipid peroxidation.
- Premature infants possess underdeveloped antioxidant defenses, increasing their susceptibility to oxygen toxicity.
- Supplemental oxygen is linked to chronic lung disease (bronchopulmonary dysplasia) and retinopathy of prematurity in neonates.
Purpose of the Study:
- To review the mechanisms of oxygen toxicity in premature infants.
- To discuss the resulting conditions, including bronchopulmonary dysplasia and retinopathy of prematurity.
- To explore strategies for minimizing oxygen-induced tissue injury and improving outcomes.
Main Methods:
- Literature review of studies on oxygen toxicity in premature infants.
- Analysis of the physiological and pathological responses to oxygen.
- Identification of potential therapeutic and preventative strategies.
Main Results:
- Oxygen induces inflammation, protease/growth factor dysregulation, fibrosis, and respiratory insufficiency in the lungs.
- Oxygen causes retinal vasoconstriction, vasoobliteration, neovascularization, and traction, leading to retinopathy of prematurity.
- Reduced antioxidant defenses exacerbate oxygen-induced damage in premature infants.
Conclusions:
- Understanding oxygen toxicity mechanisms is crucial for developing protective strategies.
- Limiting oxygen exposure, light, and utilizing antioxidants or room air resuscitation can mitigate harm.
- Optimizing oxygen management is key to improving long-term medical outcomes for 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.
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