Oxygen therapy, oxygen toxicity, and the STOP-ROP trial.

Abstract

Oxygen is essential for life. It also has proven therapeutic value in newborn infants to correct hypoxia and prevent the many complications of hypoxia, decrease the incidence and severity of apnea in premature infants, dilate the pulmonary arteries and increase pulmonary blood flow, and constrict the ductus arteriosus. Although its essential role in life is well known, oxygen also is potentially toxic. Oxygen therapy to reduce apnea in the 1940s led to an increased incidence of retinopathy of prematurity (ROP), known then as retrolental fibroplasia. Breathing higher than normal oxygen concentrations also causes pulmonary epithelial injury and has been implicated as a principal cause of chronic lung disease and bronchopulmonary dysplasia in preterm infants with respiratory distress syndrome. Within and adjacent to cells throughout the body, oxygen can react with prooxidants to produce reactive oxygen species that then produce inflammation and even cell death. In this month's issue, Dr Phelps and her colleagues report the results of the National Institutes of Health Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity (STOP-ROP) Trial,1 which examined a heretofore unproven benefit of oxygen therapy in premature infants, along with any concomitant adverse effects. This randomized clinical trial tested whether supplemental oxygen sufficient to produce high normal blood oxygen saturation values (96%–99% SpO2) would decrease the progression to threshold ROP in infants who had prethreshold ROP. The trial was inspired by evidence showing that oxygen can constrict certain blood vessels, such as those in the retina that are undergoing neovascularization after early postnatal injury, including oxygen-induced injury, and that by restraining neovascularization, oxygen can limit the resulting harmful …