Effects of oxygen on the development and severity of retinopathy of prematurity

Abstract

In 1942, when retinopathy of prematurity (ROP) first manifested as retrolental fibroplasia, the technology to monitor or regulate oxygen did not exist, and a fundus examination of preterm infants was not routinely performed. Supplemental, uncontrolled oxygen at birth has since been found to cause retrolental fibroplasia. At the same time, technological advances have made it possible to regulate oxygen and detect early forms of ROP. Nevertheless, despite our better understanding of ROP and ongoing investigations of supplemental therapeutic oxygen, including recent clinical trials (Surfactant, Positive Airway Pressure, Pulse Oximetry Randomized Trial [SUPPORT] and Benefits of Oxygen Saturation Targeting [BOOST]), the best oxygen profiles to reduce ROP risk while optimizing preterm infant health and development remain unknown. This article reviews major studies on oxygen use in preterm infants and the effects on the development of ROP.

FIG 1

Oxyhemoglobin dissociation curve: relationship between oxygen saturation and partial pressure of oxygen for fetal and adult hemoglobin curve. Decreased 2,3-DPG and increased pH can shift the curve to the left, whereas increased 2,3-DPG or decreased pH can shift the curve to the right.

FIG 2

Proposed retinal development.A, initially, there is impaired physiologic retinal vascular development from reduced growth factors from the placental circulation (line) and then a delay in retinal vascular development (dotted line). This leads to areas of avascular retina that become hypoxic once an infant is brought from supplemental oxygen into room air, given healthy lungs and other parameters. B, subsequently, hypoxic retina stimulates the production of angiogenic factors that cause vasoproliferation.