Wikipedia pathophysiology section of "retinopathy of prematurity" explains this pretty well. Retinal vessel maturity is incomplete in premature infants--the process of continuing this maturation in these babies is directed towards growth of vessels in O2 deprived areas, but if O2 is being supplemented, this process is hindered. Therefore when O2 supplementation is removed, excessive vessel proliferation going into the vitreous humor (not where it is supposed to be) leads to retinopathy of prematurity (defined as "disorganized growth of retinal blood vessels leading to scarring and retinal detachment")
"chronic high oxygen saturations can adversely affect lung and eye outcomes of preterm infants." link
agree with burak. they're trying to say that primary goal of treatment with supplemental o2 is to make sure there is no retinal damage.
why is protection of the choroid plexus, from intraventricular rupture secondary to germinal matrix hemorrhage not a possible answer?
submitted by โhyoscyamine(59)
FA pg 217. Too much oxygenation can cause free radical damage leading to retinopathy of prematurity