Animal experiments of Ashton and others * have made it possible to combine the two apparently opposite points of view concerning the role of oxygen in the pathogenesis of retrolental fibroplasia. The present concept of the etiology of the disease may be summarized as follows: Retrolental fibroplasia is the result of retinal hypoxia. This retinal hypoxia may be induced by two different mechanisms, which may operate singly or in combination:
Supplemental oxygen may cause retinal vasoconstriction. Continued vasoconstriction leads to obliteration of the newly formed retinal vessels, and continued supplemental oxygen also leads to suppression of growth of developing vessels. Retinal hypoxia results because of decreased blood supply.
Systemic diseases, such as pneumonia (especially interstitial plasma-cell pneumonia) and anemia, may result in retinal hypoxia.
The important role of the choroid in the nutrition of the retina, as emphasized by Ashton, cannot be overestimated in considering the etiology of retrolental
MANSCHOT WA. Therapy of Retrolental Fibroplasia. AMA Arch Ophthalmol. 1955;54(4):596-601. doi:10.1001/archopht.1955.00930020602014