In the early 1950's supplementary oxygen for small premature infants was implicated as a contributing factor in retrolental fibroplasia (RLF). With this new knowledge available, subsequent efforts to restrict the use of oxygen for premature infants were made and a sharp drop in the incidence of RLF resulted. Since that time, however, new cases have continued to appear. Ten patients with severe retrolental fibroplasia which developed after 1958 were reported by a research group at the Massachusetts Eye and Ear Infirmary in January 1964.1 In addition, many children who were premature at birth are now in school and have reached an age when vitreoretinal traction may cause retinal detachment. These patients have characteristic ocular changes which may include myopia and chorioretinal scarring. Because of vitreous syneresis and contraction of vitreous membranes, dragging of the retinal vessels and disc may also occur, as well as white without pressure, temporal retinal folds,