The first description of RLF as a disorder of extreme prematurity was published as a preliminary report by Terry in 1942. He stated that the condition was either "persistence of the entire vascular structure of the fetal vitreous" or a "fibroblastic overgrowth of the persistent tunica vasculosa lentis." His studies led him to conclude that an "overgrowth of embryonic connective tissue in the interstices of the persistent tunica vasculosa lentis behind the lens" accounted for the pathology observed. He stated: "It is really a retrolental fibroplasia." The terminology was used in his subsequent reports and became generally accepted, although later studies by Owens and Owens (1949) showed that RLF was not related to an embryonic abnormality but was caused by an abnormal blood vessel change in the retina.
On the basis of clinical observation, Terry (1942) concluded that the disease in its classical form was not present at birth but developed between two and six months after birth. He considered many possible factors: "Of all the probable causes listed, precocious exposure to light is considered the most tenable, and preventive measures should be taken."
The light theory was discarded after several investigators found that occluding the eyes after birth had no effect on development of the disease (Hepner et al., 1949; Crosse, 1950; Locke and Reese, 1954).
After discovering a disease that had appeared as an isolated rarity in 1942, Terry collected 117 cases of RLF during the next three years. The condition appeared to be on the increase. In 1945 Terry found that the incidence at the Boston Lying-In Hospital was approximately 12% in infants weighing 1,400 gm or less (based on fewer than 50 cases).
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