In spite of numerous human and animal studies, the etiology of retinopathy of prematurity (previously called retrolental fibroplasia) remains obscure. Prevention attempts with judicious use and careful monitoring of supplemental oxygen, while decreasing the incidence, have not eradicated this complication of prematurity. Currently, retinopathy of prematurity is a condition that cannot be prevented in certain infants, especially those of very low birth weight.
One controlled trial suggested that the prophylactic oral administration of 100 mg/kg/d of free vitamin E to babies at highest risk, while not decreasing the incidence of retinopathy of prematurity, decreases the severity in affected infants.1 Three other controlled trials showed a lower incidence of severe retinopathy of prematurity in treated groups (25 mg/kg intramuscular or 25 mg/d oral, or variable intravenous doses), but none of these differences were statistically significant.2-4 These observations have led some authors to suggest that vitamin E be routinely administered to all infants weighing less than 1,500 g at birth.5,6
It must be noted that any effective prophylaxis with vitamin E in the United States would require that 22,000 surviving infants of birth weight less than 1,500 g be treated annually to prevent approximately 2,000 infants from developing the cicatricial sequelae of retinopathy of prematurity.7 The treatment of 20,000 infants who would not develop retinopathy of prematurity would be acceptable if it were certain that the administration of vitamin E was completely safe or, at least, that the benefits of its use outweighed the risks by a substantial margin. Preliminary reports, however, suggest the possibility of complications associated with the administration of pharmacologic doses of vitamin E.8,9
- Copyright © 1985 by the American Academy of Pediatrics