Abstract
RETROLENTAL fibroplasia (RLF), the retinopathy of prematurity, first identified by Terry1in 1942, soon became one of the largest causes of child blindness. The identification of oxygen overuse as its cause in the early 1950s led to a general curtailment of oxygen therapy, and the disease virtually disappeared. During the early and mid 1960s, several reports appeared which documented the severe oxygen deprivation and the need for high concentrations of oxygen for infants with the respiratory distress syndrome. As a result, the pendulum which swung in the 1950s toward a rigid restriction in oxygen therapy for the premature infant began to swing back in the 1960s toward more liberal use of oxygen. In early 1967 I examined a significant number of new patients with RLF from several premature centers. Recalling our earlier nursery study2and the kitten studies of Ashton and Cook,3in which the majority of

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