The results of a controlled nursery study, supported by observations of others in both uncontrolled and controlled studies, clearly established the overuse of oxygen in the premature nursery as an important and probably the principal factor in the development of retrolental fibroplasia.
The clinical data is supported by observations in the newborn or young mouse, rat, kitten, and puppy where retinal lesions, identical to those seen in early human retrolental fibroplasia are produced following exposure to an enriched oxygen environment.
Fundamental to all these experiments, and apparently to the pathogenesis of human retrolental fibroplasia, is the uniform ocular susceptibility to oxygen when the retinas are immaturely vascularized, and a resistance to oxygen damage where vascularization is complete.
The animal lesions produced by oxygen are proportional to the concentration of oxygen administered and the duration of exposure, and inversely proportional to the degree of vascularization of the retina. Duration of exposure to oxygen proved to be the most important single factor in these experiments.
The ocular effects of oxygen on the immature retina can be divided into a primary phase of vasoconstriction and obliteration and a secondary phase of vascular proliferation.
These clinical and experimental data justify recommendations for a rigid supervision of oxygen administration to the premature infant to avoid any unnecessary overuse of this potentially toxic agent.
- Copyright © 1957 by the American Academy of Pediatrics