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The pathophysiology of the neonatal respiratory distress syndrome has been largely inferred from postmortem appearances in infants showing pulmonary hyaline membranes at autopsy. Little is known of earlier changes occurring soon after birth, and essentially nothing of any prenatal or perinatal disturbances of physiology. But, since roentgenological and other studies have defined the clinical entity relatively clearly, investigation of earlier phases and in infants who survive is increasingly possible. The association of nenonatal respiratory distress with an appearance of edema has been noted for some time.1Although the nature of the hyaline material composing the membranes found at autopsy has yet to be completely defined, fibrin is present.2This finding lends support to the idea that the hyaline membranes come at least in part from inside the body rather than from aspiration of foreign material. If the protein or fibrin-containing material in the alveoli is a local transudation,
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James M. Sutherland (1959) studied this question.
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