Abstract
The respiratory distress syndrome (RDS) occurs in 14% of premature infants and is twice as common and twice as lethal in males as in females. Recent work suggests that, during the intrauterine period a disturbance in nutrition of the lung resulting from fetal pulmonary vascular constriction results in alveolar-cell damage and a decrease in pulmonary surface activity with resultant atelectasis. Data on respiratory work levels, oxygen consumption and arterial oxygen tension suggest that there is an oxygen debt in the acute stage of the disease. Such data have further clarified the pathogenesis of the metabolic and respiratory components of the acidosis and the secondary effects thereof. In prevention, prophylaxis of prematurity is of major importance. A program of treatment designed to combat the various aspects of the pathophysiological disturbances is described in the form of a case profile. Modern methods of observation, biochemical control and treatment, as well as the necessity for critical evaluation, suggest that infants with RDS are best cared for in special centres.
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