Abstract
In addition to confirmation of earlier epidemiologic observations, major advances have occurred in the past few years with respect to the diagnosis and treatment of hyaline membrane disease. Prenatal assessment of the risk for developing the disorder is now routinely possible by amniocentesis and analysis of the ratio of lecithin to sphingomyelin in amniotic fluid, or by surfactant titer ("shake test"). Such predictability and numerous other lines of evidence provide strong support for the hypothesis that hyaline membrane disease fundamentally reflects a deficiency of pulmonary surfactant. In accordance with the apparent primacy of surfactant deficiency, recent improvements in management are directed toward either increasing lung volume at end expiration by application of continuous distending airway pressure, or accelerating fetal lung maturation, with respect to the synthesis and secretion of surfactant, by prenatal administration of glucocorticoids.
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