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• W1849517811 abstract "Neonatal respiratory disease remains one of the major causes of death, especially in the premature infant. In this group an estimated 10,000 to 20,000 deaths occur each year (4, 25, 29, 35). What is now called hyaline membrane disease of the newborn was first described in 1903 in Germany (16) and in 1923 in the United States (17). In spite of this, progress in establishing unequivocal pathogenesis, diagnosis, and treatment has been slow. With this in mind, we undertook a study to determine whether the diagnosis could be made before the development of clinical symptoms, thereby facilitating prompt treatment. Clinical and Pathologic Findings Infants with hyaline membrane disease are usually premature, delivered by section, or born of a diabetic mother. Their stage of development must be sufficiently advanced (1,000 or more grams weight; seven months of gestation) to permit normal pulmonary gas exchange (31). The condition occurs only in infants who breathe after birth, never in the stillborn (3, 4, 25, 35). In a matter of minutes to hours breathing becomes labored, as if against obstruction; sternal and costal retraction with cyanosis may develop, and death may ensue (3, 9, 15, 18, 21, 27, 28, 32, 35, 38, 40). Recent reports have charted the progress of the disease by recording respiratory rates (14, 28). By the time 60 per minute is reached, serious clinical disease may be expected. Since not all the infants die, the diagnosis cannot always be confirmed (31, 34, 35, 38). Grossly the lungs appear dark red to purple and markedly engorged. They contain few or no gross air-filled spaces. Microscopically the capillaries are engorged, and the alveoli and alveolar ducts may be collapsed. The few remaining air spaces are lined with a hyaline-like material (1, 5, 8, 9, 18, 24, 39). In certain stages of the disease the alveolar ducts may be dilated, which accounts for the degree of aeration seen radiographically. There has been criticism that too much emphasis has been placed on the membrane per se and not enough on the atelectasis (21). Briefly, the concept of aspiration of amniotic fluid (4, 8, 9, 21, 25) has been supplanted by many studies which favor an endogenous origin of the disease (2, 12, 13, 20, 26, 35, 36). One study showed the hyaline staining material beneath the basement membrane (12). This report also implicated both endogenous and less significant exogenous factors. Chemically, the membrane is a polysaccharide aldehyde (20, 36) which has been all inclusively termed a protein-carbohydrate (12). No specific therapy has been developed, but the treatment of choice has resolved to a simple formula of high humidity (29, 32, 35, 38, 41) without a water mist supplement (33). There has been a recent suggestion that the treatment be that of left heart failure (19). High oxygen concentrations are not advocated. A new respirator for the treatment of atelectasis, which is probably the significant clinical problem, has been described (7), but its evaluation awaits further experience." @default.
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• W1849517811 title "Hyaline Membrane Disease: Preclinical Roentgen Diagnosis" @default.
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