Hyaline membrane disease, respiratory distress, and surfactant deficiency

Clinical observations and measurements of arterial blood gas tensions and pH were made in 55 infants surviving for more than 4 hours but dying in the newborn period. After death the pressure-volume characteristics of the lung were investigated and correlated with the estimation of pulmonary surfacta...

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Veröffentlicht in:Pediatrics (Evanston) 1968-11, Vol.42 (5), p.758-768
Hauptverfasser: Reynolds, E O, Roberton, N R, Wigglesworth, J S
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Sprache:eng
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Zusammenfassung:Clinical observations and measurements of arterial blood gas tensions and pH were made in 55 infants surviving for more than 4 hours but dying in the newborn period. After death the pressure-volume characteristics of the lung were investigated and correlated with the estimation of pulmonary surfactant and the histological appearance of the lung. Infants dying with deficiency of pulmonary surfactant always had clinical respiratory distress, unless they were unable to make spontaneous respiratory efforts on which an assessment could be based, and hyaline membranes, dilatation of alveolar ducts, and atelectasis were always present in the lungs. Calculated right-to-left shunts were no greater at 4 hours of age in infants dying from hyaline membrane disease than in infants who died from other causes. Clinical respiratory distress was associated with a variety of conditions, and terminology is discussed. Normal pulmonary surface activity was found in infants who had hyaline membrane formation due to massive pulmonary hemorrhage or hydrops fetalis. Pulmonary surfactant was present in functionally significant amounts by the twenty-fourth week of gestation in infants dying from illnesses other than hyaline membrane disease and increased in amount as term was approached. It is concluded that the state at birth of the mechanism responsible for the production of pulmonary surfactant is the crucial factor determining the development of hyaline membrane disease, and that this illness arises because the synthetic mechanism is so immature that it cannot supply the demand for surfactant or because it has been damaged by prenatal or intrapartum asphyxia, or because of the interaction of these two influences.
ISSN:0031-4005
1098-4275
DOI:10.1542/peds.42.5.758