Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease

Abstract

The pathologic changes in the lungs of 112 infants dying from hyaline membrane disease (HMD) and 64 infants dying from other causes in the years 1967 to 1972 have been reviewed in order to obtain information about the pathogenesis of bronchopulmonary dysplasia (BPD). The results from the infants with HMD showed that: a) From the fourth or fifth day, the surface tension of lung extracts fell, inclusion bodies became more plentiful, and air saccules with patent airways could be inflated with air, even when severe changes due to BPD were present. b) There was a highly statistically significant correlation between the most serious lesions of BPD--damage to airways followed by excessive repair and fibrosis--and the use of high (greater than 35 cm H2O) peak airway pressures during mechanical ventilation in life. c) Damage due to oxygen breathing could not be reliably identified although some of the lesions, particularly edema and fibroplasia in intersaccular septa, may have been caused by oxygen. d) Evidence of pulmonary hypertension was present in infants surviving for more than a month with severe lung damage, and the ductus arteriosus was always open. We conclude that the most important factor in the pathogenesis of BPD following HMD is mechanical trauma to the lung from the use of excessively high peak airway pressures during mechanical ventilation.