A light-microscopic study was undertaken in 21 infants in whom the pathological diagnosis of broncho-pulmonary dysplasia had been made at autopsy. All the babies were premature, and all had been treated with ventilator and oxygen therapy for varying periods of time. The indications for ventilation were the respiratory distress syndrome in 13, and apnoea in 8. Microscopically two patterns of disease were seen: the acute phase and the chronic phase. The acute phase—days 4 to 7—was characterized by alveolar epithelial necrosis, hyaline membrane formation and ‘embryonal’ myxoid type matrix in the alveolar septa with proliferation of reticulin fibres. In the chronic phase— from day 8 onwards—the lungs showed a variegated overall appearance with emphysematous areas alternating with foci of atelectasis; subpleural fibrosis was a distinct feature. The alveolar septa were thickened with diffuse fine fibrosis. The bronchiolar mucosa showed varying degrees of hyperplasia, and there was hypertrophy of bronchiolar smooth muscle. The lymphatics were dilated, especially subpleurally. The blood vessels showed medial hypertrophy and degenerative changes in the intima and elastin. Hyaline membranes were absent. Squamous metaplasia of the bronchiolar mucosa was seen only occasionally. The vascular changes, bronchiolar muscular hyperplasia and alveolar fibrosis were more marked in those infants who survived for the longest periods. Associated complications included pulmonary air leaks in 17 infants; intraventricular haemorrhage in 8, and necrotizing enterocolitis in 4. Dr Ostor was supported by the Olive Hewitt Scholarship for Medical Research, University of Sydney. A light-microscopic study was undertaken in 21 infants in whom the pathological diagnosis of broncho-pulmonary dysplasia had been made at autopsy. All the babies were premature, and all had been treated with ventilator and oxygen therapy for varying periods of time. The indications for ventilation were the respiratory distress syndrome in 13, and apnoea in 8. Microscopically two patterns of disease were seen: the acute phase and the chronic phase. The acute phase—days 4 to 7—was characterized by alveolar epithelial necrosis, hyaline membrane formation and ‘embryonal’ myxoid type matrix in the alveolar septa with proliferation of reticulin fibres. In the chronic phase— from day 8 onwards—the lungs showed a variegated overall appearance with emphysematous areas alternating with foci of atelectasis; subpleural fibrosis was a distinct feature. The alveolar septa were thickened with diffuse fine fibrosis. The bronchiolar mucosa showed varying degrees of hyperplasia, and there was hypertrophy of bronchiolar smooth muscle. The lymphatics were dilated, especially subpleurally. The blood vessels showed medial hypertrophy and degenerative changes in the intima and elastin. Hyaline membranes were absent. Squamous metaplasia of the bronchiolar mucosa was seen only occasionally. The vascular changes, bronchiolar muscular hyperplasia and alveolar fibrosis were more marked in those infants who survived for the longest periods. Associated complications included pulmonary air leaks in 17 infants; intraventricular haemorrhage in 8, and necrotizing enterocolitis in 4. Dr Ostor was supported by the Olive Hewitt Scholarship for Medical Research, University of Sydney.
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