Bronchopulmonary Dysplasia in the Adult 1
The American review of respiratory disease (Impact Factor: 10.19). 02/1983; 127(1):117-20. DOI: 10.1164/arrd.19126.96.36.199
We describe 3 patients with adult respiratory distress syndrome that eventuated in a pathologic picture of honeycomb lung and a radiographic picture of variably cystic lung super-imposed on a background of diffuse alveolar infiltrates. All 3 patients had been treated with unusually high pressures of PEEP as well as high concentrations of oxygen for long periods of time (3 to 7 wk). Microscopically, the cystic structures in our patients appeared to be derived from collapse and fibrosis of the alveolar parenchyma with dilatation of the alveolar ducts. We suggest that this process is morphologically and radiographically similar to bronchopulmonary dysplasia as seen in the newborn.
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ABSTRACT: We have produced experimental diffuse interstitial pulmonary fibrosis in rats with a combination of low and repeated doses of paraquat plus continuous exposure to normobaric 74% O2 in the breathing air for several weeks. Pulmonary fibrosis was evaluated histologically and biochemically, through the determination of total collagen content in the lung. Our procedure is characterized by low initial mortality, the development of extensive distortion of the pulmonary architecture, and the presence of severe and diffuse interstitial fibrosis. The model was compared with bleomycin-induced pulmonary fibrosis in the same rat strain, in which the process is focal and leaves most of the lung unaffected. We conclude that lung damage produced by the combination of low doses of paraquat plus normobaric 74% O2 concentration in the breathing air is an adequate experimental model of diffuse interstitial pulmonary fibrosis as it occurs in many of the human cases of this condition.
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ABSTRACT: The effects of high pressure mechanical pulmonary ventilation at a peak inspiratory pressure of 40 cmH(2)O were studied on the lungs of healthy newborn pigs (14-21 days after birth). Forty percent oxygen in nitrogen was used for ventilation to prevent oxygen intoxication. The control group (6 pigs) was ventilated for 48 hours at a peak inspiratory pressure less than 18 cmH(2)O and a PEEP of 3-5 cmH(2)O with a normal tidal volume, and a respiratory rate of 20 times/min. The control group showed few deleterious changes in the lungs for 48 hours. Eleven newborn pigs were ventilated at a peak inspiratory pressure of 40 cmH(2)O with a PEEP of 3-5 cmH(2)O and a respiratory rate of 20 times/min. To avoid respiratory alkalosis, a dead space was placed in the respiratory circuit, and normocarbia was maintained by adjusting dead space volume. In all cases in the latter group, severe pulmonary impairments, such as abnormal chest roentgenograms, hypoxemia, decreased total static lung compliance, high incidence of pneumothorax, congestive atelectasis, and increased lung weight were found within 48 hours of ventilation. When the pulmonary impairments became manifest, 6 of the 11 newborn pigs were switched to the conventional medical and ventilatory therapies for 3-6 days. However, all of them became ventilator dependent, and severe lung pathology was found at autopsy. These pulmonary insults by high pressure mechanical pulmonary ventilation could be occurring not infrequently in the respiratory management of patients with respiratory failure.
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