The initiating event in all cases is diffuse alveolar damage, initially involving the capillary endothelium but later also the type I alveolar epithelial cells. The type II cells are more resistant to injury.
Cellular damage results in increased capillary permeability, followed by interstitial and intra-alveolar oedema, and fibrin deposition. The alveolar walls become lined with protein-rich oedema and the cellular debris of the necrosed epithelial cells. These so called hyaline membranes, in conjunction with the pulmonary oedema and consequent atelectasis, produce the characteristic "stiff" lung.
The acute oedematous stage is characterised morphologically, by large plum coloured lungs. In the ensuing organising stage, the alveolar spaces become lined by proliferating cuboidal type II cells, and there is variable degrees of interstitial and intra-alveolar fibrosis.
Recovery may occur at any stage with resorption of the oedema and re-expansion of atelectatic areas.
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