Acute respiratory distress syndrome is caused pulmonary edema that becomes protein rich. It causes severe hypoxemia and an impaired carbon dioxide excretion. The clinical disorders that are associated with ARDS include
• Aspiration of gastric contents
• Major trauma
The lung injury is caused mainly by neutrophils-dependent and platelet-dependent damage to the endothelial and epithelial barriers of the lung. Resolution is delayed because of the injury to the lung epithelial barrier that prevents removal of alveolar edema fluid and deprives the lung of adequate facilities of surfactant. Lymphocytes play an important role in the resolution of the lung injury. With a lung protective ventilatory strategy, mortality is considerably reduced.
In the acute phase of ARDS which lasts in the first week, there is evidence of interstitial and alveolar edema with accumulation of neutrophils, macrophages and red blood cells in the alveoli. There is also evidence of both endothelial and epithelial injury. In the sub-acute phase that lasts during the second week of the syndrome, some of the edema is reabsorbed and there is evidence of attempts at repair with proliferation of alveolar epithelial type II cells. There may also be infiltration of fibroblasts and some evidence of collagen deposition. In the chronic phase after a couple of weeks, there is resolution of acute neutrophilic infiltrate with more mononuclear cells and alveolar macrophages in the alveoli. In many patients, resolution progresses without fibrosis and simply with gradual resolution of the edema and acute inflammation.