The acute respiratory distress syndrome: pathogenesis and treatment.
The acute respiratory distress syndrome: pathogenesis and treatment.
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DOI：
10.1146/annurev-pathol-011110-130158
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Zemans RL
中科院分区：
文献类型：
--
作者：
Matthay MA;Zemans RL
急性呼吸窘迫综合征（ARDS）在美国每年约有20万例危重患者死亡，死亡率为40%。ARDS是由富含蛋白质的肺水肿引起的，其导致严重的低氧血症和二氧化碳排泄受损。与ARDS发展相关的临床疾病包括败血症、肺炎、胃内容物吸入和严重创伤。肺损伤主要由对肺的内皮和上皮屏障的嗜中性粒细胞依赖性和血小板依赖性损伤引起。由于肺上皮屏障损伤，阻止了肺泡水肿液的清除并剥夺了肺足够量的表面活性剂，因此消退延迟。淋巴细胞可能在肺损伤的消退中发挥作用。采用肺保护性治疗策略后，死亡率显著降低。然而，没有有效的药物治疗，尽管目前正在临床试验中测试的基于细胞的疗法和其他疗法可能为ARDS提供新的治疗方法。
The acute respiratory distress syndrome (ARDS) causes 40% mortality in approximately 200,000 critically ill patients annually in the United States. ARDS is caused by protein-rich pulmonary edema that causes severe hypoxemia and impaired carbon dioxide excretion. The clinical disorders associated with the development of ARDS include sepsis, pneumonia, aspiration of gastric contents, and major trauma. The lung injury is caused primarily by neutrophil-dependent and platelet-dependent damage to the endothelial and epithelial barriers of the lung. Resolution is delayed because of injury to the lung epithelial barrier, which prevents removal of alveolar edema fluid and deprives the lung of adequate quantities of surfactant. Lymphocytes may play a role in resolution of lung injury. Mortality has been markedly reduced with a lung-protective ventilatory strategy. However, there is no effective pharmacologic therapy, although cell-based therapy and other therapies currently being tested in clinical trials may provide novel treatments for ARDS.
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