Journal
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 6
Volume 6, Issue -, Pages 147-163Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-011110-130158
Keywords
acute lung injury; pulmonary edema
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL103772, R37HL051856, R01HL051854] Funding Source: NIH RePORTER
- NHLBI NIH HHS [K08 HL103772, R37HL51856, R37HL51854, R01 HL051854, R37 HL051856, K08 HL103772-01, R01 HL131608] Funding Source: Medline
- NIAID NIH HHS [P01AI1053194] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available