Advances in critical care for the nephrologist: acute lung injury/ARDS.
Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are a major cause of acute respiratory failure in the critically ill patient. ALI and ARDS are characterized by the acute onset of severe hypoxemia and bilateral pulmonary infiltrates in the absence of clinical evidence for left atrial hypertension. These conditions are differentiated from one another by the ratio of the partial pressure of oxygen in the arterial blood to the inspired fraction of oxygen; ARDS requires a more severe oxygenation defect. ALI and ARDS may occur in association with a number of clinical disorders, including sepsis, pneumonia, aspiration, trauma including inhalational injury, and blood transfusions. The mortality rate remains high, in the range of 25% to 40%. The pathophysiology of ALI/ARDS involves resident lung cells, including endothelial and epithelial cells, as well as neutrophils, monocytes/macrophages, and platelets. When ALI/ARDS is complicated by acute kidney injury, mortality increases substantially. Several supportive and pharmacologic therapies have been tested in clinical trials. Of these, a low tidal volume, lung protective ventilation strategy is the only strategy that has been demonstrated in a large, multicenter randomized clinical trial to reduce mortality for patients with ALI/ARDS. Based on a recent randomized trial, a conservative fluid management strategy reduces the duration of mechanical ventilation without increasing the incidence of renal failure. Pharmacologic strategies and other ventilator management strategies have not been successful to date; however, several randomized, placebo controlled treatment trials are ongoing.
Liu
Kathleen D
KD
Division of Nephrology and Critical Care Medicine, Box 0532, University of California, San Francisco, San Francisco, CA 94143-0532, USA. Kathleen.Liu@ucsf.edu
Matthay
Michael A
MA
D003422:Critical Care; D006801:Humans; D009398:Nephrology; D012128:Respiratory Distress Syndrome / Q000503:physiopathology / Q000628:therapy*