Advances in critical care for the nephrologist: acute lung injury/ARDS

Abstract

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.

Figure 1.

(A) Comparison of the alveolar and renal tubular epithelium. Left, cross section of an alveolus. The alveolar epithelium is composed of a mixture of type I and II cells. Water and ion channels are found on the apical and basolateral surfaces as shown. Right, cross section of the distal convoluted tubule. The renal tubular epithelium at this level is composed of principal cells and intercalated cells. ENaC, epithelial Na+ channel; CFTR, cystic fibrosis transmembrane conductance regulator; AQP, aquaporin. (B) Multiple pathogenic processes contribute to alveolar injury during acute lung injury/acute respiratory distress syndrome.

Figure 2.

Fluid management strategies in the FACTT trial. Left, fluid conservative strategy, in which diuretics were administered to a target central venous pressure less than 4 mmHg or pulmonary artery occlusion pressure less than 8 mmHg. Right, fluid liberal strategy in which fluids were administered to maintain a central venous pressure between 10 and 14 mmHg or pulmonary artery occlusion pressure between 14 and 18 mmHg.