Acute lung injury

Abstract

Acute lung injury (ALI), first described by Ashbaugh in 1967 (1), is a disorder with varying degrees of pulmonary cellular damage (parenchymal and vascular) that alters alveolar capillary membrane permeability, produces accumulation of noncardiogenic extravascular lung water, and results in hypoxic respiratory failure. Patients with this syndrome have dyspnea, refractory hypoxia, reduced lung compliance, and diffuse radiologic changes. Acute respiratory distress syndrome (ARDS) is a more severe subset of ALI characterized by dyspnea, refractory hypoxemia, decreased lung compliance, and diffuse radiologic changes that occur in the absence of cardiac failure or chronic lung disease. The American-European Consensus Conference on ARDS of 1994 defines ALI as “a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension.” It is associated most often with sepsis syndrome, aspiration, primary pneumonia, or multiple traumas. Much less common associations include cardiopulmonary bypass, multiple transfusions, fat embolism, and pancreatitis. ALI and ARDS are acute in onset and persistent, for example, lasting days to weeks; are associated with one or more known risk factors; are characterized by arterial hypoxemia resistant to oxygen therapy alone; and demonstrate diffuse radiologic infiltrates. Chronic lung diseases such as interstitial pulmonary fibrosis and sarcoidosis, which would technically meet the criteria for the chronicity, are excluded by this definition (2). The criteria recommended by this consensus committee are enumerated in Table 1. This definition emphasizes that ALI/ARDS is not the result of primary cardiac disease as the cause of the hypoxia and radiographic findings (2), although patients with this condition can become fluid overloaded or develop concurrent heart failure (3).