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June 19, 1991

Critical Care Medicine

JAMA. 1991;265(23):3109-3111. doi:10.1001/jama.1991.03460230059009

Considerable basic and clinical research has been devoted to understanding the natural history, pathophysiology, and pathogenesis of acute lung injury. Several neutrophil-dependent and neutrophil-independent mechanisms are probably important in mediating the initial phase of acute lung injury.1,2 The injury involves the airways, the interstitium, and the pleural spaces as well as the endothelial and the epithelial barriers of the lung.1,2 The original description of acute lung injury (also known as the adult respiratory distress syndrome) emphasized that it is a clinical syndrome of acute respiratory failure with bilateral roentgenographic infiltrates from both atelectasis and noncardiogenic pulmonary edema.3 Although this initial description was useful, it became apparent that an expanded definition was needed to achieve better precision in identifying the mechanisms responsible for acute lung injury and to determine the prognosis for survival.

An expanded definition has, therefore, been developed that includes a proposed semiquantitative scoring