Abstract

The lung responds to acute injury of diverse aetiology via a series of common pathways. The pathological changes caused by a variety of toxic and infectious agents evolve over time from endothelial and epithelial injury to alveolar consolidation and finally to fibroblast proliferation and collagen deposition. Widespread acute injury to the lung produces diffuse alveolar damage [33], a well characterized anatomical entity that forms the basis of the protean clinical picture of acute respiratory failure. This clinical picture has been identified in the past by a host of terms, creating some confusion. Recently, a panel of experts clarified the definition of acute lung injury [4]. The terms acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are proposed to describe the continuum of a syndrome of primary respiratory failure, characterized by the acute onset of dyspnoea, hypoxaemia and bilateral consolidation on the chest radiograph (table 1). ALI is considered to be the early stage of ARDS, with milder abnormalities of respiratory function, and it may subsequently evolve into the more severe and more easily diagnosed syndrome of ARDS. The major reason to define ALI is to facilitate experimental and clinical investigation of the early stages of ARDS, in order to improve the early recognition and treatment of this syndrome [4].

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