The acute respiratory distress syndrome (ARDS) was only recognised as a distinct clinical entity less than 50 years ago.¹ It arose as a consequence of the success of modern resuscitation and organ support and was first described in severely injured military personnel. It is defined by the development of rapidly progressing respiratory failure, usually within 24–48 hours of the initiating insult. Plain chest radiographs show widespread airspace shadowing with a pattern similar to cardiogenic pulmonary oedema. However, when measured, left sided cardiac pressures are normal and the pulmonary oedema fluid has a high protein content.

This picture of normal cardiac filling pressures and high air space protein content suggested that the central pathophysiology was a result of increased pulmonary epithelial/endothelial permeability. Histological examination of biopsy and autopsy specimens showed widespread epithelial and endothelial damage and radioisotope studies confirmed that lung permeability was abnormal.

Histological studies also indicated that an intense inflammatory response was occurring in the lungs of patients with established ARDS.^2,3 In addition to proteinaceous material, the air spaces were filled with acute inflammatory cells—predominantly neutrophils and macrophages. This early phase of ARDS has been characterised as the “exudative phase”. Limited studies suggest that this may be rapidly followed by the proliferation of type II pneumocytes with the beginnings of alveolar basement repair. Fibrosis is also a feature of this phase with the migration of fibroblasts and myoblasts into the fibrinous intra-alveolar exudate. A subsequent fibrotic phase can then occur with extensive lung remodelling, and this may produce a situation of irreversible end stage lung disease. It must be emphasised, however, that this orderly pattern is based on very limited biopsy material and many patients with ARDS make a very good functional recovery over a prolonged period of time.

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