Adult respiratory distress syndrome — an update

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Abstract
In adults, acute lung injury or adult respiratory distress syndrome (ARDS) may complicate a wide range of serious medical and surgical conditions, only some of which involve direct pulmonary insult. The characteristic histological feature of ARDS is an intense inflammatory process in the lungs, which may progress to fibrosis. The earliest physiological characteristic is an increase in the protein permeability across the endothelial and epithelial barriers of the lungs. This clinical syndrome is characterized by arterial hypoxaemia and bilateral radiographic infiltrates, which represent protein-rich oedema fluid. In addition there is a neutrophilic and macrophage infiltrate. Pulmonary endothelium is actively involved in the development of ARDS. It alters cell–cell adhesion as the initial step in leucocyte migration which, in turn, changes the permeability that allows protein-rich fluid to move into the interstitium. The quantity of this interstitial oedema may be sufficient to cause bulk flow through the epithelial barrier. There is probably independent epithelial injury. Finally, the endothelium can release and metabolize vasoactive and inflammatory substances, such as endothelins, nitric oxide and cytokines, etc. No single substance is responsible for acute lung injury, but rather a complex interplay exists between diverse pro- and anti-inflammatory mediators.