Key messages

• The acute respiratory distress syndrome (ARDS) is characterized by tachypnea, severe hypoxemia, and the presence of diffuse bilateral pulmonary infiltrates (a reflection of modified pulmonary capillary permeability) in the absence of signs of left ventricular failure. According to a recent consensus definition, the level of hypoxemia distinguishes acute lung injury (PaO2/FiO2 £ 300 mmHg (40 kPa)) from ARDS (PaO2/FiO2 £ 200 mmHg (27 kPa)). The cause of ARDS may be intrathoracic or extrathoracic, but it is usually the earliest sign of a generalized increase in capillary permeability, often accompanying systemic multiple organ dysfunction.

• The pathophysiological mechanisms of ARDS involve complex interactions between activated cells and both humoral and cellular mediators, and the diffusion by these cells and mediators of an initially localized inflammatory reaction, leading to a systemic inflammatory reaction syndrome.

• The principal cells implicated in these reactions are phagocytic cells and cells of the vascular endothelium. Among the mediators involved are the cytokines, active oxygen species, and elements of the complement and coagulation cascades. There are no mediators or groups of mediators specific for ARDS; early identification in bronchoalveolar lavage fluid is more useful than identification in plasma.

• The absence of specific early markers of ARDS and the complex interactions between mediators and cells render therapy using inhibitors of mediators or activated cells difficult.

• Constant improvements in the clinical treatment of ARDS have decreased the mortality of this syndrome, in particular following trauma; new therapeutic approaches are being developed using molecular biological techniques and genetic engineering.

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