Abstract

The adult respiratory distress syndrome is a condition of life-threatening organ failure triggered by blood-borne factors and challenges which arrive via the airways. Vascular damage is a necessary, but often not sufficient criterion for ARDS, which is observed in an acute and chronic form. There is a consensus that neutrophils and their products contribute to the pathogenesis of the syndrome, and that lung vascular tone regulation and endothelial and epithelial cell permeability are affected in ARDS. Whereas the precise roles of individual mediators for the development of ARDS are still ill-defined, a synergism between lipid mediators and other injurious principles is recognized. Chronic ARDS is a proliferative disorder which may require different treatment strategies than acute ARDS. Specific treatment modalities which inhibit the interaction between activated neutrophils and the lung endothelium, and surfactant replacement might have a future as early therapy approaches.

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