Pathophysiology of the adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF)--a hypothesis.
A review of the recent literature concerning the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF) is presented. We hypothesize that the two syndromes probably have a common pathophysiology, with ARDS as the first occurring organ failure. The clinical situations that may cause ARDS and MOF are characterized by massive and prolonged activation of the complement system. This results in activation of granulocytes with ensuing release of lysosomal enzymes, toxic oxygen products and prostaglandins, which collectively cause endothelial damage and permeability changes. In the lungs interstitial and alveolar edema develops, with an impaired alveolo-capillary gas exchange. Oxygen diffusion in the peripheral tissues is impeded by the same mechanism, ultimately resulting in organ failure. Hypoxia may cause additional microvascular lesions, as toxic oxygen radicals are produced during reoxygenation. The implications of this hypothesis for the prevention and therapy of ARDS and MOF are discussed.
D003167:Complement Activation; D006098:Granulocytes / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D009102:Multiple Organ Failure / Q000503:physiopathology*; D012128:Respiratory Distress Syndrome / Q000276:immunology / Q000503:physiopathology* / Q000517:prevention & control