The increased microvascular permeability of the adult respiratory distress syndrome (ARDS) results in multiple organ injury with the lungs and subsequently the kidneys as the principal targets. Direct pulmonary injury, for example aspiration of gastric contents, and indirect injury, for instance abdominal sepsis, can lead to the syndrome. The predominant infectious cause of the syndrome is gram-negative aerobic rods. Even in patients with noninfectious causes of the syndrome, the incidence of subsequent pneumonia and sepsis with gram-negative aerobic rods is high so that these organisms contribute greatly to the morbidity and mortality that result from the syndrome. Activation of polymorphonuclear leukocytes and platelets and proteolysis of complement and coagulation components contribute to the pathogenesis of the syndrome, particularly from the indirect or blood-borne causes. Therapy is largely supportive and has not progressed substantially since the introduction of positive end expiratory pressure with mechanical ventilation. The outlook for recovery of lung function of survivors is generally good, but only one in three with the syndrome survives. Because of the inflammatory properties of the syndrome, current interest for therapy centers on parenteral use of nonsteroidal antiinflammatory agents and prostaglandins of the E and I series.