Lung injury in the adult respiratory distress syndrome (ARDS) may be mediated through a variety of mechanisms and may involve the interaction of a number of systems involved in the inflammatory reaction--complement, granulocytes, prostaglandins and platelets. Studies in animals, involving the infusion of endotoxin, have produced convincing evidence that these agents can cause pulmonary vascular injury and a syndrome resembling human ARDS. Direct evidence of these pathogenic mechanisms in man is lacking, however, but some suggestive clues have emerged in the last few years that support this general scheme. Secondary lung injury through inappropriate fluid administration, sepsis, oxygen toxicity and barotrauma is potentially avoidable. Improved understanding of the pathophysiology of ARDS and improved hemodynamic monitoring should allow minimising of fluid administration and positive end-expiratory pressure in the management of these patients without dangerous impairment of cardiac output. Such an approach, combined with the avoidance of colloid in the early stages of the disease, and the use of vasoactive agents to support cardiac output if necessary, should minimise edema formation and barotrauma and maximise tissue oxygenation. Pulmonary sepsis continues to play an important role in ARDS. Patients are frequently infected after the initial pulmonary injury; such patients have a far worse prognosis than those who are not infected. Until ways are established at a cellular level to minimise colonisation of the upper respiratory tract, reliance must be placed on avoidance of cross infection by strict personal hygiene, avoidance of prophylactic antibiotics, and prompt, vigorous treatment of suspected pulmonary infection.