Adult respiratory distress syndrome. Pathogenesis and treatment

ARDS is a complication of septic and traumatic shock. It ranges from slight pulmonary dysfunction to forms so severe as to be incompatible with life. There seem to be initial pathogenic differences between sepsis-induced and trauma-induced ARDS, in that activation of granulocytes is primarily involved in the former and activation of the clotting system during a fibrinolysis-inhibition phase in the latter. In the later course the granulocyte-mediated and the coagulation-mediated injury can potentially amplify each other's effects in several positive feedback systems. In the end stage the two forms involve similar pathogenic mechanisms which may include production of oxygen radicals. Therapy aims primarily to eradicate the initiating event. Firm data support shock treatment with dextran-70 and early or prophylactic ventilator treatment using positive end-expiratory pressure. Despite lack of conclusive evidence, high-dose corticosteroids in one or two doses should be given very early, at least in sepsis-induced ARDS. Other agents which may be tried early in the course of ARDS include prostaglandin E1, cyclooxygenase inhibitors and oxygen radical scavengers.