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The Fibrinolytic Defect in Adult Respiratory Distress Syndrome: A New Therapeutic Opportunity?

Prominent alveolar fibrin deposition characterizes the adult respiratory distress syndrome (ARDS). Increased local expression of procoagulant activity and concurrently decreased fibrinolytic activity promote alveolar fibrin deposition in the lungs in ARDS. Thrombi in the lung vasculature and disseminated intravascular coagulation also occur in association with ARDS, further suggesting that disordered fibrin turnover may contribute to the pathogenesis of the syndrome. The fibrinolytic defect in ARDS potentiates alveolar fibrin deposition and organization of the fibrinous neomatrix, resulting in lung dysfunction and fibrotic repair. Similar disorders of pathways of fibrin turnover occur in systemic sepsis and these have recently been exploited to clinical advantage. Anticoagulant strategies have successfully been used in recent interventional trials in septic patients. The results of these trials suggest the possibility that this approach could be extrapolated to protect the lung in ARDS. Recent preclinical trials demonstrate that that similar anticoagulant strategies are feasible and effective in primates with evolving ARDS. Additional preclinical studies are now being performed to determine if fibrinolytic interventions likewise protect against lung injury in ARDS. Small clinical trials and case reports suggest that fibrinolysins can be of clinical benefit in selected patients with ARDS and support this approach. However, these agents increase the risk of bleeding. At this time, the use of fibrinolysins in ARDS patients is not routine and their place in the therapy of ARDS remains to be established.