Time course of procoagulant activity and D dimer in bronchoalveolar fluid of patients at risk for or with acute respiratory distress syndrome.

Intraalveolar fibrin deposition is a typical finding in acute lung injury and is not necessarily harmful. However, persistence of intraalveolar fibrin deposit may lead to hyaline membrane formation and subsequent alveolar fibrosis, a histologic hallmark of late stages of acute respiratory distress syndrome (ARDS). Thus, timing of the intraalveolar clotting disorder seems to be critical. To explore the time course of factors contributing to fibrin deposition and resolution, we sequentially analyzed procoagulant activity and fibrin degradation (by D dimer) in bronchoalveolar lavage (BAL) fluid of patients developing ARDS and those at risk for, but finally not developing, the syndrome. A total of 36 bronchoalveolar lavages were performed in 11 patients developing ARDS and 15 lavages in 10 patients at risk for but not developing this syndrome. All patients were admitted to the intensive care unit for the treatment of sepsis, trauma, or shock. In early phases of ARDS, the procoagulant activity (PCA) in BAL was significantly higher than in the patients at risk, 320 +/- 83 U (mean +/- SEM) versus 50 +/- 25 U, p < 0.05. A similar difference was noted in subacute stages (280 +/- 91 versus 46 +/- 16 U, p < 0.05). In early ARDS we observed higher levels of D dimer in BAL than in patients at risk: 1,841 +/- 827 versus 293 +/- 134 ng/ml, p < 0.05. Similarly, values of D dimer in the subacute phase were 2,776 +/- 836 versus 237 +/- 125 ng/ml, p < 0.05. In ARDS as well as in the at-risk group, D dimer in BAL fluid showed good correlation with the polymorphonuclear leukocyte count and with protein content of BAL. There was no correlation between plasma and BAL levels of D dimer. We conclude that in ARDS both the procoagulant pathway and the fibrin degradation are markedly activated compared with these in patients at risk but finally not developing this syndrome. These findings expand our understanding of intraalveolar coagulation abnormalities by providing evidence of increased fibrin breakdown in this syndrome.