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 inj ury and is not necessarily harmful. However, persistence of intraalveo lar fibrin deposit may lead to hyaline membrane formation and subseque nt alveolar fibrosis, a histologic hallmark of late stages of acute re spiratory 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 sequentia lly 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 thi s syndrome. All patients were admitted to the intensive care unit for the treatment of sepsis, trauma, or shock. In early phases of ARDS, th e 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 +/- 9 1 versus 46 +/- 16 U, p < 0.05). In early ARDS we observed higher leve ls of D dimer in BAL than in patients at risk: 1,841 +/- 827 versus 29 3 +/- 134 ng/ml, p < 0.05. Similarly, values of D dimer in the subacut e 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 cor relation with the polymorphonuclear leukocyte count and with protein c ontent 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 findi ngs expand our understanding of intraalveolar coagulation abnormalitie s by providing evidence of increased fibrin breakdown in this syndrome .