[Thromboxane A2 and granulocyte elastase after severe trauma--relationship to complications and survival rates]

Of 64 polytraumatized patients with a mean injury severity score of 33.1, 42 showed marked systemic release of thromboxane B2 and granulocyte elastase during the initial 18 hours after trauma, reaching peak arterial levels of greater than 1,000 pg/ml and ng/ml, respectively. If those patients ("responders": plasma TXB2 greater than 250 pg/ml) were compared with the remaining 22 ("non-responders": TXB2 less than 250 pg/ml) the following became obvious: "Late" mortality (greater than 3 d) was 31% in responders, which is significantly higher than in non-responders (9%). No correlation was observed between "early" mortality (less than 3 d) and mediator release. There was no difference in the incidence of the adult respiratory distress syndrome (ARDS) (38% versus 32%) or the late sepsis syndrome (17% versus 18%) between responders and non-responders. Morbidity, however, differed markedly in that ARDS in responders was associated with significantly higher elastase levels, a higher mortality and 10 times higher incidence of sepsis as compared to responders without ARDS. ARDS in non-responders, by contrast, did not change elastase maxima or the mortality rate as compared to non-responders without ARDS. It is concluded that TXB2 is not a predictor of posttraumatic ARDS, but is related to a complicated course, in particular to sepsis and mortality. Elastase with high probability predicts ARDS and/or the late sepsis syndrome. Simultaneous determination of TXB2 further enhances the predictive value of elastase.