Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma

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Abstract

Objective

To evaluate the posttraumatic course of several inflammatory mediators or markers (complement components C3, C3a, terminal complement complex, thromboxane B2, C-reactive protein, elastase, and neopterin) in relation to the development of multiple organ failure and mortality.

Design

Prospective study of a selected patient group.

Setting

Surgical intensive care units in three European trauma hospitals.

Patients

Patients (n = 56) with severe blunt trauma (Injury Severity Score of >or=to33).

Interventions

Arterial blood samples were sequentially obtained.

Measurements and Main Results

Nonsurvivors (n = 8) had significantly higher circulating C3a and elastase concentrations on the first postinjury day, compared with survivors (n = 48). No differences between these groups were found for terminal complement complex, thromboxane B2, C-reactive protein, and the neopterin/creatinine ratio.

Conclusion

In multiple trauma patients, excessive triggering of the inflammatory cascade--as expressed by complement activation and stimulation of neutrophils producing elastase--plays an important and early role in the development of multiple organ failure.

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