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

Abstract

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.

Prospective study of a selected patient group.

Surgical intensive care units in three European trauma hospitals.

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

Arterial blood samples were sequentially obtained.

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.

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.