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


METHODS
Prospective study of a selected patient group.


METHODS
Surgical intensive care units in three European trauma hospitals.


METHODS
Patients (n = 56) with severe blunt trauma (Injury Severity Score of > or = 33).


METHODS
Arterial blood samples were sequentially obtained.


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. Five patients died before day 5. Eighteen patients developed multiple organ failure, which was diagnosed from day 5 onward, leaving 33 patients without multiple organ failure. The patients with subsequent multiple organ failure showed significantly higher mean circulating concentrations of C3a (914 +/- 190 [SEM] ng/mL), terminal complement complex (57 +/- 17 U/mL), and thromboxane B2 (275 +/- 37 pg/mL) at the first postinjury day than the patients without multiple organ failure (566 +/- 110 ng/mL, 27 +/- 2 U/mL, and 169 +/- 14 pg/mL, respectively). In patients with multiple organ failure, elastase concentrations were significantly higher on days 2, 3, 4, and 5 postinjury. Neopterin/creatinine ratios, on the other hand, were significantly higher in patients with multiple organ failure when the multiple organ failure had already become established (on days 8 and 10).


CONCLUSIONS
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.
Roumen
R M
RM
Department of General Surgery, University Hospital Nijmegen, The Netherlands.
Redl
H
H
Schlag
G
G
Zilow
G
G
Sandtner
W
W
Koller
W
W
Hendriks
T
T
Goris
R J
RJ
D000293:Adolescent; D000328:Adult; D000368:Aged; D001708:Biopterins / Q000031:analogs & derivatives / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D003176:Complement C3 / Q000032:analysis; D015926:Complement C3a / Q000032:analysis; D015938:Complement Membrane Attack Complex / Q000032:analysis; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015601:Injury Severity Score; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood; D009104:Multiple Trauma / Q000097:blood* / Q000401:mortality; D019798:Neopterin; D010196:Pancreatic Elastase / Q000097:blood; D011446:Prospective Studies; D013929:Thromboxane B2 / Q000097:blood; D014949:Wounds, Nonpenetrating / Q000097:blood*
D003176:Complement C3; D015938:Complement Membrane Attack Complex; D018836:Inflammation Mediators; D001708:Biopterins; D013929:Thromboxane B2; D019798:Neopterin; D015926:Complement C3a; D002097:C-Reactive Protein; D010196:Pancreatic Elastase