title: Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma.
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.
  
  
  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.
authors.affiliation: Department of General Surgery, University Hospital Nijmegen, The Netherlands.
authors.forename: R M
authors.initials: RM
authors.lastname: Roumen
authors.forename: H
authors.initials: H
authors.lastname: Redl
authors.forename: G
authors.initials: G
authors.lastname: Schlag
authors.forename: G
authors.initials: G
authors.lastname: Zilow
authors.forename: W
authors.initials: W
authors.lastname: Sandtner
authors.forename: W
authors.initials: W
authors.lastname: Koller
authors.forename: T
authors.initials: T
authors.lastname: Hendriks
authors.forename: R J
authors.initials: RJ
authors.lastname: Goris
mesh_terms: 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*
chemical_list: 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