title: Time for changing coagulation management in trauma-related massive bleeding.
abstract: OBJECTIVE
  New insights into the pathophysiology of trauma-induced coagulopathy, the increasing availability of point-of-care devices and awareness of side effects of intravenous fluids and traditional fresh frozen plasma therapy has encouraged new concepts for managing massive blood loss.
  
  
  RESULTS
  Trauma-induced coagulopathy primarily results from blood loss, hypovolemia-induced activation of the protein C system and consequent increase of the fibrinolytic potential, whereas hemodilution, localized consumption of clotting factors and platelets, hypothermia, acidosis, anemia and hypocalcemia further decrease the hemostatic potential. The widespread use of viscoelastic devices highlighted the importance of the contribution of fibrinogen to clot firmness, a precondition for cessation of bleeding. The evidence is growing that targeted therapy using coagulation factor concentrates guided by viscoelastic measurements enables effective correction of severe coagulopathy.
  
  
  CONCLUSIONS
  During massive blood loss, viscoelastic measurements should guide aggressive treatment of deficiency or hyperfibrinolysis or both. In addition, the impact of contributing factors should be considered and as far as possible corrected. New data underscore the importance of avoiding hypoperfusion, and the use of coagulation factor concentrates should enable more effective correction of coagulopathy.
authors.affiliation: Department of General and Surgical Critical Care Medicine, Innsbruck Medical University, Austria.
authors.forename: Dietmar
authors.initials: D
authors.lastname: Fries
authors.forename: Petra
authors.initials: P
authors.lastname: Innerhofer
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schobersberger
mesh_terms: D000138:Acidosis / Q000150:complications / Q000517:prevention & control; D000740:Anemia / Q000150:complications / Q000517:prevention & control; D001778:Blood Coagulation Disorders / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*; D001779:Blood Coagulation Factors / Q000502:physiology / Q000627:therapeutic use*; D015942:Factor VIIa / Q000627:therapeutic use; D005176:Factor XIII / Q000627:therapeutic use; D005340:Fibrinogen / Q000627:therapeutic use; D006438:Hemodilution / Q000009:adverse effects; D006801:Humans; D006996:Hypocalcemia / Q000150:complications / Q000517:prevention & control; D007035:Hypothermia / Q000150:complications / Q000517:prevention & control; D010949:Plasma; D017713:Platelet Transfusion / Q000379:methods; D011994:Recombinant Proteins / Q000627:therapeutic use; D012307:Risk Factors; D014947:Wounds and Injuries / Q000150:complications / Q000503:physiopathology*
chemical_list: D001779:Blood Coagulation Factors; D011994:Recombinant Proteins; C025667:prothrombin complex concentrates; D005340:Fibrinogen; D005176:Factor XIII; C103587:recombinant FVIIa; D015942:Factor VIIa