title: Emerging treatment strategies for trauma-induced coagulopathy.
abstract: BACKGROUND
  Trauma-induced coagulopathy has a multifactorial aetiology. Coagulopathy is related to blood loss including consumption of clotting factors and platelets and haemodilution. Additionally hyperfibrinolysis, hypothermia, acidosis and metabolic changes affect the coagulation system.
  
  
  METHODS
  This is a review of pathophysiology and new treatment strategies for trauma-induced coagulopathy.
  
  
  RESULTS
  Paradigms are actively changing and there is still a shortage of data. The aim of any haemostatic therapy is to control bleeding and minimize blood loss and transfusion requirements. Transfusion of allogeneic blood products as well as trauma-induced coagulopathy cause increased morbidity and mortality. Current opinion is based on present studies and results from small case series, combined with findings from experimental studies in animals, in vitro studies and expert opinions, as opposed to large, randomized, placebo-controlled studies. A summary of new and emerging strategies, including medical infusion and blood products, to beneficially manipulate the coagulation system in the critically injured patient is suggested.
  
  
  CONCLUSIONS
  Future treatment of trauma-induced coagulopathy may be based on systemic antifibrinolytics, local haemostatics and individualized point-of-care-guided rational use of coagulation factor concentrates such as fibrinogen, prothrombin complex concentrate, recombinant factor VIIa and factor XIII. The authors speculate that timely and rational use of coagulation factor concentrates will be more efficacious and safer than ratio-driven use of transfusion packages of allogeneic blood products. Copyright © 2011 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
authors.affiliation: Centre for Haemostasis and Thrombosis, Guy's and St Thomas' NHS Foundation Trust, St Thomas' Hospital, London, UK.
authors.forename: B
authors.initials: B
authors.lastname: Sorensen
authors.forename: D
authors.initials: D
authors.lastname: Fries
mesh_terms: D000138:Acidosis / Q000209:etiology; D000740:Anemia / Q000209:etiology; D000933:Antifibrinolytic Agents / Q000627:therapeutic use; D001458:Bandages; D001778:Blood Coagulation Disorders / Q000628:therapy*; D001779:Blood Coagulation Factors / Q000627:therapeutic use; D005342:Fibrinolysis / Q000502:physiology; D006470:Hemorrhage / Q000628:therapy*; D006489:Hemostatic Techniques; D006490:Hemostatics / Q000627:therapeutic use; D006801:Humans; D007035:Hypothermia / Q000209:etiology; D010949:Plasma; D017713:Platelet Transfusion / Q000379:methods; D019095:Point-of-Care Systems; D012151:Resuscitation / Q000379:methods; D035703:Therapies, Investigational / Q000379:methods; D014148:Tranexamic Acid / Q000627:therapeutic use; D014947:Wounds and Injuries / Q000150:complications / Q000628:therapy*
chemical_list: D000933:Antifibrinolytic Agents; D001779:Blood Coagulation Factors; D006490:Hemostatics; C025667:prothrombin complex concentrates; D014148:Tranexamic Acid