Coagulopathy in traumatic brain injury

Abstract

Head injury is associated with delayed or progressive bleeding, ischemic secondary injury, and microvascular thrombosis. The general prevalence of trauma-associated coagulopathy in trauma can be as high as 97.2 %. A coagulopathy after head injury that develops within 24 h is associated with 55 % mortality, while the mortality was 23 % for those who developed coagulopathy after 24 h. It is important to understand the effects of drugs on the coagulation system. Procoagulants, Desmopressin, Cryoprecipitate fresh frozen plasma, Tranexemic acid, Aminocaproic acid, Prothrombin, Warfarin, Heparin, Apixaban, Dabigatran, Bilvalirudin, Aspirin, Clopidogrel, and Abciximab are discussed. Goal directed therapy of coagulation abnormalities diagnosed with TEG might lower the morbidity and mortality associated with trauma. Hemorrhagic contusions are the lesions most likely to expand on intracranial CT especially within the first two hours of the trauma. The greatest risk factor for progression of hemorrhagic lesion is coagulopathy. Management of bleeding and coagulopathy following traumatic brain injury is paramount to a successful outcome. Early monitoring of coagulation, early administration of FFP and platelets, maintaining adequate calcium and fibrinogen levels, treatment with desmopressin, prothrombin complex concentrate, activated factor VII, and tranexamic acid play a role in the treatment of TBI. Early therapeutic intervention of coagulopathy based on early goal directed therapeutic treatments has been shown to reduce the need for packed red blood cells, fresh frozen plasma, and platelets. Head injury patients are increasingly on new oral anticoagulants. The use of PCC carries the increased risks of both venous and arterial thrombosis during the recovery period; therefore, the risk of a thrombotic complication due to treatment with PCCs or Idarucizumab should be weighed against the need for rapid and effective correction of coagulopathy. While the CRASH-2 trial showed treatment with tranexamic acid within 1 h was associated with a significant decrease in the rate of death due to bleeding, treatment of trauma patients with tranexemic acid more than 3 h after injury was associated with an increased chance of death due to bleeding.