Blunt brain injury activates the coagulation process

Objective: To measure the prevalence of and characterize coagulopathy in patients with blunt brain injury. Design: Retrospective observation study based on review of medical records. Setting: Acutely injured patients admitted to a level I trauma center. Patients: One hundred fifty-nine patients with evidence of blunt head trauma who had computed tomography of the brain during initial evaluation and a coagulopathy score assigned based on 5 laboratory tests: platelet count, prothrombin time, partial thromboplastin time, fibrinogen level, and D-dimer level. The disseminated intravascular coagulation score ranged from 0 (no coagulopathy) to 15 (severe coagulopathy). Only individuals with intracranial injury based on computed tomography of the brain were designated as brain injured. Main Outcome Measures: Presence of coagulopathy, progression of brain injury, and death. Results: Among the 91 patients with brain injury, 41% had coagulopathy (disseminated intravascular coagulation score ≤5). Of the 68 patients without brain injury, 25% had coagulopathy. The patients with brain injury who developed profound depletion of fibrinogen did so within 4 hours of injury. There were 28 deaths (26 in the group with brain injury and 2 in the group without brain injury). Among patients with brain injury, those with coagulopathy more frequently died (P<.05 by χ² analysis). Patients with brain injury and coagulopathy deteriorated more frequently based on computed tomography criteria. Conclusions: After blunt brain injury, a disseminated intravascular coagulation syndrome can lead to consumptive coagulopathy that is associated with a higher frequency of death. The syndrome develops within I to 4 hours after injury. Therapeutic interventions need to be implemented immediately to be effective.