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ARTICLE |

Blunt Brain Injury Activates the Coagulation Process

Frieda Hulka, MD; Richard J. Mullins, MD; Edmund H. Frank, MD
Arch Surg. 1996;131(9):923-928. doi:10.1001/archsurg.1996.01430210021004.
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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 1 to 4 hours after injury. Therapeutic interventions need to be implemented immediately to be effective.Arch Surg. 1996;131:923-928

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