Hulka F, Mullins R J, Frank E H
Department of Surgery, Oregon Health Sciences University, Portland, USA.
Arch Surg. 1996 Sep;131(9):923-7; discussion 927-8. doi: 10.1001/archsurg.1996.01430210021004.
To measure the prevalence of and characterize coagulopathy in patients with blunt brain injury.
Retrospective observation study based on review of medical records.
Acutely injured patients admitted to a level I trauma center.
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.
Presence of coagulopathy, progression of brain injury, and death.
Among the 91 patients with brain injury, 41% had coagulopathy (disseminated intravascular coagulation score > or = 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 chi 2 analysis). Patients with brain injury and coagulopathy deteriorated more frequently based on computed tomography criteria.
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.
