Fibrinolytic Activation in Patients with Progressive Intracranial Hemorrhage after Traumatic Brain Injury.

Progression of intracranial hemorrhage (PICH) is a significant cause of secondary brain injury in patients with traumatic brain injury (TBI). Previous studies have implicated a variety of mediators that contribute to PICH. We hypothesized that patients with PICH would display either a hypocoagulable state, hyperfibrinolysis, or both. We conducted a prospective study of adult trauma patients with isolated TBI. Blood was obtained for routine coagulation assays, platelet count, fibrinogen, thrombelastography, markers of thrombin generation, and markers of fibrinolysis at admission and 6, 12, 24, and 48 h. Univariate analyses were performed to compare baseline characteristics between groups. Linear regression models were created, adjusting for baseline differences, to determine the relationship between individual assays and PICH. One hundred forty-one patients met entry criteria, of whom 71 had hemorrhage progression. Patients with PICH had a higher Injury Severity Score and Abbreviated Injury Scale score (head), a lower Glasgow Coma Scale score, and lower plasma sodium on admission. Patients with PICH had higher D-dimers on admission. After adjusting for baseline differences, elevated D-dimers remained significantly associated with PICH compared to patients without PICH at admission. Hypocoagulation was not significantly associated with PICH in these patients. The association between PICH and elevated D-dimers early after injury suggests that fibrinolytic activation may contribute to PICH in patients with TBI.

Blood Ethanol Levels Are Not Related to Coagulation Changes, as Measured by Thromboelastography, in Traumatic Brain Injury Patients.

BACKGROUND: Brain injury is a leading cause of death and disability in trauma patients. Ethanol (EtOH) use near the time of injury may contribute to worse outcomes in these patients by exacerbating coagulopathy. There are limited data regarding the effects of EtOH on coagulation and progression of traumatic intracranial hemorrhage (TICH). METHODS: We performed a retrospective analysis of a prospective observational study of 168 trauma patients with TBI at an urban level 1 trauma center. Thromboelastography (TEG) was performed on admission and over the subsequent 48 hours. Demographic, physiologic, and outcomes data were collected. Computed tomography imaging of the head performed within the first 48 hours of admission was analyzed for progression of TICH. RESULTS: Thirty-six percent of patients (n = 61) had positive blood EtOH on admission (median EtOH level = 198 mg/dL [range, 16-376 mg/dL]). EtOH-positive patients were less severely injured than EtOH-negative patients (P = 0.01). Other admission demographic and physiologic variables were similar between groups. There were no significant differences in TEG values between EtOH-positive and EtOH-negative patients on admission or during the subsequent 48 hours. There were no differences in radiographic progression of hemorrhage, the need for neurosurgical procedure, or mortality between EtOH-positive and EtOH-negative patients. CONCLUSIONS: EtOH use near the time of traumatic injury was not associated with alterations in coagulation, as measured by traditional coagulation tests or by TEG, in patients with TICH. Furthermore, a positive blood alcohol at admission was not associated with increased mortality or need for neurosurgical procedure these patients.