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The purpose of this study was to examine the incidence of tissue hypoperfusion in victims of severe traumatic brain injury (sTBI) and to determine the associations between hypoperfusion and TBI coagulopathy.This is a retrospective analysis of a prospectively collected cohort admitted to the surgical intensive care unit from June 2005 to December 2007 sustaining isolated sTBI, defined as sTBI [head Abbreviated Injury Scale (AIS) ≥3] with chest, abdomen, and extremity AIS <3. Criteria for TBI-associated early coagulopathy included isolated sTBI in conjunction with thrombocytopenia (platelet count <100,000 per mm3) or elevated international normalized ratio >1.2 or prolonged activated partial thromboplastin time >36 seconds at admission. Hypoperfusion was defined by the presence of an arterial base deficit (BD) >6 mmol/L. Univariate and multivariate analysis was performed to identify associations among hypoperfusion, coagulopathy, and mortality.A total of 132 patients met the study criteria. TBI-associated early coagulopathy occurred in 48 patients (36.4%). With increasing head injury severity, the incidence of coagulopathy increased in a stepwise fashion. Mean BD values and mean lactate values were significantly higher among patients with coagulopathy compared with their noncoagulopathic counterparts at hospital admission. The coagulopathic cohort presented more frequently with a BD >6 mmol/L at admission (39.6% vs. 20.2%, p = 0.016). In the stepwise logistic regression analysis, head AIS = 5 and an admission BD >6 mmol/L were independently associated with early coagulopathy. Coagulopathy was associated with increased mortality in patients after blunt head trauma, adjusted odds ratio (95% confidence interval): 3.79 (1.06–13.51); adjusted p = 0.04.Hypoperfusion is an independent risk factor for the development of early coagulopathy in patients with isolated sTBI. Nevertheless, early coagulopathy after sTBI does not occur exclusively in patients experiencing tissue hypoperfusion.