Instead, a predominance of the 349 patient

sample underwent contrast venography 1–3 weeks after admission. The authors found an overall incidence of 57.6% (95% CI 52%–62.8%) incurring DVT and 18.1% with proximal DVT, despite only 1.5% of patients displaying clinical symptoms.3 Further stratification of injury based on major location (head versus spine versus lower limbs versus face/chest/abdomen) and type yielded a framework for epidemiologic difference in risks. Subgroup analysis revealed that of 91 patients with head trauma alone or with other injury, 53.8% presented with Inhibitors,research,lifescience,medical distal deep vein clots and 19.8% presented with proximal (thigh) deep vein clots, for a total of 73% of this population. It is important to note that of the 51 patients with head trauma as their only injury, the incidence of DVT was 39%. As expected, head trauma with lower extremity trauma experienced a DVT rate of 77%, and the study found femur or tibial fractures were an independent risk factor, along with spinal cord injury, age, surgery, and blood transfusion.3 Inhibitors,research,lifescience,medical Head injuries were grouped as a whole and not

further divided. TBI-induced coagulopathy contributes risk to this population. A review by Laroche et al. from June 2012 characterizes the phenomenon as a combination of both hypercoagulable and hypocoagulable states.4 It is hypothesized that the bleeding diathesis Inhibitors,research,lifescience,medical is rooted in the elevated release of brain Inhibitors,research,lifescience,medical and systemic tissue factor (TF) due to injury. The resulting over-stimulation of the coagulation cascade can then foster a consumptive coagulopathy, though other mechanisms are being investigated.4 Additionally, in 2007 Nekludov et al. further found evidence of AZD0530 mw TF-triggered hyperfibrinolysis as well as a hypercoagulability with generation of micro-thrombosis.5 In a related review of TBI patients, evidence of hemorrhagic

progression or new development of ischemic lesions after initial Inhibitors,research,lifescience,medical emergency room presentation was found in 85% of patients with laboratory evidence of coagulopathy on admission, as compared to 31% of those with normal levels.5 Thus in a variety of analyses, diminished platelet counts, increased partial thrombin time (PTT), and elevated prothrombin time are shown to be predictive markers of mortality in severe TBI. Prothrombin time abnormality was specifically noted to be an independent predictor in the landmark multinational IMPACT study (International Cell press Mission for Prognosis and Analysis of Clinical Trials in TBI, IMPACT, 2007).5,6 However, due to small sample size, Geerts’ earliest paper was not able to state whether brain injury itself is an independent risk factor for thromboembolic events.3 Consequently, a flurry of investigational studies appeared in the past few years addressing the question. Most notable was a retrospective study of 2,000 patients by Reiff et al. in 2009.