The Relationship Between Gene Polymorphism Of FactorⅦ And Coagulopathy In Patients With Isolated Traumatic Brain Injury

Coagulopathy is common in patients with traumatic brain injury, influence on the prognosis of patients with traumatic brain injury as an important factor. Previous view that the coagulopathy is the result of tissue damage caused by trauma, hemorrhagic shock and subsequent fluid resuscitation in process of hemodilution, hyperfibrinolysis, inflammation, acidosis and hypothermia, however, these mechanisms do not fully explain this phenomenon. As the core of the extrinsic coagulation pathway, plasma FⅦa levels largely determine the coagulation status after TBI. In addition, with the development of epidemiology and molecular biology, more and more evidence demonstrate that genetic factors play an important role in the regulation of plasma levels of FⅦa. Therefore, this study analyzed the relationship of patients with isolated blunt traumatic brain injury and coagulopathy, and progressive hemorrhagic injury; Then, from the perspective of molecular biology, and expounds the association with gene polymorphisms of coagulation factor Ⅶ and coagulopathy in patients with isolated blunt traumatic brain injury; Finally, From the clinical to discuss the efficacy and safety of exogenous coagulation factor Ⅶa for coagulopathy in patients with isolated traumatic brain injury. In short, strive from a new point of view to explain the mechanism which leading of coagulopathy after traumatic braininjury,and provideaneffectivestrategyfortheclinicaltreatment.ObjectivesGiven the importance of factor Win extrinsic pathway of coagulation cascade, and thus that plasma FⅦ activity may be related to the coagulopathy induced by isolated blunt traumatic brain injury and progressive hemorrhagic injury. therefore, the purpose of this study is to investigate the associated of plasma FⅦ activity with isolated blunt traumatic brain injury and progressive hemorrhagic injury.MethodsEight-one isolated traumaticbrain patients with moderate to severe injury, aged≥16yrs, in whom plasma factor Wactivity was measured after admission between2010and2012. Blood was collected on arrival in the emergency department and analyzed with activated partial thromboplastic time, the International Normalized Ratio, platelet count, and activity offactor Ⅶ.TBI-associated coagulopathy was defined as elevated international normalized ratio>1.2or prolonged activated partial thromboplastin time>40seconds or thrombocytopenia (platelet count<120X10/L) at admission. Progressive hemorrhagic injury was present when the follow-up CT scan reported any increase in size or number of the hemorrhagic lesions. Logistic regression examined the risks for coagulopathy and progressive hemorrhagic injury after isolated traumatic brain injury.ResultsFⅦ activity in patients with coagulopathy was85.69±34.88%, which was significantly lower than patients without coagulopathy (99.57±29.37%, p=0.041). Isolated traumatic brain inury patients with FⅦactivity<77.5%have an odds ratio for coagulopathy of5.52(95%confidence interval1.82-16.68, p=0.03) relative to patients with FⅦ activity≥77.5%. FⅦ activity in patients with progressive hemorrhagic injury was70.76±18.21%, which was significantly lower than patients without progressive hemorrhagic injury (105.76±32.27%, p<0.001). A stepwise logistic regression analysis identified FⅦ<77.5%(OR=4.53;95%CI=1.62-12.67, p=0.004) as a predisposing risk factors independently associated with the presence of PHI. The overall mortality rate in the study population was7.4%(n=6). The plasma F Ⅶin death patients (91.44±47.19%) was slightly lower than that in survival patients (92.01±32.04%). But, there was no statistical difference ConclusionsDecreas of F Ⅶ activity significantly contributes to the coagulopathy and progressive hemorrhagic injury in patients with isolated traumatic brain injury. But it is not related with the mortality.