Introduction: Recent clinical studies failed to show efficacy of recombinant factor (rFVIIa) and tranexamic acid in traumatic brain injury (TBI) treatment. This failure may be caused by the pathophysiological diversity of TBI. Moreover, there is still little information on the different coagulopathic mechanisms underlying different type of TBI. The aim of this study is thus to clarify the coagulopathic mechanisms in different "pure" TBI rat models with thromboelastography (TEG), which can provide quick, simultaneous estimation of multiple coagulopathic mechanisms.
Materials and Methods: Sprague-Dawley rats (300 – 350 g) were subjected to one of three different injuries: penetrating ballistic brain injury (PBBI), lateral fluid percussion injury (FPI), and acute subdural hematoma (ASDH). In each TBI model, non-heparinized blood samples were collected at different time points (PreTBI, 2.5 h, 24 h, 7 days after TBI). TEG parameters were compared among the three TBI models, and at different time points.
Results: In the early phase (2.5 h) after injury, K-value, which indicates impairment of fibrinogenesis, was significantly higher in ASDH than in FPI (p<0.01). Moreover, MA (Maximal amplitude) and G value, which indicate the strength of platelet-fibrin interaction, were significantly lower in ASDH than FPI (p<0.05, respectively). Moreover, the Coagulation Index (CI), which indicates overall status of coagulation was the lowest in ASDH. Blood coagulation profiles of PBBI were similar to ASDH, although less severe. On the other hand, the peak of coagulopathy in FPI existed on later phase (24 h) after injury, and continued by the 7th day.
Conclusion: Our study clarified 1) The presence of acute-severe coagulopathy in ASDH, 2) gradually worsening coagulopathy in FPI, 3) acute-milder coagulopathy in PBBI. The pathophysiology and severity of coagulopathy was specific to the type of injury and the duration after injury. These results warrant a future clinical study to profile the coagulation disorders after TBI, and possibly of "TEG derived" treatment for coagulation disorder in TBI.