Discussion

Introduction: Penetrating traumatic brain injury (pTBI) management carries unique challenges due to higher risk of coagulopathy, infection and vascular injury. Development of coagulopathy is an independent predictor of outcomes. Large volume tissue destruction with release of tissue thromboplastin has been posited as a major driver for the coagulopathy. We investigate the relationship between injury related blood loss and development of consumptive coagulopathy in pTBI.

Methods: We retrospectively collected pTBI cases at our institution from 2016-2023. We collected pertinent labs collected at presentation in the trauma bay. Coagulopathy was defined as having any of the following derangements (INR>1.3, PT or PTT>1.5x normal limit, Platelet count < 150k, fibrinogen < 200).

Results: 372 patients presented with pTBI and 270 met our inclusion criteria. Based on conventional laboratory testing, 47% (127/270) developed coagulopathy at presentation. Patient characteristics are described in Table 1. 57 patients received TXA at presentation.
Coagulopathic patients were more likely to be male with worse injury (Bihemispheric or transventricular) and more likely to pass away as detailed in Table 2. Additionally, they presented with a larger base deficit. The degree of base deficit was negatively correlated with the INR (rho: -0.46, p: < 0.0001, Spreaman correlation). Coagulopathic patients were more likely to have a base deficit lower than 6 (62.8% vs 37.5%, X2: 16.2, p: < 0.0001). OR 1.56 (1.04:2.3, p: 0.03). TXA administration did not affect the development of coagulopathy.

Conclusion : Development of coagulopathy following pTBI is correlated with higher traumatic blood loss and hypotension. TXA did not change the rate of coagulopathy.