The journal of trauma and acute care surgery
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J Trauma Acute Care Surg · Jul 2017
Field and en route resuscitative endovascular occlusion of the aorta: A feasible military reality?
Severe noncompressible torso hemorrhage remains a leading cause of potentially preventable death in modern military conflicts. Resuscitative endovascular occlusion of the aorta (REBOA) has demonstrated potential as an effective adjunct to the treatment of noncompressible torso hemorrhage in the civilian early hospital and even prehospital settings-but the application of this technology for military prehospital use has not been well described. We aimed to assess the feasibility of both field and en route prehospital REBOA in the military exercise setting, simulating a modern armed conflict. ⋯ Our study demonstrates the potential feasibility of REBOA for use during tactical field and en route (flight) care of combat casualties. Further study is needed to determine the optimal training and utilization protocols required to facilitate the effective incorporation of REBOA into military prehospital care capabilities.
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J Trauma Acute Care Surg · Jul 2017
Aeromedical evacuation-relevant hypobaria worsens axonal and neurologic injury in rats after underbody blast-induced hyperacceleration.
Occupants of military vehicles targeted by explosive devices often suffer from traumatic brain injury (TBI) and are typically transported by the aeromedical evacuation (AE) system to a military medical center within a few days. This study tested the hypothesis that exposure of rats to AE-relevant hypobaria worsens cerebral axonal injury and neurologic impairment caused by underbody blasts. ⋯ Exposure of rats to blast-induced acceleration of 100G increases cerebral axonal injury, which is significantly exacerbated by exposure to hypobaria as early as 6 hours and as late as 6 days postblast. Rats exposed to underbody blasts and then to hypobaria under 100% O2 exhibit increased axonal damage and impaired motor function compared to those subjected to blast and hypobaria under 21% O2. These findings raise concern about the effects of AE-related hypobaria on TBI victims, the timing of AE after TBI, and whether these effects can be mitigated by supplemental oxygen.