J Trauma
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Over the last few years, thousands of soldiers and an even greater number of civilians have suffered traumatic injuries due to blast exposure, largely attributed to improvised explosive devices in terrorist and insurgent activities. The use of body armor is allowing soldiers to survive blasts that would otherwise be fatal due to systemic damage. Emerging evidence suggests that exposure to a blast can produce neurologic consequences in the brain but much remains unknown. ⋯ One of the major recommendations from the workshop was the need to characterize the effects of blast exposure on clinical neuropathology. Clearer understanding of the human neuropathology would enable validation of preclinical and computational models, which are attempting to simulate blast wave interactions with the central nervous system. Furthermore, the civilian experience with bTBI suggests that polytrauma models incorporating both brain and lung injuries may be more relevant to the study of civilian countermeasures than considering models with a neurologic focus alone.
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The American College of Surgeons Committee on Trauma guidelines for trauma center verification stipulate that the responsible surgeon be present within 15 minutes of the arrival of a critically injured patient. Recently, these guidelines were liberalized, extending the response time to 30 minutes in level III trauma centers. This study evaluated the potential impact of this guideline change on the delivery of care at Ohio's level III trauma centers. We hypothesized that there would be no measurable difference in the emergency department (ED) length of stay (LOS), ED disposition, and facility mortality after enactment of this mandate, which extended the surgeon response time from 15 minutes to 30 minutes at level III trauma centers. ⋯ The extension of the surgeon response time from 15 minutes to 30 minutes did not adversely affect the outcomes of trauma patients at Ohio's level III trauma centers. Furthermore, the surgeon response time was similar before and after the rule change.
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Traumatic brain injury (TBI) causes gastrointestinal dysfunction and increased intestinal permeability. Regulation of the gut barrier may involve the central nervous system. We hypothesize that vagal nerve stimulation prevents an increase in intestinal permeability after TBI. ⋯ In a mouse model of TBI, vagal stimulation prevented TBI-induced intestinal permeability. Furthermore, vagal stimulation increased enteric glial activity and may represent the pathway for central nervous system regulation of intestinal permeability.