Transmediastinal gunshot wounds in a mature trauma centre: changing perspectives.

BACKGROUND: Transmediastinal gunshot wounds are associated with a high mortality and frequently require operative intervention. The purpose of this study was to identify the diagnostic and therapeutic challenges of these injuries in a mature trauma system with decreasing prehospital time intervals. METHODS: Patients admitted to a large urban Level 1 trauma centre between 1/2006 and 12/2010 sustaining a firearm injury to the torso were identified. Transmediastinal gunshot wounds were defined as missile tracts traversing the mediastinum identified on CT images, operative notes or autopsy reports. RESULTS: Overall, 133 patients met study criteria. A total of 116 patients (87.2%) were haemodynamically unstable or had no vital signs on arrival to the Emergency Department. Ninety-seven (83.6%) of these patients required a resuscitative thoracotomy resulting in 8 survivors (6.0%). There were 17 haemodynamically stable patients (12.8%) identified, 14 of whom underwent CT scan evaluation. Six patients subsequently required operative intervention. Only 11 patients (8.3%) in the study population were successfully managed nonoperatively. The overall mortality was 78.9%, and for those who reached the hospital with vital signs, the mortality was 24.3%. CONCLUSIONS: Transmediastinal gunshot wounds encountered in a mature trauma centre are highly lethal injuries requiring resuscitative thoracotomy in most instances. Changing perspectives in these injuries may reflect the effects of an evolving prehospital care.

ß-adrenergic receptor inhibition affects cerebral glucose metabolism, motor performance, and inflammatory response after traumatic brain injury.

BACKGROUND: The purpose of this study was to evaluate how ß-adrenergic receptor inhibition after traumatic brain injury (TBI) alters changes in early cerebral glucose metabolism and motor performance, as well as cerebral cytokine and heat shock protein (HSP) expression. METHODS: Mouse cerebral glucose metabolism was measured by microPET fluorodeoxyglucose uptake and converted into standardized uptake values (SUV). Four groups of C57/Bl6 mice (wild type [WT]) were initially evaluated: sham or TBI, followed by tail vein injection of either saline or a nonselective ß-adrenergic receptor inhibitor (propranolol, 4 mg/kg). Then motor performance, cerebral cytokine, and HSP70 expression were studied at 12 hours and 24 hours after sham injury or TBI in WT mice treated with saline or propranolol and in ß1-adrenergic/ß2-adrenergic receptor knockout (BARKO) mice treated with saline. RESULTS: Cerebral glucose metabolism was significantly reduced after TBI (mean SUV TBI, 1.63 vs. sham 1.97, p < 0.01) and propranolol attenuated this reduction (mean SUV propranolol, 1.89 vs. saline 1.63, p < 0.01). Both propranolol and BARKO reduced motor deficits at 24 hours after injury, but only BARKO had an effect at 12 hours after injury. TBI WT mice treated with saline performed worse than propranolol mice at 24 hours after injury on rotarod (23 vs. 44 seconds, p < 0.01) and rearing (130 vs. 338 events, p = 0.01) results. At 24 hours after injury, sham BARKO and TBI BARKO mice were similar on rotarod (21 vs. 19 seconds, p = 0.53), ambulatory testing (2,891 vs. 2,274 events, p = 0.14), and rearing (129 vs. 64 events, p = 0.09) results. Interleukin 1ß expression was affected by BARKO and propranolol after TBI; attenuation of interleukin 6 and increased HSP70 expression were noted only with BARKO. CONCLUSION: ß-adrenergic receptor inhibition affects cerebral glucose metabolism, motor performance, as well as cerebral cytokine and HSP expression after TBI.