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.

Mortality by decade in trauma patients with Glasgow Coma Scale 3.

The aim of this study was to assess how increasing age affects mortality in trauma patients with Glasgow Coma Scale (GCS) 3. The Los Angeles County Trauma System Database was queried for all patients aged 20 to 99 years admitted with GCS 3. Mortality was 41.8 per cent for the 3306 GCS 3 patients. Mortality in the youngest patients reviewed, those in the third decade, was 43.5 per cent. After logistic regression analysis, patients in the third decade had similar mortality rates to patients in the sixth (adjusted OR, 0.88; CI, 0.68 to 1.14; P = 0.33) and seventh decades (adjusted OR, 0.96; CI, 0.70 to 1.31; P = 0.79). A significantly lower mortality rate, however, was noted in the fifth decade (adjusted OR, 0.76; CI, 0.61 to 0.95; P = 0.02). Conversely, significantly higher mortality rates were noted in the eighth (adjusted OR, 1.93; CI, 1.38 to 2.71; P = 0.0001) and combined ninth/tenth decades (adjusted OR, 2.47; CI, 1.71 to 3.57; P < 0.0001). Given the high survival in trauma patients with GCS 3 as well as continued improvement in survival compared with historical controls, aggressive care is indicated for patients who present to the emergency department with GCS 3.

Emergency department crystalloid resuscitation of 1.5 L or more is associated with increased mortality in elderly and nonelderly trauma patients.

BACKGROUND: Recent evidence suggests a survival advantage in trauma patients who receive controlled or hypotensive resuscitation volumes. This study examines the threshold crystalloid volume that is an independent risk factor for mortality after trauma. METHODS: This study analyzed prospectively collected data from a Level I Trauma Center between January 2000 and December 2008. Demographics and outcomes were compared in elderly (≥70 years) and nonelderly (<70 years) trauma patients who received crystalloid fluid in the emergency department (ED) to determine a threshold volume that was an independent predictor for mortality. RESULTS: A total of 3,137 patients who received crystalloid resuscitation in the ED were compared. Overall mortality was 5.2%. Mortality among the elderly population was 17.3% (41 deaths), whereas mortality in the nonelderly population was 4% (116 deaths). After multivariate logistic regression analysis, fluid volumes of 1.5 L or more were significantly associated with mortality in both elderly (odds ratio [OR]: 2.89, confidence interval [CI] [1.13-7.41], p=0.027) and nonelderly patients (OR: 2.09, CI [1.31-3.33], p=0.002). Fluid volumes up to 1 L were not associated with significantly increased mortality. At 3 L, mortality was especially pronounced in the elderly (OR: 8.61, CI [1.55-47.75] p=0.014), when compared with the nonelderly (OR=2.69, CI [1.53-4.73], p=0.0006). CONCLUSION: ED volume replacement of 1.5 L or more was an independent risk factor for mortality. High-volume resuscitations were associated with high-mortality particularly in the elderly trauma patient. Our finding supports the notion that excessive fluid resuscitation should be avoided in the ED and when required, operative intervention or intensive care admission should be considered.