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Background: Observational studies have demonstrated improved outcomes in TBI patients receiving in-hospital beta-blockers. The aim of this study is to conduct a randomized controlled trial examining the effect of beta-blockers on outcomes in TBI patients. Methods: Adult patients with severe TBI (intracranial AIS >= 3) were included in the study. Hemodynamically stable patients at 24 h after injury were randomized to receive either 20 mg propranolol orally every 12 h up to 10 days or until discharge (BB+) or no propranolol (BB-). Outcomes of interest were in-hospital mortality and Glasgow Outcome Scale-Extended (GOS-E) score on discharge and at 6-month follow-up. Subgroup analysis including only isolated severe TBI (intracranial AIS >= 3 with extracranial AIS <= 2) was carried out. Poisson regression models were used. Results: Two hundred nineteen randomized patients of whom 45% received BB were analyzed. There were no significant demographic or clinical differences between BB+ and BB- cohorts. No significant difference in inhospital mortality (adj. IRR 0.6 [95% CI 0.3-1.4], p = 0.2) or long-term functional outcome was measured between the cohorts (p = 0.3). One hundred fifty-four patients suffered isolated severe TBI of whom 44% received BB. The BB? group had significantly lower mortality relative to the BB- group (18.6% vs. 4.4%, p = 0.012). On regression analysis, propranolol had a significant protective effect on in-hospital mortality (adj. IRR 0.32, p = 0.04) and functional outcome at 6-month follow-up (GOS-E >= 5 adj. IRR 1.2, p = 0.02). Conclusion: Propranolol decreases in-hospital mortality and improves long-term functional outcome in isolated severe TBI. This randomized trial speaks in favor of routine administration of beta-blocker therapy as part of a standardized neurointensive care protocol. Level of evidence: Level II; therapeutic. Study type: Therapeutic study., Funding Agency:Research department of Shiraz University of Medical Sciences 1396-01-3814792

Background: Traumatic brain injury (TBI) is a major cause of death and debility following trauma. The initial brain tissue insult is worsened by secondary reactive responses including oxidative stress reactions, inflammatory changes and subsequent permanent neurologic deficits. Effective agents to improve functional outcome and survival following TBI are scarce. Selenium is an antioxidant which has shown to reduce oxidative stress. This study examines the effect of intravenous selenium (Selenase (R)) treatment in patients with severe TBI on functional outcome and survival in a prospective study design. Methods: Patients sustaining TBI were prospectively identified during a 12-month period at an academic urban trauma center. Study inclusion criteria applied were: age >= 18 years, blunt injury mechanism and admission to neurosurgical intensive care unit (NICU). Early deaths (<= 48 h) and patients suffering extracranial injuries requiring invasive interventions or surgery were excluded. All consecutive admissions during a six-month period were administered intravenous Selenase (R) for a maximum 10-day period and constituted cases. Patient demographics and outcomes up to six-months post-discharge were collected for analysis. Results: A total of 307 patients met inclusion criteria of which 125 were administered Selenase (R). Stepwise Poisson regression analysis identified five common predictors of poor functional outcome and in-hospital mortality: GCS <= 8, age <= 55 years, hypotension at admission, high Rotterdam score and invasive neurosurgical intervention. Selenase (R) significantly reduced the risk of unfavourable functional outcomes, defined as GOS-E <= 4, at both discharge (adjusted RR 0.69, 95% CI 0.51-0.92, p = 0.012) and at six months follow-up (adjusted RR 0.61, 95% CI 0.44-0.83, p = 0.002). Following adjustment for significant group differences similar results were seen for functional outcome. Selenase (R) did not improve survival (adjusted RR