Rivaroxaban versus aspirin in prevention of venous thromboembolism following total joint arthroplasty or hip fracture surgery: a meta-analysis.

OBJECTIVE: To evaluates the efficacy and safety of rivaroxaban versus aspirin in prevention of venous thromboembolism (VTE) following total hip (THA) or knee arthroplasty (TKA) or hip fracture surgery. METHODS: Major databases were systematically searched for all relevant studies published in English up to October 2020. The meta-analysis was conducted using RevMan 5.3 software. RESULTS: In total, 7 studies were retrieved which contained 5133 patients. Among these patients, 2605 patients (50.8%) received rivaroxaban, whereas 2528 patients (49.2%) received aspirin. There were no statistical difference between aspirin and rivaroxaban for reducing VTE (RR = 0.75, 95% CI 0.50-1.11, I2 = 36%, p = 0.15), major bleeding (RR = 0.94, 95% CI 0.45-2.37, I2 = 21%, p = 0.95), and all-cause mortality (RR = 0.88, 95% CI 0.12-6.44, I2 = 0%, p = 0.90) between the two groups. Compared with aspirin, rivaroxaban significantly increased nonmajor bleeding (RR = 1.29, 95% CI 1.05-1.58, I2 = 0%, p = 0.02). CONCLUSION: There was no significant difference between aspirin and rivaroxaban in prevention of venous thromboembolism following total joint arthroplasty or hip fracture surgery. Aspirin may be an effective, safe, convenient, and cheap alternative for prevention of VTE. Further large randomized studies are required to confirm these findings.

The protective effects of dexmedetomidine on ischemic brain injury: A meta-analysis.

BACKGROUND: Intracranial lesions, trauma or surgery-related damage activate immune inflammation and neuroendocrine responses, causing ischemic brain injury. Studies have shown that inflammatory cascade mediated by neuroendocrine hormones and proinflammatory mediators is implicated in the pathophysiology of ischemic brain injury. Alpha2-adrenoceptor agonists, dexmedetomidine, is widely used as neuroprotectants in anesthesia practice. However, it is still lack of a comprehensive meta-analysis to evaluate the neuroprotection of dexmedetomidine against ischemic brain injury via suppressing these two physiological responses. METHOD: Searched the Cochrane Library, Pub-Med, EMBASE, EBSCO, Ovid, Chinese biological and medical database (CBM). Related literatures published in English or Chinese before January 2017 were enrolled. We assessed the quality of eligible studies and synthesized predefined outcomes with a random-effects model or fixed-effects model. RESULT: Nineteen Randomized Controlled Trials including 879 patients were included. Findings for meta-analysis of various outcomes were summarised. Primary results shown that compared with placebo, dexmedetomidine reduced a surge of TNF-α [SMD=-2.34, 95%CI (-3.25, -1.44)], IL-6 [SMD=-2.44, 95%CI (-3.40, -1.47)], S100-ß [SMD=-2.73, 95%CI (-3.65, -1.82)], NSE [SMD=-1.69, 95%CI (-2.77, -0.61)], cortisol [SMD=-2.48, 95%CI (-3.38, -1.58)] and glucose [SMD=-1.44, 95%CI (-1.85, -1.04)]; maintained the level of SOD [SMD=1.36, 95%CI (0.62, 2.10)]; decreased the rise in CRP level at postoperative one day. In response to stress reaction, dexmedetomidine attenuated the stress-related increasing of MAP, HR and intracranial pressure without significant effects on cerebral oxygen metabolism. CONCLUSION: Alpha2-adrenoceptor agonists, dexmedetomidine, could reduce the release of inflammatory mediators and neuroendocrine hormones as well as maintain intracranial homoeostasis, alleviating ischemic brain injury and exerting an effect on brain protection.