British journal of anaesthesia
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Randomized Controlled Trial Multicenter Study
Monitoring depth of anaesthesia in a randomized trial decreases the rate of postoperative delirium but not postoperative cognitive dysfunction.
Monitoring depth of anaesthesia in those over 60 yo decreases the incidence of post-operative delirium, though not post-operative cognitive decline.
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Review Meta Analysis
Facilitatory effects of perineural dexmedetomidine on neuraxial and peripheral nerve block: a systematic review and meta-analysis.
Nerve blocks improve postoperative analgesia, but their benefits may be short-lived. This quantitative review examines whether perineural dexmedetomidine as a local anaesthetic (LA) adjuvant for neuraxial and peripheral nerve blocks can prolong the duration of analgesia compared with LA alone. All randomized controlled trials (RCTs) comparing the effect of dexmedetomidine as an LA adjuvant to LA alone on neuraxial and peripheral nerve blocks were reviewed. Sensory block duration, motor block duration, block onset times, analgesic consumption, time to first analgesic request, and side-effects were analysed. ⋯ were combined using random-effects modelling. A total of 516 patients were analysed from nine RCTs. Five trials investigated dexmedetomidine as part of spinal anaesthesia and four as part of a brachial plexus (BP) block. Sensory block duration was prolonged by 150 min [95% confidence interval (CI): 96, 205, P<0.00001] with intrathecal dexmedetomidine. Perineural dexmedetomidine used in BP block may prolong the mean duration of sensory block by 284 min (95% CI: 1, 566, P=0.05), but this difference did not reach statistical significance. Motor block duration and time to first analgesic request were prolonged for both intrathecal and BP block. Dexmedetomidine produced reversible bradycardia in 7% of BP block patients, but no effect on the incidence of hypotension. No patients experienced respiratory depression. Dexmedetomidine is a potential LA adjuvant that can exhibit a facilitatory effect when administered intrathecally as part of spinal anaesthesia or peripherally as part of a BP block. However, there are presently insufficient safety data to support perineural dexmedetomidine use in the clinical setting.
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Neuromuscular blocking drugs (NMBDs) are the most common cause of intraoperative anaphylaxis in Western Australia. Differences in the rates of anaphylaxis between individual agents have been surmised in the past, but not proven, and are an important consideration if agents are otherwise equivalent. ⋯ Rocuronium has a higher rate of IgE-mediated anaphylaxis compared with vecuronium, a result that is statistically significant and clinically important. Cisatracurium had the lowest rate of cross-reactivity in patients who had previously suffered anaphylaxis to rocuronium or vecuronium.
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Review Meta Analysis
Pharmacological perioperative brain neuroprotection: a qualitative review of randomized clinical trials.
Perioperative cerebral damage may be associated with surgery and anaesthesia. Pharmacological perioperative neuroprotection is associated with conflicting results. In this qualitative review of randomized controlled clinical trials on perioperative pharmacological brain neuroprotection, we report the effects of tested therapies on new postoperative neurological deficit, postoperative cognitive decline (POCD), and mortality rate. ⋯ None of the tested drugs was associated with a reduction in mortality rate. Drugs with various mechanisms of action have been tested over time; current evidence suggests that pharmacological brain neuroprotection might reduce the incidence of new postoperative neurological deficits and POCD, while no benefits on perioperative mortality are described. Of importance from this review is the need for shared methodological approach when clinical studies on pharmacological neuroprotection are designed.
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Ketamine-induced neuroapoptosis has been attributed to diverse stress-related mechanisms. Glycogen synthase kinase-3β (GSK-3β) is a multifunctional kinase that is active in neuronal development and linked to neurodegenerative disorders. We hypothesized that ketamine would enhance GSK-3β-induced neuroapopotosis, and that lithium, an inhibitor of GSK-3β, would attenuate this response in vivo. ⋯ Ketamine-induced neuroapoptosis is associated with a temporal decrease in GSK-3β phosphorylation, and simultaneous administration of lithium mitigated this response. These findings suggest that GSK-3β is activated during this ketamine-induced neuroapoptosis.