Department of Anesthesiology, Ohio State University Wexner Medical Center, Columbus, OH, USA.
Department of Anesthesiology and Pain Medicine, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada.
Br J Anaesth. 2018 Oct;121(4):822-841. doi: 10.1016/j.bja.2018.05.076. Epub 2018 Aug 8.
Recent reports of local-anaesthetic (LA)-induced myotoxicity after peripheral nerve blocks have increased the interest in this less commonly known complication. Basic science evidence investigating LA-induced myotoxicity seems to demonstrate a pattern, but findings from human studies vary. This systematic review summarises the existing myotoxicity evidence and empirically examines its implications. Databases were searched for all in vitro animal and human studies evaluating LA-induced myotoxicity. Studies were stratified by design. Data sought included the model examined, LA used, injury mechanisms, nature of damage, and extent of recovery. For human studies, we also aimed to estimate prevalence and recovery rates. One hundred and fifteen studies, mainly animal and ophthalmic, were included. Myotoxicity risk factors included higher concentrations and prolonged exposure to LA, and use of bupivacaine. Injury mechanisms involved early and late aberrations to cytoplasmic calcium (Ca) homeostasis by the sarcoplasmic reticulum Ca ATPase. Incidence in ophthalmic studies was 0.77% (392 of 50 618). Inflammatory changes within a few days after exposure marked the onset of myotoxicity, and myo-degeneration followed within the first week post-exposure. Time to recovery in human muscles ranged between 4 days to 1 yr. None/partial and complete recovery were observed in 61% and 38% of patients, respectively. Across all experimental models, skeletal muscles exposed to LA consistently display myotoxic effects. Evidence is robust in animal and ophthalmic studies, and displays a concerning signal with continuous adductor canal block use in human case reports. Exploring the clinical prevalence, severity, and risk-reducing strategies of myotoxicity should be prioritised.
最近有报道称,局部麻醉剂(LA)引起的周围神经阻滞后肌病增加了人们对这种不太常见的并发症的兴趣。基础科学证据似乎表明 LA 引起的肌病有一定的模式,但来自人体研究的结果却有所不同。本系统综述总结了现有的肌病证据,并对其进行了实证研究。检索了所有评估 LA 诱导肌病的体外动物和人体研究的数据库。研究按设计分层。寻求的数据包括检查的模型、使用的 LA、损伤机制、损伤性质和恢复程度。对于人体研究,我们还旨在估计患病率和恢复率。共纳入 115 项研究,主要为动物和眼科研究。肌病的危险因素包括更高浓度和更长时间暴露于 LA,以及使用布比卡因。损伤机制涉及早期和晚期通过肌浆网 CaATP 酶对细胞质钙(Ca)稳态的异常。在眼科研究中,发病率为 0.77%(50618 例中有 392 例)。暴露后几天内出现的炎症变化标志着肌病的开始,暴露后第一周内出现肌退变。人体肌肉的恢复时间在 4 天至 1 年之间不等。在 61%的患者中观察到无/部分恢复,在 38%的患者中观察到完全恢复。在所有实验模型中,暴露于 LA 的骨骼肌都显示出肌毒性作用。在动物和眼科研究中证据确凿,在人体病例报告中持续使用股神经管阻滞显示出令人担忧的信号。探索肌病的临床患病率、严重程度和降低风险的策略应优先考虑。