Zink W, Sinner B, Zausig Y, Graf B M
Zentrum Anaesthesiologie, Rettungs- und Intensivmedizin, Universitätsklinikum, Robert-Koch-Str. 40, 37075, Göttingen, Deutschland.
Anaesthesist. 2007 Feb;56(2):118-27. doi: 10.1007/s00101-006-1121-5.
Intramuscular injections of local anaesthetic agents regularly result in reversible muscle damage, with a dose-dependent extent of the lesions. All local anaesthetic agents that have been examined are myotoxic, whereby procaine produces the least and bupivacaine the most severe muscle injury. The histological pattern and the time course of skeletal muscle injury appear relatively uniform: hypercontracted myofibrils become evident directly after injection, followed by lytic degeneration of striated muscle sarcoplasmic reticulum myocyte edema and necrosis. Intriguingly, in most cases myoblasts, basal laminae and connective tissue elements remain intact which subsequently ensures complete muscular regeneration. Subcellular pathomechanisms of local anaesthetic myotoxicity are still not understood in detail. Increased intracellular Ca(2+) levels are suggested to be the most important element in myocyte injury, since denervation, inhibition of sarcolemmal Na(+) channels and direct toxic effects on myofibrils have been excluded as sites of action. Although experimental myotoxic effects are impressively intense and reproducible, only few case reports of myotoxic complications in patients after local anaesthetic administration have been published. In particular, the occurrence of clinically relevant myopathy and myonecrosis has been described after continuous peripheral blockades, infiltration of wound margins, trigger point injections, peribulbar and retrobulbar blocks.
肌肉注射局部麻醉剂通常会导致可逆性肌肉损伤,损伤程度呈剂量依赖性。所有已检测的局部麻醉剂都具有肌毒性,其中普鲁卡因造成的损伤最小,布比卡因造成的肌肉损伤最严重。骨骼肌损伤的组织学模式和时间进程相对一致:注射后立即出现肌原纤维过度收缩,随后出现横纹肌肌浆网溶解变性、肌细胞水肿和坏死。有趣的是,在大多数情况下,成肌细胞、基底膜和结缔组织成分保持完整,随后确保肌肉完全再生。局部麻醉剂肌毒性的亚细胞病理机制仍未完全了解。细胞内钙离子水平升高被认为是肌细胞损伤的最重要因素,因为去神经支配、肌膜钠通道抑制以及对肌原纤维的直接毒性作用已被排除在作用部位之外。尽管实验性肌毒性作用强烈且可重复,但关于局部麻醉剂给药后患者发生肌毒性并发症的病例报告却很少。特别是,在连续外周阻滞、伤口边缘浸润、触发点注射、球周和球后阻滞之后,已经描述了临床相关的肌病和肌坏死的发生。