Department of Anesthesiology and Pain Medicine, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada.
Department of Anaesthesia and Perioperative Medicine, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Can J Anaesth. 2021 Mar;68(3):387-408. doi: 10.1007/s12630-020-01875-2. Epub 2021 Jan 6.
The erector spinae plane (ESP) block is an emerging regional anesthetic technique with significant potential for clinical benefit. Nevertheless, its exact mechanism(s) of action has been much debated. We reviewed the available literature to explore the possible mechanisms of analgesia for the ESP block. These include neural blockade and central inhibition from direct spread of local anesthetic to the paravertebral or epidural space; analgesia mediated by elevated local anesthetic plasma concentrations due to systemic absorption; immunomodulatory effects of local anesthetics; and an effect mediated through the mechanosensory properties of thoracolumbar fascia. Based on evidence from clinical, human cadaveric, animal, and mechanistic laboratory studies, the most probable primary mechanism is a direct effect of local anesthetic via physical spread and diffusion to neural structures in the fascial plane deep to the erector spinae muscles and adjacent tissue compartments. Biological plausibility of this primary mechanism is confirmed by injectate spread to the ventral rami of spinal nerves (though quite variable) in most studies. There is consistent involvement of dorsal rami; epidural spread is a less commonly observed phenomenon. A systemic effect of local anesthetic is also plausible, but unlikely to be a major contributor to clinical analgesic efficacy. The evidence for significant analgesia due to other proposed mechanisms, such as fascia-mediated analgesia or lymphatic spread, are currently limited and thus remain speculative. Understanding the mechanisms of action could assist clinicians in further investigating and refining ESP block performance, with the ultimate goal of optimizing analgesic efficacy and improving postoperative patient outcomes.
竖脊肌平面 (ESP) 阻滞是一种新兴的区域麻醉技术，具有显著的临床获益潜力。然而，其确切的作用机制仍存在争议。我们回顾了现有文献，以探讨 ESP 阻滞的可能镇痛机制。这些机制包括局部麻醉剂向椎旁或硬膜外腔直接扩散引起的神经阻滞和中枢抑制；全身吸收导致局部麻醉剂血浆浓度升高介导的镇痛作用；局部麻醉剂的免疫调节作用；以及通过胸腰筋膜的机械感觉特性介导的作用。基于临床、人体尸体、动物和机制实验室研究的证据，最可能的主要机制是局部麻醉剂通过物理扩散和扩散到竖脊肌深筋膜平面和相邻组织间隙中的神经结构发挥直接作用。大多数研究中，注射剂扩散到脊神经腹支（尽管差异很大）证实了这种主要机制的生物学合理性。背支始终参与其中；硬膜外扩散是一种较少观察到的现象。局部麻醉剂的全身作用也是合理的，但不太可能是临床镇痛疗效的主要贡献者。由于其他提出的机制（如筋膜介导的镇痛或淋巴扩散）引起的显著镇痛的证据目前有限，因此仍具有推测性。了解作用机制可以帮助临床医生进一步研究和改进 ESP 阻滞的性能，最终目标是优化镇痛效果并改善术后患者的结局。
