Reg Anesth Pain Med. 2018 Feb;43(2):138-149. doi: 10.1097/AAP.0000000000000719.
The experimental use of lipid emulsion for local anesthetic toxicity was originally identified in 1998. It was then translated to clinical practice in 2006 and expanded to drugs other than local anesthetics in 2008. Our understanding of lipid resuscitation therapy has progressed considerably since the previous update from the American Society of Regional Anesthesia and Pain Medicine, and the scientific evidence has coalesced around specific discrete mechanisms. Intravenous lipid emulsion therapy provides a multimodal resuscitation benefit that includes both scavenging (eg, the lipid shuttle) and nonscavenging components. The intravascular lipid compartment scavenges drug from organs susceptible to toxicity and accelerates redistribution to organs where drug (eg, bupivacaine) is stored, detoxified, and later excreted. In addition, lipid exerts nonscavenging effects that include postconditioning (via activation of prosurvival kinases) along with cardiotonic and vasoconstrictive benefits. These effects protect tissue from ischemic damage and increase tissue perfusion during recovery from toxicity. Other mechanisms have diminished in favor based on lack of evidence; these include direct effects on channel currents (eg, calcium) and mass-effect overpowering a block in mitochondrial metabolism. In this narrative review, we discuss these proposed mechanisms and address questions left to answer in the field. Further work is needed, but the field has made considerable strides towards understanding the mechanisms.
脂溶性乳剂治疗局部麻醉药中毒的实验应用最初于 1998 年被发现，随后于 2006 年被应用于临床实践，并于 2008 年扩展至除局部麻醉药以外的药物。自美国区域麻醉与疼痛医学学会上次更新以来，我们对脂质复苏治疗的认识已经有了很大的进展，科学证据已经集中在特定的离散机制上。静脉内脂质乳剂治疗提供了一种多模式的复苏益处，包括清除（例如，脂质穿梭）和非清除成分。血管内脂质区室从易受毒性影响的器官中清除药物，并加速药物（例如布比卡因）的再分布到储存、解毒和随后排泄的器官。此外，脂质还发挥非清除作用，包括后处理（通过激活生存促进激酶）以及心脏毒性和血管收缩作用。这些作用可保护组织免受缺血性损伤，并在毒性恢复期间增加组织灌注。其他机制因缺乏证据而被削弱；这些机制包括对通道电流（例如钙）的直接影响以及质量效应超过线粒体代谢中的阻塞。在本叙述性综述中，我们讨论了这些提出的机制，并解决了该领域尚未解答的问题。还需要进一步的工作，但该领域在理解这些机制方面已经取得了相当大的进展。
