Moreover, the first clinical case of lipid emulsion resuscitation of a patient with toxicity induced by a non-local anesthetic drug was reported in 2008: Intralipid® infusion led to the recovery of a 17-year-old female patient with severe cardiovascular depression and seizure due to toxic doses of bupropion and lamotrigine 17. The treated patient, a 58-year-old male with seizure and asystole due to toxicity from bupivacaine and mepivacaine used in an interscalene brachial plexus block, was unresponsive to advanced cardiac life support, but lipid emulsion led to recovery 16. reported the first clinical case of lipid emulsion for treating presumed bupivacaine toxicity in 2006 16. The administration of lipid emulsion affected the central nervous system toxicity induced by local anesthetics by increasing the dosage of bupivacaine and levobupivacaine needed to produce convulsion in awake rats 15. Moreover, Intralipid® improved the survival and hemodynamics of bupivacaine-induced cardiac toxicity in dogs 14. Pretreatment with lipid emulsion reportedly increased the dosage of bupivacaine needed to produce asystole in rats, and a mixture of Intralipid® and plasma containing bupivacaine produced a high lipid-to-aqueous-phase ratio of bupivacaine (11.9 ± 1.77), suggesting that Intralipid® has a high capacity to bind bupivacaine 13. reported ventricular arrhythmia caused by the presumed intravascular migration of an epidural catheter in a 6-year-old male patient with both secondary carnitine deficiency due to long-term treatment with valproic acid and a non-toxic dose of bupivacaine (0.58 mg/ml) 12. Based on these reports, this unexpected ventricular arrhythmia was likely associated with increased susceptibility to bupivacaine toxicity due to carnitine deficiency 7 - 11. reported that subcutaneous injection of a small dose of bupivacaine (non-toxic dose: 22 mg) in a 16-year-old female patient with isovaleric acidemia yielded unexpected ventricular arrhythmia likely caused by secondary systemic carnitine deficiency 7. Pretreatment with L-carnitine before bupivacaine-induced asystole in rats decreased the susceptibility to bupivacaine-induced cardiac toxicity 11. Bupivacaine prevents long-chain fatty acid transport to the mitochondria by inhibiting carnitine-acylcarnitine translocase 8 - 10. β-Oxidation produces adenosine triphosphate (ATP) in cardiac mitochondria using long-chain fatty acids as the major energy source of the heart 9. Carnitine helps transport long-chain fatty acids into the mitochondria 7 - 9 carnitine-acylcarnitine translocase transports long-chain acyl-carnitine into the mitochondrial matrix and returns carnitine to the cytoplasm 9. However, lipid emulsion is currently used to treat local anesthetic-induced systemic toxicity 2 - 6. Lipid emulsion was originally developed for parenteral nutrition in the 1960s 1. The current review includes the following: 1) an introduction, 2) a list of the proposed mechanisms, 3) a discussion of the best lipid emulsion treatment for reversal of local anesthetic toxicity, 4) a description of the effect of epinephrine on lipid emulsion-mediated resuscitation, 5) a description of the recommended lipid emulsion treatment, and 6) a conclusion. Investigators have suggested mechanisms associated with the lipid emulsion-mediated recovery of cardiovascular collapse caused by local anesthetic systemic toxicity these mechanisms include lipid sink, a widely accepted theory in which highly soluble local anesthetics (particularly bupivacaine) are absorbed into the lipid phase of plasma from tissues (e.g., the heart) affected by local-anesthetic-induced toxicity enhanced redistribution (lipid shuttle) fatty acid supply reversal of mitochondrial dysfunction inotropic effects glycogen synthase kinase-3β phosphorylation associated with inhibition of the mitochondrial permeability transition pore opening inhibition of nitric oxide release and reversal of cardiac sodium channel blockade. A systemic review and meta-analysis confirm the efficacy of this treatment. Lipid emulsion has been shown to be an effective treatment for systemic toxicity induced by local anesthetics, which is reflected in case reports.
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