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). Based on these reports, this unexpected ventricular arrhythmia was likely associated with increased susceptibility to bupivacaine toxicity due to carnitine deficiency. 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. Pretreatment with L-carnitine before bupivacaine-induced asystole in rats decreased the susceptibility to bupivacaine-induced cardiac toxicity. Bupivacaine prevents long-chain fatty acid transport to the mitochondria by inhibiting carnitine-acylcarnitine translocase. β-Oxidation produces adenosine triphosphate (ATP) in cardiac mitochondria using long-chain fatty acids as the major energy source of the heart. Carnitine helps transport long-chain fatty acids into the mitochondria carnitine-acylcarnitine translocase transports long-chain acyl-carnitine into the mitochondrial matrix and returns carnitine to the cytoplasm. However, lipid emulsion is currently used to treat local anesthetic-induced systemic toxicity. Lipid emulsion was originally developed for parenteral nutrition in the 1960s. Keywords: lipid emulsion, local anesthetic systemic toxicity, lipid sink, lipid shuttle, bupivacaine Introduction 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. Select the file that you have just downloaded and select import option Reference Manager (RIS). Lipid Emulsion for Treating Local Anesthetic Systemic Toxicity. ✉ Corresponding author: Ju-Tae Sohn, Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, 79 Gangnam-ro, Jinju-si, Gyeongsangnam-do, 52727, Republic of Korea Tel.: +82-5 Fax: +82-5 E-mail: jts ohnac.kr More *These authors equally contributed to this study as co-first authors. Department of Anesthesia and Pain Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, Republic of Korea Institute of Health Sciences, Gyeongsang National University, Jinju-si, 52727, Republic of Koreaģ. Department of Anesthesiology and Pain Medicine, Gyeongsang National University School of Medicine, Gyeongsang National University Hospital, 15 Jinju-daero 816 Beon-gil, Jinju-si, Gyeongsangnam-do, 52727, Republic of KoreaĢ. Seong-Ho Ok 1,2*, Jeong-Min Hong 3*, Soo Hee Lee 1,2, Ju-Tae Sohn 1,2ġ. Review Lipid Emulsion for Treating Local Anesthetic Systemic Toxicity
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