Abstract

Local anesthetic toxicity is a rare, but potentially lethal, complication of regional anesthesia that cannot be prevented by any single measure. It is associated with CNS excitation and can lead to refractory cardiac dysfunction and collapse. The development of lipid emulsion for the treatment of anesthetic-induced toxicity resulted from a set of observations during a study on the potent, lipophilic drug bupivacaine and its associated clinical risk of intransigent cardiac toxicity in otherwise healthy individuals. Subsequent laboratory studies and clinical reports have shown that infusion of lipid can reliably reverse toxicity from potent local anesthetics as well as other drugs. The underlying mechanisms of lipid resuscitation may be a combination of a ‘lipid sink’ and metabolic effect. Lipid rescue has led to a reduction in fatalities associated with severe systemic toxicity, but continued research is necessary for a better mechanistic understanding. Increased physician awareness and education, as well as optimized treatment protocols, will significantly reduce the rate of morbidity and mortality from local anesthetic toxicity.

Keywords: Fat emulsion, heart arrest, intravenous, local anesthetics, overdose, resuscitation, toxicity, Antidote, CNS excitation, refractory cardiac dysfunction, lipophilic drug bupivacaine, cocaine, lipid infusion, treating cardiotoxicity, refractory cardiac arrest, American Society of Regional Anes-thesia, vascular density, tissue blood flow, cardiovascular collapse, seizure, agitation, loss of conscious-ness, nonical anesthetics, incremental injection, bupivacaine-induced cardiac, isovaleric, ventricular dysrhythmias, carnitine-dependent pathway, carnitine acylcarnitine translocase, severe hypotension, lipid therapy, mepivacaine. Advanced Cardiac Life Support (ACLS), epinephrine, atropine, amiodar-one, vasopressin, electrocardiogram, dizziness, drowsiness, generalized, lamotrigine, bupro-prion, ventricular tachycardia, fibrillation, catecholamines, amiodarone, adenosine triphosphate, beta-oxidation, The ‘lipid sink’ mechanism, physicochemical property, parti-tion coefficient, electrostatic interactions, liposomes, hemodynamic stability, clinical dilemma