Lipid emulsion treatment of systemic toxicity induced by local anesthetics or other drugs.
10.5124/jkma.2014.57.6.537
- Author:
Il Woo SHIN
1
;
Ju Tae SOHN
Author Information
1. Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju, Korea. jtsohn@nongae.gsnu.ac.kr
- Publication Type:Original Article
- Keywords:
Lipid emulsion;
Toxicity;
Local anesthetics;
Heart arrest
- MeSH:
Administration, Intravenous;
Anesthetics, Local*;
Cardiopulmonary Resuscitation;
Drug-Related Side Effects and Adverse Reactions;
Fatty Acids;
Heart Arrest;
Hemodynamics;
Humans;
Myoclonus;
Parenteral Nutrition;
Seizures;
Tachycardia, Supraventricular;
Unconsciousness;
Ventricular Fibrillation
- From:Journal of the Korean Medical Association
2014;57(6):537-544
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Although intravenous lipid emulsion (LE) is used mainly for parenteral nutrition, recently it has been used to treat patients with cardiopulmonary resuscitation (CPR)-resistant cardiovascular collapse induced by a toxic dose of local anesthetics or other drugs. Intravenous LE resolves symptoms of local anesthetic systemic toxicity, including convulsion, myoclonus, loss of consciousness, cardiac arrest, supraventricular tachycardia, and ventricular fibrillation. The main underlying mechanisms suggested to be responsible for LE-induced reversal of cardiac arrest due to drug toxicity are the lipid sink effect and the metabolic effect. The lipid sink theory posits that LE extracts a lipid-soluble toxic drug from the tissue. When a patient with cardiovascular collapse induced by a local anesthetic or another lipid-soluble drug is unresponsive to supportive treatments, including CPR and vasopressor therapy, LE administration can be considered. The suggested dosing regimen is as follows: 1) an initial intravenous bolus administration of 20% LE (1.5 mL/kg) is followed by a continuous infusion of 20% LE (0.25 mL/kg/min); and 2) when hemodynamic functions are unstable after the initial LE infusion, an intravenous administration of 20% LE (1.5 mL/kg) is repeated and followed by an increased continuous infusion of 20% LE (0.5 mL/kg/min). Further research is warranted regarding other possible mechanisms of LE's effect, the timing of LE administration, and the effect of various fatty acids on the LE-mediated reversal of cardiac arrest. This article reviews case reports and experimental evidence concerning the LE-mediated reversal of intractable cardiac arrest induced by drug toxicity, the underlying mechanism, and the dosing regimen.
