Abstract

The accidental overdose of local anesthetics may prove fatal. The commonly used amide local anesthetics have varying adverse effects on the myocardium, and beyond a certain dose all are capable of causing death. Local anesthetics are the most frequently used drugs amongst anesthetists and although uncommon, local anaesthetic systemic toxicity accounts for a high proportion of mortality, with local anaesthetic-induced cardiac arrest particularly resistant to standard resuscitation methods. Over the last decade, there has been convincing evidence of intravenous lipid emulsions as a rescue in local anesthetic-cardiotoxicity, and anesthetic organisations, over the globe have developed guidelines on the use of this drug. Despite this, awareness amongst practitioners appears to be lacking. All who use local anesthetics in their practice should have an appreciation of patients at high risk of toxicity, early symptoms and signs of toxicity, preventative measures when using local anesthetics, and the initial management of systemic toxicity with intravenous lipid emulsion. In this paper we intend to discuss the pharmacology and pathophysiology of local anesthetics and toxicity, and the rationale for lipid emulsion therapy.

Highlights

  • Local anesthetics (LAs) can be defined as drugs that reversibly block transmission of a nerve impulse, without affecting consciousness

  • Animal studies and case reports indicate a difference in cardiotoxicity between short-acting agent lignocaine and the longer-acting bupivacaine. For both agents there is dose-dependent cardiac depression but the greater toxicity potential of bupivacaine is disproportionate and does not correlate entirely with potency of inhibition of cardiac sodium channels. This difference could rely on an alternative mechanism of toxicity for bupivacaine, and we see this clinically in case reports of bupivacaine showing a more significant CVS toxicity than central nervous system (CNS), with arrhythmia and cardiac arrest often occurring without seizures

  • Vigilance is required when performing procedures that have a potential for systemic toxicity

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Summary

Introduction

Local anesthetics (LAs) can be defined as drugs that reversibly block transmission of a nerve impulse, without affecting consciousness. In 1969, articaine was synthesized by chemist Muschaweck, and with its potency and safety profile is the most common LA for dental procedures in most of Europe [2]. Despite these efforts, all of the amide LAs harbor varying levels of cardiovascular (CVS) and central nervous system (CNS) toxicity that is still a major complication seen today. Lumbar epidural anesthesia came about later in 1921 by Spanish military surgeon Fidel Pages. It was popularized by the Italian surgeon Dogliotti in the 1930s [7]. The idea of continuous infusion of epidural anesthesia, was not started until use of caudal blocks for emergency caesareans in 1942 [8], and in more recent decades the introduction of small flexible catheters has improved safety, delivery, and duration of epidural anesthesia

Mechanism of Action
Clinical Pharmacology
Pharmacokinetics and Metabolism
Local Anesthetic Systemic Toxicity
Lipid Emulsion Therapy
Prevention of Toxicity
Findings
Summary
Full Text
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