Updates in local anesthetic toxicity.

Abstract

Local anesthetics reversibly decrease the rate of depolarization and repolarization of excitable membranes (likenociceptors). They act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited Local anesthetic agents can be toxic if administered inappropriately, and in some cases may cause unintended reactions even when properly administered. The toxicity of local and infiltration anesthetics can be local or systemic. Systemic toxicity of anesthetics most often involves the central nervous system (CNS) or the cardiovascular system. CNS toxicity is biphasic. The earlier manifestations are due to CNS excitation, with problems such as seizures. Subsequent manifestations include CNS depression with a cessation of convulsions and the onset of unconsciousness and respiratory depression or arrest. Cardiovascular effects occur at higher serum concentrations of local anesthetics. These effects may include reentrant arrhythmias. Acceleration of the ventricular rate has been reported in patients with atrial arrhythmias. Treatment of local anesthetic toxicity may include: airway management, seizure suppression, management of cardiac arrhythmias. There is evidence that Intralipid, a commonly available intravenous lipid emulsion, can be effective in treating severe cardiotoxicity secondary to local anesthetic overdose, including human case reports of successful use in this way.