How is systemic local anesthetic toxicity treated?

How is systemic local anesthetic toxicity treated?

The first step in the treatment of systemic local anes-thetic toxicity is to stop the further administration of the offending agent into the central circulation. In the case of continuous intravenous infusion, for the treatment of pre-mature ventricular contractions, cessation of administration of local anesthetic is simple to accomplish. Tourniquet leak or premature deflation of the tourniquet during intravenous regional anesthesia requires tourniquet adjustment to prevent further loss of local anesthetic into the circulation.

The initial manifestations of local anesthetic toxicity are those of central nervous excitation. As neurons discharge at rapid rates, they consume oxygen and glucose. Conse-quently, oxygen should be administered early (though supplemental oxygen should already have been supplied to the patient), because the triad of hypoxemia, acidosis, and hypercarbia develops rapidly, due to the previously described respiratory and cardiovascular impairments. When positive-pressure ventilation is initiated, hyperventi-lation is preferred to prevent and treat hypercarbia. Once consciousness is lost, the patient is at increased risk for aspiration pneumonitis, thus the airway should be protected with a cuffed endotracheal tube. Diazepam, 0.1–0.3 mg/kg intravenously, suppresses seizure activity with little or no adverse cardiovascular effect. Although rapid-acting barbi-turates are also effective for seizure control, their use can be complicated by cardiovascular depression. Because local anesthetic toxicity is fraught with dysrhythmias, depressed contractility, and vasodilation, the addition of another source of cardiovascular depression, a barbiturate, is best avoided. Tonic-clonic seizure activity may prevent adequate ventilation with positive pressure and succinylcholine may need to be administered in order to facilitate oxygenation and ventilation. Although succinylcholine stops the major muscle manifestations of seizure activity, it does not treat the central nervous system source. Uncontrolled rapid neuronal dis-charge persists, with huge cerebral requirements for oxygen and glucose. During this period, oxygen delivery assumes an even greater importance than it normally does.

Cardiovascular toxicity manifests as hypotension, which is treated with intravenous fluids, the Trendelenburg position, and phenylephrine. Left ventricular dysfunction is managed with an inotropic agent such as dopamine or amrinone. Cardiac dysrhythmias may require large doses of epinephrine and atropine.