Toxicity

Toxicity is determined by the total dose and mode of LA delivered, modulated by factors influencing systemic uptake. The relative absorption of LA is site dependent. The absorption, from highest to lowest, is: intercostal/intratracheal > epidural/caudal > brachial plexus > mucosal > distal peripheral nerve > subcutaneous. Caution should be exercised with intercostal blocks: the recommended LA dose for intercostal blocks is one-tenth of maximum for peripheral blocks. Serious adverse reactions including systemic toxic reactions are more frequently encountered with the use of amide rather than ester LAs, due in part to the slower amide metabolism. However, patients with atypical plasma cholinesterase may be prone to systemic toxicity from ester LAs. The systemic toxicity of LAs is enhanced by hypercarbia, hypoxemia, and acidosis. Systemic toxicity is usually the result of rapid inadvertent intravenous injection or delivery of an excessive total dose of LA.

Serious toxicity primarily involves the CNS and cardiovascular system. CNS toxicity results from a combination of central excitatory and depressant activity of the LA, ranging from perioral tingling and numbness to confusion, seizure, and coma (see Tabje.., 32-9). Cardiovascular toxicity relates to the Na+ channel blockade and results in myocardial depression and dysrhythmias. Bupivacaine, due in part to its prolonged binding to the receptor site and slow metabolism, is particularly cardiotoxic and for this reason contraindicated for intravenous regional anesthesia. Methemoglobinemia has also been reported from excessive dosage.

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