Adverse Effects of Local Anaesthetics

Abstract

Local anaesthetics are responsible for 5 to 10% of all reported adverse reactions to anaesthetic drugs. Adverse effects may be classified as: (a) those associated directly with blocking ion channels in cell membranes, such as cardiovascular and CNS toxicity; (b) those due to other effects of drug or vehicle (mainly peripheral nerve complications); (c) allergic reactions (often a mistaken diagnosis); and (d) mechanical or other effects of technique, such as needle trauma or introduction of infection. Signs and symptoms of CNS toxicity include convulsions, followed by coma and respiratory depression. Convulsions are due to disinhibition of nervous conduction, probably by an action at the gamma-aminobutyric acid (GABA) receptor complex, while depressant effects, which predominate at higher doses, are due to blockade of sodium channels. CNS toxicity is potentiated by hypoxia and hypercapnia, so acute management must minimise these. Cardiovascular toxicity also involves sodium channel blockade, reducing contractility and interfering with conduction. Bupivacaine differs from lidocaine (lignocaine) in the sudden occurrence of dangerous ventricular arrhythmias including fibrillation at subconvulsant doses. Ropivacaine is a newer amide local anaesthetic with toxicity intermediate between these but potency similar to bupivacaine. Neurotoxic complications leading to prolonged deficit after intraspinal administration are uncommon. Causes are multifactorial, and include pH of and additives to preparations. Allergic reactions account for only 1% of untoward reactions, but anaphylactoid collapse can be lifeth-reatening and requires rapid and effective management.

Lidocaine toxicity to rat retinal ganglion cells

“…Transient loss of vision with an afferent pupillary defect has also been associated with intracameral lidocaine (9). Lidocaine is potentially toxic both systemically and to the optic nerve (10,11). There are no reports to date describing retinal pathology associated with intracameral lidocaine.…”

Newborn Tissue Concentrations of Bupivacaine following Maternal Epidural Administration during Labor in Guinea Pigs

“…Bupivacaine was administered epidurally in conjunction with induced labor to simulate obstetric use. Brain and heart were selected for analysis because they are potential sites for bupivacaine effects on ion channels and conduction [20,21]. Liver was also analyzed because it is the major site of bupivacaine metabolism in humans.…”

Beneficial effect of trimebutine and N-monodesmethyl trimebutine on trinitrobenzene sulfonic acid-induced colitis in rats

“…In contrast, bupivacaine only displays a weak and no significant activity on TNBS-induced colitis at 10mg/kg/d, and toxicity at higher dose. Cardiotoxicity of bupivacaine when overdosed is well documented (McCaughey, 1992) and association with ketamine had been described to lead to a possible inhibition of the metabolism of bupivacaine (Gantenbein et al, 1997) which could explain the observed toxicity under our experimental conditions.…”