A Comparative in Vivo Study of Local Neurotoxicity of Lidocaine, Bupivacaine, 2-Chloroprocaine, and a Mixture of 2-Chloroprocaine and Bupivacaine

Barsa, J.; Batra, Manbir S.; Br, Fink; Sm, Sumi

doi:10.1097/00132586-198308000-00053

Cited by 19 publications

(10 citation statements)

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“…Thus, the therapeutic margin seems to be approximately the same for all local anaesthetics, irrespective of whether they are esters or amides. In contrast to other studies, 17,18 ours did not find that esters were more toxic than amides.…”

Section: Discussioncontrasting

confidence: 99%

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Lipophilicity but not stereospecificity is a major determinant of local anaesthetic-induced cytotoxicity in human T-lymphoma cells

Werdehausen

Braun

Fazeli

et al. 2012

European Journal of Anaesthesiology

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Moderate correlations for cytotoxicity with lipophilicity and clinical potency of local anaesthetics can be found in nonneuronal cells that are less than those reported previously with neuronal cells. Structural factors such as ester or amide linkage or stereospecificity do not have any influence on cytotoxicity. Although S(-) enantiomers may be advantageous with regard to systemic toxicity, they have no advantage in respect of local cytotoxicity in vitro.

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Section: Discussioncontrasting

confidence: 99%

“…Esters have been considered to be more neurotoxic in comparison to amides. [16][17][18] There are conflicting results as to whether stereoisomerism affects cytotoxicity. The more recently introduced S(À) enantiomers have been shown to be less cardiotoxic after systemic administration in comparison to the R(þ) enantiomers.…”

mentioning

confidence: 99%

Lipophilicity but not stereospecificity is a major determinant of local anaesthetic-induced cytotoxicity in human T-lymphoma cells

Werdehausen

Braun

Fazeli

et al. 2012

European Journal of Anaesthesiology

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“…piperocaine, tetracaine and lidocaine, and there are many reports involving chloroprocaine. Barsa et al (1982) showed epineural cellular infiltration and fibrosis, perineural fibrosis and axonal degeneration in nerves in rabbits exposed to chloroprocaine 3% or to a mixture of chloroprocaine 1.5% with bupivacaine 0.375%. Myers et al (1986) showed that local anaesthetic solutions applied externally can alter permeability of perineurium, leading to endoneural oedema.…”

Section: Neurotoxicitymentioning

confidence: 96%

Adverse Effects of Local Anaesthetics

McCaughey¹

1992

Drug Safety

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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.

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“…Some were long lasting and neurotoxic, butprocaine and tetracaine prevailed with relative consistency, efficacy and safety, as long as certain limitations (dosage, duration of action and indication) were followed. Attempts to use larger doses (72, 73) or to prolong their efficacy by mixing them with preservatives such as glycerin, polyethylene glycol, strychnine or methylparaben usually resulted in disastrous consequences (64, 74, 75).…”

Section: Local Anestheticsmentioning

confidence: 99%

Neurologic deficits and arachnoiditis following neuroaxial anesthesia

Aldrete¹

2002

Acta Anaesthesiol Scand

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Of late, regional anesthesia has enjoyed unprecedented popularity; this increase in cases has brought a higher frequency of instances of neurological deficit and arachnoiditis that may appear as transient nerve root irritation, cauda equina, and conus medullaris syndromes, and later as radiculitis, clumped nerve roots, fibrosis, scarring dural sac deformities, pachymeningitis, pseudomeningocele, and syringomyelia, etc., all associated with arachnoiditis. Arachnoiditis may be caused by infections, myelograms (mostly from oil-based dyes), blood in the intrathecal space, neuroirritant, neurotoxic and/or neurolytic substances, surgical interventions in the spine, intrathecal corticosteroids, and trauma. Regarding regional anesthesia in the neuroaxis, arachnoiditis has resulted from epidural abscesses, traumatic punctures (blood), local anesthetics, detergents, antiseptics or other substances unintentionally injected into the spinal canal. Direct trauma to nerve roots or the spinal cord may be manifested as paraesthesia that has not been considered an injurious event; however, it usually implies dural penetration, as there are no nerve roots in the epidural space posteriorly. Sudden severe headache while or shortly after an epidural block using the loss of resistance to air approach usually suggests pneumocephalus from an intradural injection of air. Burning severe pain in the lower back and lower extremities, dysesthesia and numbness not following the usual dermatome distribution, along with bladder, bowel and/or sexual dysfunction, are the most common symptoms of direct trauma to the spinal cord. Such patients should be subjected to a neurological examination followed by an MRI of the effected area. Further spinal procedures are best avoided and the prompt administration of IV corticosteroids and NSAIDs need to be considered in the hope of preventing the inflammatory response from evolving into the proliferative phase of arachnoiditis.

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A Comparative in Vivo Study of Local Neurotoxicity of Lidocaine, Bupivacaine, 2-Chloroprocaine, and a Mixture of 2-Chloroprocaine and Bupivacaine

Cited by 19 publications

References 0 publications

Lipophilicity but not stereospecificity is a major determinant of local anaesthetic-induced cytotoxicity in human T-lymphoma cells

Lipophilicity but not stereospecificity is a major determinant of local anaesthetic-induced cytotoxicity in human T-lymphoma cells

Adverse Effects of Local Anaesthetics

Neurologic deficits and arachnoiditis following neuroaxial anesthesia

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