Methemoglobin levels following intravenous lidocaine administration

Weiss, Leon; Generalovich, Thomas; Heller, Michael; Paris, Paul M.; Stewart, Ronald D.; Kaplan, Richard M; Thompson, Denisse R.

doi:10.1016/s0196-0644(87)80180-4

Cited by 24 publications

(15 citation statements)

References 19 publications

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“…2,6-DMA has also been found in milk from cows and humans treated with lidocaine (Puente and Josephy, 2001). Following iv administration of lidocaine to patients, methemoglobinemia has been observed (Weiss et al, 1987), which is consistent with the formation of an N-hydroxy biotransformant (Kiese, 1966).…”

Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 76%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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Toxicity and carcinogenicity in the mucosa of the nasal passages in rodents has been produced by a variety of organic chemicals which are systemically distributed. In this review, 14 such chemicals or classes were identified that produced rodent nasal cytotoxicity, but not carcinogenicity, and 11 were identified that produced nasal carcinogenicity. Most chemicals that affect the nasal mucosa were either concentrated in that tissue or readily activated there, or both. All chemicals with effects in the nasal mucosa that were DNA-reactive, were also carcinogenic, if adequately tested. None of the rodent nasal cytotoxins has been identified as a human systemic nasal toxin. This may reflect the lesser biotransformation activity of human nasal mucosa compared to rodent and the much lower levels of human exposures. None of the rodent carcinogens lacking DNA reactivity has been identified as a nasal carcinogen or other cancer hazard to humans. Some DNA-reactive rodent carcinogens that affect the nasal mucosa, as well as other tissues, have been associated with cancer at various sites in humans, but not the nasal cavity. Thus, findings in only the rodent nasal mucosa do not necessarily predict either a toxic or carcinogenic hazard to that tissue in humans.

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Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 76%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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“…Benzocaine, which is used as a topical spray, is also a frequent cause. Although lidocaine is not normally expected to cause methaemoglobinaemia, low levels of methaemoglobin (up to 1.2%) have been reported with intravenous lidocaine in cardiac patients (Weiss et al 1987).…”

Section: Methaemoglobinaemiamentioning

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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“…These metabolites are hydrolyzed to DMA (http://www.dentsply.com/assets/DFU/oraqix_pi.pdf). Both lido and prilo increase formation of methemoglobin (Weiss et al, 1987;Vasters et al, 2006) probably via the corresponding N-hydroxyarylamines (Weisburger and Weisburger, 1973). This can be an acute toxicological problem associated with the use (Buckley and Benfield, 1993) and misuse (Balit et al, 2006) of these drugs and may be the basis for some effects in rats at high dosages.…”

mentioning

confidence: 99%

Assessment of the Medicines Lidocaine, Prilocaine, and Their Metabolites, 2,6-Dimethylaniline and 2-Methylaniline, for DNA Adduct Formation in Rat Tissues

Duan¹,

Jeffrey²,

Williams³

2008

Drug Metab Dispos

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ABSTRACT:The local anesthetics lidocaine (lido) and prilocaine (prilo) are metabolized to their constituent aromatic amines 2,6-dimethylaniline (DMA, 2,6-xylidine) and 2-methylaniline (MA, o-toluidine), respectively, which are both tumorigenic in rats. The capacity of lido and prilo to form DNA adducts was assessed in major target tissues for aromatic amines in male F344 rats in comparison to equimolar doses of DMA and MA using the

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Methemoglobin levels following intravenous lidocaine administration

Cited by 24 publications

References 19 publications

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Adverse Effects of Local Anaesthetics

Assessment of the Medicines Lidocaine, Prilocaine, and Their Metabolites, 2,6-Dimethylaniline and 2-Methylaniline, for DNA Adduct Formation in Rat Tissues

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