Lidocaine
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Lidocaine
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| Systematic (IUPAC) name | |
| 2-(diethylamino)- N-(2,6-dimethylphenyl)acetamide |
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| Identifiers | |
| CAS number | 73-78-9 (hydrochloride) |
| ATC code | N01 C01 D04 S02 C05 |
| PubChem | |
| DrugBank | |
| ChemSpider | |
| Chemical data | |
| Formula | C14H22N2O |
| Mol. mass | 234.34 g/mol |
| SMILES | & |
| Synonyms | N-(2,6-dimethylphenyl)-N2,N2-diethylglycinamide |
| Physical data | |
| Melt. point | 68 °C (154 °F) |
| Pharmacokinetic data | |
| Bioavailability | 35% (oral) 3% (topical) |
| Metabolism | Hepatic, 90% CYP1A2-mediated |
| Half life | 1.5–2 hours |
| Excretion | renal |
| Therapeutic considerations | |
| Pregnancy cat. | |
| Legal status | |
| Routes | IV, subcutaneous, topical |
Lidocaine (INN) (pronounced /ˈlaɪdɵkeɪn/) or lignocaine (former BAN) (/ˈlɪɡnɵkeɪn/) is a common local anesthetic and antiarrhythmic drug. Lidocaine is used topically to relieve itching, burning and pain from skin inflammations, injected as a dental anesthetic, and in minor surgery.
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[edit] History
Lidocaine, the first amino amide-type local anesthetic, was first synthesized under the name xylocaine by Swedish chemist Nils Löfgren in 1943.[1] His colleague Bengt Lundqvist made the first injection anesthesia experiments on himself.[1] It was first marketed in 1949.
[edit] Preparation
Lidocaine may be prepared in two steps by the reaction of 2,6-xylidine with chloroacetyl chloride, followed by the reaction with diethylamine:[2]
[edit] Pharmacokinetics
Lidocaine is approximately 90% metabolized (de-ethylated) in the liver by CYP1A2 (and to a minor extent CYP3A4) to the pharmacologically-active metabolites monoethylglycinexylidide and glycinexylidide.
The elimination half-life of lidocaine is approximately 1.5–2 hours in most patients. This may be prolonged in patients with hepatic impairment (average 343 minutes) or congestive heart failure (average 136 minutes).[3]
[edit] Pharmacodynamics
[edit] Anesthesia
Lidocaine alters depolarization in neurons, by blocking the fast voltage gated sodium (Na+) channels in the cell membrane[4][clarification needed]. With sufficient blockade, the membrane of the presynaptic neuron will not depolarize and so fail to transmit an action potential, leading to its anaesthetic effects. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations will also affect other modalities of neuron signaling[citation needed].
[edit] Clinical use
[edit] Indications
Topical lidocaine has been shown to relieve postherpetic neuralgia in some patients, though there is not enough study evidence to recommend it as a first-line treatment.[5] It also has uses as a temporary fix for tinnitus. Although not completely curing the illness, it has been shown to reduce the effects by around two thirds.[6]
[edit] Contraindications
Contraindications for the use of lidocaine include:
- Heart block, second or third degree (without pacemaker)[citation needed]
- Severe sinoatrial block (without pacemaker)[citation needed]
- Serious adverse drug reaction to lidocaine or amide local anaesthetics[citation needed]
- Concurrent treatment with quinidine, flecainide, disopyramide, procainamide (Class I antiarrhythmic agents)[citation needed]
- Prior use of Amiodarone hydrochloride[citation needed]
- Hypotension not due to Arrhythmia[citation needed]
- Bradycardia[citation needed]
- Accelerated idioventricular rhythm[citation needed]
- Pacemaker[citation needed]
[edit] Adverse drug reactions
Adverse drug reactions (ADRs) are rare when lidocaine is used as a local anesthetic and is administered correctly. Most ADRs associated with lidocaine for anesthesia relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, but allergic reactions can rarely occur.[citation needed].
Systemic exposure to excessive quantities of lidocaine mainly result in central nervous system (CNS) and cardiovascular effects – CNS effects usually occur at lower blood plasma concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations[citation needed]. CNS effects may include CNS excitation (nervousness, tingling around the mouth (also known as circumoral paraesthesia), tinnitus, tremor, dizziness, blurred vision, seizures) followed by depression, and with increasingly heavier exposure: drowsiness, loss of consciousness, respiratory depression and apnoea). Cardiovascular effects include hypotension, bradycardia, arrhythmias, and/or cardiac arrest – some of which may be due to hypoxemia secondary to respiratory depression.[7]
ADRs associated with the use of intravenous lidocaine are similar to toxic effects from systemic exposure above. These are dose-related and more frequent at high infusion rates (≥3 mg/minute)[citation needed]. Common ADRs include: headache, dizziness, drowsiness, confusion, visual disturbances, tinnitus, tremor, and/or paraesthesia. Infrequent ADRs associated with the use of lidocaine include: hypotension, bradycardia, arrhythmias, cardiac arrest, muscle twitching, seizures, coma, and/or respiratory depression.[7]
[edit] Insensitivity to lidocaine
Relative insensitivity to lidocaine runs in families. In hypokalemic sensory overstimulation, relative insensitivity to lidocaine has been described in people who also have attention deficit hyperactivity disorder[citation needed]. In dental anesthesia, a relative insensitivity to lidocaine can occur for anatomical reasons due to unexpected positions of nerves[citation needed]. Some people with Ehlers-Danlos syndrome are insensitive to lidocaine.[8]
[edit] Dosage forms
Lidocaine, usually in the form of lidocaine hydrochloride, is available in various forms including:
- Injected local anesthetic (sometimes combined with epinephrine)[citation needed]
- Dermal patch (sometimes combined with prilocaine)[citation needed]
- Intravenous injection (sometimes combined with epinephrine)[citation needed]
- Intravenous infusion[citation needed]
- Nasal instillation/spray (combined with phenylephrine)[citation needed]
- Oral gel (often referred to as "viscous lidocaine" or abbreviated "lidocaine visc" or "lidocaine hcl visc" in pharmacology; used as teething gel)[citation needed]
- Oral liquid[citation needed]
- Topical gel (as with Aloe Vera gels that include Lidocaine)[citation needed]
- Topical liquid[citation needed]
- Topical patch (Lidocaine 5% patch is marketed as "Lidoderm" in the US (since 1999) and "Versatis" in the UK (since 2007 by Grünenthal))[citation needed]
- Topical aerosol Spray[citation needed]
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This section requires expansion. |
[edit] Additive in cocaine
Lidocaine is often added to cocaine as a diluent.[9] Cocaine numbs the gums when applied, and since lidocaine causes stronger numbness[10], users get the impression of high-quality cocaine when in actuality, the user is receiving a diluted product.[11]
[edit] Compendial status
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This section requires expansion. |
[edit] Notes & References
- ^ a b Nils Löfgren (1948). Xylocaine: a new synthetic drug.
- ^ T. J. Reilly (1999). "The Preparation of Lidocaine". J. Chem. Ed. 76 (11): 1557. http://jchemed.chem.wisc.edu/Journal/Issues/1999/Nov/abs1557.html.
- ^ Thomson PD, Melmon KL, Richardson JA, et al. (1973). "Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans". Ann. Intern. Med. 78 (4): 499–508. PMID 4694036.
- ^ Catterall WA (2002). "Molecular mechanisms of gating and drug block of sodium channels". Novartis Found Symp 241: 206–32. doi:. PMID 11771647.
- ^ Khaliq W, Alam S, Puri N (2007). "Topical lidocaine for the treatment of postherpetic neuralgia". Cochrane Database Syst Rev (2): CD004846. doi:. PMID 17443559.
- ^ http://newsvote.bbc.co.uk/1/hi/health/7175306.stm
- ^ a b Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3
- ^ Grahame, Rodney (2005). "Local anaesthetic failure in joint hypermobility syndrome". Journal of the Royal Society of Medicine 98 (2): 84–85. doi:. PMID 15684369.
- ^ Naissa Prévide Bernardo, Maria Elisa Pereira Bastos Siqueira, Maria José Nunes de Paiva, Patrícia Penido Maia (2003). "Caffeine and other adulterants in seizures of street cocaine in Brazil". International Journal of Drug Policy 14 (4): 331–334. doi:. http://www.sciencedirect.com/science/article/B6VJX-497HGRX-5/2/3b5f81654f1e907ceb3095b4b5207362.
- ^ Howell, Kimberly. "Take a big-picture approach when dealing with corneal sensation". http://www.eyeplastics.org/topics/thyroid/thyroid_news/corneal_sensation.htm. Retrieved on 2009-04-23. "Lidocaine is more potent, with rapid diffusion and penetration."
- ^ 599 F.2d 635
- ^ The United States Pharmacopeial Convention. "Revision Bulletin: Lidocaine and Prilocaine Cream–Revision to Related Compounds Test". http://www.usp.org/USPNF/notices/lidocaineAndPrilocaine.html. Retrieved on 10 July 2009.
[edit] See also
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