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      Acute Lidocaine Toxicity; a Case Series

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          Abstract

          Introduction:

          Parenteral form of lidocaine is the best-known source of lidocaine poisoning. This study aimed to evaluate the characteristics of acute lidocaine toxicity .

          Methods:

          In this retrospective cross-sectional study, demographics, clinical presentation, laboratory findings, and outcome of patients intoxicated with lidocaine (based on ICD10 codes) admitted to Loghman Hakim Hospital, during April 2007 to March 2014 were analyzed.

          Results:

          30 cases with the mean age of 21.83 ± 6.57 year were studied (60% male). All subjects had used either 6.5% lidocaine spray or 2% topical formulations of lidocaine. The mean consumed dose of lidocaine was 465 ± 318.17 milligrams. The most frequent clinical presentations were nausea and vomiting (50%), seizure (33.3%), and loss of consciousness (16.7%). 22 (73.3%) cases had normal sinus rhythm, 4 (13.3%) bradycardia, 2 (6.7%) ventricular tachycardia, and 2 (6.7%) had left axis deviation. 11 (36.6%) cases were intubated and admitted to intensive care unit (ICU) for 6.91 ± 7.16 days. Three patients experienced status epilepticus that led to cardiac arrest, and death (all cases with suicidal intention).

          Conclusion:

          Based on the results of this study, most cases of topical lidocaine toxicity were among < 40-year-old patients with a male to female ratio of 1.2, with suicidal attempt in 90%, need for intensive care in 36.6%, and mortality rate of 10%.

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          Most cited references35

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          2015 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 33rd Annual Report.

          This is the 33rd Annual Report of the American Association of Poison Control Centers' (AAPCC) National Poison Data System (NPDS). As of 1 January 2015, 55 of the nation's poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 9.52 [7.40, 13.6] (median [25%, 75%]) minutes, creating a near real-time national exposure and information database and surveillance system.
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            Molecular mechanisms of local anesthesia: a review.

            Impulse block by LA occurs through the inhibition of voltage-gated Na+ channels. Both protonated and neutral LAs can inhibit Na+ channels though interference with the conformational changes that underly the activation process (the sequence of events that occurs as channels progress from the closed resting state to the open conducting state). The occlusion of open channels contributes little to the overall inhibition. Local anesthetic inhibition of Na+ currents increases with repetitive depolarizations in a process called phasic block. Phasic block represents increased LA binding, either because more channels become accessible during depolarization or because the channel conformations favored by depolarization bind LA with higher affinity. The details of phasic block are dependent on LA chemistry: certain LAs bind and dissociate quite rapidly, others act more slowly; some LAs interact effectively with closed states that occur intermediately between resting and open states, others favor the open channel, and still others have a higher affinity for inactivated states. Channel activation accelerates LA binding, and LAs may bind more tightly to activated and inactivated than to resting channels. In this regard, both the modulated receptor and the guarded receptor hypotheses are valid. In binding to activated and inactivated channels, LAs prevent the conformational changes of activation and antagonize the binding of activator agents that poise channels in activated, open states. These reciprocal actions are one aspect of the concerted conformational rearrangements that occur throughout Na+ channels during gating. The LA binding site may exist in the channel's pore, at the membrane-protein interface, or within the protein subunits of the channel. Judging from its susceptibility to intracellular proteases and its accessibility to LAs with limited membrane permeability (i.e., quaternary LAs in the cytoplasm), the site lies nearer to the cytoplasmic than the external surface of the membrane. Nevertheless, protons in the external medium influence the dissociation of LA from the closed channel. Binding of LAs at the inhibitory site is weak and loose. If one accounts for the membrane-concentrating effects of LA hydrophobicity that are expressed as membrane: buffer partition coefficients equal to 10(2)-10(4), then the apparent LA affinities are low. The equilibrium dissociation constants calculated on the basis of free drug in the membrane are 1-10 mM, with a correspondingly weak binding to the inhibitory LA site. The stereospecificity of LA action is also relatively nonselective, suggesting a loose fit between ligand and binding site.(ABSTRACT TRUNCATED AT 400 WORDS)
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              American Society of Regional Anesthesia and Pain Medicine checklist for managing local anesthetic systemic toxicity: 2012 version.

              In 2010, the American Society of Regional Anesthesia and Pain Medicine (ASRA) issued a practice advisory on local anesthetic systemic toxicity (LAST). The executive summary of this work contained a document that was intended to serve as a checklist for the management of LAST. Based on testing the checklist during a simulated episode of LAST, ASRA has issued an updated version that should replace the previous 2010 version. Electronic copies of the ASRA Checklist, suitable for lamination and inclusion in a local anesthetic toxicity kit, are available from the ASRA Web site (www.asra.com).
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                Author and article information

                Journal
                Emerg (Tehran)
                Emerg (Tehran)
                Emerg
                Emergency
                Shahid Beheshti University of Medical Sciences (Tehran, Iran )
                2345-4563
                2345-4571
                2018
                16 June 2018
                : 6
                : 1
                : e38
                Affiliations
                [1 ]Excellence Center of Clinical Toxicology, Department of Clinical Toxicology, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
                [2 ]Department of Forensic Toxicology, Legal Medicine Research Center, Legal Medicine Organization, Tehran, Iran.
                [3 ]School of Medicine, Shahed University, Tehran, Iran.
                Author notes
                [* ]Corresponding author: Shahin Shadnia; Department of Clinical Toxicology, Loghman-Hakim Hospital Poison Center, Kamali Avenue, South Karegar Street, Tehran, Iran. Tel/Fax: +98-21-55424041, Email: shahin1380@yahoo.com
                Article
                emerg-6-e38
                6036540
                30009240
                b845300c-2e9e-471e-b469-c6cf2ff4d38f
                Copyright (2018) Shahid Beheshti University ofMedical Sciences

                This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0)( https://creativecommons.org/licenses/by-nc/3.0/).

                History
                : February 2018
                : June 2018
                Categories
                Original Article

                lidocaine,poisoning,drug-related side effects and adverse reactions,administration

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