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      An Intentional Aconite Overdose: A Case Report

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          Abstract

          Background

          Aconite is one of the most toxic known herbs, widely used for centuries as an essential Chinese medicine, but also for deliberate poisoning throughout history. Clinically indicated in herbal medicine for a range of ailments from headaches to muscle spasm, unfortunately the narrow therapeutic window may lead to a range of toxic presentations. The mechanism of action of the pharmacologically active compounds in Aconite relate to the activation of voltage gated sodium channels within a range of tissue including myocardial, neuronal and smooth muscle leading to persistent cellular activity.

          Case presentation

          We report on a rare case of a fifty year old male with intentional aconite overdose presenting with refractory cardiovascular instability from persistent life threatening arrhythmias, respiratory failure and seizure activity.

          Conclusion

          An overview of Aconite, its history, pharmacological effects, treatment of overdose and outcomes is presented.

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          Most cited references19

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          The effects of Aconitum alkaloids on the central nervous system.

          A Ameri (1998)
          Preparations of Aconitum roots are employed in Chinese and Japanese medicine for analgesic, antirheumatic and neurological indications. The recent surge in use of phytomedicine derived from traditional Chinese medicine as well as increasing concerns about possible toxic effects of these compounds have inspired a great deal of research into the mechanisms by which certain Aconitum alkaloids may act on the central nervous system. The pharmacological effects of preparations of Aconitum roots are attributed to several diterpenoid alkaloids. The main alkaloid of these plants is aconitine, a highly toxic diterpenoid alkaloid which is known to suppress the inactivation of voltage-dependent Na+ channels by binding to neurotoxin binding site 2 of the alpha-subunit of the channel protein. In this article the pharmacology of several structurally related Aconitum alkaloids is highlighted and their therapeutic vs toxic potential is discussed. Neurochemical and neurophysiological studies will be reviewed with emphasis on the effects of the alkaloids in regions of the brain that have been implicated in pain transmission and generation of epileptic activity. Considering the chemical structure of the Aconitum alkaloids as well as their mechanism of action, a subdivision in three groups becomes obvious: the first group comprises such alkaloids which possess high toxicity due to two ester boundings at the diterpene skeleton. The members of this group activate voltage-dependent sodium channels already at resting potential and inhibit noradrenaline reuptake. Activation of sodium channels and in consequence excessive depolarization with final inexcitability and suppression of pain transmission account for their antinociceptive properties. The second group comprises less toxic monoesters which have been shown to possess strong antinociceptive, antiarrhythmic and antiepileptiform properties due to a blockade of the voltage-dependent sodium channel. Electrophysiological studies have revealed a use-dependent inhibition of neuronal activity by these alkaloids. They seem to be competitive antagonists of the group I-alkaloids. The third group of Aconitum alkaloids are lacking an ester side chain in the molecule. Toxicity is markedly reduced when compared with the two other groups. They fail to affect neuronal activity, but are reported to have antiarrhythmic actions suggesting that they may have different affinities to various subtypes of the alpha-subunit of the Na+ channel in brain and heart.
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            Aconitum sp. alkaloids: the modulation of voltage-dependent Na+ channels, toxicity and antinociceptive properties.

            Jutta Friese, Johannes Gleitz, Ulrike Gutser … (1997)
            Alkaloids from Aconitum sp., used as analgesics in traditional Chinese medicine, were investigated to elucidate their antinociceptive and toxic properties considering: (1) binding to Na+ channel epitope site 2, (2) alterations in synaptosomal Na+ and Ca2+ concentration ([Na+]i, [Ca2+]i), (3) arrhythmogenic action of isolated atria, (4) antinociceptive and (5) acute toxic action in mice. The study revealed a high affinity group (Ki 1 microM) and a low affinity group (Ki 10 microM) of alkaloids binding to site 2. The compounds of the high affinity group induce an increase in synaptosomal [Na+]i and [Ca2+]i (EC50 3 microM), are antinociceptive (ED50, 25 microg/kg), provoke tachyarrhythmia and are highly toxic (LD50 70 microg/kg), whereas low affinity alkaloids reduce [Ca2+]i, induce bradycardia and are less antinociceptive (ED50 20 mg/kg) and less toxic (LD50 30 mg/kg). These results suggest that the alkaloids can be grouped in Na+ channel activating and blocking compounds, but none of the alkaloids seem to be suitable as analgesics because of the low LD50/ED50 values.
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              A systematic review of pharmacokinetic studies on herbal drug Fuzi : Implications for Fuzi as personalized medicine

              Xiao-yan Li, Jin-jun Wu, Zhen-zhen Guo … (2018)
              Article 0 comments Cited 37 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Crit Care Med (Targu Mures)
                Journal ID (iso-abbrev): J Crit Care Med (Targu Mures)
                Journal ID (publisher-id): jccm
                Journal ID (pmc): jccm
                Title: The Journal of Critical Care Medicine
                Publisher: Sciendo
                ISSN (Print): 2393-1809
                ISSN (Electronic): 2393-1817
                Publication date Collection: April 2020
                Publication date (Electronic): 06 May 2020
                Volume: 6
                Issue: 2
                Pages: 124-129
                Affiliations
                [1 ]James Cook University Hospital , Middlesbrough, United Kingdom
                [2 ]National Poisons Information Service , Birmingham United Kingdom
                Author notes
                Article
                Publisher ID: jccm-2020-0016
                DOI: 10.2478/jccm-2020-0016
                PMC ID: 7216026
                SO-VID: 3a4a675b-14be-4150-bac7-29b041671c18
                Copyright © © 2020 Christopher Wood, James Coulson, John Thompson, Stephen Bonner, published by Sciendo
                License:

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

                History
                Date received : 23 February 2020
                Date accepted : 22 March 2020
                Page count
                Pages: 6
                Categories
                Subject: Case Report

                Keywords: aconite,cardiovascular
                Data availability:
                Keywords: aconite, cardiovascular

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