aconitine aconitum plant wolfsbane

What is the primary cause of death following ingestion of the plant pictured?

  1. Acute liver failure
  2. Arrhythmia
  3. Disseminated intravascular coagulation
  4. Status epilepticus

2. Arrhythmia

The primary cause of death from plants of the Aconitum spp (aka Monkshood, Wolfsbane) is refractory ventricular arrhythmia and asystole.

Background:

Aconitine and its related alkaloids, mesaconitine and hypaconitine, are extremely potent cardiotoxins and neurotoxins found in the Aconitum species of plants [1,2].  There are high levels of aconite alkaloids in all parts of the plant, with the highest amount found in the tubers and roots [1]. In Eastern medicine, aconite roots are processed into tinctures and pastes to treat numerous medical problems including fever and inflammation, and to stimulate cardiac contraction [1,2].  Ingestion of only a small amount can cause significant clinical effects, and the lethal dose has been reported as one teaspoon (5 mL) of aconite tincture, 1 gram of wild aconite, or 2 mg of pure aconite [1, 2, 3]. The aconitine content of plants used medicinally varies with species, place and time of harvest, method, and adequacy of processing [2]. Using higher doses than recommended or raw instead of processed aconite root in herbal meals has also led to toxicity and death [4,5].

How does aconite cause toxicity? [1,2,6]

  • Aconite alkaloids bind to voltage-dependent sodium channels in cardiac and neural tissues promoting persistent sodium channel opening affecting intracellular excitability.
  • Aconite alkaloids cause persistent opening of cardiac potassium channels (Ikr and Ikur) leading to cardiac action potential prolongation and arrhythmogenicity.
  • Aconite alkaloids block acetylcholine release and decrease vagal nerve effects on the myocardium contributing to arrhythmogenicity and neurotoxic effects.
  • Aconitine causes bradycardia and hypotension by activating the ventromedial nucleus

What are the symptoms of aconite toxicity? [1,2,3]

  • Aconite alkaloids cause a combination of cardiac, neurologic, and gastrointestinal symptoms.
  • Symptoms typically occur within 10–20 minutes but onset can range from 3 minutes to 2 hours.
  • Wild plant ingestions cause more severe cardiac effects than processed roots, likely due to higher concentrations of alkaloids in the unprocessed material.
  • Cardiac symptoms include bradycardia, sinus or ventricular tachycardia, torsade de points, ventricular fibrillation, hypotension, and chest pain. Junctional rhythms and bidirectional tachycardia have also been reported.
  • Neurologic effects include paresthesias, muscle weakness, confusion, and headaches.
  • Gastrointestinal effects include nausea, vomiting, abdominal pain, and diarrhea.

How do you diagnose aconite toxicity? [1,2]

  • Diagnosis is based on clinical suspicion or history suggesting ingestion of aconite alkaloids.
  • Patients often present with a combination of cardiac, neurologic, and gastrointestinal effects
  • There are no readily available laboratory studies to aid in real-time diagnosis.

How do you treat aconite toxicity? [1,2,6]

  • There is no antidote for aconite toxicity.
  • Vasopressors can be used for hypotension.
  • Atropine can be used for bradycardia.
  • Treating arrhythmias: [1,6]
    • Flecainide and amiodarone are the antiarrhythmics most associated with successful termination of aconite-induced ventricular arrhythmias.
      • Mexiletine and procainamide are also shown to terminate arrhythmias however small number of cases prohibit clear conclusions.
      • Lidocaine, magnesium, and epinephrine are less associated with termination of arrhythmias.
    • Cardioversion can be attempted for wide-complex arrhythmias in unstable patients; however, arrhythmias often persist due to ongoing cardiac sodium channel opening.
    • Prolonged CPR and cardiopulmonary bypass have been used successfully in patients with refractory cardiac toxicity.

Bedside Pearls

  • Aconitine and related alkaloids found in the Aconitum species are highly toxic cardiotoxins and neurotoxins.
  • Ingestion of only a small amount can cause significant clinical effects within minutes.
  • Toxicity is primarily related to persistent sodium channel opening.
  • There is no antidote for aconite toxicity.
  • Flecainide and amiodarone may be better at terminating aconite-induced cardiac arrhythmias than other antiarrhythmics.

The American College of Medical Toxicology hosts this Toxicology Visual Pearls series. The post was peer reviewed on behalf of ACMT by Drs. Michele Burns, Louise Kao, and Kristine Naňagas.

Read More in the Series

References

  1. Nelson LS and Goldfrank LW. Plants. In: Nelson LW, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS Eds. Goldfrank’s Toxicologic Emergencies. 11th edition. New York: McGraw-Hill Education, 2019.
  2. Chan TY. Aconite poisoning. Clin Toxicol 2009;47(4):279-285. PMID: 19514874.
  3. Moritz F, et al. Severe acute poisoning with homemade Aconitum napellus capsules: toxicokinetic and clinical data. Clin Toxicol. 2005;43:873-876. PMID: 16440517.
  4. Chan TY. Aconitum alkaloid poisoning related to the culinary uses of aconite roots. Toxins (Basel). 2014;6(9):2605-2611. Published 2014 Sep 2. PMID: 25184557.
  5. Chan TY. Aconitum alkaloid content and the high toxicity of aconite tincture. Forensic Sci Int. 2012;222(1-3):1-3. PMID: 22469654.
  6. Coulson JM, Caparrotta TM, Thompson JP. The management of ventricular dysrhythmia in aconite poisoning. Clin Toxicol 2017;55(5):313-321. PMID: 28421842.
Neelou Tabatabai, DO

Neelou Tabatabai, DO

Emergency Medicine Resident
UNC Health Southeastern, Lumberton, NC
Christine Murphy, MD

Christine Murphy, MD

Associate Professor of Emergency Medicine
Medical Toxicologist
Department of Emergency Medicine
Atrium Health’s Carolinas Medical Center