Aconite Poisoning

Aka: Aconite Poisoning, Aconite Toxicity, Aconite, Aconitum Poisoning, Monkshood Poisoning, Wolfsbane Poisoning, Wolfsbane, Aconitum, Aconitum napellus, Monkshood

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II. Definitions

  1. Aconite
    1. Toxic diterpenoid alkaloid root extract from plants in the Aconitum genus (esp. Aconitum napellus)
    2. Aconite contains aconitine, mesaconitine and hypaconitine
  2. Aconitum
    1. Aconitum is a plant genus within the family ranunculaceae
      1. More than 350 species of perennial flowering plants
      2. Found throughout Europe, Asia and North America in temperate, mountainous regions
      3. Common plant names include Wolfsbane and Monkshood
    2. Plants in this genus contain various toxins
      1. Diterpenoid alkaloids including aconitans
      2. All plant parts are poisonous
        1. Roots contain highest concentration of alkaloids (aconitine, mesaconitine and hypaconitine)
  3. Diterpenoid Alkaloid
    1. Group of more than 1500 identified complex substances synthesized by plants
    2. Associated with both medicinal and toxic properties

III. Background

  1. Aconite is alkaloid group extracted from Aconitum napellus root (contains aconitine, mesaconitine and hypaconitine)
  2. Aconitum was the first Diterpenoid Alkaloid group to be identified (in early 1800s by Geiger)
  3. Ancient tribes applied Aconitum to arrow tips for hunting and war

IV. Pathophysiology

  1. Accidental or intentional ingestion (e.g. foraging)
    1. Aconitum napellus (Monkshood or Wolfsbane)
      1. Deep-purple to violet, hooded flowers
      2. May appear similar to non-poisonous edibles (e.g. mountain chickory, celery)
    2. Asian medicinal ingestion
      1. Aconite root extract (A. kusnezoffi. A. carmichaeli)
  2. Aconitite binds voltage-sensitive Sodium channels in their open state (preventing inactivation)
    1. Increases Sodium influx throughout Action Potential
    2. Results in neurovascular and cardiovascular toxicity (QRS Widening, Torsades de Pointes)

V. Pharmacokinetics

  1. Rapid absorption, and symptom onset within 15-30 minutes after ingestion
  2. Half-Life: 24 hours
  3. Lethal dose
    1. Aconite 2 mg
    2. Aconite tincture (herbal medicinal wine) 5 ml
    3. Raw Aconite plant: 1 g (esp. root)

VI. Findings

  1. General
    1. Hypothermia
  2. Cardiovascular
    1. Hypotension
    2. Dysrhythmia
      1. Atrial Fibrillation
      2. Torsades de Pointes
      3. Ventricular Tachycardia
      4. Atrioventricular Blocks
  3. Respiratory
    1. Respiratory Muscle Paralysis with apnea
  4. Gastrointestinal
    1. Nausea or Vomiting
    2. Diarrhea
    3. Abdominal Pain
    4. Hypersalivation
  5. Neurologic
    1. Paresthesias (esp. perioral)
    2. Numbness (perioral, extremity)
    3. Motor weakness
    4. Seizures
    5. Agitation
    6. CNS Depression

VII. Labs

  1. See Unknown Ingestion (includes full spectrum toxicology testing)
  2. Bedside Glucose
  3. Complete Blood Count
  4. Comprehensive metabolic panel (inluding Sodium and Calcium, renal and hepatic function)
    1. Hepatorenal injury may occur
  5. Serum Magnesium
  6. Troponin level
  7. Aconitine Levels (urine and blood)
    1. Dysrhythmias occur at plasma aconitine concentrations >1.5 ng/ml

VIII. Diagnostics

  1. Electrocardiogram (EKG)
    1. Atrial Fibrillation
    2. Torsades de Pointes
    3. Ventricular Tachycardia
    4. Atrioventricular Blocks

IX. Differential Diagnosis

  1. See Accidental Poisoning Causes
  2. Digoxin Toxicity has similar findings

X. Management

  1. Gastric Decontamination if within one hour of ingestion and can control airway
    1. Oral Activated Charcoal
  2. Cardiovascular Management
    1. Symptomatic Bradycardia
      1. Atropine
    2. Hypotension
      1. Intravenous Fluids
      2. Vasopressors (e.g. Norepinephrine) for refractory Hypotension
      3. ECMO for Vasopressor refractory Hypotension
    3. Ventricular Tachycardia
      1. Flecainide (preferred first line)
        1. Dose 300 mg load, then 150 mg every 12 hours
        2. Contraindicated in underlying structural heart disease
      2. Other measures to consider (but lower efficacy)
        1. Amiodarone (preferred over Lidocaine)
        2. Magnesium
        3. Cardioversion (may be refractory)
  3. Replace Electrolytes
    1. Potassium Replacement in Hypokalemia
    2. Magnesium Replacement in Hypomagnesemia
  4. Disposition
    1. Cardiovascular effects require Intensive Care monitoring
    2. Perioral numbness or Paresthesias should be observed for 6 hours
    3. Other symptoms (e.g. gastrointestinal) should be medically monitored until resolution
    4. Asymptomatic patients may be discharged to home observation

XI. Resources

  1. Aconitum napellus(Monkshood): A Purple Poison (Poison Control)
    1. https://www.poison.org/articles/why-is-monkshood-considered-a-poison--174
  2. Aconitum (Wikipedia)
    1. https://en.wikipedia.org/wiki/Aconitum

XII. References

  1. Carroll and Yakey (2026) Crit Dec Emerg Med 40(6): 36
  2. Tomaszewski (2022) Crit Dec Emerg Med 36(4): 36
  3. Chan (2009) Clin Toxicol 47(4):279-85 +PMID: 19514874 [PubMed]
  4. Majumder (2023) Clin Case Rep 11(9):e7845 +PMID: 37636875 [PubMed]
  5. Thawabteh (2021) Molecules 26(13):4103 +PMID: 34279443 [PubMed]
  6. Wood (2020) J Crit Care Med 6(2):124-129 +PMID: 32426520 [PubMed]

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