An extremely toxic herb, aconite can result in poisoning even from small amounts found in traditional Chinese or Indian herbal mixtures.

[LFODPKM ] Letter Key

Latin Name

Aconitum napellus, A. carmichaeli, A. coreanum, A. kusnezoffii

Family

Rananculaceae

Other Common Names

Monkshood, wolfsbane, leopard killer

Description

• Aconitum species are used medicinally in traditional Chinese and Ayurvedic medicine.
• Common ingredient in herbal mixtures purchased in or imported from Hong Kong, China, Japan, and India. In Hong Kong, "chuanwu" (the main root of A. carmichaeli), and "caowu" (the root of A. kusnezoffii) are the most commonly used forms. "Fuzi" (the lateral root-tuber of A. carmichaeli) is more commonly used in mainland China (1).

Part Used

Tuber

Known Active Constituents

• Aconitine and other C₁₉ diterpenoid alkaloids, including mesaconitine and hypaconitine.
• Other cardiotonic substances include coryneine chloride (dopamine methochloride), which has -adrenergic qualities, and higenamine, a -agonist.
• Dopamine, noradrenaline, and tyramine found in some Aconitum species (1).

Mechanism/Pharmacokinetics

• Aconitum affects the voltage-sensitive sodium channels of excitable membranes and is toxic to both neurons and cardiac cells. Persistent activation of sodium channels results in increased sodium uptake, prolonged depolarization, and delayed repolarization. In cardiac cells, aconite has both negative inotropic effects (apparently vagal as they can be blocked with atropine) and positive inotropic effects (caused by prolongation of sodium influx during the action potential). Sodium-calcium exchange results in increased intracellular calcium levels: increased automaticity combined with increased vagal activity and slowed atrioventricular (A-V) conduction leads to arrhythmias (1). In nerve cells, prolonged depolarization preventing repolarization results in conduction block and muscle paralysis.
• Aconite alkaloids were quantified in the body fluids of a 40-year-old woman who committed suicide by ingesting aconite (2). Levels of the alkaloid jesaconitine were 69.1 ng/mL in blood and 237.8 ng/mL in urine. The highest levels of jesaconitine were seen in the kidneys, liver, and bile; significant amounts were also seen in the gastrointestinal tract, especially in the ileal contents. The authors suggested that aconite alkaloids are eliminated by the liver and kidneys and also in feces.

[Outline]

• LLatin Name
• FFamily
• OOther Common Names
• DDescription
• PPart Used
• KKnown Active Constituents
• MMechanism/Pharmacokinetics

[CAO ] Letter Key

Clinical Trials

• No clinical trials identified.

Animal/In Vitro

• Intraperitoneal administration of aconite extract (3 mg/kg q.d. × 7 days) or aconitine (3 µg/kg q.d. × 7 days) increased plasma corticosterone levels significantly in mice (3). Aconitine has analgesic effects in mice and antiinflammatory effects in rats (4). Aconite alkaloids can be grouped into compounds that activate or block Na⁺ channels, but the high-affinity alkaloids with antinociceptive properties were also the most toxic compounds (5). The authors of this report concluded that aconite compounds are unsuitable as analgesics because the lethal dose is too close to the effective dose.
• Aconitine applied to cat atria causes fibrillation that can be suppressed by amiodarone or atropine (6).

Other Claimed Benefits/Actions

• Antiinflammatory
• Analgesic
• Cardiotonic
• Musculoskeletal problems

[Outline]

• CClinical Trials
• AAnimal/In Vitro
• OOther Claimed Benefits/Actions

[WAD ] Letter Key

Warning

• Ingestion of any amount of aconite may result in potentially fatal cardiac arrhythmias.
• Severe poisoning has been observed following ingestion of preparations containing as little as 6 g of cured rootstocks (7).

Adverse Reactions

• Aconite poisoning
  • Mild poisoning cases may result in nausea, vomiting, and paresthesias (8). Initial symptoms usually appear within 90 minutes of ingestion (1). Most patients present with neurologic symptoms, most commonly oral numbness or burning progressing to peripheral paraesthesias and generalized muscle weakness. Nausea and vomiting are also common; other symptoms may include chest pain, abdominal pain, diarrhea, hyperventilation, respiratory distress, dizziness, sweating, confusion, headache, and excessive lacrimation (1).
  • Cardiovascular effects include bradycardia, hypotension, and a range of arrhythmias similar to that caused by cardiac glycoside toxicity (ventricular or supraventricular tachycardia, sinus bradycardia with first degree heart block, bundle branch block with junctional escape rhythm, or torsades de pointes) (1). Bidirectional tachycardia has been reported (9). In one series of 17 cases of aconite poisoning, 11 patients required high-dose inotropic support, 8 required mechanical ventilation, and 7 required cardiopulmonary resuscitation (7).
  • Several deaths have been associated with herbal medicines containing aconite (7,10); the herb has also been successfully used for suicide (2) and homicide (11). Autopsy of a homicide victim poisoned by aconite revealed hemorrhagic pulmonary edema and diffuse contraction-band necrosis in the myocardium, findings similar to that seen in epinephrine administration or release of endogenous catecholamines (11).
• Treatment of aconite poisoning
  • Patients with suspected aconite poisoning should be hospitalized and placed on cardiac monitors for at least 24 hours, the period within which ventricular arrhythmias are most likely to occur (1). Although patients with aconite poisoning are sometimes given activated charcoal, it is not known whether this treatment is effective in preventing absorption of aconitine (8). There is no specific antidote for aconite, and treatment is mainly supportive. Atropine may be given if symptoms of cholinergic excess are apparent (1).
  • Antiarrhythmics are often helpful, but cardioversion appears to be markedly unsuccessful in converting arrhythmias. In a case series of 17 cases of aconite poisoning, repeated direct-current cardioversion was unsuccessful in 10 patients (apparently all patients for whom cardioversion was attempted) (7). No single antiarrhythmic was uniformly effective. Suppression of ventricular tachycardia was eventually achieved in 5 patients receiving amiodarone, 2 patients on flecainide, and 1 each on procainamide or mexiletine. Arrhythmias resolved spontaneously in 6 patients, and 2 patients died from refractory ventricular tachycardia. The 15 other patients were stabilized within 24 hours and discharged; no sequelae were observed at a median of 15 months follow-up (7).
  • In a case report of bidirectional tachycardia, the arrhythmia was finally suppressed by 0.7 mg/kg of flecainide by slow intravenous infusion; junctional rhythm persisted for 4 hours before normal sinus rhythm was restored (9). Before administration of flecainide, other failed measures included vagotonic maneuvers or intravenous adenosine triphosphate with edrophonium hydrochloride (each suppressed the arrhythmia transiently). Neither intravenous lignocaine (lidocaine) nor synchronized direct current cardioversion (200 J) had any effect.
  • More recently, individual case reports of successful reversal of aconite-induced arrhythmias include amiodarone suppression of polymorphic ventricular tachycardia (12) and a case of magnesium treatment of long QT syndrome with torsades de pointes (13).

Drug Interactions

• None reported. The incidence and severity of adverse events would be expected to increase if aconite were combined with digoxin or other cardiac glycosides.

[Outline]

• WWarning
• AAdverse Reactions
  • Aconite poisoning
  • Treatment of aconite poisoning
• DDrug Interactions

Common Dosage Forms

• Decoction or infusion as part of a mixture of herbs.
• Recommended doses have traditionally been 8 to 12 g, but reports of toxicity have resulted in many practitioners recommending lower doses of 1.5 to 3.0 g (7).

• Doesn’t the processing done in preparing aconite for use in traditional Asian medicines reduce its toxicity?
• What is the incidence of aconite poisoning?
• What is the origin of the names monkshood and wolfsbane?

Q: Doesn’t the processing done in preparing aconite for use in traditional Asian medicines reduce its toxicity?

A: Yes. Raw aconite tubers are always processed by soaking or boiling the tubers (with or without lime or other chemicals) before slicing and drying them (1). This processing, by hydrolyzing alkaloids into less toxic benzylaconine derivatives, may reduce the alkaloid content to 10% of its original level (1). However, alkaloid types and amounts may vary with the species, where the herb was grown, time of harvest, and method of processing. In addition, dosage and preparation instructions may not be followed correctly. Poisonings are much more common when aconite is self-prescribed than when it is prescribed by a traditional Chinese medicine practitioner.

Aconite is an important and versatile herb in traditional Chinese medicine. Given that the conditions for which aconite is used are either minor conditions (musculoskeletal problems) or conditions (pain, heart failure) for which there are other effective medications, the question remains whether there is reason to use this quite toxic herb at all.

Q: What is the incidence of aconite poisoning?

A: The incidence is unknown. The diagnosis of aconite poisoning may be missed in mild cases or in areas where this sort of poisoning is rare. In one hospital in Hong Kong, at least 18 cases of known aconite poisoning were observed in a 4-year period (1).

Q: What is the origin of the names monkshood and wolfsbane?

A: The hooded flower resembles a monk’s cowl, hence the name monkshood. Aconite was a widely used arrow poison in Asia and medieval Europe and was used for both hunting and warfare (14). In ancient Rome, it was so widely used by professional poisoners that simply cultivating the plant was considered a capital offense. On the Greek island of Chios it was used for euthanasia of the old and infirm. The term wolfsbane comes from its use to poison meat laid out for wolves.

1. Chan TYK, Tomlinson B, Tse LKK et al. Aconitine poisoning due to Chinese medicine: a review. Vet Hum Toxicol 1994;36:452–455.
2. Ito K, Tanaka S, Funayama M et al. Distribution of aconitum alkaloids in body fluids and tissues in a suicidal case of aconite ingestion. J Anal Toxicol 2000;24:348–353.
3. Kimura I, Makino M, Honda R et al. Expression of major histocompatibility complex in mouse peritoneal macrophages increasingly depends on plasma corticosterone levels: stimulation by aconitine. Biol Pharm Bull 1995;18:1504–1508.
4. Bisset NG. Arrow poisons in China. Part II. Aconitum—botany, chemistry, and pharmacology. J Ethnopharmacol 1981;4:247–336.
5. Friese J, Gleitz J, Gutser UT et al. Aconitum sp. alkaloids: the modulation of voltage-dependent Na+ channels, toxicity and antinociceptive properties. Eur J Pharmacol 1997;337:165–174.
6. Winslow E. Hemodynamic and arrhythmogenic effects of aconitine applied to the left atria of anesthetized cats: effects of amiodarone and atropine. J Cardiovasc Pharmacol 1991;31:611P.
7. Tai Y-T, But PP-H, Young K et al. Cardiotoxicity after accidental herb-induced aconite poisoning. Lancet 1992;340:1254–1256.
8. Tomlinson B, Chan Tyk, Chan JCN et al. Herb-induced aconite poisoning. Lancet 1993;341:370–371.
9. Tai Y-T, Lau C-P, But PP-H et al. Bidirectional tachycardia induced by herbal aconite poisoning. PACE 1992;15:831–839.
10. Fatovich DM. Aconite: a lethal Chinese herb. Ann Emerg Med 1992;21:309–311.
11. Mori A, Mukaida M, Ishiyama I et al. [Homicidal poisoning by aconite: report of a case from the viewpoint of clinical forensic medicine]. Nippon Hoigaku Zasshi 1990;44:352–357.
12. YeihDF, Chiang FT, Huang SK. Successful treatment of aconitine induced life threatening ventricular tachyarrhythmia with amiodarone. Heart 2000;84:E8.
13. Felgenhauer N, Zilker T, Dorfmann N. Severe intoxication with aconitum. J Toxicol Clin Toxicol 1999;37:416(abst).
14. Mann J. Murder, magic, and medicine. Oxford, England: Oxford University Press, 1994:17.