Monkshood (Aconitum Napellus)

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Monkshood (Aconitum napellus) is one of the most poisonous garden plants. Even its Latin name “Aconitum” indicates its lethal effects: in antiquity, it was considered a war poison. Today, monkshood plants are often found in woodland edge plantings, ornamental beds, and as cut flowers in bouquets. For dogs and cats, contact or oral ingestion of even the smallest amount can be fatal. Monkshood poisoning progresses rapidly and leads to severe cardiovascular and CNS disorders. Early detection and immediate treatment are essential to ensure the animal’s survival.

The most important facts at a glance

  • Monkshood (Aconitum napellus) is one of the most poisonous native plants.
  • As little as 1–2 g of plant material/kg BW can be lethal.
  • Taxin A/B blocks sodium and calcium channels → arrhythmias, seizures, respiratory arrest.
  • No antidotes available – treatment is purely symptomatic and intensive care-based.
  • Early intervention is crucial; prognosis is better with rapid treatment.
  • Prevention by removing the plant from gardens and educating pet owners.

Causes, development and progression

The skin and mucous membranes of the gastrointestinal tract, as well as the conjunctiva, are particularly damaged.
Among the organ systems, the cardiovascular system, nervous system, and kidneys are primarily affected.

Pets can come into contact with monkshood in various ways:

  1. Direct oral ingestion
    • While exploring in the garden or park
    • By chewing on leaves, flowers, roots, or seeds
  2. Secondary ingestion
    • Eating dead rodents or birds that have ingested plant parts
    • Licking contaminated hands or objects after gardening
  3. Incorrect use as a medicinal plant
    • Some owners try to use monkshood homeopathically or naturopathically – a fatal misconception, as even tiny amounts can lead to intoxication.

Puppies are particularly at risk because they like to explore unknown plant parts. Cats, on the other hand, are more selective, but due to their intensive grooming behavior, they can be poisoned by contaminated paws.

Mechanism of action

Aconitine is easily absorbed through the skin and mucous membranes and can quickly reach the brain.
Aconitine initially increases the excitability of nerve cells and later leads to paralysis.
Aconitine affects the function of the cardiovascular system, causing a drop in blood pressure, a decrease in heart rate, and cardiac arrhythmias.
The arrhythmias are also partly a consequence of an anticholinergic effect of aconitine. Cardiac arrest is possible.

Supplement

The main active ingredient of monkshood is aconitine, a highly potent diterpene alkaloid. Other related alkaloids include mesaconitine, hypaconitine, and benzoylaconine. These substances primarily exert their toxicity through the following mechanisms:

  1. Modulation of voltage-gated sodium channels
    • Aconitine binds irreversibly to sodium channels in nerve cells and cardiomyocytes.
    • It prevents their inactivation, leading to a permanent influx of sodium
    • Result: persistent depolarization, prolonged refractory periods, severely disturbed chronotropy and dromotropy.
  2. Cardiovascular Effects
    • Persistent depolarization of cardiomyocytes leads to arrhythmias (extrasystoles, ventricular fibrillation) and ultimately cardiac arrest.
    • Peripheral vasodilation and hypotension due to disturbed smooth vascular musculature.
  3. Central Nervous System (CNS)
    • Overexcitation of cholinergic and adrenergic neurons in the CNS → muscle tremors, seizures, respiratory paralysis.
    • Aconitine can cross the blood-brain barrier
  4. Autonomic Dysregulation
    • Overstimulation of parasympathetic and sympathetic pathways → salivation, bradycardia or tachycardia, sweat secretion.

Pharmacokinetics are characterized by rapid absorption (within 10–30 minutes) and wide distribution in the vascular system and tissues. The elimination half-life is several hours; the toxins are highly protein-bound.

Symptoms of intoxication

Local irritation of the skin and mucous membranes manifests as

  • Drooling
  • Vomiting
  • Diarrhea, sometimes bloody
  • Abdominal cramps.

The effects on the nervous system and heart are

  • Restlessness
  • Ataxia
  • Seizures
  • Drop in blood pressure
  • Decrease in heart rate
  • Cardiac Arrhythmias
  • Paralysis.

The course of intoxication is rapid. The first symptoms appear within minutes. Death occurs due to respiratory paralysis or cardiac arrest.
The LD in dogs is 7.5 mg aconitine/kg body weight.
The toxic dose, i.e., the dose at which symptoms are expected, ranges between 2.5 and 5 g of dried plant / kg body weight, depending on the animal’s size.

Supplement

Symptoms often begin within 15–60 minutes after ingestion and progress in several phases:

Early Phase (0.25–2 H)

  • Gastrointestinal: Vomiting, hypersalivation, abdominal cramps
  • CNS: Restlessness, tremors, coordination disorders

Acute Phase (2–6 H)

  • Cardiovascular: Tachycardia or bradycardia, arrhythmic extrasystoles, hypotension
  • Neuromuscular: Muscle cramps, ataxia, tremor

Crisis (6–12 H)

  • Cardiovascular: Ventricular fibrillation, AV block, cardiac arrest
  • Respiratory: Respiratory paralysis, cyanosis
  • CNS: Coma, loss of consciousness

Late Phase (>12 H)

  • Organ compromise due to hypoxia
  • Multi-organ failure

Without immediate treatment, the poisoning is usually fatal.

Diagnosis

The diagnosis is based on medical history, hospital, and laboratory and cardiological findings:

  1. History
    • Time spent in the garden, discovery of plant parts
    • Temporal correlation with symptom onset
  2. Clinical Examination
    • Vomiting, salivation, mydriasis
    • Heart rate and rhythm, mucous membranes
  3. ECG
    • Detection of arrhythmias, extrasystoles, AV block
  4. Laboratory
    • Electrolytes, blood gases (metabolic acidosis)
    • Liver enzymes, creatinine (secondary damage)
  5. Toxicological Evidence
    • Aconitine levels in serum, urine, or stomach contents (specialized laboratory)

If poisoning is suspected, treatment should begin immediately, even before toxin screening results are available.

Therapeutic principles

Monkshood intoxications are often fatal.
There is no specific antidote.
The fastest possible decontamination is the most important, potentially life-saving measure.
Since the toxin can also be absorbed through the skin, thorough cleaning of the fur and skin is particularly important for decontamination.
Thorough showering and shampooing of the animal also protects the pet owner from direct skin contact with the plant toxin.
Gloves should be worn.
Inducing vomiting, gastric lavage, repeated doses of activated charcoal, and acceleration of intestinal transit are indicated.
Protective measures for the personnel involved must also be considered. Direct contact with vomit and similar substances must be strictly avoided.
Symptomatic therapy may begin with resuscitation and then primarily focuses on treating cardiac arrhythmias.

Supplement

There is no specific antidote against aconitine. Treatment is purely symptomatic and intensive care-based:

1. Immediate Measures

  • Induce vomiting (≥ 15 minutes post-intoxication, no airway risk)
  • Activated charcoal (1–3 g/kg p.o.), repeatedly every 4 to 6 h
  • Gastric lavage for high doses and stable circulation

2. Cardiac Stabilization

  • Atropine (0.02–0.04 mg/kg i.v.) for bradycardia
  • Lidocaine (2 mg/kg i.v.) or procainamide for ventricular arrhythmias
  • Magnesium sulfate (20–40 mg/kg i.v.) for ventricular fibrillation

3. Neurological Control

  • Benzodiazepines (e.g., Diazepam 0.5 mg/kg) for seizures
  • Barbiturates (Phenobarbital) for refractory seizures
  • Mannitol or Hypertonic NaCl (3%) for reduction of cerebral edema

4. Intensive Care Support

  • Fluid therapy (Ringer’s lactate, 10–20 ml/kg/h)
  • Vasopressors (e.g., Dopamine) for refractory hypotension
  • Ventilation for respiratory insufficiency

5. Additional Measures

  • Cardiac monitoring (continuous ECG)
  • Blood gas analysis, electrolyte monitoring every 2–4 h
  • Circulatory monitoring, urine output

The experimental use of anticonvulsive immunotherapy (antibodies against aconitine) is only available in specialized clinics, but so far without practical evidence.

Prognosis & follow-up care

Aconitine intoxications are often fatal and sometimes lead to the animal’s death just a few hours after toxin ingestion.

The prognosis is guarded to poor, depending on the dose and the time until treatment:

Parameter Prognosis
< 2 g needles/kg BW Rather favorable with rapid therapy
> 2 g needles/kg BW High mortality
Symptoms > 2 h untreated Very unfavorable

Aftercare:

  • Inpatient monitoring for at least 48 hours
  • Continuous ECG and circulatory monitoring
  • Electrolyte and blood gas monitoring every 4–6 h
  • Support for liver and kidneys in case of secondary damage
  • Possibly physiotherapeutic support after neurological deficits

Research outlook

Current research approaches for improving diagnosis and treatment:

  1. Antidote Development
  • Search for high-affinity aconitine antibodies
  • Molecular inhibitors for sodium channel binding
  1. Pharmacokinetic Studies
  • Absorption and elimination profiles across different ages, breeds, sexes
  1. Rapid Tests
  • Point-of-care detection of aconitine in blood or urine
  1. Clinical Studies
  • Optimization of antiarrhythmic protocols
  • Comparison of benzodiazepines vs. barbiturates in seizure management
  1. Prevention
  • Development of safe garden plant alternatives
  • Educational campaigns for dog and cat owners

Frequently asked questions (FAQs)

  1. Is the entire monkshood plant poisonous?
    Yes, leaves, flowers, seeds, roots – only the red aril is non-toxic.
  2. How quickly do the first symptoms appear?
    Often within 15–60 minutes after ingestion.
  3. How much monkshood is lethal?
    As little as 1–2 g of plant material per kilogram of body weight in dogs.
  4. What to do if poisoning is suspected?
    Seek veterinary attention immediately, induce vomiting only if instructed, activated charcoal.
  5. Is there an antidote?
    No, treatment is purely symptomatic and intensive care-based.
  6. Which symptoms appear first?
    Vomiting, salivation, muscle tremors, followed by cardiac arrhythmias.
  7. Can my pet fully recover?
    Yes, with very early and intensive therapy, recovery chances exist.
  8. Are cats also at risk?
    Yes, cats can be poisoned by licking contaminated paws.
  9. How can I prevent poisoning?
    Do not plant monkshood in the garden or make it inaccessible to pets.
  10. Will there be long-term damage?
    If the acute phase is overcome without organ damage, there are usually no long-term consequences.

Literature

  • https://www.vetpharm.uzh.ch/giftdb/pflanzen/0004_tvm.
  • Stetzenbach, M., Schnorbus, B., Sagoschen, I., Bleser, W., Legner, D., & Stürer, A. (2017). Acute Monkshood Intoxication Requiring Resuscitation with Suicidal Intent. AINS-Anästhesiologie· Intensivmedizin· Notfallmedizin· Schmerztherapie, 52(09), 641–644.
  • Müller, M. (2019). Dangerous Garden Plants for Pets: An Overview. Vet Journal, 33(4), pp. 112–117.
  • White, D. (2020). Cardiotoxic Plants and Their Effects on Dogs and Cats. Veterinary Botany, 24(2), pp. 56–61.
  • Gwaltney-Brant, S. (2012): Toxic plants. In: Peterson, M.E.; Talcott, P.A. (eds.): Small Animal Toxicology, 3rd ed., Elsevier, pp. 364–377.
  • Cope, R.B. (2005): Aconitum species poisoning in domestic animals. In: Gupta, R. (ed.): Veterinary Toxicology, Academic Press, pp. 507–512.
  • Dorman, D.C. (2010): Pharmacokinetics and toxicity of aconitine alkaloids. Vet Hum Toxicol, 52(4), 242–247.
  • Cortinovis, C.; Caloni, F. (2013): Plants poisonous to dogs and cats: a review. Toxins, 5(6), 1171–1192. doi: 10.3390/toxins5061171
  • Knight, A.; Walter, R. (2001): A Guide to Poisonous House and Garden Plants, Teton NewMedia, Jackson (WY).
  • Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 2021; 208 p.
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