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Plant Poisoning, Hemlock
Last Updated: June 19, 2006
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Introduction
Background:
Plant ingestions continue to be a very common exposure for humans (particularly children) and animals, and they account for nearly 100,000 calls to national poison centers annually. Pediatric patients comprise more than 80% of plant-related exposures. Only a few plants, poison hemlock and water hemlock included, are associated with potentially life-threatening toxicity, and less than 20% of plant exposures require medical management.
Hemlock poisoning may refer to poisoning by either poison hemlock (Conium maculatum) or water hemlock (Cicuta maculata). Historically, poison hemlock was reportedly used to execute Socrates and the Old Testament describes rhabdomyolysis in Israelites who consumed quail fed on hemlock.
Although related, poison hemlock and water hemlock toxicity have different pathophysiologies and clinical presentations. The root contains the greatest concentration of toxin in both species, although all plant parts are toxic. Poison hemlock causes "crooked calf disease," a congenital abnormality, among cattle formed via fetal exposure. No antidote is available for either toxin.
Poison hemlock, an exotic species introduced to the US, is a ubiquitous plant with fernlike properties that may reach a height of 2 meters. Poison hemlock grows in diverse settings, including wooded areas, ditches, and waysides throughout the US, and may be mistaken for other plants such as fool's parsley (Aethusa cynapium).
Water hemlock is typically found growing in moist habitats, such as drainage ditches, marshes, and near bodies of fresh water. Water hemlock has compound leaves, small white or green flowers, and tuberous, large, hollow roots. Water hemlock may reach a height of 2.5 meters and can also be confused with other plants such as wild carrot, also known as Queen Anne's lace (Daucus carota), or poison hemlock (C maculata).
Pathophysiology:
Poison hemlock contains several piperidine alkaloid toxins (namely coniine) that are structurally similar to nicotine. Coniine has direct effects on nicotinic (cholinergic) receptors, both agonist and antagonist. Clinically, initial manifestations include gastritis and CNS stimulation (tremor, ataxia, and seizures). Nicotine activation at autonomic ganglia can cause tachycardia, salivation, mydriasis, and diaphoresis. In severe cases, acetylcholine (nicotinic) receptor antagonism develops. This leads to bradycardia, ascending paralysis, and CNS depression (coma). Death is typically from respiratory failure.
Water hemlock contains cicutoxin, a potent, noncompetitive gamma-aminobutyric acid (GABA) receptor antagonist. Using a rat model, Uwai et al showed that cicutoxin is an antagonist of GABA-mediated chloride channels. Cicutoxin rapidly produces GI symptoms (nausea, emesis, abdominal pain) typically within 60 minutes of ingestion. CNS excitation leads to tremor and seizures, often refractory to therapy. A single bite of the root, which contains the highest concentration of cicutoxin, has been reported to kill an adult.
Frequency:
- In the US: In 2003, 77,169 plant exposures were reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System. No human deaths from hemlock ingestion were reported to US Poison Control Centers from 1997-2003. Prevalence was low for US livestock.
- Internationally: Livestock exposures in New Zealand, South America, Europe, and southern Canada have been reported. Cattle appear to be most vulnerable to hemlock toxicity.
Mortality/Morbidity: Poison hemlock poisoning is potentially lethal with large ingestions; water hemlock fatalities have occurred following a few bites of the root.
- Poison hemlock's human median lethal dose (LD50) is not known. Mortality from poison hemlock ingestion is usually secondary to respiratory paralysis.
- Water hemlock had a 30% mortality rate in one series of 86 patients. Mortality from water hemlock is usually secondary to refractory status epilepticus.
Age: Younger patients are theoretically at increased risk due to smaller body mass.
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Bibliography
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