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Hemlock Poisoning
Updated: Jan 29, 2021
Author: Daniel E Brooks, MD; Chief Editor: Michael A Miller, MD 

Overview

Practice Essentials
Hemlock poisoning may refer to poisoning by either poison hemlock (Conium maculatum; see the image below) or plants in the
water hemlock family (Cicuta species and Oenanthe crocata). Hemlocks are among the few plants that can cause life-
threatening toxicity. In both species, the root contains the greatest concentration of toxin, although all plant parts are toxic.

Hemlock. Photo by Cornell University Poisonous Plants Informational Database

Both water hemlock and poison hemlock have caused severe poisoning in both humans and livestock. Historically, poison
hemlock was reportedly used to execute Socrates, and the Old Testament describes rhabdomyolysis in Israelites who
consumed quail fed on hemlock.[1] Poison hemlock causes skeletal deformities in the offspring of livestock that eat the plants
during gestation (eg, crooked calf disease in cattle). Fatal toxicity has occurred in children who played with whistles made from
hollow stems of poison hemlock.[2, 3]

Although related, poison hemlock and water hemlock toxicity have different pathophysiologies and clinical presentations. With
water hemlock toxicity, profuse salivation, perspiration, bronchial secretion, and respiratory distress leading to cyanosis develop
soon after ingestion; severe toxicity tends to cause seizures, with death resulting from status epilepticus.[4] Poison hemlock
toxicity is characerized by rapidly progressive muscle weakness and paralysis, which may eventuate in respiratory failure.[5]

No antidote is available for either toxin. Gastrointestinal decontamination, if appropriate, and aggressive supportive care are the
mainstays of treatment.

For patient education resources, see Poisoning.

Background
Poison hemlock, an exotic species introduced to the United States, 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

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United States, 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), poison hemlock (C maculata), pignut, sweet flag, watercress, wild parsnip, wild celery, wild ginseng, and
kvanne.[6]

See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and
poisonings.

Pathophysiology
Poison hemlock

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.

Symptoms are produced with ingestion of as little as 3 mg of conline but up to 150–300 mg coniine can be tolerated, which
translates to 6–8 leaves (6 g).[7]

Water hemlock

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.[8] 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.[6]

Epidemiology
No exposures or human deaths from hemlock ingestion have been reported to US Poison Control Centers during the past 10
years.[9]  However, a case report of a death due to intentional intravenous poison hemlock injection was published in 2017.[10]  

A systematic review of 30 reported hemlock poisonings found the majoity of cases occurred in Italy (56.7%) and Greece (10%).
Males (76.7%) and those over 38 years old (66.7%) were the most commonly affected.[11]

Prevalence was low for US livestock.[2, 3]  Livestock exposures in New Zealand, South America, Europe, and southern Canada
have been reported. Cattle appear to be most vulnerable to hemlock toxicity.

Prognosis
The prognosis is good if the patient presents early and receives appropriate decontamination and supportive care.
Complications of hemlock ingestion may include the following:

Death (secondary to respiratory failure or status epilepticus)

Seizures (status epilepticus)
Rhabdomyolysis (acute kidney injury) - Hyperkalemia
Coma
Aspiration pneumonitis
Permanent neurologic sequelae
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Poison hemlock poisoning is potentially lethal with large ingestions. Water hemlock fatalities have occurred following a few bites
of the root.[4] 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. It is recognized as one of the most toxic plants in North
America. Mortality from water hemlock is usually secondary to refractory status epilepticus.
 

Presentation

History
In cases of plant toxicity, history may be obscure and ingested plants may not be available for identification.

History for poison hemlock may include the following:

Nausea and vomiting

Abdominal pain

Tachycardia

Tremor

Seizures (much more common with water hemlock)

Bradycardia (late)

Ascending paralysis (late)

Coma

Respiratory failure

History for water hemlock may include the following:

Gastrointestinal - Nausea and vomiting, excessive salivation, abdominal pain

Cardiac - Tachy/bradycardia, hypotension/hypertension, cardiac dysrhythmias/failure/arrest

Central nervous system - Delirium, convulsions, opisthotonus, hemiballismus, seizure (status epilepticus)

Physical
Poison hemlock: Signs of poison hemlock toxicity can be divided into an early stimulation phase and, in severe poisonings, a
later depressant phase.

Emesis

Salivation

Mydriasis

Tachycardia, then bradycardia

Initial fasciculations, then flaccid paralysis

Hypoventilation, respiratory arrest

Water hemlock: Signs of water hemlock toxicity begin with GI symptoms, which are rapidly followed by CNS excitation.

Emesis

Mydriasis
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Agitation

Delirium

Convulsions

Seizures

Coma

Causes
Hemlock plants may be intentionally ingested. However, most ingestions are unintentional.

Poison hemlock may be mistaken for wild carrots.

Water hemlock may be mistaken for wild parsnips or artichokes.

Birds ingesting hemlock during migratory flight may be reported to cause coturnism (human poisoning after eating quail).

DDx

Diagnostic Considerations
Other problems to be considered in the differential diagnosis of hemlock poisoning include the following:

Botulism

Nicotine (wild tobacco)

Golden chain (Laburnum anagyroides)

Strychnine

Cholinergic poisoning

Psychosis

Encephalopathy

Differential Diagnoses
Acute Hypoglycemia

Emergent Treatment of Schizophrenia

Encephalitis

Gyromitra Mushroom Toxicity

Hallucinogen Toxicity

Hallucinogenic Mushroom Toxicity

Methamphetamine Toxicity

Phencyclidine Toxicity

Toxicity, Mushrooms

Tricyclic Antidepressant Toxicity

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Workup
 

Workup

Laboratory Studies
Consider the following tests if patient is hemodynamically unstable or has altered mental status or seizures:

Basic metabolic profile including electrolytes, glucose, BUN, and creatinine

Arterial blood gas

Comprehensive drug screen to evaluate for coingestions, including serum acetaminophen level

Creatine kinase or urine myoglobin to screen for rhabdomyolysis

Consider a pregnancy test for women of childbearing age.

Imaging Studies
Perform chest radiographs if aspiration is suspected.

Other Tests
See the list below:

ECG to rule out dysrhythmias

Chemical screening test for alkaloids in plant material provides confirmation of toxicity due to poison or water hemlock.
However, a plant specimen (or ingested material) is required, and these tests are not routinely available.

Treatment

Prehospital Care
For patients with possible hemlock poisoning, maintain the airway, obtain IV access, and assist with ventilation as needed.

Emergency Department Care

Rapidly assess and correct any life-threatening conditions. Since no antidote exists for either toxin, gastrointestinal (GI)
decontamination (if appropriate) and aggressive supportive care are mainstays of treatment for hemlock poisoning. Schep et al
provide a concise review of water hemlock poisoning and management.[6]

Secure airway.

Decontaminate the GI tract if timing is appropriate.

If no contraindications exist, gastric lavage may be of limited benefit if performed rapidly after the ingestion.

Administer activated charcoal if the patient is able to protect the airway and presents within 1 hour of ingestion.
Ipecac should not be used.

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Caution should be exercised in patients exposed to water hemlock because they are at increased risk of having
seizures, and can eventually aspirate the charcoal.

Treat seizures with benzodiazepines; use barbiturates if needed.

Provide prophylaxis with water hemlock ingestion.

Benzodiazepines and barbiturates help control agitation and raise the seizure threshold.

Aggressively administer IV fluids for dehydration or rhabdomyolysis.

Replete volume if signs of hypovolemia or hypotension are present.

Correct electrolyte abnormalities.

Administer fluids with sodium bicarbonate for urinary alkalinization if evidence of rhabdomyolysis exists. If using
sodium bicarbonate, mixing it in 5% dextrose in water (D5W) is important to limit the amount of sodium load.

Potassium levels should be monitored and corrected as needed.

Administer antiemetics. Many antiemetics may lower the seizure threshold and should be used cautiously.

Provide ventilatory support, if necessary.

Observe the patient closely for at least 6 hours after presentation to evaluate for symptoms and progression. Monitor all patients
showing evidence of toxicity for possible seizures, dysrhythmias, or respiratory failure in an ICU setting. Consider transferring
the patient to a facility with a toxicology service. Counsel pregnant patients that teratogenic effects from poison hemlock
exposure have been reported in livestock.

Consultations
A regional poison center or a medical toxicologist can assist with patient treatment and potentially with plant identification. The
regional poison control center should be contacted (800-222-1222) to discuss optimal management of all known or suspected
hemlock poisonings.

Prevention
Educate patients about avoiding ingestions of hemlock and other unidentifiable or mistakenly identified plants.

Medication

Medication Summary
Do not use ipecac during gastric decontamination because of risk of inducing seizures. Other agents, if indicated, can be used.

GI Decontaminants

Class Summary
Used to limit amount of adsorbed toxin.

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Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-
1000 mg of drug per gram of charcoal. Does not dissolve in water.

For maximum effect, administer within 30 min after ingesting poison.

Antiemetics

Class Summary
Useful in treatment of symptomatic nausea. Consider risks or benefits of increased sedation and possibility of lowering seizure
threshold.

Ondansetron (Zofran)
Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally.

Metoclopramide (Reglan)
Works as antiemetic by blocking dopamine receptors in the chemoreceptor trigger zone of CNS.

Benzodiazepines

Class Summary
Can be used to control/prevent seizures and may decrease agitation. Rapid onset of action is advantageous, as is their
improved safety profile vs barbiturates.

Diazepam (Valium)
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Lorazepam (Ativan)
Sedative hypnotic with short onset of effects and relatively long half-life.

Increasing action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including
limbic and reticular formation.

Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Lorazepam contains benzyl alcohol, which may be toxic to infants in high doses.

Midazolam (Versed)
Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately three times
longer than diazepam to peak EEG effects. Thus, the clinician must wait 2-3 min to fully evaluate sedative effects before
initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered
IM if unable to obtain vascular access.

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Barbiturates

Class Summary
Can be used to control/prevent seizures and may decrease agitation. Rapid onset of action is advantageous.

Pentobarbital (Nembutal)
Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties and can produce all levels of CNS mood
alteration.

Phenobarbital (Barbita, Luminal, Solfoton)

Can be administered orally; in status epilepticus, it is important to achieve therapeutic levels as quickly as possible. IV dose may
require approximately 15 min to attain peak levels in the brain. If injected continuously until convulsions stop, brain
concentrations may continue to rise and can exceed that required to control seizures. Important to use minimal amount required
and wait for anticonvulsant effect to develop before giving a second dose.

If IM route chosen, administer into areas with little risk of encountering a nerve trunk or major artery such as one of large
muscles like gluteus maximus, vastus lateralis, or other. Permanent neurological deficit may result from injecting into or near
peripheral nerves.

Restrict IV use to conditions in which other routes are not possible, either because patient is unconscious or because prompt
action is required.

General anesthetics

Class Summary
Can be used to control seizures.

Propofol (Diprivan)
Phenolic compound unrelated to other types of anticonvulsants. Has general anesthetic properties when administered IV.

Contributor Information and Disclosures

Author

Daniel E Brooks, MD Co-Medical Director, Banner Good Samaritan Poison and Drug Information Center, Department of
Medical Toxicology, Banner Good Samaritan Medical Center

Daniel E Brooks, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American
College of Emergency Physicians, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Specialty Editor Board

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John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Chief Editor

Michael A Miller, MD Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine,
Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program

Michael A Miller, MD is a member of the following medical societies: American College of Medical Toxicology

Disclosure: Nothing to disclose.

Additional Contributors

David A Peak, MD Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician,
Massachusetts General Hospital; Assistant Professor, Harvard Medical School

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, Society for
Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, American Medical Association

Disclosure: Partner received salary from Pfizer for employment.

Acknowledgements

Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American
College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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