Hemlock Poisoning

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 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.

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]

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.

 

 

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

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.

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)

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

• Agitation

• Delirium

• Convulsions

• Seizures

• Coma

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).

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.

Perform chest radiographs if aspiration is suspected.

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.

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

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.

  • 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.

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.

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

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

Class Summary

Used to limit amount of adsorbed toxin.

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.

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.

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.

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.

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.