eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Hemlock

Daniel E Brooks, MD, Attending Physician, Department of Medical Toxicology, Co-Medical Director, Banner Poison Center, Banner Good Samaritan Medical Center

Updated: Nov 7, 2008

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).

Hemlock. Photo by Cornell University Poisonous Plants Informational Database

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.¹ 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

United States

In 2003, 77,169 plant exposures were reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System.² No human deaths from hemlock ingestion were reported to US Poison Control Centers from 1997-2003. Prevalence was low for US livestock.

International

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.

Clinical

History

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

• Poison hemlock
  • Nausea and vomiting
  • Abdominal pain
  • Tachycardia
  • Tremor
  • Seizures (much more common with water hemlock)
  • Bradycardia (late)
  • Ascending paralysis (late)
  • Coma
  • Respiratory failure
• Water hemlock
  • Nausea and vomiting
  • Abdominal pain
  • 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
  • Agitation
  • Delirium
  • Convulsions
  • Seizures
  • Coma

Causes

• Hemlock plants may be intentionally ingested. However, most ingestions are accidental.
  • 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).

Differential Diagnoses

Other Problems to Be Considered

Botulism
Nicotine (wild tobacco)
Golden chain (Laburnum anagyroides)
Strychnine
Cholinergic poisoning
Psychosis
Encephalopathy

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 co-ingestions
  • 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

• 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 airway, and assist with ventilation as needed.

Emergency Department Care

Rapidly assess and correct any life-threatening conditions. Since no antidote exists for either toxin, GI decontamination (if appropriate) and aggressive supportive care are mainstays of treatment for poison hemlock.

• Secure airway.
• Decontaminate 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 presents within 1 hour of ingestion. Ipecac should not be used.
• 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.

Consultations

A regional poison center or a medical toxicologist can assist with patient treatment and potentially with plant identification.

Medication

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

GI Decontaminants

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.

Dosing

Adult

0.5-1 g/kg PO/NG (50-100 g); no cathartic (eg, 70% sorbitol) should be given.

Pediatric

0.5-1 g/kg PO/NG (15-50 g)

Interactions

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decrease with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases adsorptive properties of activated charcoal)

Contraindications

Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies; unprotected airway with absent gag reflex

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before giving activated charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; may require NG tube for administration; may require ET intubation to control airway and prevent aspiration

Antiemetics

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.

Dosing

Adult

4-12 mg IV q8h prn nausea

Pediatric

<1 month: Not established
>1 month:
<40 kg: 0.1 mg/kg (up to 40 mg) q6h prn nausea
>40 kg: 4 mg IV q6h prn nausea

Interactions

Although there is potential for cytochrome P-450 inducers (barbiturates, rifampin, carbamazepine, and phenytoin) to change half-life and clearance of ondansetron, dosage adjustment is not usually required

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause headache; ondansetron may lead to dose-dependent increase in PR, QRS duration, QT/QTc or JT (caution in patients with known prolonged QT or congenital long QT syndrome)

Metoclopramide (Reglan)

Works as antiemetic by blocking dopamine receptors in the chemoreceptor trigger zone of CNS.

Dosing

Adult

0.4-1 mg/kg IV (10-20 mg IV) q6-8h

Pediatric

<6 years: 0.1 mg/kg IV slowly over 1-2 min
>6 years: Administer as in adults

Interactions

Anticholinergics may antagonize effects; opiate analgesics may increase toxicity in CNS; increases rate of absorption of ethanol; may not be effective in patients receiving levodopa; neuromuscular blocking effects of succinylcholine may be increased, producing prolonged respiratory depression and apnea; zalcitabine bioavailability is mildly reduced when coadministered; preanesthetic use may increase frequency and severity of neuromuscular excitation and hypotension when coadministered with thiopental; coadministration with fosfomycin lowers concentrations and urinary excretion of fosfomycin

Contraindications

Documented hypersensitivity; pheochromocytoma or GI hemorrhage, obstruction, or perforation; history of seizure disorders

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in history of mental illness and Parkinson disease; observe for tardive dyskinesia and extrapyramidal effects

Benzodiazepines

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.

Dosing

Adult

0.2 mg/kg IV at 2 mg/min, not to exceed 20 mg/dose; may repeat, monitor for respiratory depression

Pediatric

0.2-0.5 mg/kg IV
<5 years: Not to exceed 5 mg
>5 years: Not to exceed 10 mg

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, cimetidine, ethanol, disulfiram, and MAOIs

Contraindications

Documented hypersensitivity; altered mental status; low BP or RR; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); caution in altered mental status, respiratory depression, and hypotension

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.

Dosing

Adult

0.044 mg/kg (2-4 mg) IV, titrate to desired effect
Status epilepticus: 4 mg IV over 2-5 min; may repeat second dose in 10-15 min prn; not to exceed 8 mg

Pediatric

Neonates: 0.05 mg/kg IV over 2-5 min; may repeat in 10-15 min prn
Infants and children: 0.1 mg/kg over 2-5 min; second dose of 0.05 mg/kg IV at 10-15 min prn; single dose not to exceed 4 mg
Children: 0.05 mg/kg IV (0.02-0.1 mg/kg)
Adolescents: Administer as in adults
Status epilepticus: Adolescents receive 0.7 mg/kg (not to exceed 4 mg) given slowly over 2-5 min; second dose at 10-15 min prn

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; monitor for respiratory depression with high or repeated 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.

Dosing

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV given slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg followed by continuous infusion of 1 mcg/kg/min, titrating dose upward q5min until seizures controlled

Interactions

Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects due to decreased clearance; reduce dose of thiopental by 15% when using together

Contraindications

Documented hypersensitivity, sensitivity to propylene glycol (the diluent); preexisting hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and patients >60 y; monitor for respiratory depression with high or repeated doses; consider lower dosages in patients with organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, use of nicotine or taking cimetidine)

Barbiturates

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

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.

Dosing

Adult

10-20 mg/kg IV administered <50 mg/min

Pediatric

15-20 mg/kg IV administered <50 mg/min

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function, nephritis

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia since adverse reactions can occur; caution in myasthenia gravis and myxedema; monitor for hypotension, respiratory depression, and need for intubation

Follow-up

Further Inpatient Care

• 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.
• Counsel pregnant patients that teratogenic effects from poison hemlock exposure have been reported in livestock.

Transfer

• Consider transferring the patient to a facility with a toxicology service.

Deterrence/Prevention

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

Complications

Complications of hemlock ingestion may include the following:

• Death (secondary to respiratory failure or status epilepticus)
• Seizures (status epilepticus)
• Rhabdomyolysis (renal failure)
• Coma
• Aspiration pneumonitis
• Permanent neurologic sequelae

Prognosis

• The prognosis is good if the patient presents early and receives appropriate decontamination and supportive care.

Patient Education

• For excellent patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Activated Charcoal.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider diagnosis with history of wild plant ingestion
• Failure to monitor patient after diagnosis is made
• Complications following use of ipecac
• Failure to evaluate and/or treat rhabdomyolysis
• Failure to terminate seizures
• Failure to consider an intentional ingestion (eg, suicidal act)

Special Concerns

• Counsel pregnant patients after acute toxicity is treated.

Multimedia

Media file 1: Hemlock. Photo by Cornell University Poisonous Plants Informational Database

References

1. Uwai K, Ohashi K, Takaya Y. Exploring the structural basis of neurotoxicity in C(17)-polyacetylenes isolated from water hemlock. J Med Chem. Nov 16 2000;43(23):4508-15. [Medline].

2. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline].

3. Ellenhorn MJ. Poison hemlock (Conium Maculatum). In: Ellenhorn's Medical Toxicology. 2^nd ed. Williams and Wilkins; 1997:1841, 1871.

4. Furbee B, Wermuth M. Life-threatening plant poisoning. Crit Care Clin. Oct 1997;13(4):849-88. [Medline].

5. Goldfrank LR, Flomenbaum NE, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies. 6^th ed. Appleton & Lange; 1998:2, 318, 338, 1246, 1252-3.

6. Hopkins J. The glycoalkaloids: naturally of interest (but a hot potato?). Food Chem Toxicol. Apr 1995;33(4):323-8. [Medline].

7. Krenzelok EP, Jacobsen TD. Plant exposures ... a national profile of the most common plant genera. Vet Hum Toxicol. Aug 1997;39(4):248-9. [Medline].

8. Litovitz TL, Klein-Schwartz W, Caravati EM. 1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1999;17(5):435-87. [Medline].

9. Litovitz TL, Klein-Schwartz W, Dyer KS. 1997 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1998;16(5):443-97. [Medline].

10. Litovitz TL, Klein-Schwartz W, White S. 1999 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2000;18(5):517-74. [Medline].

11. Lopez TA, Cid MS, Bianchini ML. Biochemistry of hemlock (Conium maculatum L.) alkaloids and their acute and chronic toxicity in livestock. A review. Toxicon. Jun 1999;37(6):841-65. [Medline].

12. Olson KR. Hemlock. In: Poisoning and Drug Overdose. 3^rd ed. Appleton & Lange; 1999:22, 25, 30, 265-74.

13. Panter KE, James LF, Gardner DR. Lupines, poison-hemlock and Nicotiana spp: toxicity and teratogenicity in livestock. J Nat Toxins. Feb 1999;8(1):117-34. [Medline].

14. Reynolds T. Hemlock alkaloids from Socrates to poison aloes. Phytochemistry. 2005;66(12):1399-1406. [Medline].

15. Vetter J. Poison hemlock (Conium maculatum L.). Food Chem Toxicol. Sep 2004;42(9):1373-82. [Medline].

16. Watson WA, Litovitz TL, Rodgers GC, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2003;21(5):353-421. [Medline].

Keywords

hemlock, plant poison hemlock, poison hemlock, Conium maculatum, C maculatum, water hemlock, Cicuta maculata, C maculata, plant ingestion, Queen Anne's lace, wild carrot, fool's parsley

Contributor Information and Disclosures

Author

Daniel E Brooks, MD, Attending Physician, Department of Medical Toxicology, Co-Medical Director, Banner Poison Center, Banner Good Samaritan Medical Center
Daniel E Brooks, MD is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Medical Editor

David A Peak, MD, Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & 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.

Managing Editor

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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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