The correct identification of this plant is imperative. If the identity is uncertain, seek clarification from a reliable source such as a garden center or botanist.
species cause different toxic effects. Generalizations should never be made as to symptoms expected. “Hemlock” may refer to Conium maculatum
or Cicuta spp..
Both are highly toxic but have very different effects.
|California fern||Carrot fern||Deadly hemlock|
|Poison hemlock||Poison parsley||Skarntyde|
|Spotted hemlock||Winter fern|
NB: The common names of Conium maculatum are also used to refer to other genera in the Umbelliferae family. Botanic identification is crucial.
“Hemlock” most commonly refers to Conium maculatum
(poison hemlock) but can refer to Cicuta spp.
(water hemlock), which are related and significantly toxic, but contain different toxic components. Although many symptoms overlap, differentiation is important; in severe poisoning Conium maculatum
causes respiratory paralysis, whereas Cicuta spp.
plants result in profound seizures and potentially status epilepticus.
Conium maculatum is native to Europe and West Asia. It has been introduced to America, North Africa, Australia, and New Zealand.
Extracts of this species were used both as a sedative and an antispasmodic. However, because of the plants toxicity, it was discontinued by the early 20th century.
This species has no known uses and is classified as a weed.
Decontamination, if appropriate, and monitoring is recommended:
- For all known or suspected ingestions of hemlock
With environmental exposures involving dermal contact, management depends on clinical presentation. Refer all symptomatic cases to an appropriate health care facility.
All patients require medical attention.
If medical observation is required the patient must be monitored for 4 hours following exposure for onset or worsening of symptoms.
If the patient is asymptomatic at the end of the observation period, and if they have been appropriately decontaminated and any investigations
have been carried out, they may be:
Discharged into the care of a reliable observer, or
Referred for psychological assessment if the overdose or exposure was with intent to self-harm
A mousy odor is associated with Conium maculatum; this odor on the breath or in the urine can be used as a diagnostic clue. However, absence of this odor does not rule out exposure.
Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management.
Admission to an intensive care facility is required for those suffering significant signs of toxicity including:
Administration of activated charcoal may be considered within one hour of ingestion; however, benefit is unproven, and risks of seizure, vomiting, and aspiration potentially out-weigh gain.
There are no specific antidotes and no methods for enhancing elimination can be recommended.
Supportive care is the mainstay of management with primary emphasis on cardiovascular and respiratory support. In severe cases, particular care should be given to airways management and respiratory support is vital in obtaining a positive outcome, as death is usually due to respiratory paralysis. Routine supportive care should be used for the treatment of other effects.
Nausea and vomiting may persist requiring symptomatic care with IV rehydration or antiemetic drugs, appropriate fluid and electrolyte balance must be maintained. Hypotension usually responds to intravenous fluids, sympathomimetics may be needed. Rarely cardiac dysrhythmias occur and should be managed using standard electrical and/or pharmacological methods. Extreme agitation or seizures can be a complicating feature and should be treated with a benzodiazepine. Atropine may be used to control manifestations from parasympathetic stimulation, such as diarrhea, urination, bronchospasm, emesis, lacrimation, and sweating. Monitor for rhabdomyolysis and acute renal failure.
Ensure Adequate Cardiopulmonary Function
Ensure the airway is protected if compromised (intubation may be necessary).
Immediately establish secure intravenous access.
Most toxic seizures are short-lived and often do not require intervention.
Administer a benzodiazepine
as first-line treatment to patients with seizure activity.
Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, 50% dextrose
should be administered IV (preceded by thiamine
Single Dose Activated Charcoal
Decontamination with activated charcoal is recommended for recent ingestions of hemlock. However, as hemlock commonly produces vomiting, CNS or respiratory depression, the time frame for successful administration is limited and risks pulmonary aspiration. In symptomatic patients general supportive measures should take precedence over decontamination.
Administer activated charcoal up to 1 hour following a potentially toxic ingestion.
Single dose activated charcoal
1 to 2 g/kg orally
50 to 100 g orally
Nasogastric instillation of activated charcoal is not recommended unless the ingestion is considered potentially severely toxic and oral administration is not successful. Accurate placement of the nasogastric tube and protection of the airway must be ensured.
If necessary, remove contaminated clothing or jewelry. Flush the affected area with water as soon as possible. Continue to irrigate until all of the contaminant is removed.
Remove contact lenses. Irrigate immediately with water or saline for at least 15 minutes. If the eye is contaminated with solid particles, the eyelid should be completely everted and any solid material removed as quickly as possible whilst continuing to irrigate. A topical anesthetic may be necessary in some patients, especially children, to enable the patient to open the lids sufficiently for effective irrigation.
If, following irrigation, any of the following are apparent:
Ocular pain (other than mild and resolving)
Erythema (other than mild and resolving)
Decreased visual acuity
A full ophthalmologic examination should be undertaken and any injury appropriately treated.
There Are No Antidotes For This Substance
There is no specific antidote for the treatment of this poisoning. Treatment is based on symptomatic and supportive care.
Enhanced Elimination Not Recommended
Dialysis or perfusion may be indicated for secondary complications, such as acidosis or renal failure, but not for toxin removal alone.
ECG (12 lead)
Arterial blood gases (if compromised respiratory function)
On-set of paralysis
Due to nicotinic receptor over-stimulation gastrointestinal distress is common. Vomiting and diarrhea contribute to hypotension and fluid and electrolyte imbalances, potassium loss may increase the risk of cardiac dysrhythmia. Patients may require symptomatic care with antiemetic medication, IV fluids, and electrolyte replacement.
Observe patient for:
Manage gastrointestinal irritation following standard treatment protocols.
The sedation phase of hemlock toxicity can lead to reduced levels of consciousness and coma.
Closely monitor level of consciousness.
Follow standard protocols for the management of coma.
Seizures may develop after the ingestion of hemlock, though this has not been described in most case reports. Seizures should be treated with a benzodiazepine.
Observe the patient closely for onset of seizure activity.
The sedation phase of hemlock toxicity will cause weakness and paralysis, which includes muscle weakness. This can lead to respiratory arrest.
Intense respiratory support, when needed, constitutes the most vital supportive measure in preventing a poor outcome. Respiratory failure is usually the most common cause of death.
Monitoring for respiratory failure should include:
Arterial blood gases
Treat using standard protocols for respiratory failure.
The late inhibitory phase of conium toxicity will result in bradycardia.
Manage bradycardia following standard treatment protocols.
The toxic effect of conium may result in the paralysis of skeletal muscles, which may lead to rhabdomylosis;
this is characterized by an increase in muscle enzymes and the urine becoming red-brown, due to the presence of myoglobin.
Examine patient for muscle tenderness/pain and weakness.
Serum creatine kinase (increased CK-MM isoenzyme)
Acute renal failure can occur as a result of rhabdomylosis.
Patients should be monitored for the onset of renal failure:
Blood urea nitrogen (urea)
Loin pain may occur
Manage following standard treatment protocols for acute renal failure.
Patients may be discharged from hospital care when clearly asymptomatic and fully recovered from any complications. Appropriate psychiatric intervention may be necessary depending on the circumstances of the exposure.
Medical follow-up is unlikely to be required. Psychiatric intervention may be necessary depending on the circumstances of the exposure.
Following appropriate supportive care the prognosis is good.
SIGNS AND SYMPTOMS
The effects of coniine are similar to those of nicotine, but with more pronounced CNS and curare-like actions.
General signs are salivation, vomiting, dilation of the pupils, blurred vision, incoordination, myalgia, muscle fasciculations or flaccid paralysis, coldness of the extremities, and slow weak pulse. Subsequently the pulse may become rapid and thready followed by coma, convulsions, and eventually death from respiratory paralysis.
Rhabdomyolysis and subsequent renal failure have also been reported.
Systemic symptoms can occur after ingestion of fresh hemlock plant material; drying is thought to somewhat reduce toxicity, but poisonings have still occurred. Seeds of hemlock are toxic whether fresh or dried. Although the active alkaloids are oily volatile liquids, deaths have been reported after drinking liquid from boiling hemlock leaves.
Poisoning has also transpired from use of the hollow stem as a musical instrument or pea shooter.
Meat of birds, which eat hemlock seeds during migratory flights, is also poisonous to humans.
Onset/Duration of Symptoms
Symptoms could be expected to appear quite promptly, due to rapid absorption and the onset of similar compounds such as nicotine. One report describes the onset of symptoms occurring within 30 minutes of eating hemlock leaves
whereas another case reports the death of a child 3 hours after ingesting plant leaves.
Effects usually persist for between 4 to 24 hours.
Animal studies have shown an onset of 0.5 to 2 hours with duration of 3 to 7 hours.
|Mild Conium maculatum Toxicity||Moderate Conium maculatum Toxicity||Severe Conium maculatum Toxicity|
Severe GI effects
ACUTE EFFECTS (ROUTE OF EXPOSURE)
(with or without blisters)
Systemic symptoms have not been reported following skin exposure.
ACUTE EFFECTS (ORGAN SYSTEM)
Burning mouth or throat
Weak and thready pulse
Skeletal muscle paralysis
Acute tubular necrosis
(secondary to rhabdomyolysis)
The toxic content of plants may vary from year to year due to various factors that affect growth such as available moisture and spring temperatures. Thus, it is difficult to establish an association between the severity of symptoms and the ingestion of a specific amount of plant material.
The primary toxic effects of this plant are due to coniine, but the toxicity of this plant may vary considerable from that of its toxic component, due a number of different considerations, including toxic concentration, and growth factors of this plant.
Poison hemlock has been responsible for many human fatalities because of the resemblance of the seed to Anise, the leaves to parsley or carrot, and the roots to parsnips.
All parts, especially the seeds, should be regarded as poisonous, even when dried.
An adult lethal dose is 100 to 300 mg of the toxic alkaloids.
This approximately corresponds to:
40 g in a 60 kg adult
10 g in a 15 kg child
29 to 1000 g in a 60 kg adult
7 to 250 g in a 15 kg child
13 to 67 g in a 60 kg adult
3 to 17 g in a 15 kg child
20 g in a 60 kg adult
5 g in a 15 kg child
7 to 30 g in a 60 kg adult
2 to 8 g in a 15 kg child
20 to 100 g in a 60 kg adult
5 to 25 g in a 15 kg child
22 to 100 g in a 60 kg adult
6 to 25 g in a 15 kg child
Toxicity is likely to occur after any ingestion of this plant.
An estimated lethal dose in a 3 year old male has been reported to be approximately 142 g of leaf material. The child died approximately 3 hours after ingesting the plant.
A 4 year old male developed CNS depression 30 minutes after ingesting hemlock leaves and could not be roused after a further 2 hours. Following decontamination and supportive care, he became conscious 6.5 hours post ingestion.
Two adults died after ingesting an unknown amount of hemlock, which was prepared by boiling the leaves in water.
Adults have become poisoned after ingesting the meat from birds that have ingested hemlock buds. The birds themselves (robins, skylarks, chaffinches) were not susceptible to the alkaloids.
A 19 year old female required intubation 40 minutes after ingesting an unknown quantity of plant material. After 25 hours her breathing had improved sufficiently to discontinue this support.
LD50 Oral, Mouse
12 mg/kg12 mg/kg/
LD50 Oral, Mouse
100 mg/kg100 mg/kg/
LD50 Oral, Mouse
204.5 mg/kg204.5 mg/kg/
Some small birds are not susceptible to coniine poisoning, consuming the seeds as a food source, and therefore may have the potential to cause toxicity in any species ingesting them. In contrast, deaths have resulted in other larger birds such as chickens and turkeys.
Severe poisoning and fatalities in cattle, goats, horses, sheep, and pigs have resulted from poison hemlock exposure. Symptoms generally involve movement problems, increased salivation and urination, tremor, vocalization, muscle weakness, and respiratory problems, all which can occur quite rapidly.
Other animals including rabbits and elk are affected in a similar way to farm animals.
It is unknown whether coniine crosses the placenta but poison hemlock is likely to affect the infant. Any exposure to poison hemlock should be avoided during pregnancy.
No human information is available however Conium maculatum appears to act as a teratogen and abortifacient in animal poisonings.
It is unknown if exposure to, or ingestion of, this plant results in excretion of toxic substances into breast milk.
It is unknown if exposure to, or ingestion of, this plant causes impaired fertility.
Piperazine plant alkaloids include:
Coniine and gamma-coniceine are found in the largest amounts and combined account for most of the plant’s toxic activity. Coniine is about 8 times more toxic than gamma-coniceine.
These alkaloids are structurally related to nicotine, and could be expected to produce similar symptoms.
All parts of the plant contain toxic piperidine alkaloids.
Before flowering, the leaves contain the most alkaloids, but the greatest concentrations are found in the flowers and fruits/seeds. The roots, at all times, contain the least.
Younger plants have 0.3 to 0.6% in leaves and 0.15% in other plant material (excluding flowers and fruit). Older plants contain approximately 1% in all parts of the plant.
The alkaloid content, however, does vary with the climatic conditions. In good growing seasons, the average weight of the fruits and thus the quantity of alkaloids can be twice that of normal. Drying the plant reduces the alkaloid content.
Coniine alkaloids affect the neurological junction where they act as non-depolarizing neuromuscular blockers, similar to curare. However, they also act on autonomic nervous system ganglia with varying degrees of stimulator, and inhibitor (biphasic) effects (resembling the effects of nicotine).
BIOLOGICAL LEVELS - TOXIC
Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management.
No human pharmacokinetic data were found in the literature.
A coarse, erect, branched plant, that can be biennial (lives for two years and flowers in the second year), sometimes annual (lifecycle completed in one year) or perennial (lasting several years). It may exceed 2 m in height. The stem is hairless, slightly ridged and hollow with characteristic irregular purple blotches.
Appear in almost flat-topped clusters of 2 mm white flowers. Each cluster is 2 to 5 cm in diameter.
The root is generally a thick yellow or white tap root (similar to a parsnip), which may or may not have branches.
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