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Poison Hemlock

DR.A N M AL MAMUN(ROMAN)
Forensic Science
Poisonous Plants

Coniine, the
alkaloid in poison
hemlock
Conium maculatum
Conium maculatum
This plant family, also called Apiaceae or Carrot family, is one of
the best-known families of flowering plants, because of its
characteristic inflorescences and fruits and the distinctive
chemistry reflected in the odor, flavor and even toxicity of many
of its members.
The Umbelliferae seems to be the first flowering plant family to
be recognized as such by botanists about the end of the 16th
century.
Conium maculatum is a native of Europe, western Asia and North
Africa, and common in low waste places, along roadsides, edges
of cultivated fields, railroad tracks, irrigation ditches, stream
banks, etc.
It was brought to the U.S. from Europe as a garden plant.
Conium maculatum
It was introduced first into our homoeopathic pharmacopoeia by
Samuel Hahnemann.
C = Closing the eyes or as soon as one sleeps:
sweating occurs.
O = Old men and old maids: with bad effects of
suppressed sexual desire.
N = Nodular induration of stony hardness of glands.
I = Intense photophobia without inflammation
of eyes.
U = Urine: flow intermits; prostatic or uterine
affections.
M = Menses suppressed by putting hands in cold
water.
• Treatment wasn't always effective as the difference between a
therapeutic and a toxic amount is very slight.
Poison hemlock has been used as a sedative and for its
antispasmodic properties.
Also used by Greek and Persian physicians for a variety of
problems, such as arthritis.
As an inhalant it is said to relieve cough in bronchitis,
whooping-cough, asthma, etc.
Hemlock juice (Succus conii) has been prescribed as a remedy
in cases of undue nervous motor excitability, such as:
teething in children
spasms of the larynx and gullet
in acute mania

Medicinal Properties
Botanical Name
Conium maculatum.
■ The larger stems are hollow and bear numerous purple
spots that are very distinctive.
■ Leaves are fine, light-green, and fern-like. When crushed,
they give off an unpleasant “mousy” smell.
■ Fruits are smooth skinned with crenate ribs, and are
binoculated, measuring about 9 mm long, and 6 mm across.
The leaves are more dangerous in the springtime, and the
fruit is the most dangerous in the fall.

Description of Hemlock
• By far the most familiar species is Conium maculatum - the most
common of several species of hemlock characterized by their
toxicity.
• It is a herbaceous biennial plant which grows between 1.5-2.5 m tall,
with a smooth green stem, usually spotted or streaked with red or
purple on the lower half of the stem.
• The leaves are finely divided and lacy, overall triangular in shape, up
to 50 cm long and 40 cm broad.
• The flowers are small, white, clustered in umbels up to 10-15 cm
across.
• The plant is often mistaken for fennel, parsley or wild carrot although
the characteristic stem hairs of the wild carrots are missing.
• The Conium root is fleshy, white and often unbranched and can be
mistaken for parsnip.

Description of Hemlock
Description of Hemlock
The symptoms of poisoning were described by Plato (a pupil of
Socrates).
The old Roman name of the plant was Cicuta, but this name was
later applied (by Gesner, 1541) to another umbelliferous plant,
Cicuta virosa (water hemlock).
The consequent confusion was solved by the nomenclature of
Linnaeus, who restored the classical Greek name describing the
plant as Conium maculatum.
The generic name was derived from the Greek word Konas,
meaning to whirl about, because the consumption of the
plant causes ataxia, tremor and convulsions.
The specific name (maculatum) is a Latin word, meaning
spotted and refers to the very characteristic brownish–
reddish spots of stem.
The plant was used in ancient Anglo-Saxon medicine; and
the English name––hemlock––is derived from the Anglo-
Saxon words hemlic or hymelic.

Description of Hemlock
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.[33]

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.

Description of Hemlock
In its second year the plant will produce small white flowers
contained in clusters that form an umbrella-shaped head.
Toxic Part:
All parts.
Toxic Principles:
The toxins of poison hemlock are simple piperidine
alkaloids:
coniine and gamma-coniceine.
They are structurally similar to nicotine and possess similar
clinical features in toxicity.

Description of Hemlock
The plant Conium maculatum was famous as a poison and
its extract was used often to execute criminals or political
prisoners in ancient Greece.
The data on total alkaloid content in different organs of
Conium maculatum has been summarised,roots contain 0–
0.5%, shoots 0.02– 0.7%, leaves 0.3–1.5%, flowers 1.0%,
unripe fruits 1.6–3.0, ripe fruits 0.2–1.0% and seeds 0.02–
0.9%, respectively.
In the leaves of the young plants (in the phase of the active
growth) c-coniceine was the major alkaloid component with
small amounts of conhydrine.

Description of Hemlock
A useful trick to determine whether a plant is poison hemlock rather
than fennel (which it resembles) is to crush some leaves and smell the
result.
Fennel smells like liquorice, but poison hemlock smells “mouse-like” or
musty.
Discard it if you can’t tell the difference.

Poison hemlock flourishes in the spring, when most other forage is


gone.
All parts of the plant are poisonous but once the plant is dried the
poison is greatly reduced (but not gone completely).

Hemlock goes by other names such as: "poison parsley" or "spotted


parsley".

More Hemlock Info.


The piperidine alkaloids found in Conium maculatum are
acetate-derived.
The results of chemical and biochemical investigations
suggested, that Conium piperidine alkaloids are formed by
the cyclisation of an eight-carbon chain derived from four
acetate units.
Nitrogen was incorporated at some stage in the pathway to
give the piperidine nucleus.

Chemical Composition
Experiments with N-labelled amino acids showed, that L L-
alanine provided the N in a transaminase catalysed
enzymatic reaction (the presence of such a aminotransferase
which produces c-coniceine from 5-oxooctanal, was
established).
After the transamination, the 5-oxooctylamine is formed,
there is a non-enzymatic cyclisation producing c-coniceine.
c-Coniceine is the precursor of the other Conium alkaloids.

Chemical Composition
The interconversion of coniine and c-coniceine in Conium
plants indicated that these compounds are members of an
oxidation-reduction system.
The poison in water hemlock is different; it is an alcohol
called cicutoxin (from the genus name). Its effect is very
similar – violent convulsions followed by death.

Chemical Composition
Piperazine plant alkaloids include:
Conhydrine
Coniine
Gamma-Coniceine
N-Methylconiine
Pseudoconhydrine

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.

Toxic Components
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.

Routes of Exposure
An adult lethal dose is 100 to 300 mg of the toxic alkaloids.
In man, 3 mg of coniine is said to have produced symptoms,
but 150 mg have been tolerated without discomfort.
Perhaps 30-60 mg is dangerous and death may occur with
doses greater than 100 mg.
It has been reported that a lethal dose may be 6 to 8 fresh
leaves.
The onset of toxic effects is in 20 – 30 minutes.

Toxicity..
Toxicity Signs of poisoning may occur 15 minutes to an
hour after the plant is consumed.
The signs of poisoning include salivation, tremors, grinding
of the teeth, abdominal pain, dilated pupils, and elevated
body temperature.
Death may occur quickly or within about 8 hours.
There are no specific postmortem lesions.

Toxicity..
Affinity
MIND NERVES
MUSCLES GLANDS
MAMMAE OVARIES
Sexual Organs Respiration
Nicotine-like alkaloids act agonistically at nicotinic-type
acetylcholine (cholinergic) receptors (nAChRs).
These sodium-gated receptors exist widely in the central and
autonomic nervous systems, and the neuromuscular junction;
they can be present at either pre- or postsynaptic sites.
Their autonomic sites include the adrenal medulla and autonomic
ganglia; in the latter case the postsynaptic receptors are located
on the commencement of the postganglionic autonomic neurons,
whose junction with the end organs involves cholinergic
(muscarinic type) or norepinephrine.

Mechanisms of Toxicity
Mechanisms of Toxicity
The nicotinic alkaloids act as agonists on the nAChRs, causing
increased sodium ion influx through the channel, which leads to
prolonged membrane depolarization and consequently enhanced
action potential propagation.
Increased ganglionic transmission to the postganglionic
sympathetic fibers and catecholamine release from the adrenal
gland may cause tachycardia and hypertension.
Also, discharges directly from the spinal cord can cause muscle
fasciculations and tremor.
Furthermore, increased postganglionic parasympathetic
fiber activity can also occur, with risk of miosis, salivation,
lacrimation, and bronchospasm.
However, nAChRs do not play a direct role at the
neuroeffector junctions, where muscarinic cholinergic (and
noradrenergic) receptors predominate.
Indeed, because of the large number of different neuronal
receptor types, the dose–response relationships of nicotine
and related alkaloids are complicated.

Mechanisms of Toxicity
Over a substantial dose range, increasing acute doses of
these alkaloids result in proportionally more stimulation of
the nAChRs, and thus greater associated adrenergic,
somatic, cholinergic (and central) symptoms, as described
above.

However, paradoxically, at still greater doses and/or more


sustained exposures, autonomic ganglionic blockade can
occur, which, along with similar effects on central nicotinic
receptors, can lead to hypotension, bradycardia, and
respiratory depression.

Mechanisms of Toxicity
Effects of Conium..
The Conium alkaloids produce a biphasic nicotine-like
effect.
The initial stimulatory effects include nausea and vomiting,
excessive salivation, diarrhea, and abdominal pain.
Hypertension and tachycardia reflect increased adrenergic
tone but may partly relate to constriction of coronary
arteries; pallor from constriction of peripheral blood vessels
is also common.
Early neurological effects include ataxia, tremor,
restlessness, headache, visual and hearing disturbances,
confusion, dizziness, muscle fasciculations, miosis, and
seizures; deep tendon reflexes may also be diminished.
Additional early symptoms include diaphoresis and
tachypnea.

Effects of Conium..
Effects of Conium..

After the initial stimulatory phase, a period of


direct depressor effects can ensue, because of
“paradoxical” inhibition of the nicotinic
cholinergic receptors.
In this second phase circulatory effects can change
to hypotension and sinus bradycardia, cardiac
conduction abnormalities and dysrhythmias,
block, atrial fibrillation, QT prolongation, and
ventricular fibrillation.
Central effects include central nervous system depression
and coma.
Mydriasis has also been reported, which may be due to
autonomic factors.
Increasing neuromuscular blockade can lead to ptosis,
muscular weakness, and/or paralysis, with dyspnea or
apnea, respiratory failure and central nervous system
depression.

Effects of Conium..
Deaths have occurred, which appear to be due to severe
respiratory depression caused by muscular paralysis or to
cardiovascular collapse.
Coniine can produce rhabdomyolysis by either a direct toxic
effect on skeletal muscle or a strychnine-like pro-consulvant
action on the central nervous system.

Effects of Conium..
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.

Onset/Duration of
Symptoms
Mild Conium maculatum Toxicity:
GI effects
Thirst
Nausea
Vomiting
Agitation

Moderate Conium maculatum Toxicity:


Severe GI effects
Salivation Abdominal pain
Mydriasis Myalgia
Muscle weakness Muscle fasciculations
Drowsiness Tachycardia
Tachypnea Respiratory depression

Severity of Poisoning
Severe Conium maculatum Toxicity:
Bradycardia Hypotension
Seizures Paralysis
Rhabdomyolysis Renal failure
Respiratory failure Coma

Severity of Poisoning
• Skin
• Local dermatitis (with or without blisters)
• Burning sensation
• Numbness

• Systemic symptoms have not been reported following


skin exposure.

Acute Effects (Route of


Exposure)
Gastrointestinal
Burning/numbness to mouth or throat
Nausea
Vomiting
Hypersalivation
Thirst
Abdominal pain

Acute Effects (Organ


System)
Neurologic
Ataxia Agitation Tremor
Nervousness Dizziness Headache
CNS depression Dysarthria Hypotonia
Hyperreflexia Arreflexia
Absent oculocephalic reflex Absent gag reflex
Muscle paralysis Seizures
Coma

Acute Effects (Organ


System)
Respiratory
Tachypnea Dyspnea
Hypoxia Respiratory depression
Respiratory paralysis Respiratory failure
Renal
Urination Acute tubular necrosis
Renal failure (secondary to rhabdomyolysis)

Acute Effects (Organ


System)
Cardiovascular
Tachycardia Hypertension
Bradycardia Widened QRS
Weak and thready pulse Asystole
Musculoskeletal
Tremor Muscle fasciculations
Myalgia Muscle edema
Muscle weakness Decreased muscle tone
Skeletal muscle paralysis Rhabdomyolysis

Acute Effects (Organ


System)
Ocular
Mydriasis Blurred/double vision
Amblyopia
Hematologic
Elevated INR
Prolonged partial thromboplastin time
Metabolic
Fever

Acute Effects (Organ


System)
The primary action on hemlock is on the central nervous
system.
The effect of the plant is similar to poisoning with nicotine.
The general symptoms of hemlock poisoning are
nervousness, trembling, problems in movement, particularly
in the legs of humans, dilation of pupils, slow and weak
pulse (becoming later rapid), rapid respiration.

Clinical Features.
The death is most frequently caused by the cessation of
breathing at full consciousness and before cardiac arrest.
Coniine is a curare-like poison, such alkaloids block the
transmission of stimuli from motor nerve endings to striated
muscles, which subsequent leads to muscle paralysis.
The paralysis progresses from the lower limbs upwards to
respiratory muscles, and when these muscles are paralyzed,
the victim dies of asphyxia.
The brain is not affected and the victim retains
consciousness.

Clinical Features.
Clinical Features.
Conium affects very strongly:
- The sexual sphere.
- The mental sphere.
- The central nervous system.
Conium causes paralysis of the motor nerve filaments of the
cerebrospinal system.
The paralysis and weakness spreads from below, the lower giving
out before the upper.

Clinical Features.
Clinical Features.
As the action increases, other and more vital organs are involved.
The lungs are attacked; there is dyspnea; the pulse is irregular,
implicating the heart muscle.
Finally the patient dies from paralysis of respiration.
Clinical Features.
It is useful in the weakness of old people and to diseases that are
caused by a blow or fall.
Clinical Features.
We use it for swelling and induration of glands after
contusions and bruises; tumors coming on after injury, are
also helped by Conium.
Thyroid:
Stony hard thyroid enlargement.
Clinical Features.
The thing to remember is that the glands wherever affected are of
stony hardness. These indurations are quite common in the
breasts, in the testicles, and in the uterus.
Clinical Features.
It is indicated in ophthalmia - a characteristic symptom being
intense photophobia, disproportionate to the level of
inflammation.
Conium maculatum has a strong tendency for a type of paralysis
of the urinary bladder.
Clinical Features.
It is often indicated in weakness of the sexual organs, due to bad
effects from suppressed sexual desire or from excessive
indulgence.
The characteristic prostate gland symptom of Conium is a constant urge
to urinate with little or no result.
The patient has to get up at night because of this strong urge, he has to
push hard to urinate a bit.
The urination stops, while the urge remains.
This situation can be so serious that the patient becomes desperate and
anxious, so that he starts to perspire and he gets a headache and
vertigo.
Clinical Features.
Conium is the main remedy for the gland that is affected greatly
by sexual activity in man: the prostrate.
If a suppression of sexual urge occurs in a Conium man, the
first gland to be affected is the prostrate.
It can even cause prostate cancer. In addition, Conium is an
important remedy in indurated and malignant swelling of the
testes.
Clinical Features.
Weeping fits which turn into vertigo and weakness are very
characteristic of Conium.
Management….
Admission to an intensive care facility is required for those
suffering significant signs of toxicity including:
CNS depression
Convulsions
Respiratory depression
Hypotension
Bradycardia

Admission Criteria
Ensure Adequate Cardiopulmonary Function
Airway
Ensure the airway is protected if compromised (intubation may be necessary).

Cardiovascular
Immediately establish secure intravenous access.

Seizure
Most toxic seizures are short-lived and often do not require intervention.

Administer a benzodiazepine as first-line treatment to patients with seizure activity.

Emergency Stabilization
Heart rate
Respiratory rate
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 in adults).

Emergency Monitoring
Induction of emesis is also not recommended.
Benzodiazepines for convulsions.
Respiratory support.
Forced diuresis may help in preventing renal failure.

Treatment
Gastrointestinal

Gastrointestinal Irritation
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:
Nausea
Vomiting
Abdominal pain
Hematemesis
Diarrhea
Monitor:
Blood pressure
Fluid balance
Serum electrolytes (if severe)
Acid-base (if severe)

Manage gastrointestinal irritation following standard


treatment protocols.

Gastrointestinal
Neurologic

Coma
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
Seizures may develop after the ingestion of hemlock,[6] 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.
Respiratory Failure
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.
Monitoring for respiratory failure should include:
Chest auscultation
Oxygen saturation
Arterial blood gases

Treat using standard protocols for respiratory failure.

Respiratory
Bradycardia
The late inhibitory phase of conium toxicity will result in
bradycardia.

Monitor:
Heart rate/rhythm
Blood pressure
ECG

Manage bradycardia following standard treatment protocols.

Cardiovascular
Rhabdomyolysis
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.


Monitor:
Serum creatine kinase (increased CK-MM isoenzyme)
Urinalysis:
Myoglobin
pH

Musculoskeletal
Acute Renal Failure
Acute renal failure can occur as a result of rhabdomylosis.

Patients should be monitored for the onset of renal failure:


Urine output
Serum creatinine
Blood urea nitrogen (urea)
Proteinuria
Hematuria
Loin pain may occur

Manage following standard treatment protocols for acute renal failure.

Renal
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.

Management/Treatment..
Single dose activated charcoal
CHILD 1 to 2 g/kg orally
ADULT 50 to 100 g orally

Antidote:
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.

Management/Treatment..
Nasogastric Administration
Nasogastric instillation of activated charcoal is not recommended unless the ingestion is
considered potentially severely toxic and oral administration is not successful.

Skin
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.

Eye
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.

Management/Treatment..
Heart rate
Blood pressure
ECG (12 lead)
Cardiac monitoring
Respiratory function
Arterial blood gases (if compromised respiratory function)
Neurological status
Serum electrolytes
Renal function
On-set of paralysis

Monitoring
These are those of asphyxia.
The remains of the roots or leaves should be looked for in
the stomach.
When these are mixed with caustic potash and crushed in a
mortar, they give a peculiar mousy odour.

Postmortem
Appearances
Hemlock was popular in ancient times as a means of
execution.
The most famous personality executed in this fashion was
Socrates, who was condemned to death for his “crime” of
introducing new divinities.
Today, most cases of hemlock poisoning result from
accidental circumstances due to mistaken identity with
edible vegetables such as wild carrot, parsley, or anise
seeds.

Forensic Issues
Hemlock in History
In ancient Greece, hemlock was used to poison condemned
prisoners, with the most famous victim being the philosopher
Socrates. After being condemned to death for impiety in 399
BC, Socrates was given a strong solution of the hemlock plant.
Plato described Socrates' death in the “Phaedo”:

"The man … laid his hands on him and after a while examined his feet and legs, then
pinched his foot hard and asked if he felt it. He said ‘No’; then after that, his
thighs; and passing upwards in this way he showed us that he was growing cold
and rigid. And then again he touched him and said that when it reached his heart,
he would be gone. The chill had now reached the region about the groin, and
uncovering his face, which had been covered, he said – and these were his last
words – 'Crito, we owe a cock to Asclepius. Pay it and do not neglect it.' 'That,' said
Crito, 'shall be done; but see if you have anything else to say.' To this question he
made no reply, but after a little while he moved; the attendant uncovered him; his
eyes were fixed. And Crito when he saw it, closed his mouth and eyes."
Socrates was condemned to injest Conium
because of his “negative” influence on the
youth of Athens. (He was in his late
seventies.)
AVOIDING CONFUSION….

With the common name of cicuta other two species of plants are usually indicated,
both inclused in different genres:
• Minor cicuta (Aethusa cynapium), also confused with parsley. The similarity
between these plants has caused poisoning events.
• Water hemlock (Cicuta maculata) is substantially more toxic and contains a
different class of toxic components. The alkaloid responsible of water hemlock’s
effects is not coniine but cicutoxine. Although many symptoms overlap,
differentiation is important; in severe poisoning C. maculatum causes respiratory
paralysis, whereas C. maculate results in profound
Water Hemlock seizures and potentially status
epilepticus. They can be distinguished, however, on the basis of their characteristic
morphological properties: C. maculatum has a single tap root, purple and spotted
stem, whereas C. maculata has branched root systems with tubules and an absence of
purple spots.

Water hemlock (Cicuta


maculata)
Water hemlock (Cicuta maculata)
Cicuta species Family:
• Umbelliferae (Apiaceae)
Common Names:
Water Hemlock, Beaver Poison, Children’s Bane, Cicutaire, Death-of-Man,
Musquash Poison, Musquash Root, Spotted Cowbane.
Description:
• Most species of Cicuta have a similar appearance and may grow to a
height of 6 feet.
• The leaves are two or three times pinnately compound.
• The flowers are small, whitish, and heavily scented.
• In the underground portion of mature plants,there is a bundle of
chambered tuberous roots.
• A yellow,oily sap emerges from the cut stem and has a distinct odor of
raw parsnip.

Water Hemlock
These plants are found only in wet or swampy ground.
Distribution:
• Species of Cicuta are found throughout the United States (except Hawaii) and
Canada and are among the most toxic plants in North America.
Toxic Part:
• The whole plant, particularly the roots, is poisonous.
Toxin:
• Cicutoxin,an unsaturated, long-chain aliphatic alcohol,a gamma-aminobutyric
acid (GABA) receptor antagonist or potassium channel blocker.

Water Hemlock
Clinical Findings:
Toxic ingestions often occur when the plant is mistaken for a similar
appearing but edible wild plant such as Daucus carota L.
Onset of symptoms is rapid, usually within 1 hour of ingestion.

Symptoms include:
nausea, vomiting, salivation,and trismus.Generalized seizures also
may occur.

Death may occur if seizures do not terminate.

Water Hemlock
Management:
Supportive care, including airway management and protection
against rhabdomyolysis-associated complications (e.g., electrolyte
abnormalities and renal insufficiency)should be given.
Rapidly acting anticonvulsants,such as diazepam or
lorazepam,should be administered for persistent seizures.

Consultation with a Poison Control Center should be considered.

Water Hemlock