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2/15/2015
Tintinalli's Emergency Medicine: A
Comprehensive Study Guide >
Poisonous Plants
Mark A. Hostetler; Sandra M. Schneider
Poisonous Plants: Introduction
Poisonous and injurious plants number in the hundreds and have a wide variety of toxicities. This chapter focuses
on the most important plant-related exposures clinically relevant to emergency medicine (Tables 215-1 and 215-2)
and those most frequently encountered during the holiday season.1,2 Individual plants are discussed in terms of
their pathophysiology, clinical features (toxidromes), and treatment3 (Table 215-3).
Table 215-1 Most Highly Poisonous Plants
Castor bean (Ricinus communis)
Coyotillo (Karwinskia humboldtiana)
Foxglove (Digitalis purpurea)
Jequirity bean (Abrus precatorius)
Oleander (Nerium oleander)
Poison hemlock (Conium maculatum)
Water hemlock (Cicuta maculata)
Yew (Taxus species)
Table 215-2 Most Commonly Encountered Poisonous and Nonpoisonous Plants
Poisonous/Injurious
Nonpoisonous
Aloe species
African violet (Episcia reptans)
Azalea (Rhododendron species)
Coleus species
Cactus species
Dracaena species
Caladium species
Ficus plant (Ficus species)
Colchicum (autumn crocus, meadow saffron)
Honeysuckle (Lonicera species)
Jade plant (Crassula species)
Dumbcane (Dieffenbachia amoena)
Pyracantha species
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Fava beans (Vicia faba)
Rubber tree plant (Ficus elasticus)
Holly (Ilex species)
Spider plant (Chlorophytum species)
Jimsonweed (Datura species)
Umbrella plant (Schefflera species)
Lily of the valley (Convallaria majalis)
Wandering jew (Tradescantia albiflora)
Mistletoe (Phoradendron flavescens)
Nightshade (Solanum species)
Peppers (Capsicum species)
Philodendron species
Poinsettia (Euphorbia species)
Poison ivy (Toxicodendron species)
Pokeweed (Phytolacca species)
Pothos (Epipremnum species)
Table 215-3 Symptoms and Treatment of Severely Poisonous Plant Ingestions
Plant
Symptoms
Castor bean
(Ricinus
communis)
Delayed gastroenteritis, delirium, seizures, coma,
death
Coyotillo
(Karwinskia
humboldtiana)
Ascending paralysis
Treatment
Whole-bowel irrigation
Supportive care
Supportive care
GI decontamination
with activated charcoal
Foxglove
(Digitalis
purpurea)
Nausea, vomiting, diarrhea, abdominal pain,
confusion, cardiac dysrhythmias
Monitoring of
potassium level
Antidysrhythmics
Digoxin-specific Fab
antibody for
dysrhythmias
Jequirity bean
(Abrus
precatorius)
Delayed gastroenteritis, delirium, seizures, coma,
death
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Whole-bowel irrigation
Supportive care
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GI decontamination
with activated charcoal
Oleander (Nerium
oleander)
Nausea, vomiting, diarrhea, abdominal pain,
confusion, cardiac dysrhythmias
Monitoring of
potassium level
Antidysrhythmics
Digoxin-specific Fab
antibody for
dysrhythmias
Poison hemlock
(Conium
maculatum)
Tachycardia, tremors, diaphoresis, mydriasis,
muscle weakness, seizures, neuromuscular
blockade
Water hemlock
(Cicuta maculata)
Nausea, vomiting, abdominal pain, delirium,
seizures, death
Common: nausea, vomiting, abdominal pain
Yew (Taxus
species)
Rare: seizures, cardiac dysrhythmias, coma
GI decontamination
with activated charcoal
Supportive care
GI decontamination
Supportive care
GI decontamination
with activated charcoal
Consider whole-bowel
irrigation
Supportive care
Epidemiology
According to statistics gathered by the American Association of Poison Control Centers, exposures to plants are
the fourth most common reason for poison control center notification and account for 5% to 10% of all calls
received.1–3 This is likely a reflection of their wide availability rather than any high level of innate toxicity. Children
<6 years of age account for 70% to 80% of all plant-related exposures, the vast majority of which (96%) are
unintentional.4 The most common plant-related calls received by poison control centers concern completely
nontoxic plants (21%), and on average, <10% of patients require treatment in a health care facility.
Clinical Features
Dermatitis and GI irritation are the most commonly reported symptoms of plant toxicity. Vomiting is not a common
symptom after plant ingestions.5 Moderate systemic effects occur in about 1% of patients. Severe life-threatening
effects or disabling injuries are extremely uncommon and occur in only about 0.04% of patients. Death as a
consequence of plant-related exposures is rare and occurs in <0.001% of patients.
Treatment
Most plant-related exposures require no treatment, and those that do often can be managed by simple GI
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decontamination procedures to decrease the absorption of ingested toxins. Activated charcoal can adsorb
many toxins and can prevent their absorption into the body. It is the treatment of choice for most patients who
require GI decontamination. Whole-bowel irrigation using polyethylene glycol electrolyte solution should be added
when a potentially toxic intact seed has been ingested. The theory is that the bowel can be cleansed of plant
material prior to toxin release. Patients who have had a potentially serious exposure but who are asymptomatic
should be observed in the ED for about 6 hours. If patients remain asymptomatic, they may be discharged with
instructions to return to the ED if symptoms develop. Symptomatic patients require ongoing monitoring and care
and should be admitted to the hospital, because toxicity may continue to evolve. Few plant toxins have specific
antidotes.
All exposures should be reported to the regional poison control center to obtain assistance with patient
management and to enable collection of accurate data on toxic plant exposures.
Severely Poisonous Plants
Castor Bean (Ricinus communis)
Ricin is a potent toxalbumin that inhibits protein synthesis and causes severe cytotoxic effects on multiple organ
systems. It may be one of the most poisonous naturally occurring substances known.6 Although present in all
parts of the castor bean plant, ricin is concentrated mostly in the bean. Only 1% to 5% of the bean is ricin. Castor
beans are covered by a hard, relatively impervious outer shell that must be chewed or in some way broken in order
for the ricin to cause toxicity.
Symptoms develop 6 to 8 hours after exposure. Symptoms include gastroenteritis, which may be severe and
hemorrhagic, followed by delirium, seizures, coma, and death. Beans are particularly antigenic and may cause
severe hypersensitivity and cutaneous and systemic allergic reactions.
Recent attempts to use ricin as a weapon for bioterrorism have not been successful, but the possibility of its use
remains a serious threat to society. More information about ricin can be found at
http://www.bt.cdc.gov/agent/ricin/facts.asp.
Whole-bowel irrigation has been advocated to ensure rapid and complete decontamination of the GI tract. Rapid
elimination of the bean before erosion of the outer shell occurs may decrease or prevent the release of potent
toxins. Beans should be counted to ensure complete recovery. Patients should be observed for at least 12 hours.
Once symptoms develop, care is supportive.
Coyotillo (Karwinskia Humboldtiana)
Ingestion of coyotillo, which is found in Mexico, leads to ascending paralysis and in severe cases may lead to
bulbar palsy and death. There is no specific antidote, but mechanical ventilation may be necessary.
Foxglove (Digitalis purpurea)
Foxglove contains cardiac glycosides similar in structure and action to digitalis. Its toxicity lies somewhere
between that of lily of the valley and oleander (see Oleander below).
Jequirity Bean (Abrus precatorius)
Jequirity beans contain the toxalbumin abrin, one of the most lethal naturally occurring toxins known.7 Children
have died as a result of simply chewing the beans (without swallowing). Chewing and swallowing just one bean
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may also be lethal to an adult. Symptoms include delayed gastroenteritis, which may be severe and hemorrhagic,
followed by delirium, seizures, coma, demyelinating encephalitis, and death.
Recovery of the intact bean by whole-bowel irrigation is recommended. Patients should be observed for at least 12
hours. Treatment is otherwise supportive.
Oleander (Nerium oleander)
All parts of the oleander plant contain the cardiac glycosides oleandrin, oleandroside, nerioside, and digitoxigenin,
which are similar in structure and effect to digitalis. Cardiac glycosides act by inhibiting the sodium- and
potassium-activated adenosine triphosphatase pump and lead to hyperkalemia and a variety of dysrhythmias (see
Chapter 21, Fluids and Electrolytes; Chapter 22, Cardiac Rhythm Disturbances; and Chapter 23, Pharmacology of
Antiarrhythmics). Of all plants containing cardiac glycosides (lily of the valley, foxglove, and oleander), oleander is
the most toxic.8 The Cerbera odollam, or suicide tree, found in India and Madagascar also contains cardiac
glycosides similar to those in oleander.
Plant glycosides cross-react sufficiently so that a positive result on a test of serum digoxin level confirms ingestion.
However, quantitative values on the serum digoxin assay do not indicate the amount ingested or predict potential
toxicity. Effects include nausea, vomiting, diarrhea, abdominal pain, confusion, and cardiac dysrhythmias.
Potassium levels should be closely monitored. Hyperkalemia may be severe, may be refractory to the usual
treatments (insulin, glucose, bicarbonate), and may require hemodialysis.9 Calcium administration is generally not
recommended, because it may theoretically exacerbate the digitalis toxicity, although there are no published data
from human experience. In addition to GI decontamination with activated charcoal and standard antidysrhythmic
therapy, administration of digoxin-specific Fab antibody fragments is recommended for patients with ventricular
dysrhythmias.10
Poison Hemlock (Conium maculatum)
All parts of poison hemlock contain alkaloids that are similar in structure and effect to nicotine and can induce
neuromuscular blockade. Symptoms occur rapidly 15 minutes to 1 hour after ingestion and begin with complaints
of burning and dryness of the mouth. Tachycardia, tremors, diaphoresis, mydriasis, profound muscle weakness,
and seizures may develop. In severe cases, ascending paralysis, rhabdomyolysis, acute renal failure, bradycardia,
coma, and death occur. Although most ingestions are unintentional, there are some case reports of toxicity from
intentional use by patients for a presumed narcoticlike effect.11 Treatment consists of GI decontamination with
activated charcoal and supportive care, which may include administration of IV fluids, antidysrhythmics, and
anticonvulsants.
Water Hemlock (Cicuta maculata)
Cicutoxin, a C17-polyacetylene, is found in highest concentrations in the root of water hemlock, but all parts of the
plant contain the poison. Its mechanism of action appears to involve inhibition of noncompetitive γ-aminobutyric
acid antagonists of γ-aminobutyric acid receptors. One mouthful may be fatal in as soon as 15 minutes. Initial
symptoms include nausea, vomiting, and abdominal pain, followed by delirium, seizures, and death. Seizures may
be severe and refractory to conventional anticonvulsant therapy. The mortality rate may be as high as 30%.12
Treatment consists of GI decontamination with activated charcoal and supportive care with IV fluids and
anticonvulsants.
Yew (Taxus Species)
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Yew contains taxine alkaloids in the leaves and seeds, potent toxins with effects on cardiac myocytes.13 Case
reports of near-fatal human ingestions and fatal livestock ingestions have created the impression that yew berry
ingestions are highly toxic. This is not true, however. Although GI symptoms are common, moderate to lifethreatening complications are rare (<1%), and human fatalities have not been reported.14 Symptoms after
ingestion include nausea, vomiting, and abdominal pain. Rarely, seizures, cardiac dysrhythmias, and coma occur.
Treatment consists of GI decontamination, with activated charcoal, fluids, anticonvulsants, and antidysrhythmics
given as necessary. Whole-bowel irrigation may be considered.
Common Poisonous and Injurious Plants
See Table 215-4.
Table 215-4 Symptoms and Treatment of Common Poisonous Plant Ingestions or Exposures
Plant
Symptoms
Treatment
Ackee (Blighia sapida)
Hypoglycemia
Glucose
Aloe (Aloe barbadensis)
Abdominal pain, diarrhea, red urine, nephritis
Supportive care
Usually minor symptoms
GI decontamination
with activated
charcoal
Azalea (Rhododendron
species)
Cactus
Severe intoxication: salivation, lacrimation,
bradycardia, hypotension, progressive
paralysis
Pain and irritation from embedded spines
Atropine for
symptomatic
bradycardia
Fluids or
vasopressors for
hypotension
Removal of spines
Rubber cement peel
Usually minor symptoms
Caladium species
Colchicum (autumn
crocus, meadow
saffron, glory lily)
Severe intoxication: burning and irritation of
oral mucosa, swelling, drooling, dysphagia,
respiratory compromise
Delayed and severe gastroenteritis→severe
multisystem organ failure
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Ingest cold milk or
ice cream for oral
burning
Analgesics
Consider steroids if
severe symptoms
GI decontamination
with activated
charcoal
Aggressive fluid
resuscitation
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Usually minor symptoms
Dumbcane
(Dieffenbachia amoena)
Severe intoxication: burning and irritation of
oral mucosa, swelling, drooling, dysphagia,
respiratory compromise
Ingest cold milk or
ice cream for oral
burning
Analgesics
Consider steroids if
severe symptoms
Fava beans (Vicia faba)
In persons with glucose-6-phosphate
dehydrogenase deficiency: GI upset, fever,
headache, hemolytic anemia, hemoglobinuria,
jaundice
Treatment varies
depending on
degree of hemolysis
seen
Henbane (Hyoscyamus
niger)
Anticholinergic symptoms: hallucinations,
mydriasis, tachycardia, agitation, seizures,
coma
Consider
physostigmine in
severe cases
Jimsonweed (Datura
species)
Anticholinergic symptoms: hallucinations,
mydriasis, tachycardia, agitation, seizures,
coma
GI decontamination
with activated
charcoal
Consider wholebowel irrigation
Supportive care
GI decontamination
with activated
charcoal
Lily of the valley
(Convallaria majalis)
Nausea, vomiting, diarrhea, abdominal pain,
confusion, cardiac arrhythmias
Monitoring of
potassium level
Antiarrhythmics
Digoxin-specific Fab
antibody for
arrhythmias
Monkshood (Aconitum
species)
Bradycardia, heart block, torsades de pointes,
ventricular fibrillation
GI decontamination
with activated
charcoal
Supportive care
Nettle (stinging nettle,
bull nettle) (Urtica
species)
Localized burning
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Symptomatic care
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Nightshade, common or
woody (Solanum
species)
Nightshade, deadly
(Atropa belladonna)
Nausea, vomiting, diarrhea, abdominal pain
With larger doses: delirium, hallucinations,
coma
Anticholinergic symptoms: hallucinations,
mydriasis, tachycardia, agitation, seizures,
coma
Supportive care
GI decontamination
with activated
charcoal
Supportive care
Peach, apricot, pear,
crab apple, yam bean,
and hydrangea (pits or
seeds)
GI decontamination
with activated
charcoal
Acute cyanide toxicity if large amounts are
ingested: diaphoresis, nausea, vomiting,
abdominal pain, lethargy
Whole-bowel
irrigation
Cyanide antidote
therapy
Copious irrigation
with water
Pepper (Capsicum
species)
Irritation and pain on contact
Milk or ice cream for
oral irritation
Analgesics
Usually minor symptoms
Philodendron species
Pokeweed (Phytolacca
americana)
Severe intoxication: burning and irritation of
oral mucosa, swelling, drooling, dysphagia,
respiratory compromise
Mucosal irritation, abdominal pain, nausea,
vomiting, profuse diarrhea
Cold milk or ice
cream for oral
irritation
Analgesics
Consider steroids
GI decontamination
with activated
charcoal
Supportive care
Severe intoxication: coma, death
Potato, eggplant (raw)
(Solanum species)
Nausea, vomiting, diarrhea, abdominal pain
With larger doses: delirium, hallucinations,
coma
Supportive care
Cold milk or ice
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Pothos (devil’s ivy,
Epipremnum species)
Yellow sage (Lantana
camara)
Usually minor symptoms
cream for oral
irritation
Severe intoxication: burning and irritation of
oral mucosa, swelling, drooling, dysphagia,
respiratory compromise
Analgesics
Dilated pupils, vomiting, diarrhea, weakness,
coma
Consider steroids
GI decontamination
with activated
charcoal
Fluids
Skin protection
Toxicodendron species
(poison ivy, oak, and
sumac)
Holly (Ilex species)
Poinsettia (Euphorbia
pulcherrima)
American mistletoe
(Phoradendron
flavescens)
Dermatitis
Antipruritic and
topical therapies
Systemic steroids
for facial, genital, or
widespread
involvement
Gastroenteritis
GI decontamination
with activated
charcoal
Can be fatal if significant ingestion
Supportive care
Occasional local irritation
—
Gastroenteritis
GI decontamination
with activated
charcoal
Supportive care
Easter lily (Lilium
longiflorum)
Toxicity has not been reported in humans
No treatment
necessary
Ackee (Fruit of Blighia sapida)
Ingestion of unripened ackee fruit leads to hypoglycemia and encephalopathy. Treatment with glucose prevents
serious consequences. If hypoglycemia is present, administration of 50% dextrose in water IV immediately is
indicated, followed by continuous infusion with 10% dextrose in water IV to maintain euglycemia. Symptomatic
patients should be admitted for treatment of hypoglycemia.
Aloe (Aloe barbadensis)
Sap from the common succulent houseplant Aloe barbadensis contains an anthraquinone that acts as a cathartic.
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Symptoms include abdominal pain and diarrhea within 6 to 12 hours of ingestion. The substance may occasionally
turn the urine red, and large doses may cause nephritis. There is no specific antidote. IV fluid administration may
be necessary to support GI fluid losses.
Azalea (Rhododendron Species)
Andromedotoxins are found in the leaves, flowers, and nectar of azaleas. Potential symptoms after ingestion
include salivation, lacrimation, bradycardia, hypotension, progressive paralysis, and potentially (but rarely) death.
Most cases of ingestion result in minimal toxicity. In addition to GI decontamination, treatment consists of
administration of atropine for symptomatic bradycardia and fluids or vasopressors for hypotension.
Cactus
Cactus needles or spines may embed in the skin and cause direct mechanical injury. Patients typically complain of
pain and irritation at the site. Unlike other foreign bodies such as glass that are inert, spines contain proteinaceous
material and should be removed if possible. Multiple small cactus spines may be removed by applying a thin layer
of rubber cement or other similar substance over area, allowing the material to dry, and then gently peeling it off,
removing the spines that have become embedded in the adhesive. Complications such as infection and granuloma
formation occur, but are uncommon. Prickly pear cactus causes a dermatitis that can be confused with scabies.
Caladium Species
Toxicity of Caladium species is similar to that of dumbcane due to raphides but is less severe [see Dumbcane
(Dieffenbachia amoena) below].
Colchicaceae (Autumn Crocus, Meadow Saffron, Glory Lily)
Colchicine is contained in all parts of the autumn crocus, meadow saffron, and glory lily. Colchicine causes a
gastroenteritis that is severe and delayed (2 to 24 hours), followed by severe multisystem organ failure.15 Mild
toxicity is expected if GI symptoms begin >9 hours after ingestion.
Common effects include coagulopathy, bone marrow suppression with granulocytopenia and thrombocytopenia,
cardiac dysrhythmias, cardiogenic shock, adult respiratory distress syndrome, hepatic failure, delirium, seizures,
coma, and death. If patients survive, alopecia may develop.
In addition to GI decontamination with activated charcoal, treatment usually requires aggressive fluid resuscitation.
Colchicine-specific Fab fragments have been used with some success experimentally but are not commercially
available for severe poisonings.
Dumbcane (Dieffenbachia amoena)
Dumbcane plants contain calcium oxalate crystals packaged into bundles known as raphides. The plants also
contain proteolytic enzymes that have antitrypsinlike activity and stimulate histamine and bradykinin release.
Children who chew the leaves develop immediate burning and irritation of the oral mucosa. Cases of severe
swelling, drooling, dysphagia, and respiratory compromise have been reported, but are rare.16 Most cases of
human ingestion result in minor symptoms that resolve with little or no treatment. Demulsifying agents, such as
cold milk or ice cream, may help relieve oral symptoms, and analgesics may be necessary. Steroids are considered
beneficial for severe cases, although there have been no controlled trials of this therapy.
Fava Beans (Vicia faba)
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An estimated 10% to 20% of persons with glucose-6-phosphate dehydrogenase deficiency develop favism after
consuming fava beans. Symptoms include GI upset, fever, and headache, and patients may develop hemolytic
anemia with hemoglobinuria and jaundice (see Chapter 232, Acquired Hemolytic Anemia).
Henbane (Hyoscyamus niger)
Ingestion of henbane causes anticholinergic symptoms, with hallucinations, mydriasis, tachycardia, agitation,
seizures, and coma. Treatment with physostigmine may be useful in severe cases.
Jimsonweed (Datura Species)
Jimsonweed (also known as thorn apple, devil’s trumpet, or locoweed) is infamous for its hallucinogenic properties.
Exposures most commonly are intentional and occur through experimentation.17 All parts of the plant are toxic
and contain atropinelike alkaloids (hyoscyamine, atropine, and scopolamine) capable of precipitating acute
anticholinergic crises by competitive inhibition of cholinergic muscarinic receptors.
Symptoms occur within 30 to 60 minutes and may last for up to 48 hours because of anticholinergic-induced
delayed gastric motility. Symptoms include hyperthermia (“hot as a hare”), flushed skin (“red as a beet”), dry skin
and mucous membranes (“dry as a bone”), mydriasis (“blind as a bat”), and hallucinations or delirium (“mad as a
hatter”). Tachycardia and urinary retention are also common.
Treatment includes GI decontamination with activated charcoal and supportive care, including IV fluids, external
cooling, and restraints for patient protection. GI decontamination using whole-bowel irrigation may be useful for up
to 48 hours after ingestion if the patient remains symptomatic. Physostigmine, a cholinesterase inhibitor,
antagonizes both the central and peripheral effects and may be considered in patients with severe toxicity
exhibiting hyperthermia, seizures, or psychosis.17 An initial dose of 0.5 milligram for children or 1.0 to 2.0
milligrams for adults is given slowly IV over 5 minutes. Repeat doses may be required (see Chapter 182,
Hallucinogens, and Chapter 196, Anticholinergics).
Lily of the Valley (Convallaria majalis)
In addition to toxicity from ingesting the lily of the valley plant itself, which contains cardiac glycosides, toxicity has
been reported from drinking water in which the freshly cut flowers were kept [see Oleander (Nerium oleander)
above].
Marijuana (Cannabis sativa)
Ingestion of marijuana by children may lead to ataxia, seizures, hallucinations, psychosis and coma.
Monkshood (Aconitum Species)
Monkshood contains a sodium channel blocker, aconitine, that if ingested leads to bradycardia and heart block,
torsades de pointes, and ventricular fibrillation.
Nettle (Stinging Nettle, Bull Nettle) (Urtica Species)
Nettles contain a specialized system for injecting their toxins. Stinging hairs are connected to a bladder filled with
various irritants (histamine, acetylcholine, 5-hydroxytryptamine). Handling of the plant stimulates the injection of
these substances via the hair tube. An immediate burning response occurs that may last for hours. Treatment is
symptomatic.
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Nightshade, Common or Woody (Solanum Species)
The glycoalkaloid solanine is present in all parts of the common or woody nightshade. Ingestion results in nausea,
vomiting, diarrhea, and abdominal pain. Delirium, hallucinations, and coma may also occur with larger doses. There
is no specific treatment.
Nightshade, Deadly (Atropa belladonna)
Deadly nightshade contains atropinelike substances with anticholinergic properties [see Jimsonweed (Datura
Species)].
Peach, Apricot, Pear, Crab Apple, Yam Bean, and Hydrangea
Amygdalin, a cyanogenic glycoside found in the pits or seeds of the peach, apricot, pear, crab apple, yam bean,
and hydrangea, is metabolized by the enzyme emulsin to hydrocyanic acid. If large quantities are ingested, the
hydrocyanic acid created may lead to acute cyanide toxicity. Emulsin is also present in the pits or seeds of the
aforementioned plants and may be present to some degree in intestinal bacteria. Ingestion of large amounts of
seeds or pits results in diaphoresis, nausea, vomiting, abdominal pain, and lethargy that develop over hours. GI
decontamination using activated charcoal and whole-bowel irrigation is needed. Symptomatic patients should be
treated as for cyanide poisoning (see Chapter 198, Industrial Toxins).
Pepper (Capsicum Species)
Some species of Capsicum cause irritation, burning, and pain upon contact with mucous membranes as a result of
depletion of substance P from terminal nerve endings. Contact typically occurs as a result of self-inoculation while
preparing peppers or exposure to spraying of pepper extracts by police. Corneal abrasion may result if the
substance is sprayed in the eye.
Decontaminate affected areas by irrigation with copious amounts of water and gentle hand soap. For oral irritation,
demulsifying agents, such as cold milk or ice cream, may help. Analgesics may be necessary.
Philodendron Species
All parts of some Philodendron species contain oxalate raphides and may produce symptoms similar to those
caused by dumbcane, although less severe.
Pokeweed (Phytolacca americana)
All parts of the pokeweed plant are toxic, especially the roots, unripe berries, and seeds. Phytotoxins
(phytolaccotoxin and phytolaccine) cause direct mucosal irritation and GI symptoms. Patients complain of burning
in the mouth and throat, with abdominal pain, nausea, vomiting, and profuse diarrhea that may be foamy.18 Severe
intoxications may result in coma and death. Treatment is GI decontamination with activated charcoal and
supportive care consisting of fluid and electrolyte replacement.
Potato, Eggplant (Solanum Species)
Solanine is contained in green potatoes and in the sprouts, and is destroyed by cooking. It is also found in unripe
eggplant. Ingestion may cause gastroenteritis, with onset up to 12 hours after consumption [see Nightshade,
Common or Woody (Solanum Species)].
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Pothos (Devil’s Ivy, Epipremnum Species)
Pothos has toxicity similar to that associated with dumbcane, but less severe.
Yellow Sage (Lantana camara)
Leaves and unripe fruit of Lantana camara contain the toxin lantadene, which may produce dilated pupils, vomiting,
diarrhea, weakness, and coma. Symptoms may be delayed for 2 to 6 hours. Treatment is GI decontamination with
activated charcoal and fluids for dehydration.
Toxicodendron Species (Poison Ivy, Oak, and Sumac)
Poison ivy, poison oak, and poison sumac contain the antigenic resin urushiol. Once exposed, most individuals
develop sensitization as the antigenic resin binds with skin proteins and forms a complete antigen. Reexposure
then stimulates a T cell–mediated immune response. Reactions begin with itching, burning, and redness that
develop over 12 to 48 hours and may progress to varying degrees of vesiculobullous formation.
Treatment consists of antipruritic and topical therapies (oatmeal baths and topical steroids). Facial, genital, or
widespread involvement requires systemic steroid therapy for at least 10 to 14 days. Patients should be advised to
clean under their fingernails and wash all contaminated clothing. IvyBlock contains bentoquatam and binds
urushiol to prevent absorption. Zanfel also removes urushiol from the skin. Skin cleansers (such as Tecnu) may be
used up to 8 hours after exposure to decontaminate the skin. For further discussion, see Chapter 244, Treatment
of Skin Disorders in the Emergency Department.
Common Holiday or Seasonal Plants (Poisonous and Nonpoisonous)
Holly (Ilex Species)
Holly leaves are nontoxic, but the berries contain a variety of toxins known as saponins. Gastroenteritis is the most
common effect after ingestion and may occur with consumption of as few as 2 or 3 berries; ingestion of 20 to 30
berries may be fatal. Treatment is GI decontamination with activated charcoal followed by administration of IV
fluids to prevent dehydration.
Poinsettia (Euphorbia pulcherrima)
Poinsettia is not toxic. It occasionally causes local irritation to the skin, mouth, or conjunctiva.19
American Mistletoe (Phoradendron flavescens)
All parts of American mistletoe are poisonous and contain phoratoxin, a toxalbumin. Gastroenteritis may occur
following ingestion of a large number of berries, but significant morbidity is rare.20 Treatment is GI
decontamination with activated charcoal accompanied by fluid and electrolyte monitoring.
Easter Lily (Lilium longiflorum)
Toxicity from ingestion of Easter lily has not been reported in humans.
Special Considerations
Toddlers experience the world by first putting it into their mouths. Because 80% of the exposures occur among
children <6 years of age and most occur within the home, prevention is paramount. All poisonous and injurious
plants should be kept out the reach of toddlers and preschoolers. Homes should be purged of all potentially toxic
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plants, just as they are of medications and cleaning supplies, and children should be specifically instructed never
to eat plants or wild berries.4,21
References
1. Krenzelok EP, Jacobsen TD: Plant exposures: a national profile of the most common plant genera. Vet Hum
Toxicol 39: 248, 1997. [PubMed: 9251180]
2. Watson WA, Litovitz TL, Klein-Schwartz W, et al: 2004 Annual report of the American Association of Poison
Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 22: 335, 2005.
3. Mrvos R, Krenzelok EP, Jacobsen TD: Toxidromes associated with the most common plant ingestions. Vet Hum
Toxicol 43: 366, 2001. [PubMed: 11757998]
4. Lawrence RA: Poisonous plants: when they are a threat to children. Pediatr Rev 18: 162, 1997. [PubMed:
9114716]
5. Krenzelok EP, Mrvos R, Jacobsen TD: Contrary to the literature, vomiting is not a common manifestation
associated with plant exposures. Vet Hum Toxicol 44: 298, 2002. [PubMed: 12361120]
6. Audi J, Belson M, Patel M, et al: Ricin poisoning: a comprehensive review. JAMA 294: 2342, 2005. [PubMed:
16278363]
7. Kinamore PA, Jaeger RW, Castro FJ: Abrus and ricinus ingestion. Clin Toxicol 17: 401, 1980. [PubMed:
6108823]
8. Bose TK, Basu RK, Biswas B, et al: Cardiovascular effects of yellow oleander ingestion. J Indian Med Assoc 97:
407, 1999. [PubMed: 10638101]
9. Eddleston M, Persson H: Acute plant poisoning and antitoxin antibodies. J Toxicol Clin Toxicol 41: 309, 2003. [PubMed: 12807314]
10. Shumaik GM, Wu AW, Ping AC: Oleander poisoning: treatment with digoxin-specific Fab antibody fragments.
Ann Emerg Med 17: 732, 1988. [PubMed: 3382077]
11. Drummer OH, Roberts AN, Bedford PJ, et al: Three deaths from hemlock poisoning. Med J Aust 162: 592,
1995. [PubMed: 7791646]
12. Centers for Disease Control and Prevention: Water hemlock poisoning—Maine, 1992. MMWR Morb Mortal
Wkly Rep 43: 229, 1994.
13. Wilson CR, Sauer J, Hooser SB: Taxanes: a review of the mechanism and toxicity of yew (Taxus spp.). Toxicon
39: 175, 2001. [PubMed: 10978734]
14. Krenzelok EP, Jacobsen TD, Aronis J: Is the yew really poisonous to you? J Toxicol Clin Toxicol 36: 219, 1998. [PubMed: 9656977]
15. Gabrscek L, Lesnicar G, Krivec B, et al: Accidental poisoning with autumn crocus. J Toxicol Clin Toxicol 42: 85,
2004. [PubMed: 15083942]
16. Pedaci L, Krenzelok EP, Jacobsen TD, Aronis J: Dieffenbachia species exposures: an evidence-based
assessment of symptom presentation. Vet Hum Toxicol 41: 335, 1999. [PubMed: 10509443]
17. Forrester MB: Jimsonweed (Datura stramonium) exposures in Texas 1998–2004. J Toxicol Environ Health 69:
1757, 2006. [PubMed: 16905506]
18. Roberge R, Brader E, Martin ML, et al: The root of evil: pokeweed intoxication. Ann Emerg Med 15: 470, 1986. [PubMed: 3954185]
19. Krenzelok EP, Jacobsen TD, Aronis JM: Poinsettia exposures have good outcomes: just as we thought. Am J
Emerg Med 14: 671, 1996. [PubMed: 8906768]
20. Krenzelok EP, Jacobsen TD, Aronis J: American mistletoe exposures. Am J Emerg Med 15: 516, 1997. [PubMed: 9270395]
21. Krenzelok EP, Jacobsen TD, Aronis J: Those pesky berries: are they a source of concern? Vet Hum Toxicol 40:
101, 1998. [PubMed: 9554066]
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Useful Web Resources
U.S. Food and Drug Administration, Poisonous Plant Database
—http://www.accessdata.fda.gov/scripts/plantox/index.cfm
U.S. Department of Agriculture, Agricultural Research Service, Poisonous Plant Research Laboratory
—http://www.ars.usda.gov/Main/docs.htm?docid=3496
American Association of Poison Control Centers—http://www.aapcc.org
Canadian Poisonous Plants Information System—http://www.cbif.gc.ca/pls/pp/poison?p_x=px
Poisonous plants informational database (Cornell University)—http://www.ansci.cornell.edu/plants/
Poisonous Plants Homepage (University of Pennsylvania)—http://cal.vet.upenn.edu/projects/poison/index.html
Plants Toxic to Animals (University of Illinois)—http://library.illinois.edu/vex/toxic
Updated bibliography of research and articles related to plant toxicity (Jean Bruneton, Université d’Angers)
—http://ead.univ-angers.fr/~pharma/bruneton/main.php?nom=0&langue=0
Emergency Preparedness and Response: Facts about Ricin, Centers for Disease Control and Prevention
—http://www.bt.cdc.gov/agent/ricin/facts.asp
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