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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 220: Poisonous Plants Betty C. Chen; Lewis S. Nelson

INTRODUCTION

Common poisonous and injurious plants number in the hundreds and have a wide variety of toxicities. Thischapter focuses on the most important plant-related exposures clinically relevant to emergency medicine

(Tables 220-1 and 220-2).1,2 Individual plants are discussed in terms of their pathophysiology, clinical

features (toxidromes), and treatment.3 Highly poisonous plants (Table 220-1) are highlighted in depth below,and brief reviews are provided for other common poisonous plants. Table 220-2 organizes commonpoisonous plants according to toxin structure.

TABLE 220-1

Some Highly Poisonous Plants

Poison hemlock (Conium maculatum)

Yew (Taxus spp.)

Foxglove (Digitalis purpurea)

Oleander (Nerium oleander)

Castor bean (Ricinus communis)

Rosary pea (Abrus precatorius)

Water hemlock (Cicuta maculata)

Buckthorn (Karwinskia humboldtiana)

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TABLE 220-2

Classification of Poisonous Plants

Classification Mechanism of Toxicity Example Plant Species

Alkaloids Solanine and chaconine Green potato leaves, American nightshade, black

nightshade (Solanaceae)

Anticholinergics Deadly nightshade (Atropa belladonna)

Angel's trumpet or jimsonweed (Datura spp.)

Henbane (Hycoscyamus niger)

Mandrake (Mandragora o�icinarum)

Cholinergics Calabar bean (Physostigma venenosum)

Pilocarpus (Pilocarpus spp.)

Nicotinic and nicotine-like Tobacco (Nicotiana spp.)

Poison hemlock (Conium maculatum)

Golden chain (Laburnum anagyroides)

Blue cohosh (Caulophyllum thalictroides)

Lupin (Lupinus spp.)

Psychotropics Peyote (Lophophora williamsii)

Nutmeg and mace (Myristica fragrans)

Morning glory (Agyreia spp. and Ipomoea spp.)

Hawaiian baby woodrose seeds (Argyreia nervosa)

Hepatotoxic pyrrolizidines Comfrey (Symphytum o�icinale)

Sassafras (Sassafras albidum)

Ragwort (Heliotropium spp.)

Sodium channel

modulators

Monkshood (Aconitum spp.)

Larkspur (Delphinium spp.)

False or green hellebore (Veratrum spp.)

Yew (Taxus spp.)

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Classification Mechanism of Toxicity Example Plant Species

Antimitotic alkaloids and

resins

Autumn crocus (Colchicum autumnale)

Mayapple (Podophyllum peltatum)

Wild mandrake (Podophyllum emodi)

Glory lily (Gloriosa superba)

Madagascar periwinkle (Catharanthus roseus)

Glycosides Cardioactive steroids or

cardiac glycosides

Foxglove (Digitalis purpurea)

Lily of the valley (Convallaria majalis)

Oleander (Nerium oleander)

Christmas rose (Helleborus niger)

Milkweed (Asclepias spp.)

Squill (Urginea maritime and Urginea indica)

Yellow oleander (Thevetia peruviana)

Cyanogenic glycosides Almond, apricot, and cherry pits (Prunus spp.)

Tapioca plant, cassava (Manihot esculenta)

Elderberry (Sambucus canadensis)

Hydrangea (Hydrangea macrophylla)

Saponins Holly (Ilex spp.)

Salicylates Poplar species (Populus spp.)

Willow species (Salix spp.)

Proteins, peptides,

and lectins

Toxalbumins Castor bean (Ricinus communis)

Rosary pea (Abrus precatorius)

Pokeweed (Phytolacca americana)

Black locust (Robinia pseudoacacia)

American mistletoe (Phoradendron flavescens)

European mistletoe (Viscum album)

Black vomit nut (Jatropha curcas)

Hypoglycin Ackee fruit (Blighia sapida)

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Classification Mechanism of Toxicity Example Plant Species

Carboxylic acids Calcium oxalate crystals Dumbcane (Die�enbachia spp.)

Philodendron (Philodendron spp.)

Caladium (Caladium spp.)

Jack in the pulpit (Arisaema triphyllum)

Elephant's ear (Colocasia spp.)

Rhubarb (Rheum raponticum)

Alcohols Convulsants Water hemlock (Cicuta maculate)

Phenols and

phenylpropanoids

Coumarins and derivatives Sweet clover (Melilotus spp.)

Tonka beans (Dipteryx spp.)

Sweet-scented bedstraw (Galium triflorum)

Red clover (Trifolium pretense)

Capsaicin Cayenne pepper (Capsicum spp.)

Demyelination Buckthorn or coyotillo (Karwinskia humboldtiana)

Terpenoids and

resins

Grayanotoxin (sodium

channel blockers)

Azalea and rhododendron (Rhododoendron spp.),

mountain laurel (Kalmia latifolia)

Kava lactones Kava kava (Piper methysticum)

Thujone Wormwood (Artemisia absinthium)

Anisatin Star anise (Illicum spp.)

Tetrahydrocannabinol Marijuana (Cannabis sativa)

EPIDEMIOLOGY

In 2012, the American Association of Poison Control Centers received 49,374 reports of plant exposures. Ofthese cases, 31,920 involved children less than 5 years of age. There were an additional 2918 nonexposure

calls that provided information about plants to callers.2 The vast majority of exposures (96%) areunintentional ingestions. Cutaneous and ophthalmic exposures are common but generally go unreported.Although inhalational exposures are possible, they are rarely reported.

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Unfortunately, obtaining an accurate plant exposure history can be di�icult. Most exposures occur in childrenand are usually unwitnessed. Uncertainty typically surrounds these cases, particularly whether ingestiontruly occurred. The timing and amount of exposure is also di�icult to quantify in many of these situations.Furthermore, even when a plant is available, identification errors are common and may require a botanist'sexpertise. In fact, data from the National Poison Data System demonstrate that medical providers and poison

centers are unable to identify plants more than 22% of the time.2

CLINICAL FEATURES

Classification of plants and their toxicities is complex. The most straightforward approach for emergencyphysicians is to classify toxic plants by the mechanism of action of the toxin and then to further subclassifybased on the specific toxin. This will help predict the toxicologic e�ects. The reverse process can be used ifthe patient presents with clinical findings (Table 220-2). Unfortunately, attributing one toxicologic syndromeper plant oversimplifies the complexity of plant chemistry, because plants o�en contain multiple toxiccompounds, each of which produces its own toxicologic e�ects.

Moderate systemic e�ects as a consequence of plant-related exposures occur in about 1% of patients. Severelife-threatening e�ects or disabling injuries are extremely uncommon and occur in only about 0.04% ofpatients. Death occurs in <0.001% of patients.

Dermatitis and GI irritation are the most commonly reported e�ects of plant toxicity. GI complaints occurcommonly following ingestion, and additional toxic symptoms may accompany or follow. Althoughdermatitis is another commonly reported finding of plant toxicity, systemic toxicity rarely follows (see Table220-3).

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TABLE 220-3

Plant-Induced Dermatitis

Dermatitis Classification Mechanism of Injury Specific Plants

Mechanical injury

Calcium oxalate Dumbcane (Die�enbachia maculate)

Philodendron (Philodendron spp.)

Raphides and trichomes Stinging nettles (Urtica dioica)

Velvet bean or cowhage (Mucuna pruriens)

Pineapple (Bromeliaceae spp.)

Irritant dermatitis Phorbol esters Cow's horn (Euphorbia grandicornis)

Poinsettia (Euphorbia pulcherrima)

Manchineel tree (Hippomane mancinella)

Other chemical irritants Stinging nettles (U. dioica)

Velvet bean or cowhage (M. pruriens)

Pineapple (Bromeliaceae spp.)

Contact dermatitis

Urushiol oleoresins Ginkgo (Ginkgoaceae)

Poison ivy, oak, and sumac (Toxicodendron spp.)

Mango (Mangifera indica)

Pistachio (Pistacia vera)

Cashew (Anacardium occidentale)

Miscellaneous antigens Peruvian lily (Alstroemeria spp.)

Narcissus and da�odils (Narcissus spp.)

Tulips (Tulipa spp.)

Primroses (Primula spp.)

Phytophotodermatitis

Furocoumarins Cow parsnip (Heracleum lanatum)

Wild parsnip (Pastinaca sativa)

Lime (Citrus aurantiifolia)

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TREATMENT

Most plant-related exposures can be managed with supportive care. In patients able to tolerate oraladministration and believed to have potentially concerning exposures, administer activated charcoal toprevent absorption of toxin from the GI tract. Because of the uncertainty surrounding plant exposures,observe asymptomatic or minimally symptomatic patients for 4 to 6 hours in the ED. Dischargeasymptomatic patients and those with resolved minor toxicity a�er observation, with strict returnprecautions if symptoms develop. Admit those with more than minimal findings because toxicity maycontinue to evolve. This approach is generally applied to all patients with plant exposure because thescientific literature lacks adequate data to provide less conservative recommendations. There are fewantidotes available to treat poisonings by plant toxins; none are unique to plant exposures but rather aregeneralized from use in other poisonings.

Report all exposures to the regional poison control center to obtain assistance with plant identification, toobtain assistance with patient management, and to enable collection of accurate data on toxic plantexposures. Unfortunately, data reported by the National Poison Data System does not require confirmationof exposure, and the incidence of adverse e�ects is diluted by inconsequential or unconfirmed ingestions.

NICOTINIC AND NICOTINE-LIKE TOXINS (POISON HEMLOCK)

In Phaedo, Plato details the death of Socrates: a�er drinking a potion consisting of the extracts of poisonhemlock (Conium maculatum), he slowly develops paralysis and dies. All parts of poison hemlock containconiine and similar alkaloids that are structurally and functionally analogous to nicotine. Overstimulation ofnicotine receptors can rapidly progress from seemingly mild symptoms to death from respiratory failure.Symptoms may occur within hours. Mild e�ects include nervousness and tremor due to sympathomimeticstimulation. As toxicity progresses, patients exhibit more pronounced sympathomimetic features,parasympathetic findings, and paralysis from nicotinic receptor stimulation at the neuromuscular junction.Typically, ingestion of poison hemlock is due to misidentification because of its similarity in appearance towild carrot or Queen Anne's lace (Daucus carota), parsley (Petroselinum crispum), parsnip (Pastinaca sativa)roots, or anise (Pimpinella anisum). Although most ingestions are unintentional, there are case reports of

toxicity from intentional use by patients for a presumed opioid-like e�ect or for intentional self-harm.4,5,6

Treatment consists of GI decontamination with activated charcoal and supportive care, which may includerespiratory support and administration of IV fluids, antidysrhythmics, and anticonvulsants.

SODIUM CHANNEL TOXINS (YEW, RHODODENDRON, LAUREL,MONKSHOOD, LARKSPUR)

A number of plants across di�erent classifications cause sodium channel e�ects that result in cardiac,respiratory, GI, and CNS e�ects. Yew (Taxus spp.) contains taxine alkaloids in all parts of the shrub except thearil, which is the berry's red fleshy portion. The hard seed inside of the berry contains taxine alkaloids that

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block sodium and calcium channels.7,8 Few symptoms are to be expected if ingestions are small or if berriesare consumed without crushing the central seed. However, large ingestions can lead to more serious e�ects.

Grayanotoxins are terpenoids, which inhibit the opening of sodium channels, and are found in the leaves,flowers, and nectar of several plants such as azaleas and rhododendron (Rhododendron spp.). They are alsofound in in the mountain laurel (Kalmia latifolia). Ingestion of the leaves, flower, or honey from the nectar of

the flower can result in toxicity.9

Aconite, found in monkshood (Aconitum spp.) and larkspur (Delphinium spp.), is an alkaloid that activatescardiac, and less so neuronal, sodium channels. Monkshood is sometimes used in traditional Chinesemedicine as an inotrope. False or green hellebore (Veratrum spp.) is o�en confused for leeks by foragers, andthese plants contain veratridine and other assorted veratrum alkaloids, which function similarly to aconite.

Regardless of the particular alkaloid or terpenoid and its specific mechanism of cardiac toxicity, findings a�eringestion include salivation, lacrimation, bradycardia or tachycardia, cardiac dysrhythmias, hypotension,

hyperkalemia, paresthesias, muscle weakness, respiratory failure, seizures, and potentially death.8,9,10

Early a�er ingestion, activated charcoal may decrease absorption from the GI tract. No antidote is available,and symptomatic patients should receive supportive care such as IV fluids or vasopressors if hypotensive.Atropine is e�ective for bradycardia, but antiarrhythmics, such as amiodarone, carry variable e�icacy, asreported in the literature. Cardioversion for wide complex dysrhythmias can be attempted in unstablepatients with the understanding that instability may persist and dysrhythmias may recur given theunderlying channelopathy. Case reports describe successful use of extracorporeal membrane oxygenation in

treating critically ill patients with refractory cardiac toxicity from yew posioning.8,11,12

CARDIOACTIVE STEROIDS (FOXGLOVE, OLEANDER)

Cardioactive steroids are found in many plants, including foxglove (Digitalis spp.), oleander (Nerium spp.),dogbane (Apocynum cannabinum), lily of the valley (Convallaria majalis), and milkweed (Asclepias spp.).Cardioactive steroids, sometimes called cardiac glycosides, inhibit the sodium/potassium–adenosinetriphosphatase pump. Acute toxicity closely resembles that from digoxin and includes early GI symptomsfollowed by cardiac dysrhythmias. Serum digoxin concentrations may be used to qualitatively confirmcardioactive steroid exposure due to cross-reaction with the laboratory assay, but the absolute value holdslittle clinical quantitative value. Early a�er ingestion, oral activated charcoal may decrease systemic exposure

by preventing absorption.13 Assess serum potassium concentration and obtain an ECG to aid in prognosisand therapy. Administer digoxin immune Fab fragments to patients with a serum potassium >5 mEq/L a�er

an acute overdose or any cardiac dysrhythmia.14 Antidote dosing should be empiric (unlike with digoxin),and the digoxin concentration should not be used to calculate dosing, because the assay is not an accuratereflection of toxin burden. Avoid transvenous pacing and calcium administration for the increased theoreticalrisks of inducing a dysrhythmia. Traditional treatments for hyperkalemia such as insulin, calcium, sodiumbicarbonate, or hemodialysis are usually unnecessary if digoxin immune Fab is administered.

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TOXALBUMINS (CASTOR BEAN, RICIN)

Ricin and abrin are examples of toxalbumins that can be extracted from the castor bean (Ricinus communis)and rosary pea (Abrus precatorius), respectively. Ricin, in particular, is a potential biologic weapon and hasbeen implicated in a number of attempted assassinations.

These toxalbumins are proteins, peptides, or lectins, which exert their toxicity by entering cells and inhibitingprotein synthesis. The clinical syndrome associated with the toxalbumins depends on quantity as well asroute of exposure. Although one castor bean contains enough ricin to kill, its toxicity is typically limitedfollowing ingestion. Even if the castor bean is chewed to break the protective hard shell that sequesters thetoxin, the enteral absorption of ricin is poor and tends to limit toxicity to diarrhea and abdominal pain.Although delayed systemic toxicity is possible following large ingestions, these symptoms tend to occur morein parenteral exposures. Systemic organ dysfunction includes cardiac, neurologic, hepatic, and renalsequelae. Inhalational exposures are rapidly progressive and can result in life-threatening respiratory failure,

circulatory collapse, and death within 36 hours.15

Treat toxalbumin ingestion by administration of activated charcoal followed by a lengthy observation period.All routes of exposure can be fatal, but hydration and aggressive supportive care significantly reducemortality. More information about ricin can be found at the Centers for Disease Control and Prevention Website (http://www.bt.cdc.gov/agent/ricin/).

Toxalbumins are found in a number of other plants such as American mistletoe (Phoradendron flavescens)and European mistletoe (Viscum album). The leaves and stems contain phoratoxin and viscumin, both ofwhich are less potent than ricin. The berries also contain low levels of toxins that may result in gastroenteritisfollowing large doses. These berries are abundant in homes during the holiday season and are attractive tochildren. Fortunately, significant morbidity a�er berry ingestion is rare, although single incidents of seizure,

gait instability, hepatotoxicity, and death have been reported.16 Provide GI decontamination with activatedcharcoal accompanied by fluid and electrolyte monitoring for minimally symptomatic patients.

CONVULSANTS (WATER HEMLOCK)

Cicutoxin is a diol found in the water hemlock (Cicuta maculata), western water hemlock (Cicuta douglasii),and hemlock water dropwort (Oenanthe crocata). These plants are o�en mistaken for wild parsnip, turnip, orparsley, causing toxicity through dermal or enteric absorption. All parts of the plant are poisonous, with thehighest concentration of cicutoxin in the tuber. Cicutoxin's mechanism of action is not fully understood.However, it may impair γ-aminobutyric acid receptor or potassium channel function. Toxicity can manifest asearly as 15 minutes following exposure. Mild symptoms include GI discomfort, followed by bradycardia,hypotension, respiratory distress, seizures, and death. Seizures may be severe and refractory to conventional

anticonvulsant therapy. The mortality rate may be as high as 30%.17 Treatment consists of GIdecontamination with activated charcoal and supportive care. Treat seizures with γ-aminobutyric acidagonists such as benzodiazepines or barbiturates.

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DEMYELINATING ANTHRACENONES (BUCKTHORN)

Buckthorn or coyotillo (Karwinskia humboldtiana), which is found in the southwestern United States, Mexico,Central America, and the Caribbean, contains demyelinating anthracenones that lead to progressive muscleweakness that resembles Guillain-Barré syndrome. Weakness occurs weeks a�er ingestion, rendering GIdecontamination futile in symptomatic patients. In severe cases, respiratory paralysis can lead to death

without respiratory support. There is no antidote, and treatment is largely supportive until recovery.9

BELLADONNA ALKALOIDS (NIGHTSHADE, JIMSONWEED, HENBANE)

Deadly nightshade (Atropa belladonna), jimsonweed (Datura spp.), and henbane (Hyoscyamus niger) allcontain atropine-like alkaloids such as hyoscyamine and scopolamine. Ingestion or smoking results inantimuscarinic e�ects such as tachycardia, hyperthermia, mydriasis, decreased bowel sounds, urinaryretention, altered mental status, and dry, flushed skin. Severe poisoning can include seizures, coma, anddeath. Onset of e�ects depends on route of exposure, but findings should be evident within 4 hours.Exposures most commonly are intentional, such as through experimentation with the plant's hallucinogenic

properties.18

Treatment is largely supportive. Benzodiazepines are useful in calming patients, but avoid antipsychoticssuch as haloperidol to prevent further antimuscarinic activity. Physostigmine inhibits cholinesterase,resulting in increased synaptic concentrations of acetylcholine that can overcome the muscarinicantagonism from the atropine-like alkaloids. Physostigmine is generally indicated only for patients withmoderate to severe symptoms. Improvement in symptoms may be transient, and patients can require repeatdosing if symptoms recrudesce. Patients who receive physostigmine improve faster and require shorterhospitalizations than patients receiving sedative-hypnotics.

ANTIMITOTIC ALKALOIDS (AUTUMN CROCUS, GLORY LILY, MAYAPPLE)

Colchicine is contained in all parts of the autumn crocus (Colchicum autumnale) and glory lily (Gloriosasuperba). Colchicine halts cellular mitosis by inhibiting microtubule formation. Gastroenteritis, which may bedelayed (2 to 24 hours), is followed by multisystem organ failure. Common e�ects include coagulopathy,bone marrow suppression with granulocytopenia and thrombocytopenia, cardiac dysrhythmias, cardiogenicshock, acute respiratory distress syndrome, hepatic failure, delirium, seizures, coma, and death. If patientssurvive, alopecia and neuropathy may develop. Mild toxicity is expected if GI symptoms begin >9 hours a�er

ingestion.19,20

Podophyllin is an extract of the roots of the mayapple plant (Podophyllum peltatum). This extract contains amixture of toxins including podophyllotoxin, which inhibits topoisomerase II and microtubule formation.Toxicity is characterized by obtundation, coagulopathy, hematologic suppression, renal failure, GI irritation,

hepatotoxicity, and death.9

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Early a�er ingestion, pursue aggressive GI decontamination because there is no antidote and toxicity can befatal due to multisystem organ involvement. Due to its delayed onset, observe exposed patients for aprolonged period. In addition to GI decontamination with activated charcoal, treatment usually requiresaggressive fluid resuscitation and aggressive supportive care. Colchicine-specific Fab fragments have beenused in colchicine-poisoned patients with some success experimentally but are not commercially available.

CALCIUM OXALATE (ELEPHANT'S EAR)

Many common household ornamental plants contain crystalline calcium oxalate. Examples includedumbcane (Die�enbachia spp.), elephant's ear (Colocasia spp.), and philodendron (Philodendron spp.). Thecalcium oxalate crystals are needle-shaped and are packaged in raphides that also contain proteolyticenzymes and other chemicals. The contents are extruded when the plant is injured, causing both directtrauma from the crystals and inflammation due to the chemicals' e�ects.

Ingestion of calcium oxalate–containing plants results in immediate oropharyngeal pain and swelling. Thispain usually limits the amount of plant ingested. In serious cases, the swelling can involve upper airway

structures and cause respiratory compromise due to obstruction.21 Ocular exposures to the calcium oxalate–containing plants result in ocular pain, corneal injury, and conjunctivitis. Pain and swelling can last up to 8days.

Patients with oropharyngeal swelling and pain following ingestion tend to improve with supportive care.Anti-inflammatories may decrease swelling and provide analgesia. Topical treatments such as ice, ice water,and ice cream are soothing and can be given in patients with stable, patent airways. Patients at risk of airwayobstruction must be closely monitored and should be quickly intubated if progressing. Consider steroidadministration; however, there are no trials demonstrating outcome improvement with steroid use.

CYANOGENIC PLANTS (PRUNUS SPECIES)

Several thousand plants, including many common vegetables and fruits, contain cyanogenic compounds,such as amygdalin. Fortunately, the toxins are either sequestered in nonconsumed portions of the foods(seeds) or exist in quantities that are not clinically significant. Amygdalin is found in the leaves, bark, andseeds of those fruits of the Prunus species, including pears, apples, plums, peaches, and apricots. Althoughthe aril (fruit portion) of these plants is nontoxic, ingestion of the other portions of the plants and their seedscan result in the liberation of hydrogen cyanide from amygdalin in the GI tract. Linamarin and lotaustralin are

present in cassava (Manihot esculenta) and are similarly hydrolyzed to liberate hydrogen cyanide.9,22 Ifprepared correctly, the cyanogenic glycosides can be hydrolyzed prior to ingestion, thereby liberating the

cyanide prior to consumption.23,24 Initial e�ects may be slightly delayed and include GI irritation, followedby signs of tissue hypoxia. Rapid progression of toxicity can occur, and treatment for cyanide poisoningshould be initiated immediately.

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CAPSAICIN (PEPPERS)

Capsicum peppers contain capsaicin, a phenylpropanoid toxin that causes irritation, burning, and pain uponcontact with skin and mucous membranes. This toxin enhances the release of substance P from smallunmyelinated nerve fibers, which stimulate nociceptors that cause the sensation of burning or heat. Contacttypically occurs as a result of self-inoculation while preparing peppers or exposure to spraying of pepperextracts in self-defense. Decontaminate a�ected areas by irrigation with copious amounts of water andgentle hand soap. Ocular exposures may require aggressive decontamination and ophthalmologicevaluation. Analgesics may be necessary.

MISCELLANEOUS GI TOXINS

Solanine and chaconine are glycoalkaloids that are present in many common plants and vegetables of theSolanum species. Unripe eggplant, green potatoes, and their sprouts contain a small amount of these heat-labile glycoalkaloids. Ingestion may cause GI e�ects such as vomiting, diarrhea, and abdominal pain, whichcan be delayed as long as 24 hours. CNS symptoms such as hallucinations, delirium, and obtundation are

reported.25 There is no definitive antidote for solanine or chaconine poisoning, and supportive care is usuallysu�icient.

Pokeweed (Phytolacca americana) contains phytolaccatoxin and similar phytotoxins in the leaves and roots.The mature berries are less toxic. Exposures can occur when foragers mistake the roots for other nontoxicssuch as parsnips or horseradish. Pokeweed is o�en prepared in poke salad or pokeroot tea. Toxicity isavoided if prepared by parboiling young greens. Incorrect preparation results in GI upset from direct mucosalirritation. Nausea, vomiting, hemorrhagic gastritis, abdominal pain, and profuse diarrhea may last for 48

hours.26 Severe intoxications may rarely result in coma and death. Treatment is supportive. Anonconsequential lymphocytosis develops approximately 3 days a�er ingestion and typically resolves within2 weeks.

Ackee fruit grows on the Blighia sapida tree, and it is a common ingredient in West African and Jamaicancuisine. Unripe ackee fruit contains the heat-stable toxins hypoglycin A and B. Hypoglycin A inhibits free fattyacids from entering the mitochondria, impairs substrate formation for gluconeogenesis, and preventsconversion of glutamate to γ-aminobutyric acid. The resulting clinical syndrome, which is characterized bysevere vomiting and hypoglycemia, is Jamaican vomiting sickness. Severe cases develop acidemia, seizures,

and encephalopathy.9,27 Administer IV dextrose or a carbohydrate-heavy meal to hypoglycemic patients.Treat seizures liberally with benzodiazepines. However, seizures may be refractory to benzodiazepines if γ-aminobutyric acid concentrations are critically low. Rarely, chronic toxicity from hypoglycin A can lead to

cholestatic hepatitis or fulminant liver failure.9,28 Admit symptomatic patients for close monitoring andtreatment.

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Holly (Ilex spp.) exposures are in the top 10 plants reported to poison control centers.2 Although the leavesare nontoxic, the attractive berries contain a mixture of toxins. The most consequential of this mixture aresaponins, glycosides that cause abdominal pain, vomiting, and diarrhea. If fewer than six berries are

ingested, minimal toxicity should follow.29 Large ingestions with severe GI upset may result in electrolyteabnormalities. For symptomatic patients, treatment is supportive.

PLANT-INDUCED DERMATITIS

Dermal exposure to a number of plants can result in an undesired dermatitis. These exposures are some of

the most commonly reported plant-related concerns reported to poison control centers in the United States.2

Classification by mechanism of action can guide therapy (Table 220-3), but o�en, exposure to a single plantcan result in injury due to multiple mechanisms.

MECHANICAL INJURY

Specialized plant structures can injure the dermis and serve as a nidus for entry of toxins. Needle-shapedcrystals, such as calcium oxalate crystal bundles, are found in a number of common plants, includingdumbcane (Die�enbachia spp.) and philodendron (Philodendron spp.). Needles of pineapples (Bromeliaceaespp.) and the hairs of stinging nettles (Urtica dioica) directly pierce the dermis, and chemical irritants in thesestructures cause further dermal injury (see below).

IRRITANT DERMATITIS

Phorbol esters found in the sap of plants of the Euphorbiaceae (spurge) can cause dermal irritation followingcontact. Symptoms such as erythema and bullae may develop shortly a�er direct contact. The phorbol esterscan penetrate the dermis upon contact. Ocular injuries and GI injury can also occur upon exposure oringestion. Occasionally, aerosolized irritants can cause dermatitis or respiratory distress. Exposures to

poinsettia (Euphorbia pulcherrima) are typically well tolerated.30 Pineapples (Bromeliaceae spp.), stingingnettles (U. dioica), and dumbcane (Die�enbachia spp.) all introduce irritants such as proteolytic enzymes and

other proinflammatory chemicals such as histamine, acetylcholine, and 5-hydroxytryptamine.10

ALLERGIC CONTACT DERMATITIS

Many plants can cause allergic contact dermatitis a�er repeat exposure. Sensitization occurs a�er a resinbinds to skin proteins and forms an antigen. Reexposure then stimulates a T-cell–mediated immuneresponse.

Poison ivy, poison oak, and poison sumac (Toxicodendron spp.) are ubiquitous sources of the antigenic resinurushiol. Ginkgo (Ginkgoaceae), mango (Mangifera indica), pistachio (Pistacia vera), and cashew (Anacardiumoccidentale) are common foods with urushiol. In sensitized individuals, reexposure can result in urticaria andpruritus. Over 12 to 48 hours, symptoms may progress to varying degrees of vesiculobullous formation.

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1. 

2. 

3. 

4. 

5. 

6. 

Treatment usually consists of drying agents and local topical steroids, but systemic steroids may benecessary in severe cases. Some exposures can result in type I hypersensitivity or anaphylaxis.

Tulips (Tulipa spp.) and da�odils (Narcissus spp.) contain the glycoside tuliposide A. A�er hydrolysis, anallergen causes tulip fingers or da�odil itch with chronic reexposure, a painful and pruritic condition.

PHYTOPHOTODERMATITIS

Phytophotodermatitis occurs when furocoumarins are activated by sunlight and produce symptoms thatresemble sunburn in the acute phase; erythema and bullae are common. When these symptoms heal,hyperpigmentation persists for months. The mechanism is unknown. Exposure can be directly through thedermis, or furocoumarins can be deposited in the skin following ingestion and subsequent systemiccirculation. Many plants, including common foods, can cause phytophotodermatitis, including numerous

citrus fruits, celery, carrots, and herbs.9

REFERENCES

Krenzelok  EP, Jacobsen  TD: Plant exposures … a national profile of the most common plant genera. VetHum Toxicol 39: 248, 1997.

[PubMed: 9251180]  

Mowry  JB, Spyker  DA, Cantilena  LR  Jr, Bailey  JE, Ford  M: 2012 Annual Report of the AmericanAssociation of Poison Control Centers' National Poison Data System (NPDS): 30th annual report. Clin Toxicol51: 949, 2013.

[PubMed: 24359283]

Mrvos  R, Krenzelok  EP, Jacobsen  TD: Toxidromes associated with the most common plant ingestions. VetHum Toxicol 43: 366, 2001.

[PubMed: 11757998]  

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