Toxic Plant Ingestions

Published on 24/06/2015 by admin

Filed under Emergency Medicine

Last modified 24/06/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1354 times

Chapter 64 Toxic Plant Ingestions

For online only figures, please go to image

Over 63,000 plant exposures were reported to 61 American poison control centers in 2008, representing 2.5% of all human toxic exposures reported that year. The most frequently reported exposures were peace lily, pokeweed, philodendron, poison ivy and poinsettia. One death due to plant poisoning, out of 1756 deaths due to poisoning, was reported.34 A review of plant poisonings reported to American poison control centers over an 18-year period (1983 to 2000) revealed 30 fatalities, with seven due to Cicuta species (water hemlock) and five due to Datura species (jimsonweed).152 Most plant exposures are unintentional and occur in children under the age of 6 years.168 Intentional ingestions are more common in adults, due to suicidal intent or abuse, and are more likely to produce serious poisonings.34,168 Worldwide, Atropa belladonna (deadly nightshade), Hyoscyamus niger (black henbane), Conium maculatum (poison hemlock), Areca catechu (betel nut), Thevetia peruviana (yellow oleander), Nerium oleander (common oleander), Cerbera manghas (sea mango), Veratrum album (hellebore), Aconitum carmichaeli (aconite), Taxus spp. (yew), Colchicum autumnale (autumn crocus), Gloriosa superba (glory lily), Ricinus communis (castor bean), Atractylis gummifera (bird-lime or blue thistle), and Blighia sapida (ackee fruit) also cause significant morbidity and mortality.*

General Considerations

Prompt and precise identification of the plant causing toxicity may not be feasible.34 Supportive care takes priority over plant identification. Airway, breathing, and circulation are assessed, including hydration status, end-organ perfusion, and urine output. Oral administration of activated charcoal (1g/kg), up to 50 g, may aid gastrointestinal (GI) decontamination; however, recommendations on when to administer activated charcoal are challenging, because this has not been prospectively studied for most plant ingestions. If a patient is actively vomiting, activated charcoal may or may not contribute to decontamination. If the patient has a depressed mental status or is likely to seize, administration of activated charcoal may result in pulmonary aspiration of charcoal. Opinions on when to administer activated charcoal vary between toxicologists. After emergency care has been provided, a history should include time of ingestion, amount and part of plants ingested, initial symptoms, and time between ingestion and onset of symptoms. Method of preparation (e.g., drying, cooking, boiling) and number of persons who ate the same plant are also important considerations. Plant identification may be aided by communication with poison control center personnel and by Internet searches.12,273,274

Laboratory studies depend on clinical presentation and suspected plant exposure. Complications of poisoning include aspiration pneumonia, rhabdomyolysis, and deep vein thrombosis. Differential diagnosis is initially kept broad so that other illnesses, such as infection and trauma, are not missed. Table 64-1 provides signs and symptoms of toxic plant ingestions.

Central Nervous System Toxins

Anticholinergic Plants (Tropane Alkaloids)

Plants containing tropane alkaloids (often called belladonna alkaloids) include atropine, hyoscyamine (the levorotatory isomer of atropine), and hyoscine (scopolamine).* Structures of the tropane alkaloids follow:

Tropane alkaloids are found in about 25 genera and 2000 species of plants. Plants causing human toxicity include A. belladonna (deadly nightshade), Mandragora species (mandrake), H. niger (black henbane), Datura species (jimsonweed), and Brugmansia species (angel’s trumpet). The Solanaceae family includes Solanum and Scopolia carniolica, the source of scopolamine.

Anticholinergic Syndrome

Toxicity may ensue after ingesting or smoking plant parts.45 The tropane alkaloids competitively inhibit postsynaptic muscarinic receptors, producing the classic anticholinergic syndrome (Figure 64-3 and Box 64-1).104,113,203,209,230 A useful clinical sign of anticholinergic toxicity is lack of perspiration in the axillae. Anticholinergic findings suggestive of poisoning may be remembered using the following mnemonic:209,240


Datura species are generally known as jimsonweed or thorn apple, and Brugmansia species are generally known as angel’s trumpet (Figure 64-4).112,113,263 Young, thin, and tender stems of jimsonweed contain the highest concentration of tropane alkaloids.179 However, the seeds also contain high concentrations of the alkaloids, and as little as one-half a teaspoonful of seeds may cause death from cardiopulmonary arrest. The word jimsonweed is thought to be derived from Jamestown, Virginia, where British troops reportedly behaved bizarrely after consuming Datura in 1676. D. stramonium has been reportedly used in Haitian zombification rituals.45,67,112,113 Jimsonweed has been used to treat asthma, heralding the current use of ipratropium bromide.

Reports of abuse of Datura and Brugmansia as hallucinogens continue to be reported in the United States and Europe.45,113,217,255 Clusters of poisonings among adolescents are typical.* Frequently, a tea of the plant parts is brewed.138 Report of toxicity after using a homemade Datura toothpaste has also been reported.205 A mass poisoning occurred in Botswana after consumption of porridge made from sorghum flour contaminated with seeds of D. stramonium.197 Symptoms may appear within minutes and may last for days.68,203,255 Tachycardia, dry mouth, agitation, nausea, vomiting, incoherence, disorientation, auditory and visual hallucinations, mydriasis, decreased bowel sounds, slurred speech, hyperthermia, flushed skin, urinary retention, and hypertension have been reported. Blurred vision and photophobia may be secondary to mydriasis. Isolated mydriasis and cycloplegia may be seen, including anisocoria, after topical contact to the eyes.123,130,263 With severe toxicity, seizures, flaccid paralysis, and coma may ensue. Focal neurologic signs and posturing, as well as death, have also been reported. Death may occur as a result of behavioral changes, leading to trauma, drowning, or environmental exposure associated with hyper- or hypothermia.138 Autopsy has revealed edema of the brain and lungs with focal hemorrhages within the alveolar lumens, ischemic lesions and edema of the heart, and hyperemia of the sinusoidal tracts of the liver.31

Anticholinergic poisoning should be suspected when patients are observed to communicate with imaginary friends with mumbled speech, and to demonstrate repetitive picking behavior.112,242 Symptoms generally begin 30 to 60 minutes after ingestion and continue for 24 to 48 hours, but they may begin within several minutes and persist for several days. Patients are generally amnestic of events during their poisoning. Studies may show leukocytosis, mild transient elevation of liver enzymes, elevated creatine phosphokinase (CPK) levels and other evidence of rhabdomyolysis, and changes on an electrocardiogram (ECG) that are consistent with tachycardia and dysrhythmias.45,68,89,113


Treatment of anticholinergic plant exposure consists primarily of decontamination and supportive care, including airway protection, intravenous (IV) fluids, and vasopressors for hypotension resistant to IV fluids. Hyperthermia should be assessed and treated if significant. Agitation can be treated with careful administration of benzodiazepines. Haloperidol and phenothiazines should not be used because these agents may enhance toxicity. Foley catheterization or nasogastric tube placement may be necessary if there is bladder distention or decreased gut motility, respectively.104,138,140,200,230

Some recommend treating severe central anticholinergic syndrome with carefully titrated physostigmine, which is derived from the calabar bean of Physostigma venenosum. This cholinesterase inhibitor blocks acetylcholine degradation; the resultant accumulation of acetylcholine overcomes the competitive inhibition of atropinic agents, such as those found in jimsonweed. Rapid, though generally transient, reversal of peripheral and central nervous system (CNS) effects can ensue. However, bradycardia, asystole, ventricular arrhythmias, hypotension, bronchospasm, bronchorrhea, and seizures have been reported after rapid IV administration of physostigmine, limiting its routine use. Persons with cardiac conduction abnormalities are particularly susceptible to the cardiac complications. Use of physostigmine generally does not shorten the hospital stay.*

Most cases of anticholinergic poisoning can be managed safely and effectively with supportive care alone.240 Consultation with a toxicologist is recommended before using physostigmine. If physostigmine is used, the recipient should be on a cardiac monitor, with pulse oximetry, and a physician at the bedside should slowly administer graduated doses of the drug.36,104,242

Nicotinic Plants (Pyridine and Piperidine Alkaloids)

The pyridine–piperidine group contains the major alkaloids nicotine, coniine, lobeline, arecoline, piperine, and isopelletierine. Structures of some pyridine/piperidine alkaloids follow:

Nicotine alkaloids are found mainly in the Solanaceae family of plants. Other families containing nicotine alkaloids include Hippocastanaceae (horse chestnut) and Asclepiadaceae (milkweed).

Tobacco Plants

Tobacco contains both nicotine and related alkaloids with similar pharmacologic properties, such as the alkaloid anabasine, which is found in Nicotiana glauca (wild tree tobacco) (Figure 64-5). N. glauca has been mistaken for Amaranthus hybridus (marog) and eaten with porridge in South Africa. Ingestion of N. glauca is generally fatal. Anabasine, an isomer of nicotine that appears to be more toxic than nicotine, probably accounts for much of the toxicity of N. glauca, N. debneyi, and N. rotundifolia. Anabasine concentrations can be particularly high in the roots of the plants. Although there are over 60 Nicotiana species, some other more common tobacco family members include N. rustica (Mapacho), N. tabacum (cultivated or common tobacco), N. trigonophylla (desert tobacco) (Figure 64-6), and N. attenuata (coyote tobacco). N. tabacum is the major source of commercial tobacco and contains between 0.5% and 9% nicotine. N. rustica (Mapacho) tends to contain higher concentrations of nicotine than does N. tabacum. Nicotine alkaloids are rapidly absorbed from the oral and GI tracts, the respiratory tract, and the skin. The kidneys excrete nicotine fairly rapidly after biotransformation in the liver and lungs. The half-life is 1 to 2 hours. Although the lethal dose of ingested nicotine is not well established, 2 to 5 mg may cause nausea, and 40 to 60 mg may be lethal in humans. One to two cigarettes, ingested and absorbed, could be lethal in a child.176,180,228,236,247

Nicotinic Syndrome

Peripherally, acetylcholine is a neurotransmitter for autonomic and somatic motor fibers. It is stored in vesicles within the presynaptic neuron and is released by calcium-dependent exocytosis into the synapse, where it binds to receptors and is eventually degraded by acetylcholinesterase. Acetylcholine can bind to two receptor types, nicotinic and muscarinic. Nicotinic receptors are located on postganglionic autonomic neurons (NN receptors) and at skeletal neuromuscular junctions (NM receptors). Direct nicotinic agonists (e.g., arecoline, coniine, cytisine, lobeline, nicotine) prolong depolarization at these receptors and eventually cause blockade of nicotinic receptors. Clinical evidence of stimulation followed by blockade is apparent. Hypertension, tachycardia, pallor, vomiting, diarrhea, abdominal pain, salivation, bronchorrhea, tachypnea, muscle fasciculations, spasms, confusion, agitation, tremor, and convulsions (the stimulation) are followed by hypotension, bradyarrhythmias (occasionally asystole), hyporeflexia, paralysis, coma, and respiratory failure (the blockade). When death occurs, it is generally due to respiratory paralysis (Box 64-2; see also Figure 64-3).*

Green tobacco sickness is a mild form of nicotine poisoning seen in tobacco-naive field workers with dermal exposure to leaves of green tobacco in wet environments. Nicotine, a water-soluble alkaloid, is absorbed dermally. The syndrome is characterized by weakness, salivation, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, visual and hearing disturbances, respiratory depression, and occasionally fluctuations in blood pressure and heart rate. Neuromuscular blockade may result in death. A urinary nicotine metabolite, cotinine, may be helpful diagnostically.15,176,228,247

Lobeline, derived from the Indian tobacco plant Lobelia inflata, is a high-affinity nicotinic ligand. It can cause nicotine-like effects, but is generally less toxic than is nicotine.63

Poison Hemlock

C. maculatum (poison hemlock) (Figure 64-7), also known as spotted hemlock, California or Nebraska fern, stinkweed, fool’s parsley, and carrot weed, is often mistaken for an edible plant, such as parsley, parsnip, or anise; however, it has a mousy odor and an unpleasant bitter taste, and it burns the mouth and throat. The stem is hollow with purplish to reddish brown spots. Its long taproot is solid and parsnip-like. Although all plant parts are poisonous, the unripe fruit is especially toxic. Poisonings are more common in the spring and summer. Poisoning may also occur after eating birds that have consumed poison hemlock. Coniine and γ-coniceine, the principal alkaloids in C. maculatum, are pyridine derivatives similar to nicotine. Coniine is more toxic than is γ-coniceine. The alkaloid is volatile and susceptible to drying and heating.25,152,228,268,274

C. maculatum was used in ancient times for capital punishment and murder. The primary action of the toxic alkaloids is activation and then blockade of nicotinic acetylcholine receptors. Initially, stimulation causes sialorrhea, nausea, vomiting, diarrhea, abdominal cramping, tremor, ataxia, confusion, blurred vision, hypertension and tachycardia, followed by dry mucosae, GI hypotonia, lethargy, weakness, diminished cardiac contraction, hypotension, and bradycardia, as with nicotinic syndrome. Muscles rapidly swell and stiffen, with multifocal necrosis of myocytes and associated muscle pain. Muscle fasciculations may be followed by flaccid paralysis, including respiratory paralysis. Rhabdomyolysis and acute tubular necrosis with renal failure may occur. Elevated CPK and liver function tests (LFTs) may be noted. Death is usually from respiratory failure. Autopsy may reveal congestion of the lungs and liver.*

Betel Nut

Areca catechu (areca palm) (Figure 64-8) produces betel nut, a common masticatory drug in the Far East, Asia, India, and the South Pacific; it is also shipped elsewhere. An estimated 10% to 25% of the world’s population chews “betel quid.” It is generally chewed with slaked lime paste (calcium hydroxide) wrapped in leaves of betel pepper (Piper betel). known as “quid,” “punsupari,” and “pan masala.” Occasionally, tobacco is added. Quid is sucked in the lateral gingival pocket. Commercially, areca nut is marketed in the form of sweetened areca nut, known as “supari.” A. catechu contains arecoline and guvacoline, which are hydrolyzed to arecaidine and guvacine, respectively. These are strong inhibitors of gamma-aminobutyric acid (GABA) uptake. These arecal alkaloids also are nicotinic and muscarinic. Betel pepper leaves contain betel oil, which contains psychoactive phenols and cadinene. These possess cocaine-like properties. Clinical effects resemble nicotinic syndrome and cholinergic toxicity, including CNS effects (dizziness, euphoria, subjective arousal, altered mental status, hallucinations, psychosis, convulsions), cardiac effects (tachycardia, hypertension, palpitations, arrhythmias, bradycardia, hypotension, chest discomfort, and acute myocardial infarction in susceptible individuals), pulmonary effects (bronchospasm, tachypnea, dyspnea), GI effects (salivation, vomiting, diarrhea), urogenic effects (urinary incontinence), and musculoskeletal effects (weakness and paralysis). Use with calcium salts may result in hypercalcemia, hypokalemia, and metabolic acidosis with renal potassium wasting and renal insufficiency. Betel nut use is also associated with flushing, diaphoresis, warm sensations, red- or orange-stained oral mucosa and saliva, and teeth stained dark brown or black. Precancerous oral lesions may also occur with chronic use.


FIGURE 64-8 Betel nut (Areca catechu).

(Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)

Hallucinogenic Plants (Indoles, Phenylalkylamines)

About 90 of the 800,000 known plant species are hallucinogenic. Numerous rituals and religious ceremonies incorporate these plants. Many psychoactive plants are indole derivatives, which are among the most potent psychoactive compounds in nature and have the following structure:

Chemical relationships exist among serotonin, psilocybin (Psilocybe species), and D-lysergic acid diethylamide (LSD). LSD is synthesized from ergonovine (or ergometrine), derived from Claviceps purpurea. Striking structural similarities exist between the most potent psychoactive plant compounds and biochemically important neurotransmitters, as follows:

Morning Glory

The active component of the naturally occurring hallucinogen found in the seeds of morning glory (Ipomoea violacea) (Figure 64-10) is ergine, or (+)-lysergic acid amide, an indole derivative.112 About 300 seeds, or enough to fill a cupped hand, are equivalent to 200 to 300 mg of LSD, with similar systemic and hallucinatory effects. Ingestion of Hawaiian baby woodrose seeds (Argyrlia nervosa) has similar effects.105


Myristica fragrans (Figure 64-11) is used to make the spices nutmeg and mace. Mature rinds of the fruit split, revealing a bright-red, fringed, fleshy coating on the outside of its seed. The coating contains mace, and the seed contains nutmeg. Nutmeg contains myristicin, which has an indole-like structure and is metabolized to amphetamine-like compounds. Other alkylbenzene derivatives, such as safrole and elemicin, are also found in nutmeg. Nutmeg has been abused for its alleged hallucinogenic effects. A person who ingested one grated nutmeg (7 g) had weakness, loss of coordination, vertigo, fainting, nausea, and paresthesias but no hallucinations.238,265


FIGURE 64-11 Nutmeg (Myristica fragrans).

(Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)


Cannabis preparations are largely derived from the female Cannabis sativa plant. The primary psychoactive component is δ-9-tetrahydrocannabinol (THC), which is most concentrated in the flowering tops. Marijuana generally contains 0.5% to 5% THC; however, the Sinsemilla and Netherwood varieties may contain up to 20% THC, and hashish and hashish oils have higher concentrations. Cannabinoids can be smoked or ingested. A typical marijuana cigarette contains 0.5 to 1.0 g of cannabis, and the THC delivered varies from 20% to 70%, with a bioavailability of 5% to 24%. As little as 2 mg of available THC produces effects in occasional users.119

Cannabinoids bind to specific cannabinoid receptors in areas of the brain involved with cognition, memory reward, pain perception, and motor coordination. Cannabinoids act as neuromodulators in the release and action of neurotransmitters (e.g., acetylcholine, glutamate).75,119 Endogenous ligands for these receptors are endocannabinoids. The first endocannabinoid identified was anandamide, named after the Sanskrit word ananda, which means “bliss.”

Desirable effects include mild mood-altering qualities, euphoria, alteration in perceptions, time distortion, and intensification of ordinary sensory experiences (e.g., gustatory, visual, and auditory sensations). Adverse effects include impairment of short-term memory and attention, mydriasis and slowly reactive pupils, impairment of motor skills and reaction times, nausea, vomiting, and anxiety. Psychotic symptoms have been reported in persons vulnerable to psychosis. Clinically, tachycardia may occur within minutes of THC exposure and may last a few hours. Minor changes in blood pressure may also occur. Exposed toddlers may present with lethargy, slurred speech, ataxia, and shaking.27,119


The hallucinogenic peyote cactus Lophophora williamsii (Figure 64-12) contains alkaloids that are phenylethylamines or isoquinolines rather than indoles. Mescaline (3,4,5-trimethoxy-β-phenylethylamine), the primary psychoactive component of peyote, is structurally similar to the neurotransmitters norepinephrine and epinephrine and to hallucinogenic amphetamines. Pharmacologically, however, mescaline is similar to hallucinogenic indoles. Mescaline may affect the action of norepinephrine and serotonin, evidenced clinically by sympathomimetic effects, followed by marked visual hallucinations. Mescaline produces slight rises in blood pressure and heart rate, tachypnea, hyperreflexia, mydriasis, ataxia, perspiration, flushing, salivation, and urination. No deaths have been reported from peyote poisoning. Type B botulism was associated with consumption of a ceremonial tea made from peyote that was stored in a jar by members of the Native American Church. Affected members had bilaterally symmetric, flaccid weakness in all extremities, dysphagia, nasal speech, and diplopia.9,126

Mescal Bean Bush

The mescal bean bush or Texas mountain laurel (Sophora secundiflora) of the pea family (Fabaceae) produces hallucinogenic dark-red beans (mescal beans; see Figure 64-9). The beans contain the toxic alkaloid cytisine, which causes nausea, numbing sensations, hallucinations, unconsciousness, convulsions, and death through respiratory failure. The beans may be boiled in water and the mixture consumed, producing a delirium or “visionary trance.” The origin of mescalism in modern peyote religion is debated. Mescal beans are worn during some peyote ceremonies.9


The evergreen khat tree, Catha edulis, grows in East Africa and Arabia (Figure 64-13). Khat is also known as chat, qat, kat, kath, gat, eschat, miraa, murungu, qaad, and jaad. As early as 1237, khat was advocated in Arabic medical literature as a mood-elevating and hunger-suppressing agent. Khat leaves and bark continue to be chewed, with the juice of the masticated plant being swallowed for stimulatory effects. Khat contains cathinone (2-amino-1-phenyl-1-propanone), cathine (norpseudoephedrine), and norephedrine. Cathinone, a phenylalkylamine, is the major psychoactive constituent. Structurally, cathinone is similar to amphetamines, and khat has been referred to as a “natural” amphetamine. Like amphetamines, cathinone is an indirect sympathomimetic, inducing release of dopamine, serotonin, and norepinephrine.*


FIGURE 64-13 Khat (Catha edulis).

(Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)

The structures of methcathinone, cathinone, and ephedrine follow:

Cathinone in fresh plant material must be extracted by masticating laboriously; this results in gradual absorption. As the leaf wilts, cathinone content decreases and the leaf loses its potency as a psychostimulant. Because only fresh leaves produce the desired stimulatory effects, in the past, khat use was generally limited to countries where khat was produced (e.g., North Yemen, Ethiopia, Kenya); however, khat is now air-freighted to Europe and the United States, with a recent increase in use in upstate New York. Khat is transported damp, rolled in a banana leaf bundle called a marduff.

Desirable effects of khat include increased energy and alertness, feelings of increased endurance and self-esteem, enhanced imaginative ability, higher capacity to associate ideas, and euphoria. Cathinone has both positive chronotropic and inotropic effects. Tachycardia, increased blood pressure, tachypnea, and mydriasis are seen. Adverse effects include anorexia, hypomania, insomnia, delusions, paranoid psychosis, aggression, depression, anxiety, hyperthermia, stomatitis, oral lesions/cancers, gastritis, and endocrine disturbances. Khat use has also been associated with vasoconstriction, acute myocardial infarction, leukoencephalopathy and an increased incidence of acute cerebral infarction. Khat is known to be habit forming and has been classified as a substance of abuse by the World Health Organization. Cathinone is a Schedule I controlled substance under federal regulations in the United States.

Sedating Plants (Isoquinoline Alkaloids)


Papaver somniferum flowers are large and white with purple stains at the base of each petal. They yield opium, a complex of more than 20 alkaloids, including morphine, codeine, and papaverine. Morphine was the first plant alkaloid isolated, by pharmacist Friederich Wilhelm Adam Serturner in 1806.117 Seeds of P. somniferum are used in various foods and beverages, including bagels, muffins, pastries, curry sauce, rice, and teas. Opiate toxicity from poppy seed exposure occurred in a 6-month-old infant given 75 mL of strained milk made with 200 g of poppy seeds in 500 mL milk, resulting in respiratory arrest requiring ventilation. Opiate toxicity has also occurred after ingestion of a boiled poppy plant and after ingestion of spaghetti with poppy seeds. Poppy dependence has also been described. Ingestion of poppy seeds can result in detectable levels of morphine and codeine by urine drug screen testing.146,158,204,262

Convulsant Plants (Indoles, Resins)


Strychnine, an indole found in seeds of the tree Strychnos nux-vomica, is a powerful CNS stimulant. Poisoning may also occur after ingestion of rodent poisons containing strychnine, with the use of illicit drugs contaminated with strychnine, or with the use of herbal remedies contaminated with strychnine. Strychnine is especially concentrated in the seeds and roots of the plant. The bark of S. nux-vomica also contains the alkaloid brucine, which is less potent than strychnine, but produces similar toxicity when consumed. Strychnine is a selective, competitive antagonist of glycine, a major inhibitory neurotransmitter, at its postsynaptic receptors in the spinal cord and brainstem. Poisoning produces an excitatory state, with hyperreflexia, hypersensitivity to stimuli, migratory rippling movements of the muscles, twitching, rigidity, and spinal convulsions (generally, flexor spasm of the upper limbs, extensor spasm of the lower limbs, opisthotonic posturing, and spasms of the jaw muscles, all without loss of consciousness or postictal states). Minimal stimulation elicits diffuse muscle contractions. In between spasms, which last from 30 seconds to 2 minutes, muscles become completely relaxed. Respiratory and secondary cardiac failure may ensue during severe convulsions. Treatment consists of supportive care, benzodiazepines, and barbiturates. Chemical paralysis with a nondepolarizing agent, endotracheal intubation, and mechanical ventilation may be required for severely poisoned patients. Hyperthermia, rhabdomyolysis, renal failure, and acidosis may occur secondary to convulsions. These complications often require treatment. Occasionally, death ensues despite aggressive treatment.*

Some Strychnos species in Africa contain alkaloids that produce curare-like effects. These alkaloids act through nondepolarizing and competitive mechanisms at the neuromuscular junction, competing with acetylcholine for the receptor, hence blocking nerve-to-muscle transmission. This results in paralysis; however, paralysis is not seen after ingestion of these species, because the toxic alkaloids are not absorbed from the gastrointestinal tract.207

Water Hemlock

Water hemlock (Cicuta maculata) is one of the most toxic resin-containing plants. The resin of C. maculata, an unsaturated aliphatic alcohol called cicutoxin, has the following structure:

Species within the Umbelliferae (also called Apiaceae) family are divided into the Cicuta and Oenanthe genera. Nine subspecies of Cicuta of the Umbelliferae family are poisonous (Figure 64-14). C. virosa is common European water hemlock, whereas C. maculata and C. douglasii are found in North America. Oenanthe crocata, or hemlock water dropwort, is found in Europe and North America. Common names for Cicuta species include cowbane, five-finger root, snake weed, snake root, wild carrot, dead man’s fingers, death-of-man, poison parsnip, wild parsnip, beaver poison, children’s bane, muskrat weed, spotted hemlock, spotted cowbane, musquash root, false parsley, fever root, mock-eel root, wild dill, spotted parsley, and carotte à Moreau. Roots have a parsnip-like or carrot-like odor, and Cicuta species are often mistaken for edible plants, such as water parsnip. These plants have also been mistaken for pignut, sweet flag, wild carrot, wild celery, wild ginseng, and kvanne. Mature roots have air-filled chambers and are found on the ends of hollow stems. All parts of the plant are toxic, but the roots contain the highest concentration of cicutoxin. Ingestion of as little as 2 to 3 cm of the root may be fatal to an adult. The severity of poisoning and time until onset of symptoms is proportional to the amount of plant ingested. The plant is most toxic in the spring. The principal toxins, cicutoxin and oenanthotoxin, contained in these plants act as noncompetitive GABA antagonists in the central nervous system, resulting in unabated neuronal depolarization that manifiests as seizures, including status epilepticus.104,131,152,229

Water hemlock poisoning should be considered in any patient who presents with cholinergic-like poisoning and abrupt onset of seizures. Early symptoms include muscarinic effects and involve primarily the GI tract: abdominal pain, vomiting, and diarrhea. However, marked diaphoresis, salivation, and respiratory distress may also be seen. Nicotinic effects are less prominent (see Figure 64-3). Tachycardia and hypertension or bradycardia and hypotension may be seen. Dysrhythmias may occur. Ataxia, paresthesias, muscle spasms, weakness, and altered mental status have been reported. With severe poisoning, coma and epileptiform seizure activity, or spastic and tonic movements, including opisthotonus without electroencephalographic seizure activity, may occur. Rhabdomyolysis and renal failure have been reported. Deaths may be associated with persistent seizures, cerebral edema, ventricular fibrillation, pulmonary edema, cardiopulmonary arrest, and disseminated intravascular coagulation. Laboratory abnormalities include metabolic acidosis and elevated CPK and LFTs. Treatment includes securing an airway, ventilation, and treatment of seizures with benzodiazepines and barbiturates. Phenytoin is contraindicated because it is ineffective for seizure control. Anticholinergic agents are not recommended, because these agents do not reduce seizure activity. Continuous EEG monitoring is helpful. Treatment of hypoxia, acidosis, hyperthermia, rhabdomyolysis, and cerebral edema should be provided. Hypotension can be treated with intravenous fluids and vasopressors. Recovery can take up to 4 days, and some patients never completely recover. Although survival has improved with aggressive supportive care, death may still ensue. Autopsies reveal pulmonary and cerebral edema, brain hemorrhages and renal necrosis.104,131,152,229

Cardiovascular Toxins

Cardiovascular toxins found in plants are listed in Box 64-3.

Cardiotoxins that Inhibit Na+/K+ Atpase (Cardiac Glycosides)

More than 200 naturally occurring cardiac glycosides have been identified. Plant cardiac glycosides are composed of a steroid backbone, an attached five-membered unsaturated lactone ring (six-membered for Helleborus), and either a carbohydrate or sugar moiety in glycosidic linkage. The toxic aglycones are released by acid and enzymatic hydrolysis. The attached sugar moiety has no inherent cardiac action but may enhance solubility, absorption, and toxicity of the aglycone moiety. Cardiac glycosides bind to the membrane-bound enzyme Na+,K+ ATPase, increasing intracellular Na+ and Ca2+ levels and automaticity (Figure 64-15).215 Cardiac glycosides are found in Digitalis purpurea (foxglove) (Figure 64-16), Digitalis lanata, N. oleander (common oleander) (Figure 64-17), T. peruviana (yellow oleander) (Figure 64-18), Convallaria majalis (lily of the valley) (Figure 64-19), Urginea maritima (squill or sea onion) (Figure 64-20), U. indica, Cerbera manghas (sea mango), C. odollam (pink-eyed cerbera), Strophanthus gratus (ouabain), Asclepias species (balloon cotton, red-headed cotton-bush milkweeds), Calotropis procera (king’s crown), Carissa spectabilis (wintersweet), C. acokanthera (bushman’s poison), Plumeria rubra (frangipani), Cryptostegia grandifolia (rubber vine), Euonymus europaeus (spindle tree), Cheiranthus, Erysimum (wallflower), and Helleborus niger (henbane).*


FIGURE 64-16 Digitalis purpurea (foxglove).

(Courtesy Kimberlie A. Graeme, MD.)


D. purpurea grows wild in parts of the United States and is cultivated as a garden ornamental plant. D. purpurea contains only digitoxin, not digoxin. Withering reported the medical use of extracts of D. purpurea based on a recipe for treating “dropsy.”129,192 The leaves have been consumed in a risotto when they were mistaken for borage leaves, and in a salad when mistaken for dandelion leaves.38,189 Toxicity has also been reported from consumption of contaminated field water with Digitalis plants growing nearby.189 D. lanata was mistakenly substituted for plantain in herbal products, with resultant human cardiotoxicity.239 D. lanata contains lanatosides A, B, and C, which yield digoxin and digitoxin. Intentional overdoses also occur.157,189