Plant name and/or accurate species information may not always be readily available to the clinician. Historical information to be elicited includes whether the plant is an indoor or outdoor variety and a description of the plant's flower, stem, leaves, height, and location. Consultation with a botanist, medical toxicologist, or poison control center is highly recommended whenever assistance is needed in identifying an unknown plant. Transmission of digital color or facsimile images can be used to assist consultants.2 When expert consultation is unavailable, rough recognition of taxonomic families of poisonous plants and/or comparison of the species in question with pictures from a field guide may help exclude potentially life-threatening plant exposures. In general, it is useful to consider clinically relevant plants according to the predominant and most serious manifestations of toxicity.
When ingested, a wide variety of plant species causes mucous membrane irritation due to microscopic needle-shaped bundles of calcium oxalate (raphides) present throughout the plant structures. When masticated, the rhaphides release the calcium oxalate crystals, which damage mucous membranes and, in conjunction with unclarified additional mediators, cause immediate burning and inflammation. Commonly encountered plants containing calcium oxalate include philodendron (Philodendron sp.), dumb cane (Dieffenbachia) (Fig. 130–1), peace lily (Spathiphyllum sp.), pothos (Epipremnum aureum), caladium (Caladium bicolor), calla lily (Zantedeschia aethiopica), Jack-in-the-pulpit (Arisaema triphyllum), elephant's ear (Colocasia esculenta), and skunk cabbage (Symplocarpus foetidus).3 Of the species listed above, Philodendron and Dieffenbachia have historically accounted for the highest percentage of exposures.4 While oropharyngeal irritation and localized swelling can last for several days following oral exposure, one retrospective case review reported only 4/188 (2.1%) symptomatic cases, with only minor oral symptoms developing within 5 minutes of exposure.5 Although case reports exist of severe airway edema requiring tracheostomy in an adult,6 esophageal injury complicated by delayed death in a pediatric patient,7 and even aortoesophageal fistula,8 such events are exceedingly rare. A recent review of the thousands of Dieffenbachia exposures reported to poison control centers revealed that only about a third of patients developed documented symptoms, of which oral irritation was most common (18.2%). There were no reports of respiratory obstruction or death.9 For such plants, treatment is symptomatic with demulcents such as milk, popsicles, and cool drinks. Analgesics may be required and associated pruritis or dermal irritation may respond to antihistamines.
Leaves of Dieffenbachia plant.
Exposures to various Capsicum species such as the chili pepper (Capsicum annuum) continue to constitute an important source of plant exposures. In addition, the 2006 AAPCC NPDS annual report listed “pepper mace” as one of the 25 most frequent plant exposures.1 Both the Capsicum plants and “pepper spray” or “pepper mace” contain capsaicin, which is the toxin responsible for causing symptoms. Symptomatic exposures often occur after handling or ingesting the fruits or seeds of the Capsicum plants. Capsaicin causes release of substance P from nociceptive type C nerve fibers.10 Clinical effects consist of intense burning pain, hyperalgesia, irritation, and erythema. Profuse lacrimation and conjunctival inflammation may occur with ocular exposure. Capsaicin does not cause chemical burns and vesication is not seen.3,10 In some cases, contact dermatitis can develop and symptoms can persist for hours to days depending on the duration of exposure. Treatment is focused on decontamination and pain control, and exposure does not result in long-term injury. Although cold-water irrigation can provide relief, capsaicin is poorly soluble.10 A number of remedies have been suggested in the medical literature, including vinegar, topical antacids, vegetable oil, and 2% lidocaine gel.11–14
American Mistletoe (Phoradendron serotinum, Phoradendron leucarpum)
Although often thought of as highly toxic by laypersons, reports of significant toxicity from mistletoe involve Viscum album (European mistletoe), which contains cardiovascular toxins (viscotoxins) and a toxalbumin (viscumin).3,15 Based on reviews of poison center data, it seems that pediatric accidental ingestions of American mistletoe are largely asymptomatic, with essentially no major morbidity.16 Reported symptoms are mostly gastrointestinal upset, with symptoms developing within 6 hours of exposure.15 Treatment is supportive, and decontamination for small ingestions is unnecessary. In the absence of significant GI symptoms, most cases can be managed at home. Intentional or large ingestions of >20 berries or >5 leaves should be referred to the ED.16
Poinsettia (Euphorbia pulcherrima)
The 2006 AAPCC NPDS annual report listed the poinsettia as the second most common plant exposure.1 Similar to American mistletoe, the poinsettia is erroneously thought of as a highly toxic plant by laypersons, possibly because of an apocryphal report of a pediatric fatality dating from the early 20th century.17 A review of 22 793 poison center cases confirmed the relatively benign nature of poinsettia exposures. Most were accidental pediatric exposures; 96.1% were managed without ED referral and most (92.4%) remained asymptomatic. No fatalities were reported.17 Management of these exposures requires no more than supportive care and GI decontamination has not been shown to be of benefit.
Ilex species accounted for the third largest group of plant exposures in the 2006 AAPCC NPDS annual report. Ilex opaca (American holly) and Ilex aquifolium (English holly) are most frequently encountered due to their use as Christmas decorations. The plants produce green berries, which mature into red berries that highlight the foliage and are attractive to small children. It is thought that the berries are responsible for toxicity and large ingestions can cause nausea, vomiting, abdominal cramping, and diarrhea.3 Cases involving small (≤2 berries) accidental ingestions are expected to produce minimal if any symptoms. Basic supportive care with attention to hydration status is sufficient.
Pokeweed (Phytolacca americana)
Pokeweed exposures have been fairly commonly reported to the AAPCC; the most recent annual report lists pokeweed as one of the top 25 plant exposures.1 Pokeweed contains toxic saponins (phytolaccatoxin, phytolaccagenin), as well as a lymphotropic mitogen.18 All parts of the plant, particularly the root, are toxic. Most human exposures result from consumption of leaves (“poke salad”), or from mistaking the roots for horseradish or parsnips.3 Although parboiling is traditionally used to lower the toxin content when preparing “poke salad,” cases of symptomatic poisoning have nonetheless occurred.19 Pokeweed poisoning primarily causes nausea, vomiting, abdominal cramps, and diarrhea. Symptoms generally begin within 2 to 4 hours after ingestion and usually resolve within 24 to 48 hours. Severe cases with heme positive stools, tachycardia, and hypotension have also been reported.19 Rare cases with electrocardiographic (EKG) changes have been reported in adults with significant GI symptoms, although the mechanism for the EKG findings may not be related to pokeweed itself.19,20 Contemporary medical literature includes a single case of fatal ventricular fibrillation in an 18-year-old male following the ingestion of a 4 to 5 in piece of pokeweed root.21 Supportive care is the mainstay of treatment. Decontamination with activated charcoal may be considered in nonvomiting patients who present after potentially significant ingestions. Antiemetics and intravenous fluid therapy may be necessary. Admission may be required for observation and continued care in the setting of large or markedly symptomatic ingestions.
Plants Containing Anticholinergic Substances
Jimsonweed (Datura stramonium) (Fig. 130–2), deadly nightshade (Atropa belladonna), and black henbane (Hyoscyamus niger) are some of the plants that contain muscarinic antagonist alkaloids such as atropine, hyoscyamine, and scopolamine. Jimsonweed, also called locoweed and devil's trumpet, is a tall plant with a musty odor and spiny seedpods. The plant grows wild throughout the United States, and its seeds have been abused by adolescents and teenagers due to its psychotropic effects.22,23 Patients with significant ingestion will manifest an anticholinergic toxidrome: tachycardia, mydriasis, dry skin and mucous membranes, hypoactive bowel sounds, urinary retention, and hyperthermia. Central anticholinergic effects result in altered mental status, ranging from somnolence to severe agitation and delirium with hallucinations.23 Symptoms usually arise within 30 to 60 minutes of ingestion and can last for 24 to 48 hours.18 Decontamination with activated charcoal may be considered in cooperative individuals. Agitation should be initially treated with benzodiazepines. Hyperthermia should be treated supportively with cooling measures. Physostigmine has been safely and effectively used as an antidote in cases of anticholinergic plant poisoning.24–26 Physostigmine is generally reserved for patients with refractory delirium, hyperthermia, seizures, or significant arrhythmias; there is ongoing controversy regarding its effect on clinical course and outcome.27,28 Physostigmine can be given in pediatric doses of 0.02 mg/kg IV over the course of several minutes with concurrent cardiac and blood pressure monitoring. If there is no improvement, readministration after 5 to 10 minutes may be attempted, to a total of 2 mg. The dose for adolescents and adults is 1 to 2 mg IV administered slowly over 4 minutes (≤0.5 mg/min). Physostigmine's effects typically last 30 to 60 minutes and repeat dosing may be required. Patients with marked delirium, seizures, cardiopulmonary instability, or those treated with physostigmine should be admitted to an intensive care unit.
Seedpod and seeds from jimsonweed (Datura stramonium).
Plants Containing Solanine
Plants containing solanaceous alkaloids grow throughout the United States, and include the black nightshade (Solanum nigrum), Jerusalem cherry (Solanum pseudocapsicum), bittersweet (Solanum dulcamara), and potato (Solanum tuberosum). While all parts of the black nightshade and bittersweet plants are poisonous, it is the unripe berries that are the most toxic. Ingestion of sun-greened potatoes or uncooked potato sprouts may also cause illness as they contain α-solanine and the related glycoalkaloid, α-chaconine. The mechanism of solanine toxicity remains unclear. Small ingestions of these plants generally result in no more than self-limited gastrointestinal effects. Severe intoxications can manifest with CNS and respiratory depression, hyperthermia, bradycardia, hypotension, and tachycardia. The clinical picture may be clouded by the concurrent presence of anticholinergic agents in some of these plants, which may dominate the initial presentation.29,30
Plants Containing Cardiac Glycosides
Foxglove (Digitalis purpurea) (Fig. 130–3), lily-of-the-valley (Convallaria majalis), common oleander (Nerium oleander), and yellow oleander (Thevetia peruviana) all contain digitalis-like glycosides.3 Ingestion of yellow oleander results in the most significant degree of toxicity and, of plants containing digitalis-like glycosides, is responsible for the greatest number of fatalities worldwide. All parts of these plants, particularly the seeds in the case of yellow oleander, are potentially toxic. While children with small exploratory ingestions of whole plant material from lily-of-the-valley or common oleander are unlikely to develop toxicity, ingestion of only a few yellow oleander seeds can produce life-threatening poisoning. Patients may present with nausea, vomiting, dizziness, diarrhea, and abdominal pain.18 EKG findings following yellow oleander poisoning have been found to primarily consist of sinus bradycardia and conduction defects affecting the sinus or AV node.31 Hyperkalemia may also be noted, as well as a detectable serum digoxin level. While the serum digoxin level can help prove exposure, the absolute level cannot be used to guide antidotal therapy. Treatment with antidigoxin Fab fragments is safe and effective for patients with significant cardiac arrhythmias.32 It has been shown to restore sinus rhythm, correct bradycardia, and ameliorate hyperkalemia. The exact dose required is unknown and is likely much higher than those used to treat digoxin overdose.32 Decontamination with a single dose of activated charcoal is reasonable in patients not at risk for aspiration. However, the therapeutic value of multidose-activated charcoal in yellow oleander ingestion remains unclear.33,34 Patients who are asymptomatic following nontrivial ingestions should have serial EKGs, repeat electrolyte determinations, and be observed for 12 hours.
Flowers of foxglove (Digitalis purpurea) plant.
Plants Containing Sodium Channel Activators
Monkshood (Aconitum sp.), false hellebore (Veratrum sp.), azalea (Rhododendron sp.), rhododendron (Rhododendron sp.), and mountain laurel (Kalmia latifolia) all contain various toxins capable of stabilizing the open form of voltage-dependent sodium channels within the excitable membranes of neuronal and cardiac tissues.3 Aconitine is the toxic alkaloid found in Aconitum sp., while the steroidal veratrum alkaloids are contained in Veratrum sp. Exposure to grayanotoxins, found in the Rhododendron and Kalmia sp., can occur after ingestion of the leaves or via honey made from flower nectar. The resulting clinical syndromes are fairly similar, with vomiting, paresthesias, muscle weakness, hypotension, and, rarely, seizures. Bradydysrhythmias, conduction blocks, and tachydysrhythmias have been described.18 Symptom onset is generally rapid in patients with significant ingestions and often resolves within 24 to 48 hours. No antidote exists and therapy is supportive. Decontamination with activated charcoal should be initiated provided that it can be safely performed. Intubation and circulatory support with fluids and vasopressors may be needed. Aconitine has been associated with various ventricular dysrhythmias, including bidirectional ventricular tachycardia. Both lidocaine and electrical cardioversion performed poorly in published case series; amiodarone or flecainide may be reasonable alternatives.35 Bradycardia or AV block may respond to atropine, although temporary pacing has been required.18 While death is rare even in adults, and large ingestions are less likely in children, pediatric cases with significant toxicity have been reported.36
Yew plants are short evergreen shrubs commonly used in landscaping designs. The seeds and leaves of the plant, but not the fleshy red aril, contain the cardiotoxic alkaloids taxine A and B. Yew exposures in children likely result from the attractive appearance of the red aril surrounding the seed. While deaths have been reported in the medical literature, they are typically in the setting of suicidal ingestions.37 A poison center review of >11 000, largely pediatric, yew exposures revealed that the majority of cases (92.5%) were asymptomatic and no deaths were reported.38 The most frequently encountered symptoms were GI upset (65.5%), dermal irritation (8.3%), hypotension or arrhythmias (6%), and seizures (6%). There is no antidote and treatment is supportive care–driven.
Cases of significant morbidity from tobacco exposure reported in the literature resulted from exposure to green tobacco leaves or highly concentrated nicotine preparations. Most pediatric exposures involve the exploratory ingestion of cigarettes, cigarette butts, or nicotine gum.39 Symptoms usually develop within 30 to 90 minutes in children who ingest tobacco products. Patients who ingest ≥2 whole cigarettes or ≥6 cigarette butts are more likely to develop symptoms.40 Vomiting is commonly seen and patients without spontaneous vomiting in the first hour are unlikely to have ingested a toxic amount. Clinical response to nicotine intoxication may follow a biphasic course. Tachycardia, mydriasis, hypertension, tremor, and seizures may be seen. The stimulatory phase is then followed by autonomic and neuromuscular blockade from persistent stimulation, resulting in fasciculations and skeletal muscle paralysis. Death is usually because of respiratory arrest or cardiovascular collapse. Treatment is supportive, and most patients may be safely discharged after brief observation.
Poison Hemlock (Conium maculatum)
Poison hemlock can be found throughout the United States. The plant can be identified by the “mousy” odor it emits. The plant contains coniine as well as other nicotinic alkaloids, which are found particularly in the roots and seeds. Most human ingestions result from misidentification, because of its similarity to wild carrot (Daucus carota). Manifestations of toxicity are similar to those seen with nicotine, with an initial stimulatory phase that may include tachycardia, diaphoresis, tremor, and seizures. The subsequent depressant phase may involve bradycardia, hypotension, muscular paralysis, and coma. Initial gastrointestinal symptoms are often prominent. Meticulous supportive care is the mainstay of therapy. While death occurs rarely, it usually results from respiratory compromise.41 Asymptomatic patients who present with a possible ingestion should be observed for 4 to 6 hours.
Water Hemlock (Cicuta sp.)
Water hemlock is easily confused with the wild carrot (D. carota) or water parsnip (Pastinaca sativa), and may be mistaken for an edible tuber. The plant is often found growing along the borders of freshwater lakes and streams (Fig. 130–4). The plant contains cicutoxin and other toxic C17-polyacetylenes throughout, with the highest concentrations in the root. Cicutoxin is a highly potent convulsant due to its antagonism of GABAA (gamma-aminobutyric acid (subtype A)) receptors. Water hemlock is thought to be the most toxic plant in North America. Patients may suffer gastrointestinal symptoms and then rapidly develop seizures, respiratory distress, and rhabdomyolysis. Death may result from cardiopulmonary arrest complicating status epilepticus. Treatment consists of aggressive supportive care with early attention to definitive airway management and rapid escalation of anticonvulsant therapy. Benzodiazepines and phenobarbital should be used; phenytoin is unlikely to be beneficial.42 Early decontamination should be performed whenever it can be safely accomplished. Symptomatic patients should be admitted to an intensive care unit; at least 4 to 6 hours of observation is indicated for all patients with suspected ingestions.
Flowering top of water hemlock (Cicuta maculata) plant.
Plants Containing Toxalbumins
The castor bean (Ricinus communis) (Fig. 130–5) and rosary pea or jequirty bean (Abrus precatorius) contain the toxalbumins ricin and abrin, respectively. Less potent toxalbumins are also found in the physic nut (Jatropha curcas), black locust tree (Robinia pseudoacacia), and European mistletoe (Viscum album).3 Castor beans are used in the production of castor oil, and are cultivated commercially and as garden ornamentals throughout the United States.3 The bright scarlet and black seed of the rosary pea is very appealing to children, and is used for jewelry and in the making of maracas in the tropics. Because of reported fatalities after the ingestion of small numbers (range ∼2–20) of castor beans, ricin is regarded as highly toxic.43 However, the seeds of both plants have a thick waxy shell and must be chewed to liberate the toxin. Seeds swallowed whole are unlikely to produce toxicity. Ricin and abrin both inhibit ribosomal protein synthesis and exert pronounced effects on the GI tract. After oral exposure, vomiting and diarrhea leading to dehydration and delayed shock may occur. Castor bean ingestion has also been associated with GI bleeding and hemolysis. Onset of symptoms after ingestion is usually within 4 to 6 hours, but may take up to 10 hours.44 There is no antidote available, but oral castor or jequirty bean ingestions are rarely fatal in the presence of appropriate supportive care. Decontamination should be attempted in patients who are not at risk for aspiration. Symptomatic patients will require aggressive fluid resuscitation and may need vasopressor support.
Castor beans from Ricinus communis plant.
Plants Containing Colchicine
Both the autumn crocus (Colchicum autumnale) and the glory lily (Gloriosa superba) are members of the Lily family, which contain the antimitotic agent, colchicine.3 All parts of these plants contain colchicine. Poisoning, although rare, is serious and potentially fatal. Acutely, nausea, vomiting, abdominal pain, and diarrhea may result. In more severe intoxications, delayed effects may be seen, including GI hemorrhage, bone marrow suppression, multiorgan failure, and cardiovascular collapse. Fatalities have been reported in modern medical literature after the mistaken ingestion of colchicine-containing plants.45 There is no commercially available antidote, and prolonged supportive care may be required in severely poisoned patients. ED care entails circulatory support and early decontamination whenever possible, given the potential for significant morbidity and lack of an available antidote. Given the variable onset of symptoms (2–12 hours), even asymptomatic patients merit observation for an extended period.
Ackee fruit is a staple of the Jamaican diet and is grown in the West Indies, Florida, and Hawaii. The unripe fruit and seeds contain the toxins, hypoglycin A, and B, which inhibit metabolic pathways and can cause profound hypoglycemia.3 Toxicity, which also manifests severe gastrointestinal distress and CNS derangements, is known as Jamaican vomiting sickness. Lethargy, metabolic acidosis without ketonemia, seizures, and coma may occur.46 Patients can develop hepatic steatosis similar to that of Reye's syndrome. Fatalities are more common in children, possibly because of lower liver glycogen stores and a greater tendency to hypoglycemia. Treatment requires hospital admission, careful attention to blood glucose levels, antiemetics, hydration, and symptom-driven supportive care.
A variety of plants and plant products have been abused by adolescents and teenagers for their hallucinogenic effects. The seeds of morning glory (Ipomea violacea), Hawaiian baby woodrose (Argyreia nervosa), and Hawaiian woodrose (Merremia tuberosa) contain lysergic acid amides and can cause effects similar to lysergic acid diethylamide. Approximately 250 morning glory seeds must be chewed in order to achieve a psychedelic effect.47 Peyote (Lopophora williamsii) is a small, spineless cactus found in the southwestern United States and northern Mexico. The tops of the cactus are sliced off and dried, forming brown “buttons” that have a high content of mescaline. Salvia divinorum is a herb native to southern Mexico, which contains the potent hallucinogen salvinorin A. Most cases of hallucinogen intoxication are self-limited and symptoms generally subside in 4 to 6 hours.47 Intoxication may cause agitation and anxiety, requiring sedation with benzodiazepines. Patients should receive supportive treatment in a quiet, nonthreatening environment.