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Corresponding author: James H. Diaz, MD, MPH&TM, DrPH, Department of Environmental and Occupational Health Sciences, School of Public Health, and the Department of Anesthesiology/Critical Care, School of Medicine, Louisiana State University Health Sciences Center (LSUHSC) in New Orleans, 2020 Gravier Street, New Orleans, Louisiana 70112
Department of Environmental and Occupational Health Sciences, School of Public HealthDepartment of Anesthesiology/Critical Care, School of Medicine, Louisiana State University Health Sciences Center (LSUHSC) in New Orleans, New Orleans, LA
The American Association of Poison Control Centers has continued to report approximately 50,000 telephone calls or 8% of incoming calls annually related to plant exposures, mostly in children. Although the frequency of plant ingestions in children is related to the presence of popular species in households, adolescents may experiment with hallucinogenic plants; and trekkers and foragers may misidentify poisonous plants as edible. Since plant exposures have continued at a constant rate, the objectives of this review were (1) to review the epidemiology of plant poisonings; and (2) to propose a rapid toxidromic classification system for highly toxic plant ingestions for field use by first responders in comparison to current classification systems. Internet search engines were queried to identify and select peer-reviewed articles on plant poisonings using the key words in order to classify plant poisonings into four specific toxidromes: cardiotoxic, neurotoxic, cytotoxic, and gastrointestinal-hepatotoxic. A simple toxidromic classification system of plant poisonings may permit rapid diagnoses of highly toxic versus less toxic and nontoxic plant ingestions both in households and outdoors; direct earlier management of potentially serious poisonings; and reduce costly inpatient evaluations for inconsequential plant ingestions. The current textbook classification schemes for plant poisonings were complex in comparison to the rapid classification system; and were based on chemical nomenclatures and pharmacological effects, and not on clearly presenting toxidromes. Validation of the rapid toxidromic classification system as compared to existing chemical classification systems for plant poisonings will require future adoption and implementation of the toxidromic system by its intended users.
Although serious plant ingestions are uncommon, the American Association of Poison Control Centers (AAPCC) has continued to report approximately 50,000 telephone calls or 8% of incoming calls annually related to plant exposures, mostly nonlethal plant ingestions in children.
Although the frequency of plant ingestions in children is related to the presence of popular species in households, adolescents may experiment with hallucinogenic plants, and trekkers and foragers may misidentify poisonous plants as edible.
reported that only 17% of the plants could be identified by their common names, and only 13% could be identified as poisonous. Because plant exposures have continued at a relatively constant rate and the misidentification of poisonous plants has continued among outdoor enthusiasts and medical providers alike, the objectives of this review were 1) to review the epidemiology of plant poisonings and their outcomes, and 2) to propose a rapid toxidromic classification system for highly toxic plant ingestions in comparison with current classification systems.
Methods
To identify peer-reviewed, published scientific articles on herbal and plant poisonings and to develop a simplified toxidromic classification system for rapid diagnosis and management of plant poisonings for first responders and other urgent healthcare providers, Internet search engines, including PubMed, Medline, Ovid, Google, Google Scholar, and Cochrane, were queried with several key words. The key words included the following terms: plants, herbs, poisonous; poisonings, intentional, unintentional; ingestions, poisonous; foods, poisonous.
Plant poisoning reports were stratified as poisonings by either herbs or plants. Herbs were defined as seed-bearing, flowering plants without year-round woody stems as compared with other plants, shrubs, and trees with perennial woody stems. Case reports, case series, poison control center surveillance system reports, review articles, and toxicological studies were reviewed. Table 1 lists the scientific articles selected for review and stratifies them by their manuscript types.
Table 1Poisonous garden and wild plants capable of causing fatal toxicity
Solicited textbook chapters (n = 5) were used as references in this article, but were not considered peer-reviewed and were not selected as articles to be reviewed.
Number of scientific articles reviewed
Case reports
22
Case series
14
Surveillance studies, including Poison Control Center experiences
7
Reviews
6
Toxicological studies
1
Total articles selected and reviewed
50
Solicited textbook chapters (n = 5) were used as references in this article, but were not considered peer-reviewed and were not selected as articles to be reviewed.
The inclusion criteria for selected scientific articles included unintentional and intentional plant poisoning cases that were reported as individual cases or case series. The unintentional plant poisoning cases included attempted and successful suicides after plant, herb, and seed ingestions, but did not include any homicidal plant poisoning cases. Other inclusion criteria included periodic analyses of AAPCC Toxic Exposure Surveillance System (TESS) databases and other statewide poison control databases for descriptive epidemiological reviews of plant poisonings during the reporting period, 1983–2012.
Exclusion criteria for plant poisoning cases included any plant poisonings in which the toxic plant or herb was not identified and all textbook chapters that were considered solicited, not peer-reviewed scientific publications. Textbook chapters, however, provided the two different plant poisoning classification schemes for comparison with the proposed rapid toxidromic classification system (Table 2).
The well-documented cases of plant and herbal poisonings and the descriptions of their toxidromes were then identified from the selected scientific articles and classified into 4 distinctly different resultant toxidromes: 1) cardiotoxic, 2) neurotoxic, 3) cytotoxic, and 4) gastrointestinal/hepatotoxic.
Table 2A Comparison of the proposed and existing classification systems for plant poisonings
have periodically analyzed the AAPCC TESS databases on plant poisonings for more than 20 years. During the decade 1985–1994, these authors analyzed 912,534 plant exposures to determine the most common plant exposures.
Garden and household Philodendron species were the most commonly ingested species, followed by Dieffenbachia (dumb cane) species, Euphorbia pulcherrima (poinsettia), Capsicum annuum (red pepper), and Ilex (holly) species.
During the decade 2000 to 2009, these authors analyzed 668,111 plant exposures as single-substance exposures with the age of exposed patients known in most (n = 611,708) of the cases.
During the 26-year period, 1983 to 2009, there were 45 cases of fatal plant poisonings, with Datura species (family Solanaceae) and Cicuta maculata (water hemlock) responsible for 35.5% of the fatalities.
In a more recent annual analysis of the AAPCC TESS database in 2012, there were 49,373 plant exposures reported, and plants were the 19th most frequently ingested substances in human exposures, responsible for 1.84% of all substance exposures and 2.30% of single-substance exposures.
Plants were the ninth most frequently ingested foreign substance in children 5 years and younger, responsible for 2.78% of all substance exposures and 2.87% of single-substance exposures.
When stratified by plant types among all age groups, the top 3 categories responsible for 12.2% of all plant exposures in 2012 were by unknown, unspecified, or unidentified plants.
When positive plant identifications were made and reported in 2012, the top 6 most frequently confirmed plant exposures in descending order were to Phytolacca americanum (pokeweed or pokeberry), Spathiphyllum (peace lily) species, Ilex (holly) species, Philodendron species, Malus (apple and crabapple) species, and cardiac glycoside-containing plants, such as foxglove and oleander.
Several descriptive analyses of passive toxic exposure surveillance system data during the AAPCC reporting period 1983–2012 have confirmed that plant exposures are decreasing with time, but remain common and are rarely serious or fatal. Most plant exposures occurred in men and in children younger than 5 years, with a significant number of indoor exposures in children younger than 1 year. The most commonly ingested plants were popular indoor plants including Philodendron and many of the decorative holiday species, such as Ilex (holly) and Euphorbia (poinsettia). Fatal plant ingestions occurred most often in adolescents and adults intent on self-harm or hallucinogenic plant abuse.
A Toxidromic Classification System for Rapid Diagnosis of Plant Poisonings
As noted, significant confusion in properly identifying toxic vs nontoxic plants was initially reported by Harchelroad et al
in a study among emergency department staff who failed to identify poisonous plants most of the time (87%). Confusion in correctly identifying toxic plants continued in later descriptive analyses of AAPCC TESS data when the most common plant exposures were to “unknown, unspecified, or unidentified plants” in 12.2% of reported cases.
As a result, a toxidromic classification of plant poisonings was developed for use by first-responders and other urgent healthcare providers to assist in rapid identification of poisonous plant-induced toxidromes and to reduce confusion among highly toxic, less toxic, and nontoxic plants. The resultant 4 specific toxidromes of plant poisonings identified in the scientific literature could be stratified as cardiotoxic, neurotoxic, cytotoxic, and gastrointestinal/hepatotoxic poisonings, all of which have caused fatalities worldwide after both intentional and unintentional ingestions.
Table 2 compares the proposed rapid toxidromic classification system for plant poisonings with other presently used classification schemes. The current textbook classification schemes for plant poisonings were more complex, more confusing, and more cumbersome than the rapid classification system and were based on either plant chemicals or their pharmacological effects, not on plant-induced toxidromes.
The resultant 4 toxic plant ingestion toxidromes were defined as follows.
The cardiotoxic toxidrome was a constellation of digitalis toxicity–like symptoms and signs including nausea, vomiting, bradycardia, hyperkalemia, atrioventricular conduction blocks, and ventricular arrhythmias.
The neurotoxic toxidrome was a constellation of neurological symptoms and signs ranging from predominantly anticholinergic manifestations (mydriasis, facial flushing, dry skin, tachycardia, mental status changes, combative behavior, hallucinations) to nicotinic and neuromuscular manifestations (ataxia, tachycardia, hypertension, seizures, weakness, paralysis, respiratory failure).
The cytotoxic toxidrome was a constellation of abdominal pain, nausea, vomiting, watery-to-bloody diarrhea, weakness, dehydration, hypotension, metabolic acidosis, elevated serum creatinine, and multiorgan failure.
The gastrointestinal/hepatotoxic toxidrome was a constellation of manifestations ranging from upper gastrointestinal signs of drooling and dysphagia to abdominal pain with increasing hepatic enzyme levels and later jaundice.
These 4 toxidromes were further described by their mechanisms of toxicity and by examples of representative, causative species in Table 3.
Table 3Poisonous plants and herbs capable of causing fatal toxicity
Systemic toxicity
Plant poisons
Mechanisms of toxicity
Toxidromes
Antidotes; support
Genera/species
Common names
Cardiotoxic
Cardiac glycosides
Inhibit cellular Na/K ATPase, ↑ Ca in myocardium, ↑ vagal tone
Mimics digoxin toxicity: N, V, abdominal pain, sinus and junctional bradycardia, Vtach, Vfib
Digoxin-specific Fab, 10–20 vials
Convallaria majalis
Lily of the valley
Digitalis purpurea
Foxglove
Nerium oleander
Oleander
Ornithogalum umbellatum
Star of Bethlehem
Sodium channel openers
Open voltage-dependent Na channels causing persistent depolarization in cardiac conduction system and in motor neurons
AV block, bradycardia, ventricular arrhythmias, weakness, fasciculations, paralysis
None; specific antiarrhythmic therapy
Aconitum uncinatum
Monkshood, friar cap
Kalmia fatifolia
Mountain laurel
Leucothe spp
Sweet bells
Lyonia spp
Fetter bush
Pieris floribunda
Japanese Pieris
Rhododendron spp
Azalea, rhododendron
Veratrum viride
Hellebore
Zigadenus fremontii
Death camas
Sodium and calcium channel blocker with digitalis-like effects
Taxine alkaloids block Na and Ca channels and disrupt Na-K transport like digitalis glycosides
Stimulate preganglionic nicotinic receptors in the autonomic NS
↑ HR, ↑ BP, sweating, mydriasis, seizures, weakness, paralysis, coma
None; benzodiazepines for seizures
Baptisia spp
Wild indigo
Caulophyllum thalictroides
Blue cohosh
Conium maculatum
Poison hemlock
Laburnum anagryoides
Golden chaín
Lobelia siphilitica
Blue lobelia
Nicotiana longliflora
Tobacco
Other convulsants
Mechanisms include Ach imbalance, K channel block, false neurotransmitters, GABA antagonism (Cicuta, Strychnos), and hypoglycemia (Blighia)
Generalized tonic-clonic convulsions with loss of consciousness (except Strychnos opisthotonus) and postictal hypertonicity
None; benzodiazepines for seizures
Cicuta maculata
Water hemlock
Coriaria myrtifolia
Myrtle-leaved sumac
Spigelia marilandica
Pinkroot
Strychnos nux-vomica (import)
Strychnine
Blighia sapida (import)
Ackee fruit tree
Toxalbumins
Block protein synthesis by binding to the intracellular 60S ribosomal subunit
Abdominal pain, diarrhea, hematemesis, rapid multi-system organ failure, especially if abrin or ricin is aerosolized or injected
None; vasopressors
Abrus precatorius (import)
Jequirty pea, rosary pea
Mormodica spp
Balsam apple, balsam pear
Phoradendron spp
Southern mistletoe
Ricinus communis
Castor bean
Cytotoxic
Mitotic inhibitors
Block the polymerization of microtubules causing metaphase arrest of mitosis (used as cancer chemotherapeutics and to reduce inflammation in gout)
N, V, D, oral ulcers, GI bleeding, GI necrosis, initial leukocytosis followed by leukopenia
None; a colchicine Fab not available at present; consider colony-stimulating factors for BM suppression
Colchicum autumnalis
Autumn crocus
Catharanthus roseus (formerly Vinca rosea)
Periwinkle, vinca
Podophyllum pelatum
May apple
Cyanogenic glycosides
Hydrolyzed in GI tract and release CN (or hydrocyanic acid) which blocks mitochondrial electron chain with total cellular energy failure
Delayed abdominal pain, N, V, ↓ mental status, seizures, CV collapse, lactic acidosis, and multisystem organ failure
Correction of acidosis, inotropic support, and antidotal therapy with hydroxocobalamin alone, 5 grams intravenously over 15 minutes; or a combination of intravenous hydroxocobalamin and 25% sodium thiosulfate, 50 ml over 15 min.
Elderberry (leaves, stems, & roots; cooked berries are edible)
Pyrrolizidine alkaloids
Hepatically metabolized to pyrroles that damage endothelial linings of hepatic sinusoids and pulmonary vessels with centrilobular hepatic necrosis, hepatic veno-occlusion (Budd-Chiari syndrome), and pulmonary hypertension
Evidence In Support of The Four Resultant Poisonous Plant Toxidromes
Cardiotoxic poisonings
The cardiotoxic plants have been mistaken for edible herbs (dandelions) and bulbs (wild onions) or intentionally ingested in suicide attempts (foxglove, Japanese yew, and oleander) and include the cardiac glycosides, sodium channel activators, and dual sodium and calcium channel blockers. Poisonings after ingestions of plants containing cardiac glycosides resemble digitalis toxicity with initial nausea, vomiting, and abdominal pain, followed by bradycardia with predisposition to hyperkalemia, atrioventricular conduction blocks, and ventricular tachyarrhythmias.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
noted that poisonings with both common oleander (Nerium oleander) and yellow oleander (Thevetia peruviana) were frequent causes of toxicological emergencies throughout the tropical and subtropical world, with yellow oleander often ingested in suicide attempts throughout Southeast Asia, especially in India and Sri Lanka (Figure 1). The ingestion of either oleander species resulted in nausea, vomiting, abdominal pain, diarrhea, cardiac dysrhythmias, and hyperkalemia.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
The authors also noted that although digoxin-specific Fab antibody fragments were effective, but expensive, antidotes for oleander poisonings, the limited economic resources in most Southeast Asian countries restricted Fab fragment use.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
Although specifically designed for the management of digoxin toxicity, digoxin-specific Fab antibodies possess sufficient immunological cross-recognition capabilities to bind the cardiac glycoside antigens from several cardiotoxic plants, including Convallaria majalis (lily of the valley), Digitalis (foxglove) species, N oleander (common oleander), T peruviana (yellow oleander), and Ornithogalum umbellatum (star of Bethlehem) (Table 3).
Fab fragments are indicated in empiric intravenous doses (10–20 vials of 30–40 mg each) in cardiac glycoside plant poisoning cases with refractory bradycardia, hyperkalemia, and ventricular tachydysrhythmias, with or without elevated serum digoxin levels.
Although poisonings with cardiotoxic plants containing sodium channel openers, such as monkshood (Aconitum spp) and death camas (Zigadenus spp) mimic cardiac glycoside poisoning on initial presentation with bradycardia, heart blocks, and ventricular tachydysrhythmias, sodium channel activator poisonings are often accompanied by hypotension and cardiovascular collapse.
In addition, they are refractory to reversal with digoxin-specific Fab fragments, and may require intravenous atropine and sodium bicarbonate infusions, inotropic support, temporary cardiac pacing, and temporary extracorporeal life support with cardiopulmonary bypass (Figure 2).
Figure 2Zigadanus freemontii, death camas, all parts of which are toxic, contains several sodium channel activators that are refractory to reversal with digoxin-specific Fab. Source: Wikipedia (public domain).
in Delhi, India, reported 12 poisoning cases with 3 deaths after the ingestion of herbal therapy preparations containing a variety of plant cardiotoxins, including sodium channel–activating Aconitum (monkshood) species and cardiac glycoside–containing Oleander species. The authors described a poisoning toxidrome that mimicked digitalis poisoning with varying degrees of atrioventricular conduction blocks and ventricular tachyarrhythmias.
reported a series of 8 patients who ingested foothill death camas (Zigadenus paniculatus) bulbs after misidentifying them as wild onion bulbs while hiking in Juab County, Utah. All 8 patients were symptomatic with nausea, abdominal pain, dizziness, syncope, hypotension, and bradycardia, and 3 patients required hospital admission for supportive care.
Although poisonings with the sodium channel activators, such as death camas and hellebores (Veratrum spp), are refractory to Fab fragments, intravenous atropine and vasopressor administration may benefit patients with symptomatic bradycardia and hypotension.
in Manchester, New Hampshire, were among the first to report a series of Veratrum viride (false hellebore) poisoning cases (n = 6) in New England hikers who ingested false hellebores after misidentifying them as edible herbs. All patients presented with nausea, vomiting, bradycardia, and hypotension.
The authors recommended management of hellebore poisonings with atropine administration, supplemented with vasopressors as needed, for symptomatic bradycardia and hypotension.
The berries, leaves, and seeds of Taxus or yew trees contain cardiotoxic taxine alkaloids with both sodium and calcium channel blocking activities causing digitalis toxicity–like effects after ingestion, especially a predisposition to hyperkalemia and ventricular tachydysrhythmias.
Although taxine alkaloids are structurally similar to the digitalis-like plant glycosides, their hemodynamic effects, like those of the sodium channel activators, are refractory to reversal by digoxin-specific Fab.
reported the case of a 24-year-old man who chewed or swallowed 168 yew berry tree (Taxus cuspidate) seeds in a suicide attempt and was later witnessed by his parents to be diaphoretic with seizurelike activity. On arrival at the closest emergency department (ED), the patient was hypotensive, and the electrocardiogram demonstrated ventricular tachycardia that could not be cardioverted.
Although intravenous amiodarone, 300 mg, and diazepam, 5 mg, were administered, and an amiodarone infusion at 1 mg/min was instituted, ventricular tachycardia continued with resulting cardiovascular depression.
The patient was transferred to a regional intensive care unit, where an intravenous bolus of sodium bicarbonate, 100 mEq, was administered, and a sodium bicarbonate infusion was initiated at 37.5 mEq/hour.
The authors could not determine whether the correction of the cardiac tachydysrhythmias in this patient was the result of the amiodarone or sodium bicarbonate boluses and infusions, or their synergism.
Intravenous sodium bicarbonate, antiarrhythmics, and, possibly, calcium chloride with vasopressor support may be required to treat the simultaneous sodium and calcium channel blockade caused by the taxine alkaloids in yews and restore blood pressure and tissue perfusion.
All cardiotoxic plant poisonings may cause serious dysrhythmias and death and may require intensive care management with intravenous atropine and vasopressor support, antiarrhythmic therapy, temporary cardiac pacing or temporary cardiopulmonary bypass, and few specific antidotes with the exception of digoxin-specific Fab in cases of confirmed cardiac glycoside poisonings.
Neurotoxic poisonings
Like cardiotoxic plants, neurotoxic plants have also been mistaken for edible herbs (Queen Anne’s lace, parsnip, wild carrot) by hikers and foragers. They have been intentionally ingested for their stimulating, intoxicating, and hallucinogenic effects. The neurotoxic plants include the anticholinergic plants, nicotinic plants, convulsant or epileptogenic plants, and hallucinogenic plants (Table 3). In the United States, anticholinergic plant poisoning is frequently caused by several species of 3 closely related plant genera (Brugmasia, Datura, and Solandra) from the nightshade or Solanaceae family that contain combinations of 3 tropine or belladonna alkaloids including atropine, hyoscyamine, and scopolamine (Figure 3). In Europe and Asia, other members of the Solanaceae family, such as nightshade (Atropa belladonna) and mandrake (Mandragora officinarum), are frequent causes of anticholinergic plant poisonings. All of the tropine alkaloids cause central and peripheral anticholinergic toxidromes when plant parts, especially seeds, are ingested in salads or stews or brewed into teas. The tropine alkaloids inhibit acetylcholine receptors in the brain and parasympathetic nervous system, producing a classic toxidrome of flushed dry skin, fever, tachycardia, mydriasis, blurred vision, ileus, urinary retention, agitation, vertigo, and dysphoria, which may later progress to aggression, confusion, dysarthria, hallucinations, and, potentially, fatal coma.
Figure 3Brugmasia suaveolens, the angel’s chalice or trumpet plant, is a widely cultivated, flowering vine throughout the temperate world, all parts of which contain anticholinergic terpene alkaloids (atropine, hyoscyamine, and scopolamine). Teas brewed from plant leaves or flowers will cause a central and peripheral anticholinergic syndrome with delirium and hallucinations. Source: Source: Wikipedia (public domain).
reported a series of 9 cases of A belladonna berry poisonings in Turkey with all patients presenting with classic anticholinergic syndromes, and 1 patient suffering a subdural hematoma, an unusual complication. The authors noted that the berries of A belladonna could be easily mistaken for wild Caucasian blueberries in Turkey.
Another member of the Solanaceae family, mandrake or M officinarum, has been associated with witchcraft, and its berries have long been ingested in Eastern Europe as aphrodisiacs.
reported the case of a 35-year-old man in Greece who ingested unknown aphrodisiac berries and presented with a classic anticholinergic toxidrome that required 4 days of hospitalization for supportive care. Toxicological analyses of the berries and the patient’s urine detected 2 tropine alkaloids, hyoscyamine and scopolamine, and a botanist identified the aphrodisiac berries as mandrake berries.
reported a series of 7 cases in Australia of intentional ingestion of the flowers of angel’s trumpet, Datura arborea, for its intoxicating effects. All patients presented with an anticholinergic toxidrome, and 1 patient tragically drowned while hallucinating.
In addition to other varieties of angel’s trumpets (Brugmasia and Datura spp), another commonly ingested plant containing anticholinergic tropine alkaloids in the United States is Datura stramonium, also known as jimsonweed, Jamestown weed, or thorn apple.
reported a series of 9 cases of jimsonweed poisoning in teens intentionally chewing jimsonweed leaves or ingesting teas brewed from jimsonweed leaves or seed pods (thorn apples) in West Virginia. All patients presented with a classic constellation of anticholinergic effects including tachycardia, dry mouth, mydriasis, blurred vision, hallucinations, confusion, combative behavior, and difficulty urinating.
Beside accidental death while intoxicated and subdural hematoma, other serious complications of tropine alkaloid poisoning have included seizures, coma, myocardial infarction, rhabdomyolysis, pancreatitis, and tachyarrhythmias.
Physostigmine, an acetylcholinesterase inhibitor (1–2 mg intravenously, repeated as indicated every 30–60 minutes to a maximum total dose of 5–6 mg), can reverse a central anticholinergic syndrome in severe cases with coma and tachydysrhythmias.
Plants containing nicotine and nicotinelike alkaloids, such as anabasine, have also been intentionally chewed or ingested for their stimulating effects.
The plants containing nicotine and nicotinelike alkaloids that have been reported to cause human poisonings include Conium maculatum (poison hemlock), Nicotiana glauca (tree tobacco), Nicotiana tabacum (smoking tobacco), Laburnum anagyroides (golden chain tree), and Caulophyllum thalictroides (blue cohosh).
The nicotinic plant alkaloids act agonistically at nicotinic cholinergic receptors within the autonomic and central nervous systems, neuromuscular junctions, and adrenal medulla.
reported the case of a young adult man found dead in a field in Bexar County, Texas. There was no cause of death apparent at autopsy. The only positive toxicological finding was the presence of anabasine, the major nicotinic alkaloid in tree tobacco (N glauca), in the blood, liver, and other solid organs.
In addition to gastrointestinal absorption after cigarette ingestions, nicotinic plant alkaloids can also be absorbed rectally in home-remedy enemas with N tabacum (smoking tobacco) and transcutaneously during commercial tobacco harvesting, causing green tobacco sickness.
The poison hemlock plant, C maculatum, contains several neurotoxic piperidine alkaloids, primarily coniine, and has been used since antiquity as an intentional poison—most notably by the Athenians to execute Socrates.
Nicotinic plant poisoning after ingestion of poison hemlock will result in initial central nervous system (CNS) stimulation with myoclonus and hyperreflexia progressing to generalized tonic-clonic convulsions followed rapidly by weakness, neuromuscular paralysis, and respiratory failure.
They cause more serious poisonings and deaths after unintentional ingestions than most other poisonous plants worldwide every year because they are perennial weeds that resemble many frequently foraged, edible herbs including Queen Anne’s lace, parsnip, wild celery, and wild carrot.
Epileptogenic plants cause generalized tonic-clonic seizure activity through several mechanisms including gamma-aminobutyric acid antagonism in the CNS (water hemlock), postsynaptic inhibition of inhibitory glycine receptors in the spinal cord (strychnine), and profound hypoglycemia (imported unripe ackee or breadfruit tree fruit).
In 1992, a 23-year-old man and his 39-year-old brother were foraging for wild ginseng root in Maine and identified some similar herbs growing in a swampy area.
The younger man collected several of the plants and took 3 bites from the root of one. The older man took 1 bite of the root of the same plant (Figure 4).
Emergency medical personnel arrived 45 minutes after the younger man became ill and found him unresponsive with dilated pupils, cyanotic, profusely salivating, and having tonic-clonic convulsions separated by periods of apnea.
Figure 4The hollow stem of Cicuta maculata, water hemlock, has been used to make toy whistles, which have caused fatal cicutoxin poisonings after oral mucosal contact. Source: Personal collection.
Unintentional ingestions of the water hemlock plant, C maculata, cause most of the fatalities attributed to the misidentification of poisonous plants in the United States and Europe because the plant resembles many edible herbs and roots, including ginseng, parsnip, and wild carrot; it is lethal in very small quantities (2–3 cm of its root); and it grows in low-lying, marshy areas worldwide (Figure 4).
According to the US Centers for Disease Control and Prevention:Water hemlock causes most of the fatalities attributed to misidentification of poisonous plants because the plant is lethal in small quantities, resembles edible plants, and is found throughout North America … Persons who forage for edible wild plants [need] to be aware of and able to recognize poisonous plants in their area.
Water hemlock poisoning will produce initial abdominal pain and nausea within 15 to 90 minutes followed by vomiting, flushing, diaphoresis, salivation, vertigo, bronchorrhea, dyspnea, and cyanosis.
Loss of consciousness, seizures, and status epilepticus may follow initial symptoms and, if not lethal, may result in rhabdomyolysis, myoglobinuria, and acute renal failure.
Although derived from a nonnative Asian plant, Strychnos nux-vomica, strychnine is now cultivated in Hawaii and has been used for decades in the United States and Southeast Asia as a rodenticide, antiparasitic, antipyretic, and heroin adulterant.
Strychnine poisoning is unique among epileptogenic plant poisonings because it causes initial CNS stimulation manifested by fasciculations and hyperreflexia followed by severe tonic-clonic muscle spasms with opisthotonic posturing without loss of consciousness.
Severe muscular spasms can result in tendon ruptures and vertebral fractures and are often associated with hyperpyrexia, rhabdomyolysis, and acute renal failure.
There are no antidotes for the epileptogenic plant poisonings, and successful management strategies have included early airway protection and sedation and muscular relaxation with benzodiazepines and neuromuscular blockers, especially in strychnine poisonings.
Although now banned by several countries and controlled in most US states, Salvia or S divinorum is often marketed on the Internet as a legal alternative to marijuana and illicit drugs.
The psychoactive agent in Salvia is salvinorin A, a diterpene and selective kappa-opioid receptor agonist, which produces psychomimetc effects after ingestion of teas brewed from leaves resembling the adverse effects caused by serotonergic agonists, selective serotonin reuptake inhibitors, and N-methyl-d-aspartate glutamate (NMDA) antagonists.
The psychoactive agents in morning glory seeds include the ergot alkaloids, ergonovine and lysergic acid amide, which resemble lysergic acid diethylamide stereochemically and cause similar psychomimetic effects.
The psychedelic effects of Salvia leaf teas and morning glory seeds or brews are similar with blunted affect, déjà vu, dissociation, uncontrollable laughter, multidimensional motion sensation, merging objects, colorful visual hallucinations, and paranoia.
The cytotoxic plants include 1) the toxalbumins, the toxin (ricin) of one of which, the castor bean (Ricinus communis) has been weaponized; 2) the mitotic inhibitors, many of which are highly effective as cancer chemotherapeutics; and 3) the cyanogenic plant glycosides contained in the kernels of several fruits, including apples, apricots, cherries, peaches, and plums (Table 3). Many are popular household (crocus) and garden (crocus, vinca) plants that have been used to make anti-inflammatory drugs (colchicine from crocus) and jewelry (castor bean, jequirity or rosary pea) and to treat cancer (vinblastine and vincristine from vinca, podophyllotoxin from mayapple).
The toxalbumins are all plant lectins usually concentrated in seeds that inhibit protein synthesis by binding to intracellular 60S ribosomal subunits and resulting in initial gastrointestinal toxicity followed by multiorgan failure.
The toxalbumin-containing plants include the castor bean plant (R communis), formerly grown commercially for castor oil–containing pharmaceuticals and motor oils; the jequirity pea or rosary plant (Abrus precatorius), a Caribbean tropical vine introduced into South Florida; the balsam apple (Mormordica spp), a tropical, creeping vine with fruit used in home remedies topically for wound healing and orally for diabetes; and several varieties of mistletoe (Phoradendron spp), the parasitic epiphytes of deciduous trees and popular Christmas decorations.
Ricin and abrin can be released in highly toxic amounts when the hard seeds of castor bean plants or jequirity pea vines are chewed, swallowed, and ingested, or when these toxalbumins are weaponized for injection or for aerosolization.
Both castor bean and jequirity pea seeds are still used by Caribbean and West African folk artists to make colorful jewelry and rosary beads that are frequently imported and may be accidently ingested by children (Figure 5, Figure 6).
There are no antidotes or vaccines for toxalbumin toxicity, and management of poisonings must begin immediately with intravenous fluid resuscitation and vasopressor support for cardiovascular collapse.
Figure 5Colorful Ricinus communis or castor bean seeds often used in tropical native jewelry will release the toxalbumin, ricin, a powerful protein synthesis inhibitor, when chewed, with severe gastrointestinal toxicity and potential multisystem organ failure. However, the ingestion of intact seeds does not cause toxicity and will not require therapy. Source: United States Department of Agriculture (USDA).
Figure 6Colorful Abrus precatorius or jequirity or rosary pea seeds often used in tropical native jewelry will release the toxalbumin, abrin, when chewed, with severe gastrointestinal toxicity and potential multisystem organ failure. However, the ingestion of intact seeds does not cause toxicity and will not require therapy. Source: United States Department of Agriculture (USDA).
Ricin is among the most lethal natural toxins known, and the castor bean plant, R communis, from which it can be easily obtained, grows throughout the world. The lethal dose of ricin may be as little as 500 μg or 4 chewed beans in an adult and 3 chewed beans in a child.
Ricin gained attention as a weapon when a ricin pellet fired by an umbrella gun was used to assassinate Bulgarian dissident Geogi Markov in London in 1978.
reported 2 cases of ricin poisoning in children in the United States who had chewed and swallowed brightly colored castor beans (Figure 5). The patients presented with repeated vomiting, diarrhea, dehydration, and elevated serum creatinine levels.
reported the fatal case of a 42-year-old Saudi man who ingested an herbal mixture containing castor bean powder and presented with bloody diarrhea and hypovolemic shock that progressed to cardiorespiratory arrest.
Abrin contained in jequirity or rosary pea seeds is another natural toxalbumin with a lethal dose in man as low as 0.1 to 1.0 μg/kg.
reported the case of an 18-month-old boy who presented to the ED with abrupt onset of fever, vomiting, diarrhea, and dehydration. The parents observed 3 consecutive diapers that contained colorful red seeds with black end bands later identified by the regional poison control center as A precatorius seeds (Figure 6).
reported the case of a 19-year-old man in India who ingested crushed rosary pea seeds after a family quarrel and presented with abdominal pain, vomiting, and bloody diarrhea, followed by mental status changes and seizures. Magnetic resonance imaging of the brain demonstrated demyelination bilaterally in the medial temporal lobes, an unusual complication of abrin poisoning.
reported the attempted suicide in a 20-year-old man who chewed and swallowed 10 rosary pea seeds that he had obtained by mail order over the Internet. He presented to the ED with vomiting and watery diarrhea for 6 to 8 hours.
The indigenous plants containing mitotic inhibitors include autumn crocus (Colchium autumnalis), vinca or periwinkle (Catharanthus roseus), and mayapple (Podophyllum pelatum).
The mitotic inhibitors all contain similar cytotoxic plant alkaloids that can inhibit polymerization of microtubules and cause metaphase arrest of mitosis, especially in rapidly dividing cells in the gastrointestinal tract and bone marrow.
Cytotoxic alkaloids derived from these plants have been used to treat gout (colchicine), condylomata acuminata (podophyllin), and cancer (vinblastine, vincristine, paclitaxel, podophyllotoxin).
Ingestions of any parts of these plants will cause initial oropharyngeal pain followed by severe gastrointestinal symptoms within hours, including intense abdominal pain and severe, profuse, and persistent diarrhea that may lead to volume depletion and electrolyte imbalance.
Delayed toxic effects may include bone marrow toxicity, manifesting initially as leukocytosis followed by leukopenia, peripheral neuropathy, ataxia, seizures, and encephalopathy.
There are no antidotes for mitotic inhibitor toxicity, and management of poisonings must begin immediately with intravenous fluid resuscitation and vasopressor support for cardiovascular collapse.
reported the case of a 68-year-old woman who had picked, cooked, and eaten leaves of colchicine-containing Colchium autumnale (autumn crocus) that she had mistaken outdoors for edible wild leeks. A few hours later, she developed abdominal pain, nausea, vomiting, and diarrhea with dehydration.
By day 3, the patient had developed cardiogenic shock with multiorgan failure and was admitted to a regional intensive care unit with a mean arterial pressure of 50 mm Hg and left ventricular ejection fraction of 5% to 10%.
Pancytopenia and coagulopathy developed on day 4 and required massive transfusion with blood products including red blood cell (15 units) and platelet (13 units) concentrates and 7 units of fresh-frozen plasma.
The authors concluded that ECLS might be useful as a bridge to recovery in severely poisoned patients with colchicine poisoning and refractory circulatory shock.
Many edible fruits of the Malus (apple, crabapple) and Prunus (apricots, cherries, peaches, plums) species contain cyanide-releasing glycosides within their kernels.
In addition, some ornamental plants, such as hydrangeas, and even trees (elder) also contain cyanogenic glycosides in their flowers (hydrangeas) or leaves, stems, and roots (elder).
After ingestion of toxic parts of cyanogenic plants, cyanogenic glycosides have to be hydrolyzed in the gastrointestinal tract before they release cyanide ion, which inhibits the final step in the mitochondrial electron transport chain and causes cytotoxicity from limited adenosine triphosphate production and cellular energy failure.
After an incubation period of several hours, a constellation of lethargy, diaphoresis, abdominal pain, nausea, and vomiting ensues and is followed by mental status changes, ataxia, vertigo, stupor, seizures, cardiovascular instability, and multisystem organ failure.
On August 26, 1983, 8 persons with acute gastrointestinal (acute abdominal pain, nausea, vomiting) and neurological (weakness, dizziness, numbness, stupor in 1 patient) were evacuated from a remote, rural religious center in Monterey County, California, to a regional hospital for treatment of possible cyanide poisoning.
Two days before the outbreak, religious center staff had prepared a fruit juice drink in a stainless steel press made from the crushed berries, leaves, and stems of elder trees, Sambucus mexicana (Figure 7).
The juice was served the next day to a group of 25 people, and the severity of the presenting symptoms was correlated with the amount of fruit juice consumed.
Figure 7Ripe elderberries on the American elder tree, Sambucus mexicana. Although the ripe berries are edible and often used in juices and jams, the leaves, stems, bark, and roots of elderberry trees contain cyanogenic glycosides capable of causing symptomatic cyanide poisoning. Source: Wikipedia (public domain).
Although elderberries are safe to consume, especially when cooked, the leaves, stems, and roots should not be crushed when preparing juices from wild elderberries.
Initial management should include correction of acidosis, inotropic support, and antidotal therapy with hydroxocobalamin alone, 5 g intravenously over 15 minutes, or a combination of intravenous hydroxocobalamin and 25% sodium thiosulfate, 50 mL over 15 minutes.
The plants causing gastrointestinal toxicity include the hepatotoxic pyrrolizidine alkaloids and the calcium oxalate injectors, which are popular household plants and include many cultivars of Caladium, Dieffenbachia, Philodendron, Schefflera, and Spathiphyllum.
Because intense oropharyngeal pain from mucosal injection of calcium oxalate crystals will limit further ingestion, chewing, and swallowing, most calcium oxalate plant ingestions are not very hazardous and can be managed with copious irrigation, demulcents, viscous lidocaine, and oral analgesics.
Ocular exposures to the sap of calcium oxalate–containing plants may cause severe eye pain, which should be managed with copious irrigation, topical anesthesia, and referral to an ophthalmologist for slit-lamp evaluation and follow-up, if indicated.
For many years, there was consensus that the scientific literature ascribed significantly more morbidity to household Dieffenbachia (dumb cane) exposures than could be supported by observations made by experienced clinical practitioners.
In a study designed to determine whether the symptoms of Dieffenbachia exposures described in case reports and published in the scientific literature were consistent with years of clinical experience, Pedaci et al
conducted an Internet-based comparative study of 23 published reports of Dieffenbachia exposures with the symptom information obtained from the AAPCC TESS database for the period 1993–1996. There were some consistent similarities in the symptoms of Dieffenbachia exposures reported in the literature and in the TESS data, eg, the concordance of oral irritation was 92.6% in the case reports vs 18.2% in the TESS data.
Similar wide disparities, however, continued throughout the concordances between other symptoms reported in the scientific literature vs the TESS data, such as throat irritation (22.2% vs 2.3%), ocular irritation (44.4% vs 1.7%), and many others.
The authors of the study concluded that the scientific literature did indeed portray Dieffenbachia exposures as associated with more morbidity than what was reported in the AAPCC TESS clinical practice database.
later (2005) reported a case of an aortoesophageal fistula with exsanguinating hemorrhage in a 12.5-year-old girl 5 weeks after eating 1 leaf of Dieffenbachia picta in a suicide attempt. Emergency exploration of the cervical esophagus, laparotomy, and thoracotomy were required to identify the source of the massive gastrointestinal hemorrhage as an aortoesophageal fistula between the ascending aorta and thoracic esophagus, control the bleeding surgically, and save the child’s life.
Although calcium oxalate injectors rarely cause potentially fatal poisonings, they are responsible for the most frequent plant ingestions, rarely with any serious consequences, and have been used in suicide attempts.
The indigenous plants containing pyrrolizidine alkaloids in all parts include the very fragrant and popular ornamental house and garden species of Crotalaria (yellow rattlebox) and Sesbania (scarlet rattlebox).
Chronic low-dose ingestions of plant pyrrolizidine alkaloids in herbal teas and dietary supplements may result in insidious hepatotoxicity from veno-occlusive disease indistinguishable from the Budd-Chiari syndrome.
After ingestion, the pyrrolizidine alkaloids are hepatically metabolized to highly alkaline pyrroles that can cause caustic burns of the lining epithelium of hepatic sinusoids and, less commonly, of pulmonary vessels.
There are no antidotes for pyrrolizidine toxicity; supportive management may allow time for hepatic regeneration, and hepatic transplantation may be indicated for acute or chronic liver failure.
Because most plant exposures are to nontoxic plants or to relatively nontoxic amounts of toxins in poisonous plants, the general management of poisonings by unknown plants should be supportive and based on the 4 presenting toxidromes. With the exception of animal-derived digoxin-specific Fab antibodies (Digibind, DigiFab) to inactivate ingested plant-derived cardiac glycosides and physostigmine to reverse plant toxin-induced central anticholinergic syndromes, there are few effective antidotes for most plant toxins. Most gastrointestinal decontamination techniques for management of plant poisonings are no longer indicated. Oral activated charcoal administration may be indicated if the poisoned patient is conscious, alert, and cooperative, and presents within 60 minutes of potentially dangerous or lethal plant ingestions. Whole bowel irrigation does offer an opportunity to completely cleanse the gastrointestinal tract of poisonous plant matter but should be reserved only for patients who have ingested significant amounts of poisonous plant matter that will release toxins slowly over time in the gastrointestinal tract such as chewed apple, cherry, or apricot kernels containing cyanogenic glycosides or oleander seeds containing cardiotoxic glycosides. Severe poisonings with cardiotoxic plants, toxalbumins, and colchicine may result in cardiovascular collapse and multiorgan failure and require extracorporeal life support.
Conclusions
Colorful cultivated and wild plants and their fruits and seeds, some of which may be highly toxic, will continue to attract the mouthing behaviors of infants and toddlers.
Even experienced trekkers, foragers, and chefs may occasionally misidentify poisonous plants and herbs as edible. A simple toxidromic classification system of plant poisonings designed for urgent-care first-responders may permit more rapid differential diagnoses of highly toxic vs nontoxic plant ingestions both in households and outdoors, direct earlier management of potentially serious plant ingestions, and reduce costly inpatient evaluations for inconsequential plant ingestions. Validation of a rapid toxidromic classification system as compared with existing, cumbersome classification systems for plant poisonings will require future adoption and implementation of the toxidromic system by its intended users with time.
References
Watson W.A.
Litovitz T.L.
Klein-Schwartz W.
et al.
2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System.
A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
☆Financial support: Support was provided by departmental and institutional sources. The author has no financial interests or other acknowledgments to disclose.
Solicited textbook chapters (n = 5) were used as references in this article, but were not considered peer-reviewed and were not selected as articles to be reviewed.
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