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Poisoning by Herbs and Plants: Rapid Toxidromic Classification and Diagnosis

  • James H. Diaz
    Correspondence
    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
    Affiliations
    Department of Environmental and Occupational Health Sciences, School of Public Health

    Department of Anesthesiology/Critical Care, School of Medicine, Louisiana State University Health Sciences Center (LSUHSC) in New Orleans, New Orleans, LA
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      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.

      Key words

      Introduction

      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.
      • 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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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.
      • Bohnert A.S.
      • Fudalej S.
      • Ilgen M.A.
      Increasing poisoning mortality rates in the United States, 1999–2006.
      • Harchelroad F.
      • Scalise J.A.
      • Dean B.S.
      • Krenzelok E.P.
      Identification of common houseplants in the emergent care setting.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.M.
      Plant exposures: a state profile of the most common species.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      In a study designed to assess the ability of emergency department staff doctors and nurses to correctly identify poisonous plants, Harchelroad et al
      • Harchelroad F.
      • Scalise J.A.
      • Dean B.S.
      • Krenzelok E.P.
      Identification of common houseplants in the emergent care setting.
      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
      Types of scientific articles selected for review
      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 reports22
      Case series14
      Surveillance studies, including Poison Control Center experiences7
      Reviews6
      Toxicological studies1
      Total articles selected and reviewed50
      low asterisk 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.
      • 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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.M.
      Plant exposures: a state profile of the most common species.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      • Vohra R.
      • Seefeld A.
      • Cantrell F.L.
      • Clark R.F.
      Salvia divinorum: exposures reported to a statewide poison control system over 10 years.
      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).
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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
      Classification systemsProposed new classificationGoldfrank et al classification
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Nelson et al classification
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      Classification methodsClassification by toxidromesClassification by “pharmacognosy”Classification by chemical compounds
      Classification categoriesCardiotoxicAlkaloidsAnticholinergics (antimuscarinics)
      NeurotoxicGlycosidesCalcium oxalate crystals
      CytotoxicTerpenes and resinsCardioactive steroids and glycosides
      Gastrointestinal/hepatotoxicProteins, peptides, and lectinsCyanogenic compounds
      Phenols and phenylpropanoidsGastrointestinal poisons
      Mitotic inhibitors
      Nicotinelike alkaloids
      Pyrrolizidine alkaloids
      Sodium channel activators
      Toxalbumins

      Results and Discussion

      The Epidemiology and Outcomes of Plant Poisonings

      Krenzelok et al
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.M.
      Plant exposures: a state profile of the most common species.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      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.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.M.
      Plant exposures: a state profile of the most common species.
      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.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.M.
      Plant exposures: a state profile of the most common 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.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      Male patients accounted for 52.2% of the plant ingestions and more than 60% of the moderate and severe outcomes.
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      The most severe outcomes occurred in those who intentionally ingested plants for their hallucinogenic effects or to commit suicide.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      Children younger than 5 years accounted for 81.2% of the plant exposures.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      Within the pediatric exposure category during the decade 2000 to 2009, 57.8% of the plant exposures occurred in children younger than 1 year.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and fatalities.
      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.
      • Krenzelok E.P.
      • Mrvos R.
      Friends and foes in the plant world: a profile of plant ingestions and 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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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
      • Harchelroad F.
      • Scalise J.A.
      • Dean B.S.
      • Krenzelok E.P.
      Identification of common houseplants in the emergent care setting.
      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.
      • Mowry J.B.
      • Spyker D.A.
      • Cantilena L.R.
      • Bailey J.E.
      • Ford M.
      2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report.
      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.
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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 toxicityPlant poisonsMechanisms of toxicityToxidromesAntidotes; supportGenera/speciesCommon names
      CardiotoxicCardiac glycosidesInhibit cellular Na/K ATPase, ↑ Ca in myocardium, ↑ vagal toneMimics digoxin toxicity: N, V, abdominal pain, sinus and junctional bradycardia, Vtach, VfibDigoxin-specific Fab, 10–20 vialsConvallaria majalisLily of the valley
      Digitalis purpureaFoxglove
      Nerium oleanderOleander
      Ornithogalum umbellatumStar of Bethlehem
      Sodium channel openersOpen voltage-dependent Na channels causing persistent depolarization in cardiac conduction system and in motor neuronsAV block, bradycardia, ventricular arrhythmias, weakness, fasciculations, paralysisNone; specific antiarrhythmic therapyAconitum uncinatumMonkshood, friar cap
      Kalmia fatifoliaMountain laurel
      Leucothe sppSweet bells
      Lyonia sppFetter bush
      Pieris floribundaJapanese Pieris
      Rhododendron sppAzalea, rhododendron
      Veratrum virideHellebore
      Zigadenus fremontiiDeath camas
      Sodium and calcium channel blocker with digitalis-like effectsTaxine alkaloids block Na and Ca channels and disrupt Na-K transport like digitalis glycosidesMydriasis, abdominal pain, weakness, emesis, diaphoresis, seizures, ↓ BP, refractory Vtach, ↑ KNone; digoxin-specific Fab ineffective; amiodarone and NaHCO3Taxus spp.yews only. Paclitaxel, a mitotic inhibitor derived from bark of Pacific yew (T. brevifolia) is used to treat and prevent breast cancerAll evergreen yew trees and shrubs
      AnticholinergicBlock Ach at muscarinic receptors in brain and parasympathetic NSFever, dry flushed skin, mydriasis, tachycardia, dysphoria, delirium, ileus, atonic bladder, seizures, paralysisPhysostigmine, 1–2 mg IV; children, 0.02 mg/kgAtropa belladonnaDeadly nightshade
      Brugmasia candidaAngel’s trumpet
      Datura stramoniumJimson weed
      NeurotoxicHallucinogenicSalvinorin A is a complete opioid kappa receptor agonist; lysergimides in morning glory seeds inhibit serotonin reuptakeInebriation, laughter, depersonalization, dissociation, visual hallucinations, paranoiaNone; benzodiazepinesSalvia divinorumDiviner’s (seer’s) sage
      Morning glories:
      Ipomoea tricolorHeavenly blue morning glory
      Turbina (Rivea) corymbosaChristmas vine morning glory
      NicotinicStimulate preganglionic nicotinic receptors in the autonomic NS↑ HR, ↑ BP, sweating, mydriasis, seizures, weakness, paralysis, comaNone; benzodiazepines for seizuresBaptisia sppWild indigo
      Caulophyllum thalictroidesBlue cohosh
      Conium maculatumPoison hemlock
      Laburnum anagryoidesGolden chaín
      Lobelia siphiliticaBlue lobelia
      Nicotiana longlifloraTobacco
      Other convulsantsMechanisms 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 hypertonicityNone; benzodiazepines for seizuresCicuta maculataWater hemlock
      Coriaria myrtifoliaMyrtle-leaved sumac
      Spigelia marilandicaPinkroot
      Strychnos nux-vomica (import)Strychnine
      Blighia sapida (import)Ackee fruit tree
      ToxalbuminsBlock protein synthesis by binding to the intracellular 60S ribosomal subunitAbdominal pain, diarrhea, hematemesis, rapid multi-system organ failure, especially if abrin or ricin is aerosolized or injectedNone; vasopressorsAbrus precatorius (import)Jequirty pea, rosary pea
      Mormodica sppBalsam apple, balsam pear
      Phoradendron sppSouthern mistletoe
      Ricinus communisCastor bean
      CytotoxicMitotic inhibitorsBlock 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 leukopeniaNone; a colchicine Fab not available at present; consider colony-stimulating factors for BM suppressionColchicum autumnalisAutumn crocus
      Catharanthus roseus (formerly Vinca rosea)Periwinkle, vinca
      Podophyllum pelatumMay apple
      Cyanogenic glycosidesHydrolyzed in GI tract and release CN (or hydrocyanic acid) which blocks mitochondrial electron chain with total cellular energy failureDelayed abdominal pain, N, V, ↓ mental status, seizures, CV collapse, lactic acidosis, and multisystem organ failureCorrection 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.Eriobotrya japonicaJapanese plum, loquat (fruit pits)
      Hydrangea macrophyllaHydrangea
      Malus sppApple, crab apple (fruit pits)
      Manihot esculentaCassava, tapioca (roots)
      Prunus sppApricot, cherry choke cherry, peach, plum (fruit pits)
      Sambucus mexicanaElderberry (leaves, stems, & roots; cooked berries are edible)
      Pyrrolizidine alkaloidsHepatically 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 hypertensionAbdominal pain, jaundice, cirrhosis, hepatic necrosis, hepatoma, coagulopathy, pulmonary and portal hypertensionNone; supportive therapy for liver failure, liver transplantCrotalaria sppYellow rattlebox
      Heliotropium curassavicumSeaside heliotrope
      Senecio sppRagwort, groundsel
      Sesbania grandifloraScarlet wisteria, scarlet rattlebox
      GI/hepatotoxicCalcium oxalate crystal injectorsA large group of common interior plants, all parts of which when chewed will launch calcium oxalate crystals from specialized launchers (raphides)Intense oral and pharyngeal pain, salivation, laryngeal edema, upper GI perforation possible (aorto-duodenal fistula has been reported)Demulcents or cold water, irrigation, viscous lidocaine; endoscopy to rule out mucosal injuriesCaladium sppCaladium
      Dieffenbachia sppDumb cane, mother-in-law’s tongue
      Epipremnum (Pothos) aureumGolden pothos, devil’s ivy
      Philodendron sppPhilodendron
      Schefflera (Brassia) actinophyllaSchefflera, umbrella tree
      Spathiphyllum sppPeace lily, white anthurium
      Ach, acetylcholine; AV, atrioventricular; BM, bowel movement; BP, blood pressure; CN, cyanide (hydrocyanic acid); CV, cardiovascular; D, diarrhea; GABA, gamma-aminobutyric acid; GI, gastrointestinal; HR, heart rate; N, nausea; NS, nervous system; V, vomiting; Vfib, ventricular fibrillation; Vtach, ventricular tachycardia.

      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Bandara V.
      • Weinstein S.A.
      • White J.
      • Eddleston M.
      A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
      • DeSilva H.A.
      • Fonseka M.M.D.
      • Pathmeswaran A.
      • et al.
      Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomized, placebo-controlled trial.
      • Ohuchi S.
      • Izumoto H.
      • Kamata J.
      • et al.
      A case of aconitine poisoning saved with cardiopulmonary bypass [in Japanese].
      • Peterson M.C.
      • Rasmussen G.J.
      Intoxication with foothill camas (Zigadenus paniculatus).
      • West P.
      • Horowitz B.Z.
      Zigadenus poisoning treated with atropine and dopamine.
      • Dwivedi S.
      • Aggarwal A.
      • Sharma V.
      Cardiotoxicity from ‘safe’ herbomineral formulations.
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      • Schep L.J.
      • Schmierer D.M.
      • Fountain J.S.
      Veratrum poisoning.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      In a 2010 review, Bandara et al
      • Bandara V.
      • Weinstein S.A.
      • White J.
      • Eddleston M.
      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.
      • Bandara V.
      • Weinstein S.A.
      • White J.
      • Eddleston M.
      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.
      • Bandara V.
      • Weinstein S.A.
      • White J.
      • Eddleston M.
      A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
      Most oleander poisoning cases in Southeast Asia were managed with oral activated charcoal administration and supportive care.
      • Bandara V.
      • Weinstein S.A.
      • White J.
      • Eddleston M.
      A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning.
      • DeSilva H.A.
      • Fonseka M.M.D.
      • Pathmeswaran A.
      • et al.
      Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomized, placebo-controlled trial.
      Figure thumbnail gr1
      Figure 1Nerium oleander, a Mediterranean native, contains the cardiac glycoside, oleandrin, in all of its parts. Source: Wikipedia (public domain).
      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).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Ohuchi S.
      • Izumoto H.
      • Kamata J.
      • et al.
      A case of aconitine poisoning saved with cardiopulmonary bypass [in Japanese].
      • Peterson M.C.
      • Rasmussen G.J.
      Intoxication with foothill camas (Zigadenus paniculatus).
      • West P.
      • Horowitz B.Z.
      Zigadenus poisoning treated with atropine and dopamine.
      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).
      • Ohuchi S.
      • Izumoto H.
      • Kamata J.
      • et al.
      A case of aconitine poisoning saved with cardiopulmonary bypass [in Japanese].
      • Peterson M.C.
      • Rasmussen G.J.
      Intoxication with foothill camas (Zigadenus paniculatus).
      • West P.
      • Horowitz B.Z.
      Zigadenus poisoning treated with atropine and dopamine.
      Figure thumbnail gr2
      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 2011, Dwivedi et al
      • Dwivedi S.
      • Aggarwal A.
      • Sharma V.
      Cardiotoxicity from ‘safe’ herbomineral formulations.
      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.
      • Dwivedi S.
      • Aggarwal A.
      • Sharma V.
      Cardiotoxicity from ‘safe’ herbomineral formulations.
      In 2003, Peterson and Rasmussen
      • Peterson M.C.
      • Rasmussen G.J.
      Intoxication with foothill camas (Zigadenus paniculatus).
      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.
      • Peterson M.C.
      • Rasmussen G.J.
      Intoxication with foothill camas (Zigadenus paniculatus).
      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.
      • West P.
      • Horowitz B.Z.
      Zigadenus poisoning treated with atropine and dopamine.
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      • Schep L.J.
      • Schmierer D.M.
      • Fountain J.S.
      Veratrum poisoning.
      The Veratrum species hellebores are also sodium channel openers and can cause significant bradycardia and hypotension on ingestion.
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      • Schep L.J.
      • Schmierer D.M.
      • Fountain J.S.
      Veratrum poisoning.
      In 1990, Jaffe et al
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      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.
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      The authors recommended management of hellebore poisonings with atropine administration, supplemented with vasopressors as needed, for symptomatic bradycardia and hypotension.
      • Jaffe A.M.
      • Gephardt D.
      • Courtemanche L.
      Poisoning due to ingestion of Veratrum viride (false hellebore).
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      In 2009, Pierog et al
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      The amiodarone infusion was discontinued when the wide complex tachycardia resolved and normal sinus rhythm and blood pressure were restored.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • Pierog J.
      • Kane B.
      • Kane K.
      • Donovan J.W.
      Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy.
      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.
      • McHenry L.E.
      • Hall R.C.
      Angel’s trumpet. Lethal and psychogenic aspects.
      • Hayman J.
      Datura poisoning—the Angel’s Trumpet.
      • Greene G.S.
      • Patterson S.G.
      • Warner E.
      Ingestion of angel’s trumpet: an increasingly common source of toxicity.
      • Francis P.D.
      • Clarke C.F.
      Angel trumpet lily poisoning in five adolescents: clinical findings and management.
      • Firestone D.
      • Sloane C.
      Not your everyday anisocoria: angel’s trumpet ocular toxicity.
      • Andreola B.
      • Piovan A.
      • Da Dalt L.
      • Filippini R.
      • Cappelletti E.
      Unilateral mydriasis due to Angel’s trumpet.
      • Cikla U.
      • Turkmen S.
      • Karaca Y.
      • et al.
      An Atropa belladonna L. poisoning with acute subdural hematoma.
      • Nikolaou P.
      • Papoutsis I.
      • Stefanidou M.
      • et al.
      Accidental poisoning after ingestion of “aphrodisiac” berries: diagnosis by analytical toxicology.
      • Urich R.W.
      • Bowerman D.L.
      • Levisky J.A.
      • Pflug J.L.
      Datura stramonium: a fatal poisoning.
      Centers for Disease Control and Prevention (CDC)
      Jimsonweed poisoning associated with a homemade stew—Maryland, 2008.
      • Spina S.P.
      • Taddei A.
      Teenagers with Jimson weed (Datura stramonium) poisoning.
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      • Tiongson J.
      • Salen P.
      Mass ingestion of jimson weed by eleven teenagers.
      • Thabet H.
      • Brahmi N.
      • Amamou M.
      • Ben Salah N.
      • Hédhili A.
      • Yacoub M.
      Datura stramonium poisonings in humans.
      Figure thumbnail gr3
      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).
      In 2012, Cikla et al
      • Cikla U.
      • Turkmen S.
      • Karaca Y.
      • et al.
      An Atropa belladonna L. poisoning with acute subdural hematoma.
      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.
      • Cikla U.
      • Turkmen S.
      • Karaca Y.
      • et al.
      An Atropa belladonna L. poisoning with acute subdural hematoma.
      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.
      • Nikolaou P.
      • Papoutsis I.
      • Stefanidou M.
      • et al.
      Accidental poisoning after ingestion of “aphrodisiac” berries: diagnosis by analytical toxicology.
      In 2012, Nikolaou et al
      • Nikolaou P.
      • Papoutsis I.
      • Stefanidou M.
      • et al.
      Accidental poisoning after ingestion of “aphrodisiac” berries: diagnosis by analytical toxicology.
      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.
      • Nikolaou P.
      • Papoutsis I.
      • Stefanidou M.
      • et al.
      Accidental poisoning after ingestion of “aphrodisiac” berries: diagnosis by analytical toxicology.
      In 1985, Hayman
      • Hayman J.
      Datura poisoning—the Angel’s Trumpet.
      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.
      • Hayman J.
      Datura poisoning—the Angel’s Trumpet.
      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.
      • Urich R.W.
      • Bowerman D.L.
      • Levisky J.A.
      • Pflug J.L.
      Datura stramonium: a fatal poisoning.
      Centers for Disease Control and Prevention (CDC)
      Jimsonweed poisoning associated with a homemade stew—Maryland, 2008.
      • Spina S.P.
      • Taddei A.
      Teenagers with Jimson weed (Datura stramonium) poisoning.
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      • Tiongson J.
      • Salen P.
      Mass ingestion of jimson weed by eleven teenagers.
      • Thabet H.
      • Brahmi N.
      • Amamou M.
      • Ben Salah N.
      • Hédhili A.
      • Yacoub M.
      Datura stramonium poisonings in humans.
      In 1982, Urich et al
      • Urich R.W.
      • Bowerman D.L.
      • Levisky J.A.
      • Pflug J.L.
      Datura stramonium: a fatal poisoning.
      reported a fatal case of jimsonweed ingestion in a 20-year-old man. In 1997, Dewitt et al
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      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.
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      There were no deaths.
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      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.
      • Hayman J.
      Datura poisoning—the Angel’s Trumpet.
      • Cikla U.
      • Turkmen S.
      • Karaca Y.
      • et al.
      An Atropa belladonna L. poisoning with acute subdural hematoma.
      • Urich R.W.
      • Bowerman D.L.
      • Levisky J.A.
      • Pflug J.L.
      Datura stramonium: a fatal poisoning.
      The management of anticholinergic poisonings may include benzodiazepines for sedation for agitation and beta-blockers for tachydysrhythmias.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Most patients will recover within 24 hours with benzodiazepine sedation alone for anxiety and combativeness.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Plants containing nicotine and nicotinelike alkaloids, such as anabasine, have also been intentionally chewed or ingested for their stimulating effects.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      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).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      The nicotinic plant alkaloids act agonistically at nicotinic cholinergic receptors within the autonomic and central nervous systems, neuromuscular junctions, and adrenal medulla.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      Early nicotinic cholinergic toxidromes resemble anticholinergic toxidromes with mydriasis, diaphoresis, restlessness, tremors, tachycardia, hypertension, abdominal pain, and, possibly, seizures.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      The later phases are characterized by bradycardia, hypotension, dyspnea, neuromuscular paralysis, respiratory failure, and cardiorespiratory arrest.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      • Castorena J.L.
      • Garriott J.C.
      • Barnhardt F.E.
      • Shaw R.F.
      A fatal poisoning from Nicotiana glauca.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      In 1987, Castorena et al
      • Castorena J.L.
      • Garriott J.C.
      • Barnhardt F.E.
      • Shaw R.F.
      A fatal poisoning from Nicotiana glauca.
      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.
      • Castorena J.L.
      • Garriott J.C.
      • Barnhardt F.E.
      • Shaw R.F.
      A fatal poisoning from Nicotiana glauca.
      The authors concluded that the decedent had been lethally poisoned by nicotinic alkaloids in tree tobacco absorbed transmucosally or transcutaneously.
      • Castorena J.L.
      • Garriott J.C.
      • Barnhardt F.E.
      • Shaw R.F.
      A fatal poisoning from Nicotiana glauca.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Castorena J.L.
      • Garriott J.C.
      • Barnhardt F.E.
      • Shaw R.F.
      A fatal poisoning from Nicotiana glauca.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Schep L.J.
      • Slaughter R.J.
      • Beasley D.M.
      Nicotinic plant poisoning.
      The convulsant or epileptogenic plants include water hemlock, strychnine, and ackee or breadfruit.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      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.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      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).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      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.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      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).
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      Within 30 minutes, the younger man vomited and began to have a seizure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      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.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      He was transported to a local ED where he was treated with gastric lavage and activated charcoal.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      Three hours after ingesting the root of the plant, he experienced ventricular fibrillation that could not be reversed and died.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      The older brother presented to the ED with seizures and delirium 2 hours after taking 1 bite of the plant root.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      He was stabilized and recovered uneventfully.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      The plant was later identified by an expert as water hemlock, C maculata (Figure 4).
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      Figure thumbnail gr4
      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).
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      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.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      Water hemlock’s primary toxin, cicutoxin, is present in all its parts, and reaches its highest concentrations in roots and stems.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      Oral mucosal contact with toy whistles made from the hollow stems of water hemlock has been associated with deaths in children (Figure 4).
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Driesbach R.
      Handbook of Poisoning.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      Loss of consciousness, seizures, and status epilepticus may follow initial symptoms and, if not lethal, may result in rhabdomyolysis, myoglobinuria, and acute renal failure.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      Centers for Disease Control and Prevention (CDC)
      Water hemlock poisoning—Maine, 1992.
      • Schep L.J.
      • Slaughter R.J.
      • Becket G.
      • Beasley D.M.
      Poisoning due to water hemlock.
      • Driesbach R.
      Handbook of Poisoning.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      Severe muscular spasms can result in tendon ruptures and vertebral fractures and are often associated with hyperpyrexia, rhabdomyolysis, and acute renal failure.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Philippe G.
      • Angenot L.
      • Tits M.
      • Frédérich M.
      About the toxicity of some Strychnos species and their alkaloids.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Additional supportive care with mechanical ventilation and hemofiltration or hemodialysis for renal failure are often indicated in severe cases.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Carlton B.E.
      • Tufts E.
      • Girard D.E.
      Water hemlock poisoning complicated by rhabdomyolysis and renal failure.
      The frequently abused hallucinogenic plants include the herb diviner’s sage (Salvia divinorum) and morning glory vine, especially its seeds.
      • Vohra R.
      • Seefeld A.
      • Cantrell F.L.
      • Clark R.F.
      Salvia divinorum: exposures reported to a statewide poison control system over 10 years.
      • Musshoff F.
      • Madea B.
      Ricin poisoning and forensic toxicology.
      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.
      • Bohnert A.S.
      • Fudalej S.
      • Ilgen M.A.
      Increasing poisoning mortality rates in the United States, 1999–2006.
      • DeSilva H.A.
      • Fonseka M.M.D.
      • Pathmeswaran A.
      • et al.
      Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomized, placebo-controlled trial.
      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.
      • Singh S.
      Adolescent salvia substance abuse.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Morning glory seeds, like S divinorum, may also be purchased on the Internet, but unlike Salvia, have not been criminalized.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Vohra R.
      • Seefeld A.
      • Cantrell F.L.
      • Clark R.F.
      Salvia divinorum: exposures reported to a statewide poison control system over 10 years.
      • Singh S.
      Adolescent salvia substance abuse.
      There are no antidotes for Salvia and morning glory seed intoxication, and sedation with benzodiazepines and antipsychotics are often indicated.
      • Bohnert A.S.
      • Fudalej S.
      • Ilgen M.A.
      Increasing poisoning mortality rates in the United States, 1999–2006.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Singh S.
      Adolescent salvia substance abuse.

      Cytotoxic poisonings

      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.
      • Musshoff F.
      • Madea B.
      Ricin poisoning and forensic toxicology.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      • Lim H.
      • Kim H.J.
      • Cho Y.S.
      A case of ricin poisoning following ingestion of Korean castor bean.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Musshoff F.
      • Madea B.
      Ricin poisoning and forensic toxicology.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      • Lim H.
      • Kim H.J.
      • Cho Y.S.
      A case of ricin poisoning following ingestion of Korean castor bean.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      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.
      • Singh S.
      Adolescent salvia substance abuse.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      • Lim H.
      • Kim H.J.
      • Cho Y.S.
      A case of ricin poisoning following ingestion of Korean castor bean.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      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).
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      • Musshoff F.
      • Madea B.
      Ricin poisoning and forensic toxicology.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      • Lim H.
      • Kim H.J.
      • Cho Y.S.
      A case of ricin poisoning following ingestion of Korean castor bean.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      As long as seeds are not chewed before ingestion, they will not release their toxalbumins and cause significant gastrointestinal toxicity.
      • Nelson L.S.
      • Shih R.D.
      • Balick M.J.
      Handbook of Poisonous and Injurious Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      Figure thumbnail gr5
      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 thumbnail gr6
      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.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      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.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      In additional criminal uses, ricin has reputedly been weaponized for aerosol dispersion.
      • Audi J.
      • Belson M.
      • Patel M.
      • Schier J.
      • Osterloh J.
      Ricin poisoning: a comprehensive review.
      In 1986, Wedin et al
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      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.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      The children recovered uneventfully with supportive care.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      In 2012, Assiri
      • Assiri A.S.
      Ricin poisoning causing death after ingestion of herbal medicine.
      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.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      Most cases of abrin poisoning have occurred after chewing and swallowing the very colorful A precatorius (rosary pea) seeds (Figure 6).
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      In 2015, Alhamdani et al
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      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).
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      The child recovered uneventfully with intravenous rehydration and supportive care.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      Rosary pea seeds have been chewed and swallowed intentionally in suicide attempts.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      In 2008, Sahoo et al
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      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.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      The patient recovered uneventfully after corticosteroid therapy and supportive care.
      • Sahoo R.
      • Hamide A.
      • Amalnath S.D.
      • Narayana B.S.
      Acute demyelinating encephalitis due to Abrus precatorius poisoning-complete recovery after steroid therapy.
      Today, rosary pea seeds can be easily obtained over the Internet.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      In 2015, Jang et al
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      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.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      The patient recovered uneventfully with supportive care and was discharged to outpatient psychiatric follow-up.
      • Jang D.H.
      • Hoffman R.S.
      • Nelson L.S.
      Attempted suicide by mail order: Abrus precatorius.
      The indigenous plants containing mitotic inhibitors include autumn crocus (Colchium autumnalis), vinca or periwinkle (Catharanthus roseus), and mayapple (Podophyllum pelatum).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Cytotoxic alkaloids derived from these plants have been used to treat gout (colchicine), condylomata acuminata (podophyllin), and cancer (vinblastine, vincristine, paclitaxel, podophyllotoxin).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      Delayed toxic effects may include bone marrow toxicity, manifesting initially as leukocytosis followed by leukopenia, peripheral neuropathy, ataxia, seizures, and encephalopathy.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      Death may result from direct toxic effects, coagulopathy, cardiovascular collapse, or latent sepsis.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      In 2015, Boisramé-Helms et al
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      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.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      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%.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      Mechanical ventilation and venous-arterial extracorporeal life support (ECLS) were instituted for cardiogenic shock refractory to vasopressors.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      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.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      By day 10, coagulation and cardiac status had been restored, and the patient was weaned from mechanical ventilation and ECLS.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      The authors concluded that ECLS might be useful as a bridge to recovery in severely poisoned patients with colchicine poisoning and refractory circulatory shock.
      • Boisramé-Helms J.
      • Rahmani H.
      • Stiel L.
      • Tournoud C.
      • Sauder P.
      Extracorporeal life support in the treatment of colchicine poisoning.
      Many edible fruits of the Malus (apple, crabapple) and Prunus (apricots, cherries, peaches, plums) species contain cyanide-releasing glycosides within their kernels.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      On arrival, all patients had normal arterial blood gases, received supportive care with rehydration, and were discharged uneventfully the next day.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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).
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      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.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Those who drank tea only remained well.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Figure thumbnail gr7
      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).
      The elder tree is indigenous to the Western United States and produces globular black berries that are edible when mature (Figure 7).
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Elderberry extracts are used in fruit juices, cough and cold syrups, and alcoholic beverages, and cooked elderberries are used in jams and pies.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Elder tree leaves, stems, bark, and roots all contain cyanogenic glycosides that can release hydrocyanic acid in the gastrointestinal tract.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Although elderberries are safe to consume, especially when cooked, the leaves, stems, and roots should not be crushed when preparing juices from wild elderberries.
      Centers for Disease Control and Prevention (CDC)
      Poisoning from elderberry juice—California.
      Laboratory results in cyanide poisoning will demonstrate lactic acidosis and elevated cyanide and thiocyanate levels.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.

      Gastrointestinal/hepatotoxic poisonings

      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      • Snajdauf J.
      • Mixa V.
      • Rygl M.
      • Vyhnánek M.
      • Morávek J.
      • Kabelka Z.
      Aortoesophageal fistula—an unusual complication of esophagitis caused by Dieffenbachia ingestion.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      The closest concordances were in dermal edema (3.7% vs 2.2%), dermal erythema (5.3% vs 2.5%), and cough/choke (3.7% vs 1.1%).
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      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.
      • Francis P.D.
      • Clarke C.F.
      Angel trumpet lily poisoning in five adolescents: clinical findings and management.
      Despite the findings of the study by Pedaci et al,
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      Snajdauf et al
      • Snajdauf J.
      • Mixa V.
      • Rygl M.
      • Vyhnánek M.
      • Morávek J.
      • Kabelka Z.
      Aortoesophageal fistula—an unusual complication of esophagitis caused by Dieffenbachia ingestion.
      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.
      • Snajdauf J.
      • Mixa V.
      • Rygl M.
      • Vyhnánek M.
      • Morávek J.
      • Kabelka Z.
      Aortoesophageal fistula—an unusual complication of esophagitis caused by Dieffenbachia ingestion.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Pedaci L.
      • Krenzelok E.P.
      • Jacobsen T.D.
      • Aronis J.
      Dieffenbachia species exposures: an evidence-based assessment of symptom presentation.
      • Snajdauf J.
      • Mixa V.
      • Rygl M.
      • Vyhnánek M.
      • Morávek J.
      • Kabelka Z.
      Aortoesophageal fistula—an unusual complication of esophagitis caused by Dieffenbachia ingestion.
      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).
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.
      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.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.
      Massive acute ingestions can cause right upper quadrant pain, acute hepatitis, ascites, elevated liver enzymes, and coagulopathy.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.
      Chronic low-level exposures may result in cirrhosis, hepatic veno-occlusive disease, and pulmonary hypertension.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.
      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.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Palmer M.E.
      • Betz J.M.
      Plants.
      • Stewart M.J.
      • Steenkamp V.
      Pyrrolizidine poisoning: a neglected area in human toxicology.

      Poisonings By Unknown Plants

      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.
      • Wedin G.P.
      • Neal J.S.
      • Everson G.W.
      • Krenzelok E.P.
      Castor bean poisoning.
      • Alhamdani M.
      • Brown B.
      • Narula P.
      Abrin poisoning in an 18-month-old child.
      Teenagers will continue to experiment with naturally hallucinogenic plants.
      • Spina S.P.
      • Taddei A.
      Teenagers with Jimson weed (Datura stramonium) poisoning.
      • Dewitt M.S.
      • Swain R.
      • Gibson Jr, L.B.
      The dangers of jimson weed and its abuse by teenagers in the Kanawha Valley of West Virginia.
      • Tiongson J.
      • Salen P.
      Mass ingestion of jimson weed by eleven teenagers.
      • Singh S.
      Adolescent salvia substance abuse.
      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.

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