Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 129. Plants and Mushrooms

Edward P  Krenzelok


• The vast majority of plant exposures are unintentional and involve small quantities and are typically asymptomatic.

• Gastrointestinal upset is the most common manifestation of symptomatic exposures.

• Foxglove, oleander, and lily of the valley are among several species of plants that contain cardiac glycosides and may cause toxicity similar to digoxin poisoning.

• The typical mushroom ingestion by children involves the “backyard mushroom” and toxicity is unlikely.

• The majority of toxic mushrooms taken belong to the gastrointestinal irritant group, and symptoms occur within the first few hours of ingestion.

• Most potentially life-threatening mushrooms will have an onset of symptoms 6–8 hours, or even longer, after ingestion.


Exposure to potentially toxic plants is a common occurrence in children, especially among those who are ≤5 years of age.1 The risk associated with plant exposures is very low, resulting in minimal morbidity and nearly no mortality.1The American Association of Poison Control Centers report that plant exposures are the 12th most common causes of toxicity in children ≤5 years.1,2 There were only four plant-related fatalities. One involved the unintentional ingestion of the highly toxic Conium maculatum (poison hemlock) while the other three were the consequence of children being administered home remedies that were produced from manipulating botanical material.1 Ingestion is the most common route of exposure, and unless stated otherwise, all of the information in this chapter will pertain to the ingestion route of exposure.

Although most plant exposures have a positive outcome and do not require medical attention, the exposures often result in caretaker anxiety and emergent interaction with the health care system. Children ≤5 years are vulnerable to unintentional plant exposures for a variety of reasons, which include carelessness by adults (placing plants in areas that are accessible to children), curiosity and hand-to-mouth activity of children, attractive plant colors and fragrances, and associating household and exterior plants as food. Contrary to poisoning exposures in general, where only 52.1% of the exposures involve children ≤5 years, 81.2% of all plant exposures occur in children ≤5 years.1Even more noteworthy is the preponderance of those exposures in children ≤1 year of age where nearly 60% of the plant exposures occurred.1Children in this age group are vulnerable due to their rapidly developing mobility, hand-to-mouth activity, and improving motor skills, which allow them to ingest plant material such as leaves, stems, and berries that have fallen onto the floor or low tables.

Unintentional (accidental) plant exposures are uncommon in children aged 6–12. Fatalities, rarely, if ever occur and the outcomes of exposures are generally positive. However, in the 13–19-year age group, plant exposure is typically due to recreational substance use. Morbidity increases, and there are rare fatalities.


The physician managing a child who has ingested a plant is faced with four challenges: identification of the plant, determining if it is toxic, determining whether the ingestion was accidental, intentional, or if the botanical material was prepared as a home remedy, and if emergent intervention is necessary. Plant identification is often difficult. Consider sending a digital photo of the plant to a resource with expertise such as a regional poison center, a florist or a botanist. Be wary of common names for plants because nicknames and regional common names can refer to different plants. The regional poison information center is a valuable resource to advise whether intervention is indicated. In the United States and its territories’ regional poison information centers provide 24/7/365 service and can be accessed by calling 1-800-222-1222.

Another consideration is the reason for the exposure. Toxicity is more likely and more pronounced if the ingestion is intentional for either abuse or medicinal purposes because larger doses are involved.1

Most plant exposures are nontoxic and can be managed with reassurance. If the young child is seen soon after ingestion of the plant, check the mouth for residual plant debris and remove if present. It may be useful to provide the child with a beverage to eradicate the adverse taste of the plant and to dilute any irritants within the oral cavity and stomach. Gastrointestinal decontamination utilizing emesis or lavage does not change patient outcome since most of the exposures are nontoxic and because those interventions have no demonstrated utility.3,4 The administration of activated charcoal may be beneficial if administered within the first hour after the ingestion, but its use should be restricted to the treatment of plant ingestions that are associated with significant toxicity or life-threatening potential.5 Antidote use is limited to a minimal number of rare indications that will be discussed in this chapter.


Thousands of plants have the potential to be toxic, but the majority of the exposures involve a limited number of species that are found in and around the home. In Table 129-1, the 15 most common plant exposures are listed by rank with their botanical name and a common name.1 Frequency of exposure is a function of the prevalence of the plant in and around homes.

TABLE 129-1

Fifteen Most Common Plant Exposures in Children1


Potentially toxic plants will be grouped by toxic effect, for example, gastrointestinal irritant or by specific toxin such as oxalate.


The majority of plants with the potential for at least minor toxicity belong to this category and it is the general caveat for most plant ingestions. These plants have the potential, if ingested in significant quantity, to produce nausea, vomiting, abdominal cramping, and diarrhea. Examples of this group are found in Table 129-2.611

TABLE 129-2

Gastrointestinal Irritants



When ingested, a wide variety of plant species cause oral mucous membrane irritation due to the presence of microscopic needle-shaped bundles of calcium oxalate (raphides) present throughout the plant structures.12 When masticated, the raphides release the calcium oxalate crystals, which damage mucous membranes and, in conjunction with unclarified additional mediators, cause the rapid onset of burning and inflammation. The administration of milk or a cool drink and sucking on a popsicle or ice cubes helps to relieve the local irritation. Commonly encountered plants that contain calcium oxalate are found in Table 129-3.1315

TABLE 129-3




Plants containing solanaceous alkaloids grow throughout the United States and include: Solanum americanum (American Nightshade); Solanum dulcamara (Bittersweet); Solanum nigrum (Black Nightshade), and Solanum tuberosum (Potato). The ingestion of a small quantity of any of these plants rarely results in the development of symptoms. When symptoms occur they are generally self-limited gastrointestinal effects. Severe intoxication, while rare, may be manifested with CNS and respiratory depression, hyperthermia, bradycardia, hypotension, and tachycardia.16



Few plants are associated with significant morbidity and mortality. An exception are the members of genus Datura.1,17 Datura stramonium is the most prevalent of the species in North America and is known commonly as jimsonweed.17 Other common names include angel’s trumpet, devil’s apple, Jamestown weed, la reina de la noche, locoweed, moonflower, stinkweed, and thornapple.17 The plants contain significant quantities of belladonna alkaloids, namely, atropine and scopolamine.17 Jimsonweed is an opportunistic plant and grows wild throughout the United States. The seeds are abused, especially by adolescents and teenagers, for to their psychotropic effects, but toxicity often occurs when the green leaves are mistaken for other edible plants.18 Patients with a significant ingestion will manifest an anticholinergic toxidrome: tachycardia, mydriasis, dry skin and mucous membranes, hypoactive bowel sounds, urinary retention, and hyperthermia. Central anticholinergic effects result in altered mental status, ranging from somnolence to severe agitation, delirium, and hallucinations.17,19 Symptoms usually arise within 30–60 minutes of ingestion and can persist for 24–48 hours.17 Approximately 80% will experience adverse effects.17 Minor agitation may respond to benzodiazepines. Hyperthermia should be treated supportively with cooling measures. Since the basis of toxicity is muscarinic antagonism, the use of a cholinesterase inhibitor such as physostigmine may help to restore autonomic balance and should be considered in patients with refractory delirium and agitation; however, there is ongoing controversy regarding its effect on clinical course and outcome and injudicious use may be complicated with cholinergic toxicity.17,20 Physostigmine may be used in pediatric doses of 0.02 mg/kg IV at a rate not to exceed 0.5 mg/min—it must not be administered rapidly or via IV push as seizures and arrhythmias may occur.17 If there is no improvement after 5–10 minutes, additional doses may be attempted, to a total of 2 mg. The dose for adolescents and adults is 0.5–2 mg IV administered no more rapidly than 1 mg/min.17 Physostigmine has a short half-life and the effects typically last for 30–60 minutes and repeat dosing may be required. A constant infusion of physostigmine should not be used.17 Patients with marked delirium, seizures, cardiopulmonary instability, or those treated with physostigmine should be admitted to an intensive care unit.


This group includes Digitalis purpurea (Foxglove)21Convallaria majalis (Lily of the Valley),21 and Nerium oleander (Common Oleander).22 It is unlikely that the casual ingestion of plant parts will be toxic to children. The greatest risk comes when it is brewed as a tea and used as a home remedy or used with suicidal intention.21 If toxicity occurs, the child should be treated conventionally for digoxin toxicity. Supportive care and, if indicated, the administration of digoxin immune Fab may be beneficial.21 Unlike foxglove, the cardiac glycosides of the lily of the valley (convallatoxins) are less potent.21 If serious oleander toxicity develops, digoxin immune Fab may be effective.23


Taxus species (Yew): Yew plants contain the cardiotoxic alkaloids taxine A and B. Morbidity and mortality are associated with suicidal ingestions.24 A poison center review of over 11,000 largely pediatric yew exposures revealed that the majority of cases (92.5%) were asymptomatic, and no deaths were reported.25

Conium maculatum (Poison Hemlock): Poison hemlock contains coniine, as well as other nicotinic alkaloids.26 Manifestations of toxicity are similar to those observed with nicotine, with an initial stimulatory phase that may include tachycardia, diaphoresis, tremor, and seizures. The subsequent depressant phase may involve bradycardia, hypotension, muscular paralysis, and coma.26,27 Supportive care is the mainstay of therapy. Asymptomatic patients who present with a possible ingestion should be observed for a minimum of 4–6 hours.

Cicuta maculata and Cicuta douglasii (Water Hemlock): Water hemlock contains a variety of toxins, including cicutoxin, with the highest concentrations in the root.28 Cicutoxin is a highly potent convulsant. Patients may first suffer gastrointestinal symptoms and then rapidly develop seizures, progressing on to status epilepticus. Treatment consists of aggressive supportive care with early attention to definitive airway management and rapid escalation of anticonvulsant therapy (see Chapter 52). Asymptomatic patients should be observed closely for a minimum of 4–6 hours.


The typical mushroom ingestion by children involves the “backyard mushroom,” and toxicity is unlikely. The majority of toxic mushrooms taken belong to the gastrointestinal irritant group, and symptoms occur within the first few hours of ingestion. Most potentially life-threatening mushrooms will have an onset of symptoms 6–8 hours, or even longer, after ingestion.

Toxic mushrooms range from those that produce gastrointestinal distress to those that have fatal outcomes. While there are 14 groups of mushrooms that have the potential to produce toxicity, most toxic mushroom species fall into one of eight distinct classifications or groups (Table 129-4). These groups contain toxins that give rise to distinct clinical syndromes that are characterized by the time of onset after ingestion and the nature of the symptoms. The more severely toxic and potentially life-threatening species generally have a delayed onset of symptoms. For Groups I and II, symptoms usually begin 6–24 hours after ingestion; Group VIII can cause symptoms 24 hours to 2 weeks after ingestion. Less toxic species, comprising Groups III–VII, usually cause symptoms within 30 minutes to 3 hours after ingestion. Most unintentional “backyard mushroom” ingestions by children do not result in toxicity. Serious mushroom poisoning typically occurs in adults in the context of foraging for edible mushrooms. Other than for groups I, II, and III, toxicity is typically short term and self-resolving and treatment is supportive.

TABLE 129-4




1. Krenzelok EP, Mrvos R. Friends and in the plant world: a profile of ingestions and fatalities. Clin Toxicol. 2011;49:142.

2. Bronstein AC, Spyker DA, Cantilena LR, Rumack BA, Dart RC. 2011 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th annual report. Clin Toxicol. 2012;50:911.

3. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: ipecac syrup. J Toxicol Clin Toxicol. 2004;42:133.

4. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: gastric lavage. J Toxicol Clin Toxicol. 2004;42:933.

5. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: single-dose activated charcoal. Clin Toxicol. 2005;43:61.

6. Barceloux DB. Holly (Ilex species). In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:861.

7. Krenzelok EP, Jacobsen TD, Aronis JM. Poinsettia exposures have good outcomes... just as we thought. Am J Emerg Med. 1996;14:671.

8. Krenzelok EP, Jacobsen TD, Aronis J. American mistletoe exposures. Am J Emerg Med. 1997;15:516.

9. Spiller HA, Willias DB, Gorman SE, Sanftleban J. Retrospective study of mistletoe ingestion. J Toxicol Clin Toxicol. 1996;34:405.

10. Barceloux DB. Pokeweed (Phytolacca americana L.). In: Barcelouxed DB. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:800.

11. Roberge R, Brader E, Martin ML, et al. The root of evil-pokeweed intoxication. Ann. Emerg Med. 1986;15:490.

12. Barceloux DB. Dieffenbachia and other oxalate-containing plants. In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:768.

13. Krenzelok EP, Jacobsen TD: Plant exposures... a national profile of the most common plant genera. Vet Hum Toxicol. 1997;39:248

14. Mrvos R, Dean BS, Krenzelok EP. Philodendron/dieffenbachia ingestions: are they a problem? J Toxicol Clin Toxicol. 1991;29:485.

15. Pedaci L, Krenzelok EP, Jacobsen TD, Aronis J. Dieffenbachia species exposures: an evidence-based assessment of symptom presentation. Vet Hum Toxicol. 1999;41:335.

16. Barceloux DB. European bittersweet and other Solanum species. In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:803.

17. Krenzelok EP. Aspects of Datura poisoning and treatment. Clin Toxicol. 2010;48:104.

18. Papoutsis J, Nikolaou PA, Athanaselis S, et al. Mass intoxication with Datura innoxia-case series and confirmation by analytical toxicology. Clin Toxicol. 2010;48:143.

19. Spina SP, Taddei A. Teenagers with jimson weed (Datura stramonium) poisoning. Can J Emerg Med. 2007;9:467.

20. Krenzelok EP. Datura poisoning and the use of physostigmine. Clin Toxicol. 2010;48:575.

21. Barceloux DB. Digitalis-containing flowers In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:773.

22. Barceloux DB. Dogbane family and cardenolides. In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:847.

23. Eddleston M, Rajapakse S, Rajakanthan JS, et al. Antidigoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomized controlled trial. Lancet. 2000;355:967.

24. Van Ingen G, Visser R, Peltenburg H, et al. Sudden unexpected death due to Taxus poisoning. A report of five cases, with review of the literature. Forensic Sci Int. 1998;56:81.

25. Krenzelok EP, Jacobsen TD, Aronis J. Is the yew really poisonous to you? J Toxicol Clin Toxicol. 1998;36:219.

26. Barceloux DB. Poison hemlock (Conium maculatum L). In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:796.

27. Fiesseler FW, Shih RD. Poison hemlock. In: Brent J, Wallace KL, Burkhart KK, et al, eds. Critical Care Toxicology. Philadelphia, PA: Elsevier Mosby; 2005:1319.

28. Barceloux DB. Water hemlock and water dropwort. In: Barceloux DB, ed. Medical Toxicology of Natural Substances. Hoboken, NJ: John Wiley and Sons, Inc.; 2008:821.

29. Mrvos R, Swanson-Biearman B, Krenzelok EP. Backyard mushroom ingestions: no gastrointestinal decontamination-no effect. J Emerg Med. 2007;33:381.