6/11/2019 Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e Chapter 220: Poisonous Plants Betty C. Chen; Lewis S. Nelson INTRODUCTION Common poisonous and injurious plants number in the hundreds and have a wide variety of toxicities. This chapter focuses on the most important plant-related exposures clinically relevant to emergency medicine (Tables 220-1 and 220-2).1,2 Individual plants are discussed in terms of their pathophysiology, clinical features (toxidromes), and treatment.3 Highly poisonous plants (Table 220-1) are highlighted in depth below, and brief reviews are provided for other common poisonous plants. Table 220-2 organizes common poisonous plants according to toxin structure. TABLE 220-1 Some Highly Poisonous Plants Poison hemlock (Conium maculatum) Yew (Taxus spp.) Foxglove (Digitalis purpurea) Oleander (Nerium oleander) Castor bean (Ricinus communis) Rosary pea (Abrus precatorius) Water hemlock (Cicuta maculata) Buckthorn (Karwinskia humboldtiana) 1/17 6/11/2019 TABLE 220-2 Classification of Poisonous Plants Classification Mechanism of Toxicity Example Plant Species Alkaloids Solanine and chaconine Green potato leaves, American nightshade, black nightshade (Solanaceae) Anticholinergics Deadly nightshade (Atropa belladonna) Angel's trumpet or jimsonweed (Datura spp.) Henbane (Hycoscyamus niger) Mandrake (Mandragora oicinarum) Cholinergics Calabar bean (Physostigma venenosum) Pilocarpus (Pilocarpus spp.) Nicotinic and nicotine-like Tobacco (Nicotiana spp.) Poison hemlock (Conium maculatum) Golden chain (Laburnum anagyroides) Blue cohosh (Caulophyllum thalictroides) Lupin (Lupinus spp.) Psychotropics Peyote (Lophophora williamsii) Nutmeg and mace (Myristica fragrans) Morning glory (Agyreia spp. and Ipomoea spp.) Hawaiian baby woodrose seeds (Argyreia nervosa) Hepatotoxic pyrrolizidines Comfrey (Symphytum oicinale) Sassafras (Sassafras albidum) Ragwort (Heliotropium spp.) Sodium channel Monkshood (Aconitum spp.) modulators Larkspur (Delphinium spp.) False or green hellebore (Veratrum spp.) Yew (Taxus spp.) 2/17 6/11/2019 Classification Mechanism of Toxicity Example Plant Species Antimitotic alkaloids and Autumn crocus (Colchicum autumnale) resins Mayapple (Podophyllum peltatum) Wild mandrake (Podophyllum emodi) Glory lily (Gloriosa superba) Madagascar periwinkle (Catharanthus roseus) Glycosides Cardioactive steroids or Foxglove (Digitalis purpurea) cardiac glycosides Lily of the valley (Convallaria majalis) Oleander (Nerium oleander) Christmas rose (Helleborus niger) Milkweed (Asclepias spp.) Squill (Urginea maritime and Urginea indica) Yellow oleander (Thevetia peruviana) Cyanogenic glycosides Almond, apricot, and cherry pits (Prunus spp.) Tapioca plant, cassava (Manihot esculenta) Elderberry (Sambucus canadensis) Hydrangea (Hydrangea macrophylla) Saponins Holly (Ilex spp.) Salicylates Poplar species (Populus spp.) Willow species (Salix spp.) Proteins, peptides, Toxalbumins Castor bean (Ricinus communis) and lectins Rosary pea (Abrus precatorius) Pokeweed (Phytolacca americana) Black locust (Robinia pseudoacacia) American mistletoe (Phoradendron flavescens) European mistletoe (Viscum album) Black vomit nut (Jatropha curcas) Hypoglycin Ackee fruit (Blighia sapida) 3/17 6/11/2019 Classification Mechanism of Toxicity Example Plant Species Carboxylic acids Calcium oxalate crystals Dumbcane (Dieenbachia spp.) Philodendron (Philodendron spp.) Caladium (Caladium spp.) Jack in the pulpit (Arisaema triphyllum) Elephant's ear (Colocasia spp.) Rhubarb (Rheum raponticum) Alcohols Convulsants Water hemlock (Cicuta maculate) Phenols and Coumarins and derivatives Sweet clover (Melilotus spp.) phenylpropanoids Tonka beans (Dipteryx spp.) Sweet-scented bedstraw (Galium triflorum) Red clover (Trifolium pretense) Capsaicin Cayenne pepper (Capsicum spp.) Demyelination Buckthorn or coyotillo (Karwinskia humboldtiana) Terpenoids and Grayanotoxin (sodium Azalea and rhododendron (Rhododoendron spp.), resins channel blockers) mountain laurel (Kalmia latifolia) Kava lactones Kava kava (Piper methysticum) Thujone Wormwood (Artemisia absinthium) Anisatin Star anise (Illicum spp.) Tetrahydrocannabinol Marijuana (Cannabis sativa) EPIDEMIOLOGY In 2012, the American Association of Poison Control Centers received 49,374 reports of plant exposures. Of these cases, 31,920 involved children less than 5 years of age. There were an additional 2918 nonexposure calls that provided information about plants to callers.2 The vast majority of exposures (96%) are unintentional ingestions. Cutaneous and ophthalmic exposures are common but generally go unreported. Although inhalational exposures are possible, they are rarely reported. 4/17 6/11/2019 Unfortunately, obtaining an accurate plant exposure history can be diicult. Most exposures occur in children and are usually unwitnessed. Uncertainty typically surrounds these cases, particularly whether ingestion truly occurred. The timing and amount of exposure is also diicult to quantify in many of these situations. Furthermore, even when a plant is available, identification errors are common and may require a botanist's expertise. In fact, data from the National Poison Data System demonstrate that medical providers and poison centers are unable to identify plants more than 22% of the time.2 CLINICAL FEATURES Classification of plants and their toxicities is complex. The most straightforward approach for emergency physicians is to classify toxic plants by the mechanism of action of the toxin and then to further subclassify based on the specific toxin. This will help predict the toxicologic eects. The reverse process can be used if the patient presents with clinical findings (Table 220-2). Unfortunately, attributing one toxicologic syndrome per plant oversimplifies the complexity of plant chemistry, because plants oen contain multiple toxic compounds, each of which produces its own toxicologic eects. Moderate systemic eects as a consequence of plant-related exposures occur in about 1% of patients. Severe life-threatening eects or disabling injuries are extremely uncommon and occur in only about 0.04% of patients. Death occurs in <0.001% of patients. Dermatitis and GI irritation are the most commonly reported eects of plant toxicity. GI complaints occur commonly following ingestion, and additional toxic symptoms may accompany or follow. Although dermatitis is another commonly reported finding of plant toxicity, systemic toxicity rarely follows (see Table 220-3). 5/17 6/11/2019 TABLE 220-3 Plant-Induced Dermatitis Dermatitis Classification Mechanism of Injury Specific Plants Mechanical injury Calcium oxalate Dumbcane (Dieenbachia maculate) Philodendron (Philodendron spp.) Raphides and trichomes Stinging nettles (Urtica dioica) Velvet bean or cowhage (Mucuna pruriens) Pineapple (Bromeliaceae spp.) Irritant dermatitis Phorbol esters Cow's horn (Euphorbia grandicornis) Poinsettia (Euphorbia pulcherrima) Manchineel tree (Hippomane mancinella) Other chemical irritants Stinging nettles (U. dioica) Velvet bean or cowhage (M. pruriens) Pineapple (Bromeliaceae spp.) Contact dermatitis Urushiol oleoresins Ginkgo (Ginkgoaceae) Poison ivy, oak, and sumac (Toxicodendron spp.) Mango (Mangifera indica) Pistachio (Pistacia vera) Cashew (Anacardium occidentale) Miscellaneous antigens Peruvian lily (Alstroemeria spp.) Narcissus and daodils (Narcissus spp.) Tulips (Tulipa spp.) Primroses (Primula spp.) Phytophotodermatitis Furocoumarins Cow parsnip (Heracleum lanatum) Wild parsnip (Pastinaca sativa) Lime (Citrus aurantiifolia) 6/17 6/11/2019 TREATMENT Most plant-related exposures can be managed with supportive care. In patients able to tolerate oral administration and believed to have potentially concerning exposures, administer activated charcoal to prevent absorption of toxin from the GI tract. Because of the uncertainty surrounding plant exposures, observe asymptomatic or minimally symptomatic patients for 4 to 6 hours in the ED. Discharge asymptomatic patients and those with resolved minor toxicity aer observation, with strict return precautions if symptoms develop. Admit those with more than minimal findings because toxicity may continue to evolve. This approach is generally applied to all patients with plant exposure because the scientific literature lacks adequate data to provide less conservative recommendations. There are few antidotes available to treat poisonings by plant toxins; none are unique to plant exposures but rather are generalized from use in other poisonings. Report all exposures to the regional poison control center to obtain assistance with plant identification, to obtain assistance with patient management, and to enable collection of accurate data on toxic plant exposures. Unfortunately, data reported by the National Poison Data System does not require confirmation of exposure, and the incidence of adverse eects is diluted by inconsequential or unconfirmed ingestions. NICOTINIC AND NICOTINE-LIKE TOXINS (POISON HEMLOCK) In Phaedo, Plato details the death of Socrates: aer drinking a potion consisting of the extracts of poison hemlock (Conium maculatum), he slowly develops paralysis and dies. All parts of poison hemlock contain coniine and similar alkaloids that are structurally and functionally analogous to nicotine. Overstimulation of nicotine receptors can rapidly progress from seemingly mild symptoms to death from respiratory failure. Symptoms may occur within hours. Mild eects include nervousness and tremor due to sympathomimetic stimulation. As toxicity progresses, patients exhibit more