Highlights & Basics
- Common toxic plant ingestion may be intentional (consumption/smoking of concentrated extracts) or accidental.
- Severe or life-threatening clinical consequences are rare.
- The most lethal plants are the most uncommon and rarely reported exposures: water hemlock, jimson weed seeds, castor bean, rosary pea, monkshood, autumn crocus, and oleander.
- There may be physiologic effects in the gastrointestinal, cardiac, neurologic, pulmonary, dermatologic, and hematologic systems.
- Unusual plant ingestions may cause intractable seizures, acidosis, liver necrosis, heart block, hypotension, tachycardia, or hypertension.
- Asymptomatic patients are observed for several hours and efforts are made to correctly identify the plant.
- The majority are treated with symptomatic and supportive care.
- Antidotes are usually only required for digoxin-like plants and cyanide-containing plants.
Quick Reference
History & Exam
Key Factors
tachycardia
hypertension
hypotension
miosis
mydriasis
bradycardia
altered mental state
hallucinations
seizures
Other Factors
nausea
vomiting
abdominal pain
diarrhea
dyspnea
skin flushing
dermatitis
dermatologic/mucosal irritation
visible bleeding: epistaxis, melena, hematuria, hematemesis, hemoptysis
headache
chest pain
muscle pain/swelling
skin pallor
easy bruising
petechial spotting
jaundice
asterixis
ascites
palmar erythema
spider angiomata
diaphoresis
dry skin
fever
urinary retention
constipation
hyperventilation
fasciculations
neuromuscular weakness
altered sensation
Diagnostics Tests
1st Tests to Order
ECG
CBC
serum electrolytes
serum creatinine
serum lactate
serum BUN/creatinine ratio
liver function tests
INR
ABG
chest x-ray
Other Tests to consider
troponin
serum digoxin levels
response to physostigmine
Treatment Options
acute
all patients
all patients
with GI symptoms
with hepatic toxicity
with tachycardia/hypertension
with bradycardia/hypotension
with QRS prolongation >100 milliseconds
with seizures
with ingestion of cyanogenic glycoside-containing plants
with hematologic toxicity/myelotoxicity
with bleeding/elevated INR
with dermatologic toxicity
with nicotinic toxicity
with antimuscarinic toxicity
with muscarinic toxicity
with aconitine-related ventricular dysrhythmia
Definition
Classifications
Common toxic North American plants
Gastrotoxic plants
- Pokeweed/inkberry (Phytolacca americana): contains phytolacca toxin and mitogen; highest concentrations are in the roots.
- North American mistletoe (Phoradendron flavescens) and European mistletoe (Viscum album): when concentrated into teas or extracts, both cause vomiting and severe abdominal cramps. Isolated reports of illness from eating small quantities of mistletoe berries are most likely isolated idiosyncratic occurrences; systematic analyses demonstrate little evidence of any toxicity other than gastroenteritis.[5]
- Ipecac (Cephaelis ipecacuanha): the syrup contains emetine and cephaline alkaloids, which cause violent vomiting and cramping.
- Ginkgo (Ginkgo biloba): ingestion of seeds/leaves/leaf extracts can cause nausea, diarrhea, and gastrointestinal upset.Image
- Plants containing ribosome-inactivating protein 2 (e.g.,castor bean [contains ricin; Ricinus communis], rosary pea [contains abrin; Abrus precatorius], black locust [Robinia pseudoacacia]) are directly cytotoxic with early signs of severe gastroenteritis.
- Sesbania species (bagpod, rattlebox) contain saponins and cytotoxic sesbanimide. There was one death reported in 2021.[7]
Hepatotoxic plants
- Distaff thistle (Atractylis gummifera): contains atractyloside.
- Kava kava (Piper methysticum): contains kavalactone, kavain, flavokavain B, all shown to be hepatotoxic.
- Creosote bush (Larrea tridentate): contains nordihydroguaiaretic acid.
- Blue-green algae: contains peptide microcystin.
- Pennyroyal (Mentha pulegium) and Hedeoma pulegioides: contains pulegone.
- Germander (Teucrium chamaedrys): contains teucrin A.
- Senna contains sennosides, which are metabolized by colonic bacteria to rhein anthrone, a reactive hepatotoxic compound.
Cardiotoxic plants
- Monkshood contains aconitine, mesaconitine, and hypaconitine, all alkaloids that cause dysrhythmias by activating sodium channels.[12]
- Green tea (Camellia sinensis), yerba mate (Ilex paraguariensis), bala (Sida cordifolia), and ma huang (Ephedra) species: contain stimulants such as caffeine, theophylline, and ephedrine, which can cause tachyarrhythmias and hypertension.
- Tejocote (Crataegus mexicana) and candlenut (Aleurites moluccanus), sold as a dietary supplement online, are often substituted with Oleander peruviana.
- Blue cohosh (Caulophyllum thalictroides), poison hemlock (Conium maculatum), golden chain (Laburnum anagyroides), Indian tobacco (Lobelia inflata), lupin (Lupinus species), and tobacco (Nicotiana tabacum): contain nicotine-like alkaloids and may cause tachyarrhythmias.
- Khat (Catha edulis): contains cathinone, which may cause tachyarrhythmias.
- Bitter orange (Citrus aurantium): contains synephrine, an alpha-receptor agonist that may cause tachyarrhythmias.
Neurotoxic plants
- Opium poppy seeds (Papaver somniferum): contain opium and many refined opiates, including morphine, thebaine, codeine, papaverine, and noscapine.
- Marijuana (Cannabis sativa): contains tetrahydrocannabinol.
- Coca (Erythroxylum coca): contains cocaine alkaloids.
- Absinthe (Artemisia absinthium): contains thujone.
- Peyote cactus (Lophophora williamsii): contains mescaline (hallucinations may occur after ingestion of very small amounts).
- Nutmeg (Myristica fragrans): in very large doses nutmeg can cause delirium, a sense of blood rushing to the head, euphoria, and dissociation.[15]
- Hawaiian baby woodrose (Argyreia nervosa): contains lysergic acid.
- Morning glory (Rivea corymbosa, Ipomoea violacea, Argyreia): contains lysergic acid amide and ergonovine.
- Salvia divinorum contains salvinorin A, a potent hallucinogen.
- Kratom (Mitrogyna speciosa): contains mitragynine, an indole alkaloid that stimulates mu and delta opiate receptors.
- Some herbal blends are adulterated with unlabeled chemicals with hallucinogenic properties, such as JWH018, HU210, and mephedrone.
- Khat (Catha edulis): contains cathinone, which may cause central nervous system (CNS) stimulation.
- Calea zacatechichi, for reasons that are not clear, produces CNS depression.
- Ayahuasca is a mixture of Banisteriopsis caapi (containing harmine and harmaline - monoamine oxidase [MAO] inhibitors) and Psychotria viridis (containing N,N-dimethyltryptamine).
- Gelsemium sempervirens contains indole alkaloids (gelsemine) that block nicotinic receptors and may cause ataxia, profound muscle weakness, and seizures.[16]
- Rambutan (Nephelium lappaceum) seeds contain gamma-aminobutyric acid (GABA), an alpha-glucosidase inhibitor, and a glycoprotein that can cause anaphylaxis.[17]
- Monkshood, wolfsbane, and devil helmet (Aconitum species): contain aconitine alkaloids.
- Poison nut, quaker button, strychnos seed (Strychnos nux-vomica): contain strychnine alkaloids and brucine alkaloids.
- Chondrodendron tomentosum and Strychnos toxifera: contain curare alkaloids.
- Azalea (Rhododendron species), fetterbush (Leucothoe fontanesiana), and Kalmia species: contain grayanotoxin.
- Buckthorn, coyotilla, tullidora (Karwinskia humboldtiana): contain Karwinskia toxin.
- Wormwood (Artemisia absinthium), absinthe (Artemisia absinthium), tansy (Tanacetum vulgare), sage (Salvia officinalis), and arborvitae tree: contain thujone.Images
- Japanese star anise (Illicium anisatum , Illicum lanceolatum): contains anisatin, while Chinese star anise (Illicum verum) contains veranisatins.Images
- Poison nut, quaker button, and strychnos seed (Strychnos nux-vomica): contain strychnine alkaloids.
- Blue cohosh (Caulophyllum thalictroides), poison hemlock (Conium maculatum), golden chain (Laburnum anagyroides), Indian tobacco (Lobelia inflata), lupin (Lupinus species), laburnum, and tobacco (Nicotiana tabacum): all contain nicotine-like alkaloids that can cause overstimulation of the nicotine receptors.
- Ginkgo (Ginkgo biloba): uncooked ginkgo seeds contain ginkgotoxin, and consumption of large quantities of seeds over time can cause death; ginkgo leaf and ginkgo leaf extracts appear to contain little ginkgotoxin.Image
Nephrotoxic plants
- Aristolochia species: contain aristolochic acid, which causes irreversible interstitial nephritis.
- Ephedra species: contain ephedrine, which crystallizes in concentrated urine, causing kidney stones.
- Carambola (Averrhoa carambola): contains soluble oxalates that may cause oxalate nephropathy and encephalopathy.
- Ackee fruit (Blighia sapida): contains hypoglycin A and B, which may cause hypoglycemia and seizures.
Dermatotoxic plants
- Philodendron, Caladium, and peace lily (Spathiphyllum) species: contain oxalate crystals that cause immediate pain when chewed or crushed.[22]
- Chili or cayenne peppers (Capsicum annuum): contain a phenylpropanoid that releases substance P from local sensory nerve endings, causing intense burning pain in whatever part of the body comes into contact with the plant.Images
- Ginkgo (Ginkgo biloba): ingestion of seeds/leaves/leaf extracts can cause allergic skin reactions due to urushiol-like alkylphenols.Image
- Stinging nettles (Urtica dioica) have stinging hairs that release histamine, acetylcholine, and serotonin. Tree nettles (Dendrocnide or Laportea species) have stinging hair that contain calcium oxalate.
- St John's wort (Hypericum perforatum) contains hypericin, a photosensitizer.
- Various plants contain furocoumarins or psoralens that are photosensitizers (celery, parsnip, limes, bergamot, figs, dill, mustard, carrot, giant hogweed [Heracleum mantegazzianum]).
- Common ivy (Hedera helix) contains a contact sensitizer, falcarinol.
- Plants causing photodermatitis such as pawpaw (Asimina triloba), parsnip (Pastinaca sativa), and rue (Ruta graveolens).
- Some wild grasses produce a grass inflorescence (flower-bearing part) called foxtail. The plant contains a pointed anterior section and barbed posterior section, which facilitates progressive forward movement after force application. Retrograde movement is prevented by stiff trailing spikelets. Children play with it by making the grass move on the tongue, causing aspiration. Because the grass spike migrates while in the body, it has caused airway obstruction, bronchiectasis, lung abscess, and migration through the pleural cavity.[23]
Hematotoxic plants
- Sweet vernal grass (Anthoxanthum odoratum), tonka beans (Dipteryx odorata), bedstraw (Galium triflorum), sweet clover (Melilotus), red clover (Trifolium pratense), and horse chestnut (Aesculus hippocastanum) species: contain coumarin or coumarin derivatives, and ingestion of large amounts of the plants may result in severe bleeding.[24]
- Ginkgo (Ginkgo biloba): uncooked ginkgo seeds contain ginkgotoxin, which can increase bleeding risks (particularly in people who take anticoagulants); consumption of large quantities of seeds over time can cause death; ginkgo leaf and ginkgo leaf extracts appear to contain little ginkgotoxin.Image
- Autumn crocus, meadow saffron (Colchicum autumnale): contain colchicine alkaloids.
- Madagascar periwinkle (Catharanthus roseus/Vinca rosea): contains vincristine and vinblastine alkaloids.
- North American mayapple (Podophyllum peltatum), Southwestern Chinese Podophyllum aurantiocaule, and Podophyllum delavayi, and other Podophyllum species: contain podophyllum alkaloids.
- Castor bean (Ricinus communis): contains ricin, a type 2 RIP.Image
- Rosary pea (Abrus precatorius) contains abrin, a type 2 RIP.
- Black locust (Robinia pseudoacacia) contains robin, a type 2 RIP.
Multiorgan toxic plants
- Jimsonweed/locoweed (Datura stramonium), belladonna (Atropa belladonna), henbane (Hyoscyamus niger), and European or true mandrake (Mandragora officinarum) all contain belladonna alkaloids, ingestion of which can cause severe antimuscarinic symptoms.[18]
- Betel nut (Areca catechu), calabar bean/ordeal bean (Physostigma venenosum) and Pilocarpus species all contain muscarinic alkaloids, ingestion of which can cause muscarinic symptoms.[26]
- Blue cohosh (Caulophyllum thalictroides) contains methylcytisine.
- Poison hemlock (Conium maculatum) can cause rhabdomyolysis and renal failure secondary to consumption either of a plant or of birds who have eaten the plant.
- Golden chain (Laburnum anagyroides), Indian tobacco (Lobelia inflata), lupin (Lupinus species), laburnum, and tobacco (Nicotiana tabacum) all contain nicotine-like alkaloids that can cause overstimulation of the nicotine receptors.[10]
- Cassava (Manihot esculenta) and Prunus species contain cyanogenic glycosides amygdalin and linamarin, respectively, which are released when seeds are chewed.[27]
- Colchicine alkaloids from autumn crocus and glory lily.
- Podophyllotoxin from mayapple.
- Vincristine/vinblastine from periwinkle.
- Taxol from yew.
Vignette
Common Vignette 1
Common Vignette 2
Other Presentations
Epidemiology
Etiology
Pathophysiology
- Phytolacca toxin and mitogen (from pokeweed and inkberry)
- Saponin glycosides (from holly berries)Image
- Viscumin (from mistletoe)
- Emetine and cephaline alkaloids (from ipecac syrup)
- Solanine from solanaceous plants
- Ribosome-inactivating protein 2 (castor bean [contains ricin; Ricinus communis], rosary pea [contains abrin; Abrus precatorius], black locust [Robinia pseudoacacia]).
- Atractyloside (e.g., from distaff thistle): a glycoside that inhibits oxidative phosphorylation in the liver.
- Peptide microcystins (e.g., from blue-green algae): cyanotoxins that cause liver necrosis by dissociation of the hepatocytes, hydropic degeneration, and intrahepatic pooling of blood.
- Pyrrolizidine alkaloid (e.g., from ragworts, other Senecio species, rattleweeds, and Heliotropium species): metabolized to pyrroles that bind both proteins and nucleic acids within hepatocytes. The pyrroles have an antimitotic effect on hepatocytes, forming megalocytes, which die and are replaced with fibrous tissue instead of normal hepatocytes. Ultimately, the liver fails due to hepatocellular death and fibrosis.Image
- Kavalactone, kavain, and flavokavain B (e.g., from kava kava): the exact mechanism of liver injury is unclear. Cytotoxicity can be demonstrated in animal models.
- Nordihydroguaiaretic acid (e.g., from creosote bush): a polyphenol that causes peroxidation of hepatocyte membrane lipids and DNA double-strand breaks. Administration is associated with a time- and dose-dependent increase in serum alanine aminotransferase levels and lactate dehydrogenase, suggesting liver damage.
- Cardiac glycosides (e.g., from lily of the valley, foxglove, oleander, and red squill species): cardioactive steroids with actions on the heart that are virtually identical to those of digoxin. Digoxin-like cardioactive steroids cause bradycardia by increasing intracellular calcium, which results in slowed transmission through the atrioventricular node.Image
- Taxine alkaloids (e.g., from yew leaves and seeds): causes sodium channel blockade.Images
- Aconitine alkaloids (from monkshood): causes sodium channel opening and calcium channel blockade.
- Saponins from pokeweed: causes heart block due to vagal stimulation.
- Nicotine-like alkaloids (e.g., from blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, laburnum, and tobacco): bind to nicotinic acetylcholine receptors, increase levels of several neurotransmitters, and increase release of epinephrine from splanchnic nerves in the adrenal medulla.[30]
- Caffeine, theophylline, synephrine, norephedrine (phenylpropanolamine), and ephedrine-like stimulants (e.g., from green tea, yerba mate, bitter orange, bala, ma huang): ephedrine is a sympathomimetic amine that increases postsynaptic noradrenergic receptor activity, resulting in increased heart rate and blood pressure. Because ephedrine does not cross the blood-brain-barrier well, the effects are most pronounced in the peripheral nervous system.
- Cathinone (e.g., from khat) and synthetic cathinone derivatives (mephedrone): a monoamine alkaloid chemically similar to amphetamines. It induces the release of dopamine, which causes increased heart rate and blood pressure.
- Aconitine alkaloids (e.g., from monkshood): cause opening of sodium channels in neurons, resulting in decreased transmission of the action potential.
- Strychnine alkaloids (e.g., from poison nut, quaker button, strychnos seed): act as antagonists at the inhibitory glycine receptor (a ligand-gated chloride channel in the spinal cord and the brain). This results in loss of control of large muscle groups with an intact mental status.
- Curare alkaloids (e.g., from Chondrodendron tomentosum, and Strychnos toxifera): competitive antagonists at the nicotinic acetylcholine receptor (nAChR), one of the two types of acetylcholine (ACh) receptors. D-tubocurare occupies the same position as ACh, resulting in muscle fasciculation, weakness, and seizures.
- Brucine alkaloids (e.g., from poison nut, quaker button, strychnos seed): structurally and chemically similar to strychnine alkaloids, with similar toxicities (antagonism of glycine receptors in the brain and spinal cord).
- Grayanotoxins (e.g., from azalea, fetterbush, Kalmia species): bind to specific sodium ion channels in cell membranes (receptor sites involved in activation and inactivation). They prevent inactivation of the cell membranes, leaving excitable cells depolarized and paralyzed.
- Karwinskia toxins (e.g., from buckthorn, coyotilla, tullidora): cause the destruction of Schwann cells.
- Cicutoxin (e.g., from water hemlock, other Cicuta species): believed to be a gamma-aminobutyric acid (GABA) antagonist that prevents inhibitory inward chloride currents in the central nervous system (CNS), resulting in CNS stimulation and seizures.Images
- Nicotine (e.g., blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, laburnum, or tobacco): causes CNS stimulation via stimulation of the nicotinic parasympathetic nervous system.
- Thujone (e.g., from wormwood, tansy, sage, absinthe): a GABA-A receptor antagonist. Inhibition of GABA receptor disrupts the balance between excitatory and inhibitory neurotransmission, leading to uninterrupted stimulation causing muscle spasms and convulsions.Images
- Anisatin (e.g., from Japanese star anise): suspected of being a strong GABA antagonist, preventing inhibitory inward chloride currents in the CNS, resulting in CNS stimulation and seizures.Images
- Strychnine alkaloids (e.g., from poison nut, quaker button, strychnos seed): act as antagonists at the inhibitory glycine receptor (ligand-gated chloride channel in the spinal cord and the brain), which results in loss of control of large muscle groups with an intact mental status.
- Hypoglycins A and B (e.g., from ackee fruit, litchi [lychee] fruit): cause hypoglycemia.
- Cyanogenic glycoside amygdalin (e.g., from cassava): can cause acidosis via mitochondrial interference and uncoupling of oxidative phosphorylation when seeds are chewed.
- Cyanogenic glycoside linamarin (e.g., from Prunus species): can cause acidosis via mitochondrial interference and uncoupling of oxidative phosphorylation when seeds are chewed.
- Gelsemine blocks nicotinic receptors and can cause seizures.[16]
- Lysergic acid/LSA (e.g., from Hawaiian baby woodrose and morning glory): has psychedelic effects thought to be due to a strong partial agonist effect at 5-HT2A receptors, which is believed to result in increased glutamate release and excitation in the cerebral cortex.
- Mescaline alkaloid (e.g., from peyote cactus): psychedelic effects of mescaline are thought to be similar to LSA and are due to a strong partial agonist effect at 5-HT2A receptors, resulting in increased glutamate release and excitation in the cerebral cortex.
- Thujone (e.g., from wormwood oil, sage oil, cedar oil): a GABA-A receptor antagonist. Inhibition of GABA receptors disrupts the balance between excitatory and inhibitory neurotransmission leading to uninterrupted stimulation causing muscle spasms and convulsions.
- Opiates (e.g., from opium poppy seeds): cause activation of opiate mu receptors.
- Tetrahydrocannabinol (e.g., from marijuana) and synthetic CB1 agonists (JWH 018): an agonist at the cannabinoid receptor CB1 (most abundant G protein-coupled receptor in the brain).
- Cocaine alkaloid (e.g., from coca): a dopamine reuptake inhibitor, a norepinephrine reuptake inhibitor, and a serotonin reuptake inhibitor, which collectively causes CNS hyperexcitability.
- Nutmeg: in very large doses can cause delirium, a sense of blood rushing to the head, euphoria, and dissociation.
- Salvinorin A is a selective kappa opiate receptor agonist with no effect at 5-HT2A receptors.
- Delirium and hallucinations may occur from central antimuscarinic effects of plants containing belladonna alkaloids (jimson weed, Datura, Brugmansia species).
- Cathinone (from khat) and synthetic cathinones (mephedrone) have amphetamine-like CNS stimulation.
- Coumarin-containing phenylpropanoids/ginkgolides (e.g., from sweet vernal grass, tonka beans, bedstraw, sweet clover, red clover, and horse chestnut): inhibit platelet aggregation.
- Colchicine alkaloids (e.g., from autumn crocus, meadow saffron): have antimitotic effects.
- Vincristine and vinblastine alkaloids (e.g., from Madagascar periwinkle): have antimitotic effects.
- Podophyllum alkaloids (e.g., from North American mayapple, Podophyllum species): have antimitotic effects.
- Ricin-like (type 2) ribosome-inactivating proteins (e.g., from castor bean [Ricinus communis]): have cytotoxic effects.Image
- Hypoglycins A and B (e.g., from ackee fruit): have cytotoxic effects.
- Oxalate raphide (from philodendron, caladium, or peace lily): is typically injected via needle-like apparatus; causes immediate pain on ingestion; may contain proteolytic enzymes, histamine, and acetylcholine. The raphides are the needle-shaped crystals of calcium oxalate or carbonate.
- Furocoumarins or psoralens that are photosensitizers (celery, parsnip, limes, bergamot, figs, dill, mustard, carrot, giant hogweed [Heracleum mantegazzianum]).
- Pulmonary toxicity (bronchiolitis obliterans) may occur following the chronic consumption of Sabah vegetables (Sauropus androgynus).
- Cyanogenic glycoside amygdalin (e.g., from cassava): can cause acidosis via mitochondrial interference and uncoupling of oxidative phosphorylation when seeds are chewed.
- Cyanogenic glycoside linamarin (e.g., from Prunus species): can cause acidosis via mitochondrial interference and uncoupling of oxidative phosphorylation when seeds are chewed.
- Any plant that causes cardiac arrest, shock, or seizures.
- Nicotine-like alkaloids (e.g., from blue cohosh, poison hemlock, golden chain, laburnum, and Indian tobacco): cause overstimulation of nicotine receptors.
- Solanine alkaloids (e.g., from betel nut, calabar bean/ordeal bean, and pilocarpus plants): cause muscarinic effects by muscarinic receptor stimulation.
- Belladonna alkaloids (e.g., from jimsonweed/locoweed, belladonna, henbane, and European/true mandrake): cause antimuscarinic effects by muscarinic receptor inhibition.
- Colchicine- or podophyllotoxin-containing plants (autumn crocus, glory lily, or mayapple).
- Vincristine/vinblastine from periwinkle.
- Taxol from yew.
Images
Diagnostic Approach
Historical factors
- Patients who have ingested pokeweed, inkberry, holly berries (usually ≥6 berries), mistletoe berries, oxalis, or ipecac may complain of gastrointestinal cramping, vomiting, and/or diarrhea.Images
- Patients who have ingested blue-green algae, ragworts, other Senecio species, rattleweeds, Heliotropium species, distaff thistle, kava kava, or green tea capsule may complain of symptoms of acute liver failure (e.g., skin yellowing, confusion, poor memory, personality change, lethargy).Image
- Patients who have ingested monkshood, lily of the valley, foxglove, oleander, red squill, blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, tobacco, green tea, yerba mate, bala, ma huang, or khat may complain of cardiovascular symptoms (e.g., fainting, dizziness, shortness of breath, fatigue, palpitations).Image
- Patients who have ingested, snorted, or inhaled morning glory seeds, Jimson weed seeds, poppy seeds, absinthe, marijuana, coca, peyote (only small amount required), Hawaiian baby woodrose, Calea, Salvia divinorum, Kratom, or very large amounts of nutmeg may complain of hallucinations and/or confusion.
- Patients who have ingested monkshood, wolfsbane, devil helmet, poison nut, quaker button, strychnos seed, Chondrodendron tomentosum, Strychnos toxifera, wireweed, azalea, fetterbush, Kalmia species, buckthorn, coyotilla, or tullidora may complain of limb weakness, numbness, or pain.
- Patients who have ingested water hemlock, other Cicuta species, wormwood, absinthe, tansy, sage, poison nut, quaker button, strychnos seed, Carolina jessamine (Gelsemium sempervirens), or Japanese star anise may present after having seizures. The seizures are characterized as generalized muscular spasm and myoclonus with mental status changes.Images
- Patients who have ingested philodendron, caladium, oxalis, peace lily, chili, or cayenne pepper plants may complain of dermatologic irritation or mucous membrane pain/burning.Images
- Patients who have ingested sweet vernal grass, tonka beans, bedstraw, sweet clover, red clover, or horse chestnut may complain of symptoms of severe bleeding. Bleeding may be visible (e.g., epistaxis, melena, vaginal hemorrhage, hematuria, hematemesis, hemoptysis, petechial spotting) or nonvisible, manifesting according to the origin of the bleeding (e.g., headache, altered mental status, syncope, shortness of breath, chest pain, abdominal pain, or muscle pain and swelling).
- Patients who have ingested autumn crocus, meadow saffron, Madagascar periwinkle, North American mayapple, Podophyllum species, castor bean (Ricinus communis), or ackee fruit may complain of symptoms associated with bone marrow suppression, which will manifest clinically as weakness, shortness of breath, pale skin, easy bruising, petechiae, abdominal pain, fever, rash, and diarrhea.Image
- Patients who have ingested, snorted, or inhaled jimsonweed, locoweed, belladonna, henbane, or European/true mandrake may complain of antimuscarinic symptoms (e.g., fever, dry skin, skin flushing, hallucinations, inability to pass urine, and vomiting).[18]
- Patients who have ingested betel nut, calabar bean, ordeal bean, and pilocarpus plants may complain of muscarinic symptoms (e.g., sweating, fainting, dizziness, shortness of breath, fatigue, palpitations, and diarrhea).[26]
- Patients who have ingested blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, or tobacco may complain of symptoms of violent vomiting, sweating, tremors, fever, palpitations, seizures, and shortness of breath.[10]
- Patients who have ingested cassava or prunus plants may complain of nausea, vomiting, abdominal pain, shortness of breath, hyperventilation, and, depending on the severity, headache and altered mental status.[27]
Physical exam
- Patients who have ingested blue-green algae, ragworts, other Senecio species, rattleweeds, Heliotropium species, distaff thistle, kava kava, or green tea capsules may have signs of liver failure (e.g., jaundice, impaired consciousness, asterixis, ascites, palmar erythema, spider angiomata).Image
- Patients who have ingested monkshood, lily of the valley, foxglove, oleander, or red squill may have weak pulses, be bradycardic, and/or be hypotensive.Image
- Patients who have ingested blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, tobacco, green tea, yerba mate, bala, ma huang, bitter orange, or khat may be tachycardic and hypertensive.
- Patients who have ingested monkshood, wolfsbane, devil helmet, poison nut, quaker button, strychnos seed, Chondrodendron tomentosum, Strychnos toxifera, wireweed, azalea, fetterbush, Kalmia species, buckthorn, coyotilla, or tullidora may have weakness, and reduced sensation on neurologic exam.
- Patients who have ingested jimsonweed, locoweed, belladonna, henbane, or European/true mandrake may demonstrate antimuscarinic signs including mydriasis (dilated pupils), fever, dry skin, skin flushing, tachycardia, and urinary retention.[18]
- Patients who have ingested betel nut, calabar bean, ordeal bean, or pilocarpus plants may demonstrate cholinomimetic signs including miosis (constricted pupils), diaphoresis, bradycardia, hypotension, and basal crackles on lung auscultation.[26]
Investigations
- ECGs of patients who have ingested monkshood, lily of the valley, foxglove, oleander, red squill, blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, green tea, yerba mate, bala, or ma huang may show dysrhythmias.Image
- ECGs of patients who have ingested monkshood, lily of the valley, foxglove, oleander or red squill may show bradyarrhythmias with/without heart block.
- ECGs of patients who have ingested blue cohosh, poison hemlock, golden chain, Indian tobacco, lupin, tobacco, green tea, yerba mate, bala, ma huang, or khat may show tachyarrhythmias.
- ECGs of patients who have ingested yew leaves or seeds may show ventricular arrhythmias.Images
- CBC can help evaluate plant-induced bone marrow suppression or provide evidence of internal bleeding; serum electrolytes, BUN, and creatinine may be useful for the evaluation of plant-induced gastroenteritis/nephrotoxins.
- Arterial blood gas and serum lactate may be necessary after ingestion of cyanogenic glycoside-containing plants or after plant-induced seizure in order to assess for acidosis.
- Serum digoxin levels may be positive after ingestion of cardiac glycoside-containing plants, but due to differences in binding affinity to the assay, levels are not useful and treatment is determined according to symptom severity. Negative results may occur despite ingestion of cardiac glycoside.
- Liver function tests are useful after ingestion of potentially hepatotoxic plants, and INR is useful after ingestion of plants with the potential to cause bleeding/hepatotoxicity.
- Serum calcium levels may be decreased after ingestion of soluble oxalate-containing plants (rhubarb, sorrel, dock, star fruit).
- Serum glucose may be decreased after ingestion of unripe ackee fruit.
- Troponins may be prognostic for cardiotoxicity in colchicine ingestions.
- Patients who have ingested betel nut, calabar bean (ordeal bean), or pilocarpus plants may have noncardiogenic pulmonary edema. Depending on the severity, this may be visible on chest x-ray.
- Physostigmine is an acetylcholinesterase inhibitor that lasts for a short period (0.5 to 6 hours) and may reverse the antimuscarinic effects of certain medications and toxins for a short period of time.
- Physostigmine may be useful in antimuscarinic plant poisoning as a diagnostic aid, when the etiology of the patient's fever, tachycardia, and altered mental status are unknown. Response to physostigmine can help differentiate between an antimuscarinic poisoning and another etiology such as infection or poisoning via a sympathomimetic. Physostigmine may be used as treatment and may control agitation more effectively than benzodiazepines.[34]
Plant identification
Risk Factors
History & Exam
Tests
Differential Diagnosis
Viral gastroenteritis
Differentiating Signs/Symptoms
- Usually insidious onset, accompanied by fever and other constitutional signs and symptoms. Self-limiting. Commonly caused by rotaviruses, noroviruses, and certain adenoviruses.
Differentiating Tests
- Viral stool culture: positive for causative organism.
Bacterial gastroenteritis
Differentiating Signs/Symptoms
- Usually accompanied by ingestion of spoiled food contaminated with Staphylococcus, Salmonella, Campylobacter, or other bacterial pathogens.
Differentiating Tests
- Stool culture and culture of suspected food: positive for causative organism.
Acute myocardial infarction
Differentiating Signs/Symptoms
- May be difficult to differentiate clinically.
- History of coronary artery disease, presence of cardiac risk factors.
Differentiating Tests
- ECG: ischemic changes.
- Cardiac enzymes: elevated.
Epilepsy
Differentiating Signs/Symptoms
- May have known history of seizures.
Differentiating Tests
- electroencephalogram (EEG): epileptiform activity or focal, localizing abnormality.
Differentiating Signs/Symptoms
- May be difficult to differentiate clinically (chronic cassava or prunus seed ingestion can cause cyanide toxicity). History of occupational exposure.
- Cherry-red color to lips and skin may occur. May rarely smell bitter almonds on breath. Hypotension.
Differentiating Tests
- ABG: acidosis, elevated lactate.
Acetaminophen poisoning
Differentiating Signs/Symptoms
- History of deliberate overdose or chronic ingestion. May cause various degrees of liver injury including fulminant hepatic failure and hepatorenal syndrome.
Differentiating Tests
- Serum acetaminophen levels: may be elevated.
Treatment Approach
Gastrointestinal effects
Hepatotoxic effects
Cardiac effects
Neurologic effects
Cyanide poisoning
Hematologic toxicity and myelotoxicity
Bleeding
Dermatologic toxicity
Multiorgan toxicity: nicotinic toxicities
Multiorgan toxicity: antimuscarinic toxicities
Multiorgan toxicity: muscarinic toxicities
Treatment Options
all patients
observation and symptomatic care
Comments
- The mainstay of treatment for most plant poisoning is symptomatic and supportive care. Very few plant exposures require any specific treatment or antidote.[38]
- Asymptomatic patients who present for evaluation after consuming a potentially poisonous plant should be observed for several hours after ingestion, and efforts should be made to correctly identify the plant.
with GI symptoms
antiemetics ± intravenous fluids
Primary Options
- prochlorperazine maleate
children >2 years of age: 0.4 mg/kg/day orally given in divided doses every 6-8 hours; adults: 10 mg orally every 6 hours when required, maximum 40 mg/day
- prochlorperazine maleate
- prochlorperazine edisylate
children >2 years of age: 0.1 to 0.15 mg/kg intramuscularly every 6-8 hours when required; adults: 5-10 mg intravenously/intramuscularly every 4 hours when required, maximum 40 mg/day
- prochlorperazine edisylate
- diazepam
children: 0.12 to 0.8 mg/kg/day orally given in divided doses every 6-8 hours when required; adults: 5-10 mg orally/intravenously every 4-6 hours when required
- diazepam
- droperidol
children: 5 mg/m2 intravenously every 2-4 hours when required, maximum 6 doses in 24 hours; adults: 1.25 to 2.5 mg intravenously every 4 hours when required
- droperidol
- ondansetron
children 8-14 kg of weight: 2 mg orally; children 15-30 kg of weight: 4 mg orally; children >30 kg of weight: 8 mg orally; adults: 0.15 mg/kg intravenously/intramuscularly every 8 hours
- ondansetron
- granisetron
children: 10-20 micrograms/kg orally; adults: 2-4 mg orally once or twice daily
- granisetron
- metoclopramide
children: 0.1 mg/kg intravenously/orally every 2-6 hours, maximum 10 mg; adults: 5-10 mg intravenously/orally every 4-6 hours when required
- metoclopramide
- promethazine
children >2 years of age: 0.25 to 1 mg/kg intramuscularly/orally every 4-6 hours when required; adults: 12.5 to 25 mg intramuscularly/orally every 4-6 hours when required
- promethazine
Comments
- Control of nausea, vomiting, abdominal cramping, and diarrhea caused by plant toxin can be difficult. Treatment modalities including intravenous fluid, antiemetics, and gastric acid-reducing agents may be employed, but are frequently inadequate to control the symptoms of plant-induced gastroenteritis.
- Nausea may be treated with antiemetics such as phenothiazines, benzodiazepines, metoclopramide, or 5HT3-antagonists. Using phenothiazines for nausea or vomiting caused by plants that induce seizures or cardiac conduction delays (e.g., monkshood, yew, pennyroyal) should be avoided.
gastric acid-reducing agents
Primary Options
- bismuth subsalicylate
children 3-6 years of age: 5 mL orally every 2-4 hours when required, maximum 8 doses/day; children 7-9 years of age: 10 mL orally every 2-4 hours when required, maximum 8 doses/day; children 10-12 years of age: 15 mL orally every 2-4 hours when required; maximum 8 doses/day; children >12 years of age and adults: 30 mL orally every 2-4 hours when required
- bismuth subsalicylate
- aluminum hydroxide/magnesium hydroxide/simethicone
adults: 5-10 mL orally every 4 hours when required
- aluminum hydroxide/magnesium hydroxide/simethicone
Secondary Options
- famotidine
neonates and infants <3 months: 0.5 to 1 mg/kg orally once daily; children ≥3 months of age: 0.5 to 1 mg/kg orally twice daily, maximum 80 mg/day; adults: 20-40 mg orally once or twice daily
- famotidine
- cimetidine
neonates: 5-20 mg/kg intravenously/intramuscularly/orally every 6-12 hours; infants: 10-20 mg/kg intravenously/intramuscularly/orally every 6-12 hours; children: 20-40 mg/kg intravenously/intramuscularly/orally every 6 hours; adults: 300 mg intravenously/intramuscularly/orally every 6 hours, maximum 2400 mg/day
- cimetidine
Tertiary Options
- omeprazole
children: 0.6 to 0.7 mg/kg orally once daily; adults: 20 mg orally once daily
- omeprazole
- esomeprazole
adults: 20-40 mg intravenously once daily
- esomeprazole
- pantoprazole
adults: 40 mg intravenously once daily
- pantoprazole
Comments
- Antacids, H2 antagonists, or proton-pump inhibitors may be used.
- Note that cimetidine is metabolized through CYP 450 3A4 and has multiple pharmacodynamic drug interactions.
with hepatic toxicity
N-acetylcysteine
Primary Options
- acetylcysteine
adults: 150 mg/kg intravenously over 1 hour, followed by 50 mg/kg over 4 hours, followed by 100 mg/kg over 16 hours; OR 140 mg/kg orally, followed by 70 mg/kg orally/intravenously every 4 hours
- acetylcysteine
Comments
- Patients who develop hepatic toxicity and injury caused by hepatotoxic plants, or who are at risk for hepatotoxicity, may benefit from intravenous or oral N-acetylcysteine.[39]
referral to liver transplant center
Comments
- Patients who demonstrate continued acidosis (pH <7.3) despite maximal resuscitative efforts, or who demonstrate continued deterioration of hepatic synthetic function (coagulopathy), should be referred to a liver transplant center for optimal management of their hepatotoxicity. Evidence of liver injury and elevation of serum aminotransferases or bilirubin are not in and of themselves reasons for liver transplantation.
with tachycardia/hypertension
benzodiazepine
Primary Options
- lorazepam
children: 0.05 mg/kg intravenously every 4-8 hours when required; maximum 2 mg/dose; adults: 2 mg intravenously every 1-2 hours when required
- lorazepam
- diazepam
children: 0.04 to 0.2 mg/kg every 2-4 hours when required; maximum 0.6 mg/kg each 8 hours; adults: 5-10 mg intravenously every 1-2 hours when required
- diazepam
- midazolam
children 6 months to 5 years of age: 0.05 to 0.1 mg/kg intravenously every 2-3 min, maximum 6 mg; children 6-12 years of age: 0.025 to 0.05 mg/kg intravenously every 2-3 min, maximum 10 mg; adults: 2-4 mg intravenously every 1-2 hours when required, maximum total dose 10 mg
- midazolam
Comments
- Standard treatments of tachycardia, including intravenous benzodiazepines to sedate the patient and reduce catecholamine outflows, are indicated in poisonings that cause sympathomimetic or antimuscarinic cardiac effects.
with bradycardia/hypotension
atropine
Primary Options
- atropine
children: 0.02 mg/kg intravenously every 5 minutes, maximum 1 mg; adults: 0.5 mg intravenously every 3-5 minutes, maximum 3 mg
- atropine
Comments
- Bradycardia should be treated according to the severity of hemodynamic embarrassment and presence of intraventricular conduction delays, with the use of atropine and vasopressors/inotropes or pacemaker as indicated.
vasopressor/inotropes or pacemaker
Comments
- Bradycardia should be treated according to the severity of hemodynamic embarrassment and presence of intraventricular conduction delays, with the use of atropine and vasopressors/inotropes or pacemaker as indicated.
digoxin immune Fab
Primary Options
digoxin immune Fab
consult specialist for guidance on dose
Comments
- Several case reports describe the use of digoxin immune Fab for the treatment of bradycardia and hypotension in patients poisoned after ingesting concentrates of plants that contain cardiac glycosides. It is best documented for oleander ingestions.
- Dosing is administered intravenously over 15 to 30 minutes with maximum effect seen within 1 to 3 hours. End-point is determined by resolution of dysrhythmia, hypotension, and normokalemia.
- Because the serum digoxin level is not 100% cross-reacting in plant poisonings, the level should not be used to dose digoxin immune Fab. The dosing is similar in children as adults; however, fluid overload must be considered when higher doses are required.[49]
with QRS prolongation >100 milliseconds
sodium bicarbonate ± potassium repletion if hypokalemic
Comments
- Patients who have ingested cardiotoxic plants that cause a prolongation of the QRS complex to >100 milliseconds should receive serum alkalinization with intravenous sodium bicarbonate.
- Sodium bicarbonate should be administered by direct intravenous injection at 1-2 mEq/kg, followed by a continuous infusion of 150 mEq/L of sodium bicarbonate in 5% dextrose injection at 200-250 mL/minute (1/5-2X maintenance fluids). Titrate to serum pH between 7.45-7.55. Hypokalemia (potassium <3.8 mEq/L) may be induced by sodium bicarbonate shifting potassium intracellularly; therefore, potassium repletion is needed.
with seizures
benzodiazepine
Primary Options
- lorazepam
children: 0.05 mg/kg intravenously every 4-8 hours when required, maximum 2 mg/dose; adults: 2 mg intravenously every 1-2 hours when required
- lorazepam
- diazepam
children: 0.04 to 0.2 mg/kg intravenously every 2-4 hours when required, maximum 0.6 mg/kg every 8 hours; adults: 5-10 mg intravenously every 1-2 hours when required
- diazepam
- midazolam
children 6 months to 5 years of age: 0.05 to 0.1 mg/kg intravenously every 2-3 min, maximum 6 mg; children 6-12 years of age: 0.025 to 0.05 mg/kg intravenously every 2-3 min, maximum 10 mg; adults: 2-4 mg intravenously every 1-2 hours when required, maximum 10 mg
- midazolam
Comments
- Neurologic toxicity caused by plant poisoning should be treated with benzodiazepines to reduce catecholamines and elevate the seizure threshold.
phenobarbital or propofol
Primary Options
- phenobarbital
5 mg/kg intravenously every 15-30 min to a total dose of 15-20 mg/kg
- phenobarbital
- propofol
5 micrograms/kg/min intravenously for 10-15 minutes, then increase by 5-10 micrograms/kg/min increments every 10-15 minutes when required to achieve a state of general anesthesia and EEG burst suppression
- propofol
Comments
- Because much of plant-induced seizure activity is related to gamma-aminobutyric acid (GABA) inhibition, other GABA agents besides benzodiazepines may be helpful. This includes the barbiturates such as phenobarbital. Phenobarbital is an anticonvulsant that may be useful because it has a long duration of action and may control multiple, repeat seizures caused by plants. It also acts synergistically with benzodiazepines. Respiratory depression is possible at high doses.
- Propofol may be an alternative agent because of its GABA agonism and N-methyl-D-aspartate (NMDA) receptor antagonism. However, the anticonvulsant effect of propofol will cease when the drug is discontinued.
with ingestion of cyanogenic glycoside-containing plants
cyanide antidote
Primary Options
- sodium nitrite and sodium thiosulfate
refer to local specialist protocol for dosing
- sodium nitrite and sodium thiosulfate
- hydroxocobalamin
refer to local specialist protocol for dosing
- hydroxocobalamin
Comments
- Although not described in the literature, symptomatic patients poisoned with cyanogenic glycosides (e.g., cassava or prunus plants) should be treated with a cyanide antidote.
- Dosing recommendations should follow those for routine use of the cyanide antidotes.
- Nithiodote® contains sodium nitrite and sodium thiosulfate. Cyanokit® contains hydroxocobalamin. Sodium nitrite may cause hypotension. Hydroxocobalamin can cause red discoloration of the skin and affect colorimetric lab tests (creatinine, LFTs).
- If cyanide antidotes are not available, good supportive measures (including oxygenation and intubation) are often associated with good outcomes.
with hematologic toxicity/myelotoxicity
transfusions as required + monitoring for infection
Comments
- If the patient exhibits anemia, blood transfusion may be necessary.
- If the patient exhibits thrombocytopenia, then platelets may need to be transfused.
- Pancytopenia and a general decrease in all blood cell lines including leukocytes (neutropenia) will result in the patient becoming immunocompromised, requiring exquisite vigilance to monitor for infections. The use of erythropoietin or a granulocyte-stimulating factor may be a useful adjunct.
with bleeding/elevated INR
vitamin K as required
Primary Options
phytonadione (vitamin K1)
refer to local specialist protocol for dosing
Comments
- If bleeding is caused by ingestion of plant-derived coumarin compounds, vitamin K (phytonadione) may have a role in helping to reverse the coagulopathy. Recommendations regarding the management of patients on vitamin K antagonist therapy with elevated INR can be amended to apply to individuals who have developed coagulopathy as a result of ingestion of plant-derived coumarin derivatives, according to local specialist protocol.[45]
with dermatologic toxicity
topical emollient and corticosteroid
Primary Options
- hydrocortisone topical
(1% to 2.5%) apply to affected area(s) three to four times daily when required
- hydrocortisone topical
Comments
- After decontamination with soap and water, most dermatologic manifestations of plant toxicity can be treated with topical emollients and corticosteroids.
with nicotinic toxicity
cardiopulmonary monitoring + fluid resuscitation
Comments
- Supportive care is paramount, with careful cardiac and pulmonary monitoring and intravenous fluid supplementation and replacement to correct acidemia.
with antimuscarinic toxicity
cardiopulmonary monitoring, temperature monitoring, fluid resuscitation ± physostigmine or rivastigmine
Primary Options
- physostigmine
refer to local specialist protocol for dosing
- physostigmine
Secondary Options
- rivastigmine
refer to local specialist protocol for dosing
- rivastigmine
Comments
- Antimuscarinic toxicity is treated primarily with supportive care, cardiopulmonary and temperature monitoring, and intravenous fluid hydration.
- Physostigmine may be indicated in patients with a clear antimuscarinic toxidrome and serious central toxicity with an altered mental status, particularly delirium, requiring chemical and/or physical restraint. The use of physostigmine for antimuscarinic toxicity is increasing, and there is growing evidence that it is safe and has minimal cholinergic side effects.[46] [47] Physostigmine is not commercially available in the US, but it may be available via a temporary importation service via the Food and Drug Administration.[36] [37]
- An ECG is recommended prior to using physostigmine as it can cause arrhythmias. It is not recommended in patients with suspected or known tricyclic antidepressant intoxication. It may cause nausea, vomiting, diarrhea, seizures which can be treated with atropine. Consultation with a poison center is recommended prior to using physostigmine, and it should be given in a monitored environment.
- If physostigmine is not available, some experts recommend using rivastigmine; however, this is an off-label use.[48]
with muscarinic toxicity
cardiopulmonary monitoring, temperature monitoring + fluid resuscitation
Comments
- Cholinomimetic poisonings are treated primarily with supportive care, cardiopulmonary and temperature monitoring, and intravenous fluid hydration.
atropine or ipratropium
Primary Options
- atropine
children: consult specialist for guidance on dose; adults: 2 mg intravenously initially, followed by double dose increments (e.g., 4 mg, 8 mg, 16 mg, etc.) every 5 minutes until secretions are controlled
- atropine
- ipratropium bromide inhaled
(17-34 micrograms) 1-2 puffs every 6-8 hours: or 250-500 micrograms nebulized every 6-8 hours
- ipratropium bromide inhaled
Comments
- Atropine is used to treat bronchorrhea, bronchospasm, bradycardia, and pulmonary edema; it is given along with supplemental oxygen, adjunctive respiratory assistance, endotracheal intubation, and mechanical ventilation if necessary.
- Ipratropium may be useful in relieving bronchospasm.
with aconitine-related ventricular dysrhythmia
chemical cardioversion or external circulatory assist (intraaortic balloon pump assist or extracorporeal membrane oxygenation or left ventricular assist device or cardiopulmonary bypass)
Primary Options
- magnesium sulfate
children: 25-50 mg/kg intravenously over 10-20 minutes, maximum 2 g/dose; adults: 1-2 g intravenously over 5-20 minutes initially, followed by 3-20 mg/minute infusion (maximum 12 g/24 hours)
- magnesium sulfate
- amiodarone
children and adults: consult specialist for guidance on dose
- amiodarone
- flecainide
children: consult specialist for guidance on dose; adults: 200-300 mg orally as a single dose
- flecainide
Comments
- Magnesium sulfate, flecainide, and amiodarone are first-choice therapies for aconitine-related ventricular dysrhythmia, which is frequently refractory to cardioversion. If ventricular dysrhythmia occurs with prolonged QTc, amiodarone may not be appropriate because it blocks potassium cellular flux. If these treatments fail and cardiogenic shock is present, intraaortic balloon pump assist, extracorporeal membrane oxygenation, left ventricular assist device, or cardiopulmonary bypass may be considered.[12] [41] [42] [43] [44]
Prevention
Primary Prevention
- People should avoid foraging/collecting wild plants unless they have intimate familiarity with all parts of the specific plant and methods to prepare it for consumption.
- Potentially poisonous plants should not be used as decorative houseplants.
- Pokeweed leaves can be safely consumed after parboiling.[33]
Follow-Up Overview
Prognosis
Plant poisonings with cardiac consequences
Plant poisonings with neurologic consequences
Plant poisonings with gastrointestinal consequences
Monitoring
Complications
Citations
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Burkhard PR, Burkhardt K, Haenggeli CA, et al. Plant-induced seizures: reappearance of an old problem. J Neurol. 1999 Aug;246(8):667-70.[Abstract]
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