CRACKCast E164 – Plants, Mushrooms, and Herbal Medications

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This episode of CRACKCast covers Rosen’s 9th Edition Chapter 158, Plants, Mushrooms, and Herbal Medications. Most of these ingestions occur in children, and much more commonly in the developing world. However, many of these species and herbals are available in North America, especially with out global trade industry, so we must be vigilant and aware of these uncommon but potentially deadly presentations.

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KEY CONCEPTS

  • Most botanical exposures result in minimal toxicity and management is largely symptom-based, supportive care.
  • Most serious toxicity results from exposure to plants with anticholinergic, antimitotic, cardiovascular, or convulsive properties
  • Most cases in which gastrointestinal (GI) symptoms begin within the first 2 hours after an unknown mushroom ingestion will prove to involve a non–life-threatening substance
  • GI symptoms that onset in more than 6 to 8 hours suggest a potentially life-threatening ingestion, such as the cyclopeptide and gyromitrin groups
  • Use local poison control centers, mycologists, and botanists to help identify serious plants and mushrooms that have been ingested. We recommend digital photography with expert consultation
  • Herbal medications are unregulated and may have inherent toxicity, herb-drug interactions, or contaminants. Clinicians should advise against the routine use of herbal medications.

Rosen’s in Perspective

  • Since ancient times plants have been used for nutritional, therapeutic, psychoactive, and toxic properties
  • Ancient Greeks recognized the lethal effects plants for eg sentencing Socrates to death by ingestion of a hemlock-based liquid
  • 65% plant exposures involve children younger than 6 years old
  • Majority of plant exposures result in minimal toxicity and death is exceedingly rare
  • The most common severe and occasionally fatal poisonings= anticholinergic, antimitotic, cardiotoxic, or convulsive properties

[1] For each of the following, describe the expected toxicity.

Jequirity pea / Rosary, Castor Beans

  • Toxalbumins
  • Contain the toxins abrin and ricin
  • Inhibit ribosomal protein synthesis, leading to cell death.
  • Seeds or beans swallowed whole with the hard outer shell intact typically prevent absorption of significant toxin
  • Chewed or crushed=may release the toxin and cause local toxicity in the GI tract
  • Symptoms may progress to severe neurologic toxicity (seizure, coma, cerebral edema, demyelinating encephalitis), multi-organ failure, and death
  • Purified ricin derived from the castor bean is highly toxic and lethal in small doses

 Jequirity pea

 Castor Beans

Umbrella tree (Schefflera arboricola), Dumb cane (Dieffenbachia)

  • These plants are commonly found in homes / offices – hard to kill ‘em and look good
  • Toxicity with these plants comes down to the presence of Raphides
  • Raphides= needle-shaped, calcium oxalate crystals
  • Ingestions can result in vomiting, mucosal irritation, ulceration, and edema
  • Look for airway compromise in severe ingestions
  • Dermal exposures may lead to contact dermatitis
  • Treatment = supportive, including maintenance of a patent airway.
  • Corticosteroids and antihistamines = adjunctive therapies
    • diphenhydramine (25 to 50 mg intravenous push [IVP]) and dexamethasone (4 to 8 mg IVP)

 Umbrella Tree (Schefflera arboricola)

 Dumb cane (Dieffenbachia)

Capsicum annuum aka all those peppers you love (jalapeno, bell, cayenne)

  • Basically comes down to capsaicin
  • Vanilloid 1 receptor (TRPV1) agonist
  • These receptors activate nociceptive nerve fibers
  • Potent burning sensation
  • Causes GI / Mucosal / Dermal irritation

Capsicum annuum

Water Hemlock

  • Cicutoxin
  • Neurotoxicity / seizures (GABA antagonist)
  • Supportive / Benzos

 Water Hemlock

Jimson Weed, Deadly Nightshade

  • Anticholinergic Toxicity
  • Commonly mistaken for blueberries
  • Supportive care, consider physostigmine

 Deadly Nightshade

Eucalyptus oil

  • High doses eucalyptol = ingestion, skin contact, or inhalation
  • Usually cause GI or dermal irritation
  • However, large doses of essential oil preparations have been reported for causes of status epilepticus

 Eucalyptus Tree

Poinsettia

  • Mild GI toxicity when plants ingested (N/V/D)
  • Can cause temporary blindness when exposed to eyes

 Poinsettia

Oleander, Foxglove, Lily of the valley, Milkweed

  • Cardiac glycoside
  • Digitalis tox / digoxin toxicity
  • Bind to cell transmembrane Na+-K+-ATPases
  • Leads to a rise in intracellular Ca2+ concentrations
  • Depresses the AV/SA nodes, increased contractility and myocardial irritability
  • Low & slow toxidrome

 Oleander

 Foxglove

 Lily of the Valley

 Milkweed

Tobacco

  • Nicotinic
  • SLUDGE / BBB + Neuromuscular Weakness → Looks more sympathomimetic initially than does a regular cholinergic toxidrome
  • Supportive care, atropine, benzos

 Tobacco Plant

Pokeweed

  • Can be lethal in Children and to adults in large amounts
  • Highest concentrations= rootstock > leaves > stems > ripe fruit
  • Berries can be very toxic, even when immature

 Pokeweed (Phytolacca americana)

Rhododendron

  • Rhododendron species contain grayanotoxin
  • AKA “Mad Honey”
  • Present in honey that is produced from their nectar
  • Presents w/ GI symptoms, hypersalivation, diaphoresis, and cardiac effects.
  • Grayanotoxin = sodium channel “openers” – hold Na channels in their open state and keep cells in a depolarized state
  • Watch for Low & Slow
    • Bradydysrhythmias (including sinus bradycardia, AV blocks, and atrial fibrillation with slow ventricular response)
    • Hypotension
    • Seizures
  • Tx w/ fluids, atropine & pacing

 Rhododendron

Yew

  • Taxus species = coniferous trees and shrubs
  • taxine pseudoalkaloids = sodium and calcium channel blockade
  • hypotension, dysrhythmias, and cardiac arrest.
  • Management = supportive. Consider ECMO

 European yew / common yew (Taxus baccata)

[2] List 5 mushrooms with early onset toxicity and 3 with late onset – and describe the toxicity expected

  • Classified as
    • Early = 0-4hrs
    • Late onset = > 6hrs
    • Think most lethal = late
  • Early = C-GIMPS
    • Coprine
    • GI Toxin
    • Ibotenic Acid / muscimol
    • Psilocybin
  • Late = GOAA
    • Gyromitrin
    • Orellanine
    • Allenic norleucine
    • Amanita (cyclopeptides)
  • CNS / Hallucinogenic
    • Amanita Muscara (Ibotenic Acid / muscimol)
    • Psilocybe cubenis (Psilocybin)
  • Cholinergic
    • Clitocybe (muscarine)
  • Hepatotoxicity
    • Amanita philloides (cyclopeptides/amatoxin) “Death cap/angel”
    • Amnita Verosa
    • Lepiota
  • Disulfiram-like reaction w/ ETOH
    • Coprinus (Coprine)
  • Seizures
    • Gyrometria (GABA antagonist)
  • Renal
    • Cortinarius (orellanine)

MNEMONIC: GO A PIC EM (relevant mushroom toxins)

G: Gyrometrin O: Orellanine A: Amatoxin P: Psilocybin I: Ibotenic Acid  C: Coprine  E: Emetogenic (early GI group) M: Muscamol

[3] List 4 mechanisms of toxicity resulting from the use of herbal medicine

  • Ephedra
    • sympathomimetic
  • Ma huang
    • sympathomimetic
  • Jimsonweed
    • anticholinergic
  • St John’s Wart
    • MAOI
    • SS, decreases INR

[4] List 4 plants containing cardiac glycosides

FOLM

  • Foxglove
  • Oleander
  • Lilly of the Valley
  • Milkweed

[5] What is Buckthorn?

Poisonous fruit from the karwinskia humbold tianna commonly seen in SW USA and Mexico.

  • Toxicity
    • Exposure: Ingestion
    • Toxic agent: T-544 (Tullidinol)
    • May uncouple oxidative phosphorylation
  • Epidemiology
    • Ingestion of buckthorn fruit: Karwinskia humboldtiana
    • Distribution: Southwestern U.S. & Mexico
    • Children, cattle & goats most commonly affected
      • Animal disease called “Limberleg”: Incoordination & Ataxia
      • Cattle most susceptible
    • Severity of toxicity proportionate to amount of fruit ingested
    • External links: Medicinal Plants; NatureServe
  • Neuropathy
    • Onset
      • Latent period: 5 to 20 days after ingestion
      • Rapidly progressive
      • General features: Fever; Cramps; Diarrhea; Headache
    • Weakness
      • Early: Legs > Arms
      • Progression: Severe quadriparesis; Bulbar & respiratory involvement
      • Cranial nerves: Normal
    • Sensory loss: Mild; Distal
    • CSF: Normal
    • Course
      • May improve spontaneously if supported through paralysis
      • Over 3 to 12 months
    • Pathology
      • Segmental demyelination ± Axonal swelling & loss
      • Experimental: Axonal loss (Motor) more prominent with systemic administration
    • Diagnosis: History of ingestion of fruit; Exclusion of other causes
  • Systemic features
    • Liver necrosis
    • Occasional degeneration of skeletal & cardiac muscle fibers
    • Micturition difficulty
    • Muscle: Cramps; Cardiac change

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Chris Lipp
Chris Lipp is one of the founding Fathers for CrackCast. He currently divides his time as an EM Physician in Calgary (SHC/FMC) and in Sports Medicine. His interests are in endurance sports, exercise as medicine, and wilderness medical education. When he isn’t outdoors with his family, he's brewing a coffee or dreaming up an adventure…..
Adam Thomas

Adam Thomas

CRACKCast Co-founder and newly minted FRCPC emergency physician from the University of British Columbia. Currently spending his days between a fellowship in critical care and making sure his toddler survives past age 5.
Adam Thomas
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