From the Garden to Gurney: Plant Poisoning in the Emergency Department

Dr Neeraj Manikath , claude.ai

Abstract

Plant poisonings represent a diagnostic and therapeutic challenge in emergency medicine, bridging toxicology, ethnobotany, and clinical acuity. While often underestimated, plant-related exposures account for approximately 5-7% of all poisoning cases presenting to emergency departments globally. This review synthesizes current evidence on common and life-threatening plant poisonings, emphasizing bedside clinical assessment, pattern recognition, and practical management strategies. We highlight the "toxidromes" of plant poisoning, diagnostic pearls often missed in standard teaching, and evidence-based interventions that can prevent morbidity and mortality.

Introduction

The romanticization of "natural" products has paradoxically increased plant poisoning incidents in the 21st century. Unlike pharmaceutical toxicity where the agent is usually known, plant poisonings present unique challenges: delayed presentation, misidentification, variable toxin concentrations, and patients' reluctance to disclose herbal remedy use. As internists and emergency physicians, we must maintain a high index of suspicion and master the art of toxidrome recognition—often our only diagnostic tool when laboratory confirmation is unavailable or delayed.

Clinical Pearl #1: Always ask about plant exposures separately from "medications." Patients don't consider herbal teas, garden plants, or traditional remedies as relevant medical information unless specifically prompted.

Classification by Toxidrome: A Bedside Approach

1. Anticholinergic Syndrome: The "Hot, Dry, Mad, Blind" Plants

Key Plants: Datura stramonium (Jimson weed), Atropa belladonna (deadly nightshade), Hyoscyamus niger (henbane), Brugmansia species (angel's trumpet)

Toxin: Tropane alkaloids (atropine, scopolamine, hyoscyamine)

Clinical Presentation: The classic anticholinergic toxidrome manifests as hyperthermia, anhidrosis, mydriasis with loss of accommodation, urinary retention, decreased bowel sounds, tachycardia, and delirium. However, several nuances deserve emphasis:

Oyster #1: Unlike pharmaceutical anticholinergic poisoning, plant-derived tropane alkaloids have higher lipophilicity, resulting in more prominent CNS effects—particularly visual hallucinations and agitated delirium that can persist for 24-72 hours. Patients may pick at invisible objects (carphology) or engage in "phantom behaviors" like smoking imaginary cigarettes.

Bedside Hack: The "ice cube test"—apply an ice cube to the patient's axilla. Complete absence of sweating despite hyperthermia strongly suggests anticholinergic toxicity rather than sympathomimetic toxidrome, where sweating is typically present.

Diagnostic Pitfall: Unilateral mydriasis from accidental ocular contamination (after handling crushed Jimson weed seeds then rubbing the eye) can mimic stroke or intracranial pathology. The affected pupil will NOT respond to pilocarpine 1% drops—a useful bedside test called the "pharmacologic denervation test."

Management Pearls:

• Physostigmine remains controversial but can be life-saving in severe agitated delirium with risk of injury. Dose: 0.5-2 mg IV slowly (over 5 minutes) with continuous cardiac monitoring. Contraindications include cardiac conduction abnormalities, asthma, and co-ingestion of tricyclic antidepressants.
• Clinical Hack: If physostigmine is unavailable or contraindicated, consider benzodiazepines (lorazepam 2-4 mg IV) for agitation, but avoid antipsychotics which may worsen anticholinergic toxicity and lower seizure threshold.
• Urinary catheterization is often necessary; be prepared for significant retention (>1000 mL).

2. Cardioactive Glycoside Toxicity: When the Garden Attacks the Heart

Key Plants: Digitalis purpurea (foxglove), Nerium oleander (oleander), Convallaria majalis (lily of the valley), Thevetia peruviana (yellow oleander), Cerbera odollam (suicide tree)

Toxin: Cardiac glycosides (digoxin-like and more potent analogues)

Clinical Presentation: The presentation mimics digoxin toxicity but is often MORE severe due to higher potency and lipophilicity of plant glycosides.

Oyster #2: Unlike pharmaceutical digoxin, plant cardiac glycosides (especially oleandrin from oleander) are NOT reliably detected by standard digoxin immunoassays, which may show falsely low or negative results. However, a positive digoxin level in a digoxin-naive patient confirms plant glycoside exposure.

Bedside Recognition: Look for the triad of:

1. Gastrointestinal symptoms (nausea, vomiting, abdominal pain)—often the first manifestation
2. Cardiac dysrhythmias—classically atrial tachycardia with AV block, but ANY rhythm disturbance can occur
3. Hyperkalemia—a critical prognostic marker (K+ >5.5 mEq/L associated with increased mortality)

Clinical Pearl #2: The "yellow-green vision" (xanthopsia) classically associated with digoxin toxicity is rarely reported acutely in plant poisoning but may develop over hours.

ECG Pearls:

• "Regularized irregular" rhythm: atrial fibrillation with complete heart block and junctional escape rhythm
• Bidirectional ventricular tachycardia—highly specific for cardiac glycoside toxicity
• ST depression with characteristic "Salvador Dali mustache" or "reverse tick" appearance

Critical Management Decisions:

Hack #2: Hyperkalemia in cardiac glycoside poisoning should NOT be treated with standard hyperkalemia protocols (calcium, insulin/dextrose). Calcium administration can precipitate fatal dysrhythmias ("stone heart"). Insulin/glucose and sodium bicarbonate are preferred.

Digoxin-Specific Fab Fragments: The cornerstone of treatment for life-threatening toxicity:

• Indications: Hemodynamically significant dysrhythmias, K+ >5.0-5.5 mEq/L, cardiac arrest
• Dosing challenge: Without knowing serum digoxin levels in acute plant ingestion, use empiric dosing: 10-20 vials IV over 30 minutes
• Pearl: Response to Fab fragments is usually dramatic within 30-60 minutes. Lack of response should prompt consideration of other co-toxins or misdiagnosis.
• Cost and availability remain significant barriers; contact poison control early for sourcing assistance

Oyster #3: Rebound toxicity can occur 12-24 hours after Fab administration as unbound glycoside redistributes from tissue stores. Admit all patients for minimum 24-hour observation even if initial response is excellent.

3. Calcium Oxalate Crystal-Containing Plants: Mechanical and Chemical Injury

Key Plants: Dieffenbachia (dumb cane), Caladium, Philodendron, Colocasia (elephant ear), Arisaema triphyllum (Jack-in-the-pulpit)

Toxin: Insoluble calcium oxalate raphides (needle-shaped crystals) + proteolytic enzymes

Clinical Presentation: Immediate intense burning pain of lips, tongue, oral mucosa, and pharynx. The pathognomonic feature is mechanical injury from thousands of microscopic "needles" injected into tissue, causing intense inflammation.

Bedside Diagnosis: Simply ask the patient to show you their tongue—you'll see edema, erythema, and tiny white punctate areas representing crystal embedment.

Clinical Hack #3: Use a Wood's lamp or dermatoscope to visualize calcium oxalate crystals in oral tissue—they fluoresce under UV light, confirming diagnosis at bedside.

Major Complication: Angioedema with airway compromise, though less common than the pain suggests.

Management:

• Cool liquids or ice chips for symptomatic relief
• Pain control: viscous lidocaine, systemic analgesics if needed
• Controversial intervention: Some toxicologists advocate cold milk or dairy products theoretically to bind oxalates, though evidence is anecdotal
• Monitor airway for 4-6 hours; intubation rarely necessary but have difficult airway equipment ready
• Corticosteroids and antihistamines have minimal proven benefit but often given for severe edema

Pearl #3: Avoid inducing emesis or gastric lavage—this increases exposure to oropharyngeal mucosa and worsens injury.

4. Cholinergic Crisis: The Nicotinic Plants

Key Plants: Nicotiana species (tobacco, tree tobacco), Conium maculatum (poison hemlock), Laburnum anagyroides (golden chain tree)

Toxins: Nicotine, coniine, cytisine

Clinical Presentation: Biphasic toxicity is characteristic:

• Phase 1 (nicotinic stimulation): Tachycardia, hypertension, mydriasis, fasciculations, diaphoresis
• Phase 2 (nicotinic blockade): Bradycardia, hypotension, paralysis, respiratory failure

Oyster #4: Poison hemlock (Conium maculatum) contains coniine, which causes ascending paralysis resembling Guillain-Barré syndrome but with PRESERVED consciousness—a terrifying presentation. Patients are "locked in" with flaccid paralysis but fully aware.

Historical Note: This is the poison that killed Socrates, described by Plato: "...the coldness was spreading about as far as his waist... his feet and legs were stiff..."

Bedside Recognition: Look for the "mousy" or "musty" odor of poison hemlock on the patient's breath or in vomitus—highly characteristic if present.

Management:

• Aggressive supportive care is primary treatment
• Secure airway early if respiratory muscle involvement evident
• Atropine may help muscarinic symptoms (salivation, bronchorrhea) but does NOT reverse nicotinic effects (paralysis)
• Benzodiazepines for seizures if they occur
• No specific antidote exists—supportive care until toxin elimination (typically 24-72 hours)

Hack #4: Maintain euvolemia and avoid vasopressors initially for hypotension—these patients often respond to fluid resuscitation alone, and vasopressors may worsen nicotinic receptor stimulation effects.

5. Hepatotoxic Plants: The Delayed Disaster

Key Plants: Amanita phalloides (death cap mushroom), Senecio species (ragwort), Heliotropium (heliotrope), Crotalaria species

Toxins: Amatoxins (mushrooms), pyrrolizidine alkaloids (other plants)

Clinical Presentation: The insidious nature of these poisonings makes them particularly dangerous—patients present feeling well initially, then deteriorate rapidly days later.

Amatoxin Poisoning Phases:

• Phase 1 (6-24 hours): Severe gastroenteritis with cholera-like diarrhea, vomiting, abdominal cramps
• Phase 2 (24-48 hours): False recovery—patients feel better while hepatocellular injury progresses
• Phase 3 (48-96 hours): Fulminant hepatic failure, coagulopathy, encephalopathy, renal failure
• Phase 4: Death or recovery (if liver transplant performed)

Oyster #5: By the time transaminases rise significantly (typically day 2-3), massive hepatocyte injury is already irreversible. Early recognition based on history and clinical pattern is crucial.

Diagnostic Pearl #4: If a patient presents with severe gastroenteritis after a wild mushroom meal, assume amatoxin poisoning until proven otherwise—even if they feel better. The "latency period" of >6 hours between ingestion and symptoms is highly characteristic.

Critical Management Strategy:

Multi-targeted therapy (though evidence is mostly observational):

1. Silibinin (milk thistle extract): 20-50 mg/kg/day IV in divided doses

   • Mechanism: Inhibits amatoxin hepatocyte uptake, acts as antioxidant
   • Must start within 48 hours (ideally sooner)
   • Availability limited in many countries; contact poison control for access

2. High-dose penicillin G: 300,000-1,000,000 units/kg/day IV

   • Mechanism: Competitively inhibits amatoxin uptake into hepatocytes
   • Start immediately if amatoxin suspected

3. N-acetylcysteine: Standard dosing as per acetaminophen overdose protocol

   • Antioxidant support for hepatocytes

4. Activated charcoal: Multiple-dose activated charcoal (MDAC) every 4 hours

   • Interrupts enterohepatic circulation of amatoxins
   • Continue for 48-72 hours

5. Early liver transplant evaluation: Contact transplant center on day 1-2, not day 4 when fulminant failure manifests

Hack #5: Use the "Meixner test" if available—add dilute hydrochloric acid and a drop of newspaper pulp to patient's urine. A blue-green color suggests amatoxin presence (though sensitivity is limited).

Pearl #5: "When in doubt, dose it out"—if there's any suspicion of amatoxin ingestion based on history, start treatment immediately. The toxicity of interventions (penicillin, silibinin, NAC) is far less than the mortality of untreated amatoxin poisoning (50-90%).

6. Sodium Channel Activators: The "Electric" Plants

Key Plants: Aconitum species (aconite, monkshood, wolfsbane), Veratrum species (false hellebore)

Toxins: Aconitine, veratridine—among the most potent plant toxins known

Clinical Presentation: Rapid onset (minutes to 2 hours) of:

• Perioral paresthesias spreading to extremities—often described as "electric" or "tingling"
• Profound bradycardia or ventricular dysrhythmias
• Hypotension
• Muscle weakness
• Altered mental status

Oyster #6: Aconite poisoning can present with refractory ventricular tachycardia or fibrillation resistant to standard ACLS protocols. The toxin holds sodium channels in an open state, causing persistent depolarization.

ECG Finding: Progressive QRS widening with bidirectional VT similar to digoxin toxicity, but occurring within hours rather than days.

Management:

• Immediate cardiac monitoring and IV access
• Atropine for symptomatic bradycardia (though often incompletely effective)
• Amiodarone is the antiarrhythmic of choice (300 mg IV bolus, then infusion)
• Avoid class Ia and Ic antiarrhythmics (may worsen sodium channel dysfunction)
• Flecainide has been reported effective in case reports but is counterintuitive
• Intralipid therapy: 20% lipid emulsion (1.5 mL/kg bolus, then 0.25 mL/kg/min infusion) for refractory cardiovascular collapse—case reports suggest benefit

Bedside Hack #6: The combination of paresthesias + cardiac dysrhythmia in a patient who ingested a wild plant or herbal preparation should trigger immediate consideration of aconitine poisoning. Have the crash cart ready.

The Diagnostic Approach: When Plants are Poisonous but Unknown

The Systematic Assessment

1. Focused History (often from family/EMS):

   • Recent outdoor activities, gardening, foraging
   • New herbal supplements or teas
   • Intentional ingestion (suicide attempt, recreational)
   • Cultural practices (traditional medicines, religious ceremonies)
   • Occupation (farmers, landscapers, florists)

2. Toxidrome Recognition (as detailed above)

3. Associated Clues:

   • Smell on breath or vomitus
   • Plant material in emesis or gastric contents
   • Peculiar symptoms (e.g., yellow vision, electric paresthesias)
   • Temporal patterns (immediate vs. delayed)

4. Laboratory Evaluation:

   • Basic metabolic panel (potassium is crucial)
   • Hepatic function tests (transaminases, INR, bilirubin)
   • ECG (rhythm, intervals, morphology)
   • Consider: digoxin level even if patient not on digoxin, creatine kinase, lactate, osmolal gap
   • Save serum and urine for potential send-out toxicology

Clinical Pearl #6: Take photographs of any plant material brought by family or found with the patient. Send photos to poison control center or local botanist/toxicologist. Time is critical, and physical plant specimens can be analyzed later.

Regional Poison Control: Your Lifeline

Hack #7: Program your regional poison control number into your phone NOW (1-800-222-1222 in the US). These specialists are available 24/7, have access to toxicologists and databases, and can guide management including sourcing rare antidotes.

Controversial and Emerging Therapies

Extracorporeal Elimination

Oyster #7: Most plant toxins are highly protein-bound and lipophilic, making hemodialysis ineffective. However, hemoperfusion has been reported successful in aconite poisoning and may be considered for refractory cases.

Fomepizole in Grayanotoxin Poisoning

Grayanotoxins from Rhododendron species ("mad honey" poisoning) cause bradycardia and hypotension. Recent case reports suggest fomepizole may have efficacy, though mechanism remains unclear. Consider in refractory bradycardia unresponsive to atropine.

Therapeutic Plasma Exchange

Reported in severe cardiac glycoside poisoning when Fab fragments are unavailable, though evidence is limited to case reports.

Special Populations

Pediatric Considerations

• Children have higher morbidity due to smaller body mass and faster toxin absorption
• Most pediatric exposures are accidental, single-plant-part ingestions with lower toxicity
• However: Intentional poisonings (child abuse) must be considered if presentation is severe or recurrent
• Decontamination in children is challenging; focus on supportive care

Pregnancy

• Many plant toxins cross the placenta and can cause fetal toxicity even without maternal symptoms
• Oxytocic effects: Caulophyllum (blue cohosh), ergot alkaloids can cause uterine contractions and fetal distress
• Fetal monitoring is essential in significant maternal exposures
• Decision-making regarding antidotes in pregnancy requires toxicology consultation

Prevention and Public Health

Hack #8: Educate patients about high-risk situations:

• Never eat wild plants or mushrooms without expert identification
• Don't assume herbal products are safe—many contain toxic plants
• Keep toxic ornamental plants away from children and pets
• Be aware of "lookalike" plants (wild carrot vs. poison hemlock)

The Forensic Angle

Oyster #8: Plant poisonings have a high rate of intentional ingestion (suicide or homicide). Maintain chain of custody for specimens if foul play is suspected. Document meticulously. Some plants (oleander, aconite, amatoxins) are virtually undetectable without specific testing.

Conclusion: Mastery Through Pattern Recognition

Plant poisoning requires synthesis of history, toxidrome recognition, and aggressive supportive care. While we've discussed specific antidotes and interventions, the foundation remains:

1. Maintain high index of suspicion—ask about plants explicitly
2. Recognize toxidromes at the bedside—ECG, physical exam, temporal pattern
3. Call poison control early—don't wait for deterioration
4. Support, support, support—airway, breathing, circulation
5. Consider rare antidotes early—sourcing takes time
6. Document thoroughly—medicolegally important

Final Pearl: The plants most likely to kill are often the most beautiful—foxglove, oleander, monkshood. Teach your patients that botanical elegance doesn't equal safety.

Key References

1. Palmer ME, Betz JM. Plants. In: Nelson LS, et al. Goldfrank's Toxicologic Emergencies, 11th ed. McGraw-Hill; 2019:1537-1560.

2. Schep LJ, et al. Aconitum poisoning. Clin Toxicol. 2009;47(4):279-285.

3. Enserink R, et al. A review of cardiac glycosides: Structure, toxicity, and antidote. Crit Care. 2020;24:102.

4. Santi L, et al. Acute liver failure caused by Amanita phalloides poisoning. Int J Hepatol. 2012;2012:487480.

5. Chan TY. Aconite poisoning presenting as hypotension and bradycardia. Hum Exp Toxicol. 2009;28(12):795-797.

6. Holstege CP, et al. Oxalate-containing plants. J Toxicol Clin Toxicol. 2002;40(6):697-698.

7. Krenzelok EP, Jacobsen TD. Plant exposures: A national profile of the most common plant genera. Vet Hum Toxicol. 1997;39(4):248-249.

8. Lapoint J, et al. Grayanotoxin poisoning from rhododendron honey. Clin Toxicol. 2013;51(4):301-302.

9. Eddleston M, et al. Management of acute yellow oleander poisoning. QJM. 2000;93(7):483-492.

10. Dart RC, et al. Expert consensus guidelines for stocking of antidotes in hospitals treating acute poisonings. Ann Emerg Med. 2018;71(3):314-325.

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Author's Note: This review emphasizes practical, bedside decision-making based on current evidence and extensive clinical experience. Readers are encouraged to consult local poison control centers and update protocols based on institutional resources and emerging evidence.