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Emergency And Acute Medicine – Plant Poisoning
Plant exposure is one of the most common reasons for contacting a poison center, and the majority of cases involve unintentional ingestion in children younger than 6 years. Accurate identification of the ingested plant is critical whenever possible, as toxicity varies widely depending on species and toxin class. Plants may produce toxicity through anticholinergic compounds, cardiac glycosides, nicotine-like alkaloids, cyanogenic compounds, calcium oxalate crystals, pyrrolizidine alkaloids, sodium channel activators, or toxalbumins.
Plants with anticholinergic properties such as jimson weed and deadly nightshade act as competitive antagonists at muscarinic receptors and produce the classic toxidrome of dry, warm, flushed skin, urinary retention, absent bowel sounds, and agitated delirium. Plants containing cardiac glycosides such as foxglove and oleander inhibit the sodium–potassium ATPase pump and cause digoxin-like toxicity, including gastrointestinal symptoms, bradycardia, tachydysrhythmias, and hyperkalemia. Nicotine-like alkaloid–containing plants such as tobacco and poison hemlock stimulate nicotinic receptors, leading to hypertension and tachycardia early, followed by bradycardia, muscle weakness, and respiratory failure in severe cases.
Cyanogenic plants such as apricot, cherry, and cassava are metabolized to cyanide and interfere with cellular respiration, causing abdominal pain, altered mental status, lactic acidosis, seizures, cardiovascular collapse, and multiorgan failure. Calcium oxalate–containing plants such as dumb cane and philodendron release microscopic crystals that cause immediate burning pain, oral swelling, and potential airway compromise; ocular exposure results in keratoconjunctivitis. Pyrrolizidine alkaloid–containing plants may cause acute hepatitis and, with chronic exposure, hepatic veno-occlusive disease. Sodium channel–activating plants such as aconite and rhododendron may produce gastrointestinal symptoms, bradycardia with atrioventricular block, tachydysrhythmias, seizures, and cardiovascular instability. Toxalbumin-containing plants such as castor bean interfere with ribosomal function and can cause severe systemic toxicity depending on route and dose.
In pediatric patients, lip, tongue, and oropharyngeal irritation is common, especially with calcium oxalate plants, and airway compromise is a concern. Children often ingest concentrated plant parts such as seeds or berries, which increases toxicity risk. Even small amounts of certain plants, such as yellow oleander leaves or jimson weed seeds, may be life-threatening.
Diagnosis is primarily clinical and depends on history, plant identification, and toxidrome recognition. Laboratory evaluation may include electrolytes, renal function, glucose, liver function tests, and blood gas analysis for acid–base status. Digoxin levels should be obtained in suspected cardiac glycoside poisoning. Lactate measurement is useful in suspected cyanogenic toxicity. Electrocardiography is essential in patients with suspected cardiotoxic plant ingestion.
Prehospital care focuses on airway, breathing, and circulation. Syrup of ipecac is not recommended. Plant material should be collected in a paper bag for identification.
Emergency department management is largely supportive. Airway protection and cardiac monitoring are priorities. Intravenous fluids should be administered for dehydration or hypotension, with vasopressors initiated if fluid resuscitation fails. Anticholinergic agitation is treated with benzodiazepines, and physostigmine may be considered for severe delirium. Cardiac glycoside toxicity with significant bradycardia, tachydysrhythmias, or hyperkalemia warrants digoxin-specific antibody fragments. Cyanogenic toxicity with severe lactic acidosis or hemodynamic instability should be treated with hydroxocobalamin or a cyanide antidote kit. Atropine is indicated for bradycardia associated with sodium channel–active plant toxins. Calcium oxalate exposures are managed with irrigation, analgesia, and airway monitoring. Toxalbumin and pyrrolizidine alkaloid exposures require supportive care and specialist consultation.
Patients require admission if they develop dysrhythmias, refractory hypotension, altered mental status, intractable vomiting, metabolic acidosis, or evidence of end-organ damage. Children should be admitted with a lower threshold due to smaller lethal doses and less specific symptoms. Patients may be discharged if they return to baseline mental status, tolerate oral intake, demonstrate stable cardiac function, and have no anticipated delayed toxicity.
Death from unintentional plant ingestion is rare, but intentional ingestion, misuse of herbal preparations, or consumption of highly toxic species can be fatal. Early recognition of toxidromes and consultation with poison control or a medical toxicologist are essential to optimize outcomes.
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