B. Zane Horowitz
EPIDEMIOLOGY
Plants are very common ingestions; young children account for 70% to 80% of all plant-related exposures. Fatalities are extremely rare.
Mushroom ingestions account for 8000 exposures annually, and less than 5 deaths per year.
Amanita species are responsible for 95% of fatalities associated with mushrooms in the United States.
PATHOPHYSIOLOGY
Toxins found in plants and mushrooms produce effects that range from mild gastrointestinal (GI) symptoms to organ failure and death.
Mushrooms with psilocybin- and psilocin-containing toxins have neuroactive chemicals with effects similar to lysergic acid diethylamide (LSD), producing hallucinogenic effects; they are often intentionally ingested for their mind-altering effects.
Mushrooms that contain gyromitrin, a compound that is broken down to monomethyl hydrazine, can cause seizures. It inhibits the enzyme pyridoxal phosphate, which is responsible for formation of vitamin B6 Without vitamin B6the CNS neurotransmitter GABA cannot be formed, and refractory seizures occur.
Amanita phalloides contain amanitin, which is well absorbed in the intestines, is actively transported into the liver, and undergoes enterohepatic circulation. Amanitin binds to hepatocytes and inhibit formation of messenger RNA, leading to delayed onset of liver failure.
Coprinus atramentarius (inky cap) mushrooms contain the amino acid coprine, which is converted to L-aminocyclopropanol by the liver. This compound inhibits aldehyde dehydrogenase, preventing breakdown of alcohol, identical in its mechanism of action to an Antabuse (disulfiram) reaction.
Ricin, a potent toxalbumin found in castor beans, produces severe cytotoxic effects in multiple organ systems.
Amygdalin, found in the pits of peaches, apricots, pears, crab apples, and hydrangea, is metabolized to hydrocyanic acid, and can lead to acute cyanide poisoning if the pits are crushed and ingested in sufficient quantities.
Cardiogenic glycosides are found in foxglove, oleander, and lily of the valley (Table 130-1).
TABLE 130-1 Symptoms and Treatment of Severely
CLINICAL FEATURES
Cicutoxin, found in water hemlock, produces severe GI symptoms, followed by delirium, seizures, and death.
Direct irritation and chemical burns to the oropharynx have been reported after ingestion of Abrus (rosary pea), Capsicum (ornamental peppers), Daphne, Dieffenbachia, and Rhododendron.
Cardiovascular symptoms, including hypotension, dysrhythmias, and conduction defects, have been reported after ingestion of aconitine, Convallaria, Taxus, Rhododendron, and oleander, and may be life threatening.
Jimson weed, henbane, and nightshade berries contain atropine-like alkaloids that can cause an acute anti-cholinergic crisis.
Urushiol, found in Toxicodendron species (poison ivy, oak, and sumac), produces a contact dermatitis in sensitized individuals.
Seizures may be seen after ingestion of Conium, water hemlock, and gyromitrin-containing mushrooms.
Ingestion of Amanita species of mushrooms produces delayed onset of GI symptoms 6 to 48 hours after ingestion. Manifestations of hepatic failure develop 1 to 3 days after exposure.
Cortinarius orellanus and Amanita smithiana mushrooms contain nephrotoxic compounds, which result in delayed onset of renal failure.
Consuming alcohol after ingestion of coprine-containing mushrooms will result in a disulfiram-like reaction. Facial flushing, nausea and vomiting, diaphoresis, palpitations, hypotension, and weakness can be observed 2 to 72 hours after ingestion.
Mushrooms with ibotenic acid and muscimol cause early-onset stimulatory neurologic symptoms, followed by sedation.
Inocybe and Clitocybe species containing muscarine cause early-onset cholinergic effects, characterized by the SLUDGE syndrome (salivation, lacrimation, urination, defecation, gastrointestinal hypermotility, and emesis).
DIAGNOSIS AND DIFFERENTIAL
Diagnosis of plant and mushroom poisoning is clinical, based on history of ingestion, with confirmation by a mycologist or botanist.
Early GI toxicity of mushroom poisoning (within 1-2 hours of ingestion) generally indicates a benign course.
Delayed GI toxicity of mushroom poisoning (greater than 6 hours) suggests a more toxic ingestion, which can lead to hepatic failure, renal failure, and even death (Table 130-2).
Physical examination should include a search for evidence of cholinergic, anticholinergic, or sympathetic nervous system stimulation.
If delayed-onset GI symptoms suggest cytotoxic mushroom poisoning, electrolytes, blood urea nitrogen, creatinine, liver enzymes, and coagulation studies should be obtained.
Ingestion of cardiotoxic plants warrants ECG monitoring and serial potassium levels.
TABLE 130-2 Mushrooms: Symptoms, Toxicity, and Treatment
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Initial treatment for plant-related and mushroom poisoning is supportive, with priority given to airway management, ventilation, fluid resuscitation, and seizure control.
Activated charcoal should be considered only for suspected plants and mushrooms of high toxicity if presenting within 1 to 2 hours of ingestion.
Controversy exists as to the best treatment for amanitin-containing mushrooms but generally utilized modalities include silimarin, 1 gram PO four times daily, or its purified alkaloid, silibinin, 5 milligrams/kg IV over 1 hour, followed by 20 milligrams/kg/d as a constant infusion.
High-dose penicillin therapy, 0.3 to l.0 millionunits/kg/d of penicillin G, is recommended for amatoxin poisoning; it blocks the uptake of amatoxin into the liver.
Intravenous N-acetylcysteine is often used for amanitin toxins at the same doses used to treat acetaminophen poisoning.
Rapid progression to hepatic encephalopathy, hepatorenal syndrome, and coagulopathy are indications for liver transplantation. Consider transfer to a liver transplant setting and ICU care early in the course of mushroom ingestions.
High-dose pyridoxine, 25 milligrams/kg IV, is recommended for patients presenting with neurologic symptoms and seizures associated with gyromitrin.
Fluid and electrolyte replacement and hemodialysis are the mainstays of treatment for renal failure.
Patients with potential amanitin, gyromitrin, or orel-lanine poisoning, or those with refractory symptoms, require admission and monitoring for at least 48 hours. All other patients who are asymptomatic after 6 to 8 hours of treatment and observation can be discharged.
Atropine may be administered to patients with severe muscarinic symptoms.
Digoxin-specific Fab antibodies can be used for heart block and dysrhythmias from cardiogenic glycoside containing plants.
Jimson weed ingestions with anticholinergic delirium may be treated with physostigmine.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 214, “Mushroom Poisoning,” by Anne F. Brayer, Sandra M. Schneider, and Arif Alper Cevik, and Chapter 215, “Poisonous Plants,” by Mark A. Hostetler and Sandra M. Schneider.