Version May 2024
INTRODUCTION — This topic discusses the management of mushroom poisoning. The clinical manifestations and evaluation of mushroom poisoning and more detailed discussion of diagnosis and treatment of poisoning with amatoxin-containing mushrooms are discussed in greater detail separately:
●(See "Clinical manifestations and evaluation of mushroom poisoning".)
APPROACH TO MANAGEMENT — Ingestion of potentially poisonous mushrooms occurs frequently, but serious toxicity is uncommon [1]. There are 12 groups of identified mushroom toxins with 14 described clinical syndromes (table 1). Defining which clinical syndrome predominates, initiating general supportive care, and administering any specific treatments for that syndrome are the key steps in the initial management for mushroom ingestion [2].
Supportive care and gastrointestinal decontamination with activated charcoal suffice for proper management of most patients with mushroom poisoning [3].
Patients who ingest potentially lethal mushrooms (eg, Amanita virosa, Amanita phalloides, Cortinarius orellanus, Gyromitra esculenta) typically develop signs of toxicity more than six hours after ingestion [2,4]. However, clinical manifestations of poisoning that occur less than six hours after ingestion do not exclude the potential for life-threatening toxicity, especially when more than one type of mushroom has been eaten. When specific therapy is necessary, it is guided by clinical presentation (table 1). (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Mushroom poisoning syndromes' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Mushroom identification'.)
A regional poison control center should be contacted to discuss likely mushroom species ingested based upon clinical findings, identification of any mushrooms available for analysis, and treatment of specific toxic effects. Most poison control centers maintain active call lists of mycologists who are knowledgeable concerning local prevalence of mushroom genera and species and can assist in mushroom identification. (See 'Additional resources' below.)
SUPPORTIVE CARE — Recommendations for care of children and adults with mushroom poisoning are primarily derived from case series and reports and are driven by physical findings. After initial assessment and support of airway, breathing, and circulation as needed, the clinician should anticipate and aggressively manage fluid losses caused by vomiting and diarrhea, which are common findings after toxic mushroom ingestion. The clinician should also be ready to treat symptoms caused by any of the toxic mushrooms (table 1). (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Mushroom poisoning syndromes'.)
GASTROINTESTINAL DECONTAMINATION — We recommend that patients who are alert and present for care within one hour of a potentially toxic mushroom ingestion receive activated charcoal (AC). The recommendation of AC administration following toxic mushroom exposure derives from indirect evidence of benefit in volunteers and in animal studies, as well as from evidence of benefit following ingestions of other medications. Mushrooms, like most complex xenobiotics, bind well to AC. Because of adverse effects, such as vomiting and volume depletion, the combination of a cathartic (eg, sorbitol) and AC should be used sparingly, if at all, and only a single dose of a cathartic should ever be given to any patient. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Activated charcoal' and "Gastrointestinal decontamination of the poisoned patient", section on 'Cathartics'.)
The greatest benefit occurs if AC is given within one hour. The efficacy of AC as a function of time from ingestion is discussed in detail separately. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Evidence of efficacy and adverse effects'.)
We recommend that patients who ingest potentially toxic mushrooms not undergo gastric emptying by gastric lavage or syrup of ipecac in the emergency department. Syrup of ipecac administered in remote locations far from medical treatment soon after pediatric ingestion may prevent toxicity [5]. Most serious mushroom poisonings are only detected hours after ingestion, and exploratory ingestions by children typically consist of small ingestions that rarely have serious consequences [5]. Furthermore, randomized controlled trials show minimal benefit and possible risk to patients who undergo gastric emptying after poisoning. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Indications' and "Gastrointestinal decontamination of the poisoned patient", section on 'Syrup of Ipecac'.)
ELIMINATION ENHANCEMENT — Multiple dose activated charcoal (MDAC) does not appear to improve poisoning outcomes after ingestion of mushrooms other than amatoxin-containing mushrooms. The use of MDAC for management of poisoning after ingestion of amatoxin-containing mushrooms is discussed separately. (See "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment", section on 'Management'.)
Hemodialysis or hemoperfusion do not remove significant amounts of mushroom toxins.
SPECIFIC CLINICAL SYNDROMES
Vomiting and diarrhea — Vomiting and diarrhea may be caused by any of the toxic mushrooms and can also occur when certain edible species are not cooked prior to eating (Morchella species in particular) [2-4,6].
Vomiting may be safely treated with an antiemetic (eg, ondansetron 0.15 mg/kg intravenously) and does not increase the amount of absorbed toxin. Antispasmodic agents (eg, loperamide) should be avoided in patients with diarrhea. Intravenous fluids should be given based upon clinical assessment of losses and evidence of dehydration. Patients with signs of shock should receive prompt fluid resuscitation (algorithm 1) (see "Treatment of severe hypovolemia or hypovolemic shock in adults" and "Shock in children in resource-abundant settings: Initial management" and "Maintenance and replacement fluid therapy in adults" and "Treatment of hypovolemia (dehydration) in children in resource-abundant settings").
If more serious mushroom poisoning cannot be excluded, patients should undergo initial baseline laboratory testing and be admitted for 24 to 48 hours to rule out progression to more serious conditions (eg, liver failure, renal failure). (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Ancillary studies' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed symptom onset (>6 hours after ingestion)' and 'Disposition' below.)
Disulfiram-like reaction — Vomiting, headache, flushing, pruritus, chest pain, palpitations, tachypnea, confusion, and anxiety can occur with coingestion of coprine-containing mushrooms and ethanol. The onset of symptoms is rapid, occurring within hours of drinking ethanol. It can also occur when ethanol is consumed days after the mushroom is ingested because coprine has prolonged duration of action since its metabolites irreversibly inhibit aldehyde dehydrogenase. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Disulfiram-like reaction'.)
Patients suspected to have a disulfiram reaction and who have chest pain require evaluation for myocardial infarction and other serious etiologies. (See "Evaluation of the adult with chest pain in the emergency department".)
Disulfiram reactions are self-limited and managed with supportive care. The severity and duration of the reaction depends upon the amount of ethanol ingested and can last for several hours but as long as one day. Supportive therapies include the following [7]:
●Vomiting – Ondansetron; avoid promethazine or metoclopramide, which may worsen hypotension
●Orthostatic hypotension/shock – Trendelenburg positioning and boluses of crystalloid solution (eg, 1 L normal saline or lactated Ringer); continuous infusion of norepinephrine if hypotension is unresponsive to fluid therapy
●Skin flushing and pruritus – Diphenhydramine
Some experts would administer fomepizole (4-methylpyrazole) to a patient who develops a serious or life-threatening disulfiram reaction (severe, persistent vomiting; chest pain; or shock) and has a detectable serum ethanol concentration. Fomepizole inhibits alcohol dehydrogenase and prevents the metabolism of ethanol to acetaldehyde. Small case series have found that fomepizole reversed severe disulfiram reactions in patients with co-ingestion of disulfiram and ethanol, including those with nonspecific electrocardiogram (ECG) changes and chest pain and those with hypotension unresponsive to fluid administration and norepinephrine [8-10]. Although not specifically studied for co-ingestion of coprine and ethanol, the positive evidence for disulfiram and ethanol co-ingestion can be extrapolated to this scenario since coprine and disulfiram have a similar pharmacologic mechanism of action.
Agitation, delirium, and/or hallucinations — Central nervous system (CNS) excitation with hallucinations may occur after ingestion of mushrooms that contain psilocybin, psilocin, muscimol, or ibotenic acid [2,11-13]. Patients with these findings should initially receive benzodiazepines (eg, midazolam 0.05 mg/kg, typical maximum single dose 2 mg or lorazepam 0.05 to 0.1 mg/kg, typical maximum single dose 2 to 4 mg) and be placed in a quiet room. In some cases, physical restraints may also be necessary. Physostigmine should be avoided since CNS excitation is not caused by anticholinergic effects. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Hallucinations' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'CNS excitation and depression' and "Intoxication from LSD and other common hallucinogens", section on 'Agitation and dysphoria'.)
Seizures — Seizures are associated with ingestion of mushrooms that contain gyromitrin, or in children, muscimol or ibotenic acid [5,14]. Initial treatment includes oxygenation, support of airway and breathing, and administration of benzodiazepines (eg, lorazepam 0.05 to 0.1 mg/kg, typical maximum single dose 2 to 4 mg) (table 2 and algorithm 2). Pyridoxine (eg, 70 mg/kg intravenously up to 5 g) should be given to patients with possible ingestion of gyromitrin-containing mushrooms and patients with unknown mushroom ingestion whose seizures are not controlled with standard anticonvulsant therapy including benzodiazepines [14]. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed gastroenteritis, seizures, and liver toxicity' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'CNS excitation and depression'.)
Cholinergic excess — Cholinergic symptoms include vomiting, diarrhea, salivation, bronchorrhea, bronchospasm, and bradycardia [15]. Treatment consists of administration of anticholinergic medications until drying of respiratory secretions has occurred (eg, in adults, atropine 1 to 2 mg intravenously; in children, 0.02 mg/kg intravenously up to single dose maximum of 2 mg, or glycopyrrolate 10 mcg/kg intravenously, typical maximum single dose: 0.2 mg). (See "Organophosphate and carbamate poisoning", section on 'Atropine'.)
Persistent vomiting may be treated with ondansetron (eg, 0.1 mg/kg intravenously, maximum typical single dose 4 mg).
Bronchospasm may be treated with inhaled albuterol combined with ipratropium bromide using typical dosing for children (table 3 and table 4) and adults (table 5). Intravenous fluids should be given based upon clinical assessment of losses and evidence of dehydration. Patients with signs of shock should receive prompt fluid resuscitation (algorithm 1). (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Cholinergic poisoning' and "Treatment of severe hypovolemia or hypovolemic shock in adults" and "Shock in children in resource-abundant settings: Initial management" and "Maintenance and replacement fluid therapy in adults" and "Treatment of hypovolemia (dehydration) in children in resource-abundant settings".)
Rhabdomyolysis — Patients with rhabdomyolysis typically present with the triad of pigmented granular casts in the urine, a red to brown color of the urine supernatant, and a marked elevation in the plasma creatine kinase (CK) concentration one to three days after eating the mushroom Tricholoma equestre [16] (see "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed rhabdomyolysis').
A more rapid-onset rhabdomyolysis has been associated with ingestion of certain Russula species of mushroom (Russula subnigricans). In addition to fatigue and muscle weakness, elevation of the CK can occur within hours in some patients who ingest these mushrooms, although delayed rhabdomyolysis has been reported as well [17]. It is thought that the toxin cyclprop-2-ene carboxylic acid is the causative agent for the myotoxic Russula species.
The primary treatment goals are similar to rhabdomyolysis from other causes and are discussed in detail elsewhere. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)
●Fluid repletion with normal saline infusion (20 to 40 mL/kg per hour up to 1 to 2 L per hour) – The emergency provider should closely monitor urine output with the goal of maintaining a minimum urine flow of 4 mL/kg per hour; 200 mL per hour in adults. Alkalinization of the urine or the use of mannitol to increase diuresis may be associated with adverse effects and the efficacy of these strategies is uncertain. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Bicarbonate in selected patients' and "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Mannitol'.)
●Evaluation for significant electrolyte abnormalities (hyperkalemia, hyperphosphatemia, and hypocalcemia) – Management of hyperkalemia is of particular importance. Hypocalcemia is usually transient and calcium administration should be avoided unless severe symptoms (eg, tetany) are present. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Metabolic abnormalities'.)
Liver failure — Patients who have evidence of liver toxicity or who develop signs of delayed gastroenteritis or seizures after mushroom ingestion have a high risk of developing acute liver failure caused by amatoxin- or gyromitrin-containing mushrooms. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed gastroenteritis and liver toxicity' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed gastroenteritis, seizures, and liver toxicity'.)
Early consultation with a regional poison control center is strongly encouraged. Initial management consists of intensive fluid resuscitation if hypovolemic shock is present, initiation of elimination enhancement with multiple-dose activated charcoal, and supportive care of liver toxicity. (See "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment", section on 'Symptomatic (gastroenteritis, delayed hepatotoxicity)' and "Acute liver failure in adults: Management and prognosis".)
Because of the complexities involved, patients with acute liver failure should be managed in an intensive care unit in centers with an active liver transplant program. Patients admitted to hospitals without a transplant program should be transferred as soon as possible and ideally before the onset of the severe coagulopathy and increased intracranial pressure that may make later transfer dangerous.
Renal failure — Delayed renal insufficiency is associated with ingestion of mushrooms that contain orellanine or allenic norleucine [18,19]. The major complications of renal failure include volume overload, hyperkalemia, metabolic acidosis, hypocalcemia, and hyperphosphatemia. The initial assessment therefore includes the careful evaluation of volume status and measurement of serum electrolytes, particularly potassium and bicarbonate, and evaluation of a complete blood count and serum phosphate, calcium, albumin and uric acid. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Acute gastroenteritis and delayed renal failure' and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed renal failure'.)
Accepted indications for dialysis in patients with renal failure generally include (see "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose"):
●Fluid overload that is refractory to diuretics
●Hyperkalemia (serum potassium concentration >6.5 mEq/L) or rapidly rising serum potassium, as can occur in rhabdomyolysis
●Metabolic acidosis (arterial pH less than 7.1)
●Signs of uremia, such as pericarditis, neuropathy, or an otherwise unexplained decline in mental status
Erythromelalgia — Erythromelalgia is characterized by burning pain, swelling, and reddening or flushing in the extremities. Ingestion of Clitocybe species including acromelalga and amoenolens has been associated with the development of erythromelalgia. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Erythromelalgia'.)
Treatment consists of supportive care (eg, elevation of the extremities to reduce edema) and pain control. One case of rapid improvement in pain and erythema after intravenous and oral nicotinic acid therapy has been described [20,21].
Shitake dermatitis — Dermatitis is characterized by pruritic, erythematous, flagellate eruptions on either the trunk or the extremities 2 hours to 5 days after ingestion of raw or undercooked shitake mushrooms (Lentinula edodes). (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Shiitake dermatitis'.)
Treatment is supportive. Corticosteroids and antihistamines can be used in severe cases.
Immune-mediated hemolytic anemia — Care is supportive and includes treatment of shock, transfusion for low hemoglobin and bleeding, and management of intravascular hemolysis and organ injury, primarily kidney and liver failure. Plasmapheresis has been proposed for severe cases [22,23].
ANTIDOTES — For most mushroom poisonings, supportive care is the main treatment. However, specific antidotes are available for some mushroom poisonings and may be helpful for patients with seizures and delayed gastroenteritis, methemoglobinemia, cholinergic excess, or severe disulfiram reactions:
●Patients who have ingested mushrooms that contain gyromitrin and who develop seizures should receive pyridoxine (70 mg/kg, maximum dose: 5 g) in addition to standard anticonvulsant therapy (eg, lorazepam) (algorithm 2). This therapy reverses pyridoxal-5-phosphate deficiency in the CNS mediated by the toxic metabolite, monomethylhydrazine [3]. (See 'Seizures' above and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Delayed gastroenteritis, seizures, and liver toxicity'.)
●Patients who develop methemoglobinemia after consumption of mushrooms that contain gyromitrin may benefit from the administration of methylene blue (1 to 2 mg/kg slowly infused over five minutes) if methemoglobin is above 20 percent or causing symptoms. (See "Methemoglobinemia", section on 'Management (acquired/toxic)'.)
●Patients with evidence of cholinergic excess and respiratory distress should receive anticholinergic agents (eg, atropine intravenously, 0.02 mg/kg intravenously, minimum single dose: 0.1 mg, typical maximum single dose: 1 mg, or glycopyrrolate 10 mcg/kg intravenously, typical maximum single dose: 0.2 mg). (See 'Cholinergic excess' above and "Clinical manifestations and evaluation of mushroom poisoning", section on 'Cholinergic poisoning' and "Organophosphate and carbamate poisoning", section on 'Atropine'.)
●Some experts would administer fomepizole (15 mg/kg intravenously) to patients with suspected serious or life-threatening disulfiram reactions (severe, persistent vomiting; chest pain; or shock) with a detectable serum ethanol concentration after ingestion of coprine-containing mushrooms. (See 'Disulfiram-like reaction' above.)
DISPOSITION — Consultation with a regional or international poison control center is advised to assist with disposition decisions. (See 'Additional resources' below.)
The following patients warrant hospital admission [2]:
●Patients with delayed symptoms more than six hours after mushroom ingestion
●Patients with early symptoms less than three hours after mushroom ingestion who remain symptomatic beyond six hours despite supportive care or who ingested more than one type of mushroom
●Patients with evidence of rhabdomyolysis, liver toxicity, or renal insufficiency
●Asymptomatic patients in whom ingestion of amatoxin-containing mushrooms is strongly suspected
●Asymptomatic patients in whom follow-up at 24 hours cannot be assured
Asymptomatic patients in whom evaluation at 24 hours is assured may be discharged. Patients with early symptoms that resolve and in whom the ingestion of delayed toxicity mushrooms can be reliably excluded based upon history, clinical manifestations, and when possible, mushroom identification, may also be discharged with follow-up by phone or in person at 24 hours.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
SUMMARY AND RECOMMENDATIONS
●Approach – Mushroom poisoning occurs frequently, but serious toxicity is uncommon. In most cases, the specific species of mushroom consumed is unknown. Classification of poisoning based upon clinical presentation (table 1) is most helpful in guiding further treatment and more quickly arrives at the type of mushroom ingested in most instances. A regional poison control center should be contacted to help determine likely mushroom species ingested based upon clinical findings, identification of any mushrooms available for analysis, and treatment of specific toxic effects. (See 'Approach to management' above.)
●Supportive care – After careful assessment and support of airway, breathing, and circulation as needed, the clinician should anticipate and aggressively manage fluid losses caused by vomiting and diarrhea, which are common findings after toxic mushroom ingestion. (See 'Supportive care' above.)
●Gastrointestinal decontamination – In an alert patient who presents for care within one hour of a potentially toxic mushroom ingestion, we recommend treatment with activated charcoal (Grade 1B). (See 'Gastrointestinal decontamination' above.)
In a patient who ingests a potentially toxic mushroom, we recommend they not undergo gastric emptying by gastric lavage or syrup of ipecac in the emergency department (Grade 1B). (See 'Gastrointestinal decontamination' above.)
●Specific clinical syndromes – The table (table 1) presents the specific clinical syndromes of mushroom poisoning and their treatment. (See 'Specific clinical syndromes' above.)
●Antidotes – Specific antidotes are available for some mushroom poisonings and may be helpful for patients with seizures and delayed gastroenteritis, methemoglobinemia, or cholinergic excess (see 'Antidotes' above):
•Seizures from gyromitrin – Treat with pyridoxine (70 mg/kg, maximum dose: 5 g) in addition to standard anticonvulsant therapy (eg, lorazepam) (algorithm 2). (See 'Seizures' above.)
•Methemoglobinemia from gyromitrin – Treat with methylene blue (1 to 2 mg/kg slowly infused over five minutes) if methemoglobin is above 20 percent or causing symptoms. (See "Methemoglobinemia", section on 'Management (acquired/toxic)'.)
•Cholinergic excess and respiratory distress – Treat with anticholinergic agents (eg, atropine 0.02 mg/kg intravenously, minimum single dose: 0.1 mg, typical maximum single dose: 1 mg; or glycopyrrolate 10 mcg/kg intravenously, typical maximum single dose: 0.2 mg). (See 'Cholinergic excess' above.)
•Disulfiram reaction - Some experts would administer fomepizole (15 mg/kg intravenously) to a patient with suspected serious or life-threatening disulfiram reaction (severe, persistent vomiting; chest pain; or shock) with a detectable serum ethanol concentration after ingestion of coprine-containing mushrooms. (See 'Disulfiram-like reaction' above.)
●Disposition – The following patients warrant hospital admission (see 'Disposition' above):
•Patients with delayed symptoms more than six hours after mushroom ingestion
•Patients with early symptoms less than three hours after mushroom ingestion who remain symptomatic beyond six hours despite supportive care or who ingested more than one type of mushroom
•Patients with evidence of rhabdomyolysis, liver toxicity, or renal insufficiency
•Asymptomatic patients in whom ingestion of amatoxin-containing mushrooms is strongly suspected
•Asymptomatic patients in whom follow-up at 24 hours cannot be assured
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