Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

MUSHROOMS-GENERAL

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management covers general mushrooms and is most useful when the identification of the mushroom is NOT proved. Other POISINDEX Managements discuss various mushroom toxins in more detail and should be used for the specific mushrooms that have been identified as species that contain the appropriate mycotoxin. The specific mushroom toxins will vary, depending on the genus and species of the mushroom involved (Barbato, 1993). Because of this, accurate identification of the mushroom is of utmost importance.
    1) For Cyclopeptides-containing mushrooms (Amatoxins): See management Mushrooms-cyclopeptides
    2) For Gyromitrin-containing mushrooms: See management Mushrooms-monomethylhydrazine
    3) For Muscarine-containing mushrooms: See management Mushrooms-muscarine/histamine
    4) For Coprine-containing mushrooms: See management Mushrooms-coprine
    5) For Ibotenic acid- and muscimol-containing mushrooms: See management Mushrooms-muscimol/ibotenic acid
    6) For Psilocybin-containing mushrooms: See management Mushrooms-hallucinogenic
    7) For Gastrointestinal toxins-containing mushrooms: See management Mushrooms-gastrointestinal
    8) For Orellanine-and orellinine-containing mushrooms: See management Mushrooms-orellanine/orelline
    9) For Amanita smithiana; Amanita proxima; Amanita pseudoporphyria; Amanita boudieri; Amanita echinocephala; Amanita gracilior mushrooms: See management Mushrooms-select Amanita species/acute renal failure
    10) For Rhabdomyolysis-associated mushrooms: See management Mushroom-induced rhabdomyolysis
    11) For Erythromelalgia-associated mushrooms: See management Mushroom-induced erythromelalgia
    12) For Immunohemolytic syndrome-associated mushrooms: See management Mushroom-induced immunohemolytic syndrome

Specific Substances

    1) General mushrooms
    2) Mushrooms-Unspecified
    3) Unspecified mushrooms

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Wild mushrooms are ingested by adults for sustenance, as delicacy foods, and as drugs of abuse. Children ingest mushrooms while exploring the environment. The mushroom should be identified by a qualified mycologist whenever possible (most often available through a poison center). Obtain a thorough patient history including description of the sample, the location where it was picked, and the timing of the onset of any symptoms. If no mushroom sample is available, the history and description may give clues to expected effects. The specific appropriate Poisindex management should be used if the mushroom has been identified. This document should be used to assist in the case of a patient who has ingested a mushroom that has not been identified.
    B) TOXICOLOGY: The toxins vary depending upon the mushroom ingested.
    C) EPIDEMIOLOGY: Mushroom ingestions in both children and adults are common. Severe toxicity is uncommon and death is extremely rare.
    D) WITH POISONING/EXPOSURE
    1) Adverse effects depend on the type of mushroom ingested. In general, the mushrooms that produce serious, potentially life-threatening toxicity are characterized by a delayed onset of signs and symptoms (6 hours or more). Patients who develop signs and symptoms within 3 hours of mushroom ingestion have generally ingested a mushroom that does not cause life-threatening toxicity.
    2) CYCLOPEPTIDE-CONTAINING MUSHROOMS - AMATOXINS
    a) PHASE 1 (6 to 24 hours postingestion): sudden onset of sharp colicky abdominal pain, nausea, vomiting, thirst, and stools containing blood and mucous shreds, lasting several hours.
    b) PHASE 2: a period of well being, lasting a few hours. This phase may be lacking in extreme cases.
    c) PHASE 3 (2 to 4 days postingestion): abdominal pain recurs; jaundice, renal shutdown, seizures, coma, and death.
    3) GYROMITRIN-CONTAINING MUSHROOMS - MONOMETHYLHYDRAZINE (MMH)
    a) After a latent period of 6 to 12 hours, the patient experiences a feeling of fullness in the stomach, which precedes vomiting, and watery diarrhea, which may persist for 2 days. Seizures may rarely occur following ingestion of MMH-containing mushrooms.
    b) Headache, lassitude, cramps, muscle spasms, and intense pain in the region of the liver and stomach are followed by jaundice and cyanosis unresponsive to oxygen.
    4) MUSCARINE-CONTAINING MUSHROOMS
    a) Onset usually 15 to 30 minutes postingestion; signs include excessive perspiration, salivation, lacrimation, bradycardia, miosis, blurred vision, increased peristalsis, crampy abdominal pain, watery stools, reduced blood pressure, pulmonary congestion, and asthmatic wheezing.
    5) COPRINE-CONTAINING MUSHROOMS
    a) Onset usually occurs within 20 minutes to 2 hours of ingestion of alcohol up to 5 days after the mushroom is eaten. Additional symptoms include flushing of the face and neck with throbbing distention of neck veins; swelling and paresthesia in the hands and feet; metallic taste; tachycardia; and chest pains. Later symptoms include nausea, vomiting, and sweating. Severe reactions may lead to hypotension, angioedema, and bronchospasm.
    6) IBOTENIC ACID AND MUSCIMOL-CONTAINING MUSHROOMS
    a) Onset usually occurs within 30 to 90 minutes (most marked at 2 to 3 hours) postingestion; the patient experiences a feeling of drowsiness, which is followed by a state resembling alcohol intoxication. Following this is a state of confusion, dizziness, ataxia, euphoria (may progress to hyperkinetic activity), muscle cramps or spasms, delirium, visual disturbances, and hallucinations lasting 4 to 12 hours. Vomiting is the most commonly reported symptom in Amanita muscaria cases, while vomiting is rare in Amanita pantherina cases. Drowsiness and coma-like sleep follow. Recovery is often rapid.
    7) PSILOCYBIN-CONTAINING MUSHROOMS
    a) Onset usually occurs within 30 to 60 minutes (occasionally as late as 3 hours). Signs include mood pleasant or apprehensive, impaired judgement, poor performance ability, unmotivated hyperkinetic compulsive movements, laughter, mydriasis, vertigo, ataxia, paresthesias, muscle weakness, and drowsiness progressing to sleep.
    8) GASTROINTESTINAL IRRITANT MUSHROOMS
    a) Onset usually occurs within 30 minutes to 2 hours; signs include nausea, vomiting, abdominal cramps, and diarrhea (mild to severe). In many cases the symptoms subside spontaneously in 3 to 4 hours, and recovery is usually complete within 1 to 2 days.
    9) ORELLANINE AND ORELLININE-CONTAINING MUSHROOMS
    a) Onset usually occurs in 36 hours to 14 days; signs include gastrointestinal upset, nausea, anorexia, headache, rigors, severe thirst, muscle aching, polyuria or oliguria, and acute renal failure.
    0.2.21) CARCINOGENICITY
    A) Some mushrooms, such as members of the "False Morel," genus Gyromitra, have been proven to be carcinogenic in animals. Other genera, such as Agaricus, may also contain carcinogenic substances.

Laboratory Monitoring

    A) Labs are not indicated in the majority of patients.
    B) Patients with significant gastrointestinal toxicity, or patients in whom the mushroom cannot be identified or who have onset of symptoms 6 hours or more after ingestion should have a basic metabolic panel and liver enzymes monitored.
    C) Urinalysis and urine electrolytes should be obtained in patients with evidence of renal insufficiency.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) The specific appropriate Poisindex management should be used if the mushroom has been identified. Treatment should be focused on symptomatic management and supportive care. Overall, drug intervention is rarely required.
    B) DECONTAMINATION
    1) PREHOSPITAL: No prehospital decontamination is indicated.
    2) HOSPITAL: Activated charcoal should be given to patients that present early and do not have significant gastrointestinal toxicity or CNS depression. Gastric lavage should be considered in patients presenting early with confirmed ingestion of mushrooms containing amatoxin.
    C) AIRWAY MANAGEMENT
    1) Airway management should be considered for patients with angioedema or bronchospasm unresponsive to IV antihistamines. Airway protection should be employed as needed for airway protection in patients with significant CNS depression.
    D) ANTIDOTE
    1) Penicillin G should be considered for treatment of amatoxin induced hepatotoxicity. It may displace amatoxin from plasma protein binding sites and possibly inhibit its uptake into hepatocytes. The dose is 300,000 to 1,000,000 units/day. The medication silibinin is currently undergoing clinical trials for amatoxin-induced hepatotoxicity. The dose ranges from 20 to 50 mg/kg/day until there is clinical improvement. Pyridoxine 5 grams IV should be given for seizures associated with Gyromitra mushroom ingestion.
    E) HYPOTENSION
    1) Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULTS: begin infusion at 0.5 to 1 mcg/min: CHILDREN: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    F) SEIZURES
    1) Administer a benzodiazepine IV; DIAZEPAM (ADULTS: 5 to 10 mg, repeat every 10 to 15 min as needed. CHILDREN: 0.2 to 0.5 mg/kg, repeat every 5 min as needed) or LORAZEPAM (ADULTS: 2 to 4 mg; CHILDREN: 0.05 to 0.1 mg/kg). It is important to avoid overtreatment, especially in Ibotenic acid/muscimol poisonings in which hyperactivity/aggression typically alternate with periods of lethargy/coma. Oversedation can result in severe CNS depression. MONOMETHYLHYDRAZINE-CONTAINING MUSHROOMS (Gyromitra spp.) - PYRIDOXINE: Administer pyridoxine (empiric dose: 5 g IV) for persistent seizures despite benzodiazepine therapy. Consider phenobarbital or propofol if seizures are persistent despite benzodiazepine and pyridoxine treatment.
    G) NAUSEA AND VOMITING
    1) Patients with nausea and vomiting should be given antiemetics (ADULTS: Ondansetron 4 mg IV or orally, CHILDREN: 0.15 mg/kg).
    H) DISULFIRAM-LIKE REACTION
    1) Patients with disulfiram-like reaction should be treatment with fluids and antihistamine administration (ADULTS: diphenhydramine 25 to 50 mg IV or orally, CHILDREN: 1 mg/kg).
    I) RENAL INSUFFICIENCY
    1) Patients should be hydrated with isotonic fluids. Dialysis is rarely necessary and should only be considered in oliguric or anuric patients.
    J) AGITATION
    1) Patients should be kept in a dimly lit room with little sensory stimulation. Rarely sedatives, such as benzodiazepines or antipsychotics are necessary to control agitation.
    K) ENHANCED ELIMINATION
    1) There is no role for extracorporeal elimination of mushroom toxins.
    L) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients in whom the ingestion of amatoxin containing mushrooms can be excluded (either because they do not grow in the area, or because the onset of gastrointestinal toxicity is within 2 hours and only one type of mushroom was ingested, or by a mycologist identifying the mushroom in question) may be managed at home. Patients with mild nausea and vomiting symptoms can be managed at home.
    2) OBSERVATION CRITERIA: Patients who ingested hallucinogenic mushrooms may be observed until asymptomatic. Patients with significant gastrointestinal toxicity should be observed until they are rehydrated and can tolerate oral fluids.
    3) ADMISSION CRITERIA: Patients that develop seizures, renal failure, or hepatotoxicity, should be admitted to the hospital. Patients who may have ingested amatoxin containing mushrooms should be admitted, even if not yet symptomatic.
    4) CONSULT CRITERIA: A mycologist should be consulted in regions where toxic mushroom species are endemic. A toxicologist should be consulted for patients with seizures, renal failure, severe disulfiram-like reaction, or hepatotoxicity. A hepatologist or transplant surgeon should be consulted in cases of hepatic failure.
    M) PITFALLS
    1) In regions where toxic mushroom species are not endemic, sending asymptomatic patients to healthcare facilities is not necessary. However, in regions where amatoxin containing mushrooms are found, adequate history must be sought to reasonably exclude ingestion of these species prior to making a decision to keep patients at home since decontamination is time-dependent. Oversedating patients with ibotenic acid/muscimol containing mushrooms may lead to a prolonged hospital stay. Failure to treat a monomethylhydrazine-containing mushroom ingestion with pyridoxine may lead to recalcitrant seizures. If patients have eaten more than one type of mushroom, the timing of the onset of symptoms cannot be used to exclude the possibility of amatoxin containing mushroom ingestion.
    N) TOXICOKINETICS
    1) Dependent upon the specific mushroom and the specific species ingested.
    O) DIFFERENTIAL DIAGNOSIS
    1) Ingestion of other plant species may yield to gastrointestinal or anticholinergic toxicity. In patients ingesting mushrooms for abuse purposes, other illicit drug ingestions should be considered.
    0.4.3) INHALATION EXPOSURE
    A) Inhalation of the fumes of monomethylhydrazine (MMH) from cooking mushrooms of genus Gyromitra may lead to MMH intoxication.
    B) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Contrary to popular belief, handling toxic mushrooms should NOT lead to the dermal absorption of mushroom toxins. However, RARELY, heavy exposure to Ibotenic acid/Muscimol containing Amanita muscaria has caused symptoms.

Range Of Toxicity

    A) TOXICITY: Mushroom species range from being nontoxic to lethal, depending on the type of mushroom toxin present, and the amount present in the particular mushroom ingested. For more specific information, consult the POISINDEX Management on the particular mushroom toxin.

Clinical Effects

Summary Of Exposure

    A) USES: Wild mushrooms are ingested by adults for sustenance, as delicacy foods, and as drugs of abuse. Children ingest mushrooms while exploring the environment. The mushroom should be identified by a qualified mycologist whenever possible (most often available through a poison center). Obtain a thorough patient history including description of the sample, the location where it was picked, and the timing of the onset of any symptoms. If no mushroom sample is available, the history and description may give clues to expected effects. The specific appropriate Poisindex management should be used if the mushroom has been identified. This document should be used to assist in the case of a patient who has ingested a mushroom that has not been identified.
    B) TOXICOLOGY: The toxins vary depending upon the mushroom ingested.
    C) EPIDEMIOLOGY: Mushroom ingestions in both children and adults are common. Severe toxicity is uncommon and death is extremely rare.
    D) WITH POISONING/EXPOSURE
    1) Adverse effects depend on the type of mushroom ingested. In general, the mushrooms that produce serious, potentially life-threatening toxicity are characterized by a delayed onset of signs and symptoms (6 hours or more). Patients who develop signs and symptoms within 3 hours of mushroom ingestion have generally ingested a mushroom that does not cause life-threatening toxicity.
    2) CYCLOPEPTIDE-CONTAINING MUSHROOMS - AMATOXINS
    a) PHASE 1 (6 to 24 hours postingestion): sudden onset of sharp colicky abdominal pain, nausea, vomiting, thirst, and stools containing blood and mucous shreds, lasting several hours.
    b) PHASE 2: a period of well being, lasting a few hours. This phase may be lacking in extreme cases.
    c) PHASE 3 (2 to 4 days postingestion): abdominal pain recurs; jaundice, renal shutdown, seizures, coma, and death.
    3) GYROMITRIN-CONTAINING MUSHROOMS - MONOMETHYLHYDRAZINE (MMH)
    a) After a latent period of 6 to 12 hours, the patient experiences a feeling of fullness in the stomach, which precedes vomiting, and watery diarrhea, which may persist for 2 days. Seizures may rarely occur following ingestion of MMH-containing mushrooms.
    b) Headache, lassitude, cramps, muscle spasms, and intense pain in the region of the liver and stomach are followed by jaundice and cyanosis unresponsive to oxygen.
    4) MUSCARINE-CONTAINING MUSHROOMS
    a) Onset usually 15 to 30 minutes postingestion; signs include excessive perspiration, salivation, lacrimation, bradycardia, miosis, blurred vision, increased peristalsis, crampy abdominal pain, watery stools, reduced blood pressure, pulmonary congestion, and asthmatic wheezing.
    5) COPRINE-CONTAINING MUSHROOMS
    a) Onset usually occurs within 20 minutes to 2 hours of ingestion of alcohol up to 5 days after the mushroom is eaten. Additional symptoms include flushing of the face and neck with throbbing distention of neck veins; swelling and paresthesia in the hands and feet; metallic taste; tachycardia; and chest pains. Later symptoms include nausea, vomiting, and sweating. Severe reactions may lead to hypotension, angioedema, and bronchospasm.
    6) IBOTENIC ACID AND MUSCIMOL-CONTAINING MUSHROOMS
    a) Onset usually occurs within 30 to 90 minutes (most marked at 2 to 3 hours) postingestion; the patient experiences a feeling of drowsiness, which is followed by a state resembling alcohol intoxication. Following this is a state of confusion, dizziness, ataxia, euphoria (may progress to hyperkinetic activity), muscle cramps or spasms, delirium, visual disturbances, and hallucinations lasting 4 to 12 hours. Vomiting is the most commonly reported symptom in Amanita muscaria cases, while vomiting is rare in Amanita pantherina cases. Drowsiness and coma-like sleep follow. Recovery is often rapid.
    7) PSILOCYBIN-CONTAINING MUSHROOMS
    a) Onset usually occurs within 30 to 60 minutes (occasionally as late as 3 hours). Signs include mood pleasant or apprehensive, impaired judgement, poor performance ability, unmotivated hyperkinetic compulsive movements, laughter, mydriasis, vertigo, ataxia, paresthesias, muscle weakness, and drowsiness progressing to sleep.
    8) GASTROINTESTINAL IRRITANT MUSHROOMS
    a) Onset usually occurs within 30 minutes to 2 hours; signs include nausea, vomiting, abdominal cramps, and diarrhea (mild to severe). In many cases the symptoms subside spontaneously in 3 to 4 hours, and recovery is usually complete within 1 to 2 days.
    9) ORELLANINE AND ORELLININE-CONTAINING MUSHROOMS
    a) Onset usually occurs in 36 hours to 14 days; signs include gastrointestinal upset, nausea, anorexia, headache, rigors, severe thirst, muscle aching, polyuria or oliguria, and acute renal failure.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) There have been occasional reports of contact dermatitis or allergic reactions to inhaled spores involving a wide range of species. Probably the most common species associated with contact dermatitis are Suillus spp, especially those with viscid cap cuticles, including Suillus americanus, S luteus, S granulatus, S tomentosus; Phallus impudicus; P hadriani, and possibly other "stink horn" species, apparently caused by contact with the slime covering the heads (Rietschel et al, 2008; Beug et al, 2006; Bruhn & Soderberg, 1991).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) There have been occasional reports of contact dermatitis or allergic reactions to inhaled spores involving a wide range of species. Probably the most common species associated with contact dermatitis are Suillus spp, especially those with viscid cap cuticles, including Suillus americanus, S luteus, S granulatus, S tomentosus; Phallus impudicus; P hadriani, and possibly other "stink horn" species, apparently caused by contact with the slime covering the heads (Rietschel et al, 2008; Beug et al, 2006; Bruhn & Soderberg, 1991).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) Some mushrooms, such as members of the "False Morel," genus Gyromitra, have been proven to be carcinogenic in animals. Other genera, such as Agaricus, may also contain carcinogenic substances.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Labs are not indicated in the majority of patients.
    B) Patients with significant gastrointestinal toxicity, or patients in whom the mushroom cannot be identified or who have onset of symptoms 6 hours or more after ingestion should have a basic metabolic panel and liver enzymes monitored.
    C) Urinalysis and urine electrolytes should be obtained in patients with evidence of renal insufficiency.

Methods

    A) CHROMATOGRAPHY
    1) Some mushroom toxins can be identified by utilization of high pressure liquid chromatography (HPLC).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients that develop seizures, renal failure, or hepatotoxicity, should be admitted to the hospital. Patients who may have ingested amatoxin containing mushrooms should be admitted, even if not yet symptomatic.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients in whom the ingestion of amatoxin containing mushrooms can be excluded (either because they do not grow in the area, or because the onset of gastrointestinal toxicity is within 2 hours and only one type of mushroom was ingested, or by a mycologist identifying the mushroom in question) may be managed at home. Patients with mild nausea and vomiting symptoms can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A mycologist and toxicologist should be consulted as soon as possible in order to guide proper treatment.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients who ingested hallucinogenic mushrooms may be observed until asymptomatic. Patients with significant gastrointestinal toxicity should be observed until they are rehydrated and can tolerate oral fluids.
    B) The mushroom specimen should be kept in a paper bag in the refrigerator (DO NOT FREEZE) for 24 hours in case more detailed identification is warranted.

Monitoring

    A) Labs are not indicated in the majority of patients.
    B) Patients with significant gastrointestinal toxicity, or patients in whom the mushroom cannot be identified or who have onset of symptoms 6 hours or more after ingestion should have a basic metabolic panel and liver enzymes monitored.
    C) Urinalysis and urine electrolytes should be obtained in patients with evidence of renal insufficiency.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) No prehospital decontamination is indicated.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Activated charcoal should be given to patients that present early and do not have significant gastrointestinal toxicity or CNS depression. Gastric lavage should be considered in patients presenting early with confirmed ingestion of mushrooms containing amatoxin.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    1) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    D) PRECAUTIONS:
    1) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    2) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    E) LAVAGE FLUID:
    1) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    2) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    3) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    F) COMPLICATIONS:
    1) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    2) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    G) CONTRAINDICATIONS:
    1) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) SUPPORT
    1) The specific appropriate Poisindex management should be used if the mushroom has been identified. Treatment should be focused on symptomatic management and supportive care. Overall, drug intervention is rarely required.
    B) ANTIDOTE
    1) Penicillin G should be considered for treatment of amatoxin induced hepatotoxicity. It may displace amatoxin from plasma protein binding sites and possibly inhibit its uptake into hepatocytes. The dose is 300,000 to 1,000,000 units/day. The medication silibinin is currently undergoing clinical trials for amatoxin-induced hepatotoxicity. The dose ranges from 20 to 50 mg/kg/day until there is clinical improvement. Pyridoxine 5 grams IV should be given for seizures associated with Gyromitra mushroom ingestion.
    C) MONITORING OF PATIENT
    1) Labs are not indicated in the majority of patients.
    2) Patients with significant gastrointestinal toxicity should have a basic metabolic panel and liver enzymes monitored.
    3) Urinalysis and urine electrolytes should be obtained in patients with evidence of renal insufficiency.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) NOTE: It is important to avoid overtreatment, especially in Ibotenic acid/muscimol poisonings in which hyperactivity/aggression typically alternate with periods of lethargy/coma. Oversedation can result in severe CNS depression.
    3) MONOMETHYLHYDRAZINE-CONTAINING MUSHROOMS (Gyromitra spp.) - PYRIDOXINE: Administer pyridoxine (empiric dose: 5 g IV) for persistent seizures despite benzodiazepine therapy.
    4) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    5) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    6) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    7) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    8) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    F) NAUSEA AND VOMITING
    1) Patients with nausea and vomiting should be given antiemetics (ADULTS: Ondansetron 4 mg IV or orally, CHILDREN: 0.15 mg/kg).
    G) DISULFIRAM ADVERSE REACTION
    1) Patients with disulfiram-like reaction should be treatment with fluids and antihistamine administration (ADULTS: diphenhydramine 25 to 50 mg IV or orally, CHILDREN: 1 mg/kg).
    H) PSYCHOMOTOR AGITATION
    1) Patients should be kept in a dimly lit room with little sensory stimulation. Rarely sedatives, such as benzodiazepines or antipsychotics are necessary to control agitation.
    2) INDICATION
    a) If patient is severely agitated, sedate with IV benzodiazepines.
    3) DIAZEPAM DOSE
    a) ADULT: 5 to 10 mg IV initially, repeat every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    4) LORAZEPAM DOSE
    a) ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed (Manno, 2003).
    b) CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    5) Extremely large doses of benzodiazepines may be required in patients with severe intoxication in order to obtain adequate sedation. Titrate dose to clinical response and monitor for hypotension, CNS and respiratory depression, and the need for endotracheal intubation.
    I) DELIRIUM
    1) Sedatives may be administered for anxiety, hysteria, or hallucinations. Seizures may occasionally occur in children.

Inhalation Exposure

    6.7.2) TREATMENT
    A) FUME
    1) Inhalation of fumes from cooking Gyromitra may cause acute symptoms of Monomethyhydrazine (MMH) poisoning since the toxin is very volatile, with a boiling point of 87.5 degrees C.
    B) PNEUMONITIS
    1) Inhalation of large numbers of spores of mushrooms or other nonpathogenic fungi (molds, rusts, smuts, mildews, etc) may cause a syndrome resembling bronchopneumonia similar to "dust pneumonia." These cases have been reported as "respiratory disease of Mushroom Workers-Farmer's Lung" (Bringhurst et al, 1959), or "Mushroom Worker's Pneumonitis" (Lockey, 1974).
    2) Workers in the commercial production of mushrooms have been involved but probably NOT from the inhalation of spores of the mushrooms themselves (since these are harvested before full maturity or appreciable release of spores) but more likely from the inhalation of dust and spores from the compost used to grow the mushrooms (Bringhurst et al, 1959). This dust has been shown to contain many microorganisms, both bacterial and fungal, both pathogenic and saprophytic (Kleyn & Wetzler, 1981).
    3) At far greater risk are individuals involved in the handling of other moldy vegetable products such as hay, straw, soybean vines, compost, grain, etc. Such illnesses have been described as "Farmer's Lung" (Dickie & Rankin, 1958) or "Thresher's Lung" (Tornell, 1946) when caused by handling moldy or spoiled hay, "Silo-Filler's Disease" (Delaney et al, 1956) Lowry & Schuman, 1956; (Grayson, 1956) when caused by inhalation of smut spores in the fodder or nitrogen dioxide produced in the fermentation of silage, or "pulmonary moniliasis" (Zettergren, 1950) when pathogenic fungus spores are inhaled.
    a) Chronic inhalation of fungus spores may result in chronic obstructive lung disease, "Farmer's Lung," again NOT a poisoning or a condition for which a treatment management is provided in POISINDEX.
    b) The diagnosis and management of these diseases is NOT within the scope of this management. Nor are the allergic diseases, "mold induced asthma," (Salvaggio & Aukrust, 1981) respiratory, or skin diseases produced by pathogenic fungi, or the effects of mycotoxins (Hayes, 1980) (especially the carcinogenic aflatoxins) produced by fungus infections of food-producing plants discussed here.
    4) The only known cases of acute pneumonitis produced by the inhalation of mushroom spores are those in which the old folk-remedy of staunching blood flow with the contents of puffballs has been used to stop nosebleeds. In these cases, large quantities of puffball spores were inhaled and an acute pneumonitis resulted (Strand et al, 1967).
    a) For the acute phase of this inhalation pneumonitis, treat as any other case of inhalation pneumonitis; corticosteroid therapy may be helpful.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL ABSORPTION
    1) Merely handling poisonous mushrooms is NOT sufficient to cause intoxications. There should be NO dermal absorption of the mycotoxins.
    B) DERMAL DECONTAMINATION
    1) Wash hands well before eating, after handling mushroom specimens.

Enhanced Elimination

    A) SUMMARY
    1) There is no role for extracorporeal elimination of mushroom toxins.

Abstracts

Case Reports

    A) OTHER
    1) MUSHROOM POISON CASE REGISTRY
    a) MUSHROOM POISON CASE REGISTRY
    1) Mushroom poisoning cases may be reported to the North American Mycological Association's Mushroom Poisoning Case Registry. Reporting is voluntary and patient confidentiality is maintained.
    2) Forms may be obtained from the website and completed forms or questions may be sent to:
    3) Dr. Michael W. Beug, PO Box 116, Husum, WA 98623; phone: (509) 493-2237
    4) Alternatively, reports may be submitted online at www.sph.umich.edu/~kwcee/mpcr. The website also contains a list of volunteers from different regions of North America willing to assist in the identification of mushrooms.
    B) Encephalopathy has occurred in patients with renal failure who ingested Pleurocybella porrigens. This is an edible mushroom, but in Japan it has been reported to cause encephalopathy. This effect has not been observed in the United States (Saviuc & Danel, 2006).

Range Of Toxicity

Summary

    A) TOXICITY: Mushroom species range from being nontoxic to lethal, depending on the type of mushroom toxin present, and the amount present in the particular mushroom ingested. For more specific information, consult the POISINDEX Management on the particular mushroom toxin.

Minimum Lethal Exposure

    A) Mushroom species range from being nontoxic to lethal, depending on the type of mushroom toxin present, and the amount present in the particular mushroom ingested. For more specific information, consult the POISINDEX Management on the particular mushroom toxin.

Maximum Tolerated Exposure

    A) Mushroom species range from being nontoxic to lethal, depending on the type of mushroom toxin present, and the amount present in the particular mushroom ingested. For more specific information, consult the POISINDEX Management on the particular mushroom toxin.
    B) It should be understood that the synthesis of poisons in a species is subject to the same laws that govern variation in other characteristics, such as in anatomical and morphological details. Not every fruiting body of a mushroom should be expected to contain as much poison as every other fruit body of the same size and weight (Smith, 1978).

Pharmacology Toxicology

Toxicologic Mechanism

    A) Mushroom toxins are chemicals that are produced and stored within the mushroom fruiting body. Although they are present in small amounts, their potency can allow for symptoms to be produced with the ingestion of small amounts.

Animal Toxicology

Clinical Effects

    11.1.13) OTHER
    A) OTHER
    1) Effects in animals will most often be the same as in humans.

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Treatment is essentially the same as for human victims.
    2) SUMMARY
    a) Begin treatment immediately.
    b) Keep animal warm and do not handle unnecessarily.
    c) Remove the patient and other animals from the source of contamination or remove dietary sources.
    3) Treatment should always be done on the advice and with the consultation of a veterinarian.
    4) Additional information regarding treatment of poisoned animals may be obtained from a Veterinary Toxicologist or the National Animal Poison Control Center.
    5) ASPCA ANIMAL POISON CONTROL CENTER
    a) ASPCA Animal Poison Control Center, 1717 S Philo Road, Suite 36 Urbana, IL 61802
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) Contact information: (888) 426-4435 (hotline) or www.aspca.org (A fee may apply. Please inquire with the poison center). The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) EMESIS/GASTRIC LAVAGE -
    1) CAUTION: Carefully examine patients with chemical exposure before inducing emesis. If signs of oral, pharyngeal, or esophageal irritation, a depressed gag reflex, or central nervous system excitation or depression are present, EMESIS SHOULD NOT BE INDUCED.
    2) HORSES OR CATTLE: DO NOT attempt to induce emesis in ruminants (cattle) or equids (horses).
    3) DOGS AND CATS
    a) IPECAC: If within 2 hours of exposure: induce emesis with 1 to 2 milliliters/kilogram syrup of ipecac per os.
    b) APOMORPHINE: Dogs may vomit more readily with 1 tablet (6 milligrams) apomorphine diluted in 3 to 5 milliliters water and instilled into the conjunctival sac or per os.
    1) Dogs may also be given apomorphine intravenously at 40 micrograms/kilogram, although this route may not be as effective.
    4) LAVAGE: In the absence of a gag reflex or if vomiting cannot be induced, place a cuffed endotracheal tube and begin gastric lavage.
    a) Pass large bore stomach tube and instill 5 to 10 milliliters/kilogram water or lavage solution, then aspirate. Repeat 10 times.
    b) ACTIVATED CHARCOAL/CATHARTIC -
    1) ACTIVATED CHARCOAL: Administer activated charcoal. Dose: 2 grams/kilogram per os or via stomach tube. Avoid aspiration by proper restraint, careful technique, and if necessary tracheal intubation.
    2) CATHARTIC: Administer a dose of a saline or sorbitol cathartic such as magnesium or sodium sulfate (sodium sulfate dose is 1 gram/kilogram). If access to these agents is limited, give 5 to 15 milliliters magnesium oxide (Milk of Magnesia) per os for dilution.
    3) ACTIVATED CHARCOAL/HORSES: Administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube. Neonates: administer 250 grams (one-half pound) activated charcoal in up to 2 quarts water.
    4) ACTIVATED CHARCOAL/RUMINANTS: Administer 2 to 9 grams/ kilogram of activated charcoal in a slurry of 1 gram charcoal/3 to 5 milliliters warm water via stomach tube. Sheep may be given 0.5 kilogram charcoal in slurry.
    5) CATHARTICS/HORSES: Mineral oil is administered 30 minutes after activated charcoal. DOSE: 4 to 6 liters in adult horses and 1 to 4 liters in neonates or foals.
    a) Magnesium sulfate: 0.2 to 0.9 grams/kilogram (500 grams for adults).
    b) The sulfate laxatives are especially effective when given 30 to 45 minutes after mineral oil administration.
    c) Carbachol (lentin): administer 1 milligram to an adult.
    6) CATHARTICS/RUMINANTS & SWINE: Adult cattle: administer 500 grams sodium or magnesium sulfate. Other ruminants and swine: administer 1 to 2 grams/kilogram.
    a) The sulfate laxatives are especially effective when given 30 to 45 minutes after cathartic administration.
    b) Mineral oil: Do not administer within 30 minutes of activated charcoal. DOSE: small ruminants and swine, 60 to 200 milliliters; cattle, 0.5 to 1 gallon.
    c) Magnesium oxide: (Milk of Magnesia) Small ruminants, up to 0.25 gram/kilogram in 1 to 3 gallons warm water; adult cattle up to 1 gram/kilogram in 1 to 3 gallons warm water or 2 to 4 boluses MgOH per os.
    d) Give these solutions via stomach tube and monitor for aspiration.
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) This agent may cause hepatotoxicity. Monitoring liver function tests is suggested for patients with significant exposure.

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Treatment is essentially the same as for human victims.
    2) SUMMARY
    a) Begin treatment immediately.
    b) Keep animal warm and do not handle unnecessarily.
    c) Remove the patient and other animals from the source of contamination or remove dietary sources.
    3) Treatment should always be done on the advice and with the consultation of a veterinarian.
    4) Additional information regarding treatment of poisoned animals may be obtained from a Veterinary Toxicologist or the National Animal Poison Control Center.
    5) ASPCA ANIMAL POISON CONTROL CENTER
    a) ASPCA Animal Poison Control Center, 1717 S Philo Road, Suite 36 Urbana, IL 61802
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) Contact information: (888) 426-4435 (hotline) or www.aspca.org (A fee may apply. Please inquire with the poison center). The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) EMESIS/GASTRIC LAVAGE -
    1) CAUTION: Carefully examine patients with chemical exposure before inducing emesis. If signs of oral, pharyngeal, or esophageal irritation, a depressed gag reflex, or central nervous system excitation or depression are present, EMESIS SHOULD NOT BE INDUCED.
    2) HORSES OR CATTLE: DO NOT attempt to induce emesis in ruminants (cattle) or equids (horses).
    3) DOGS AND CATS
    a) IPECAC: If within 2 hours of exposure: induce emesis with 1 to 2 milliliters/kilogram syrup of ipecac per os.
    b) APOMORPHINE: Dogs may vomit more readily with 1 tablet (6 milligrams) apomorphine diluted in 3 to 5 milliliters water and instilled into the conjunctival sac or per os.
    1) Dogs may also be given apomorphine intravenously at 40 micrograms/kilogram, although this route may not be as effective.
    4) LAVAGE: In the absence of a gag reflex or if vomiting cannot be induced, place a cuffed endotracheal tube and begin gastric lavage.
    a) Pass large bore stomach tube and instill 5 to 10 milliliters/kilogram water or lavage solution, then aspirate. Repeat 10 times.
    b) ACTIVATED CHARCOAL/CATHARTIC -
    1) ACTIVATED CHARCOAL: Administer activated charcoal. Dose: 2 grams/kilogram per os or via stomach tube. Avoid aspiration by proper restraint, careful technique, and if necessary tracheal intubation.
    2) CATHARTIC: Administer a dose of a saline or sorbitol cathartic such as magnesium or sodium sulfate (sodium sulfate dose is 1 gram/kilogram). If access to these agents is limited, give 5 to 15 milliliters magnesium oxide (Milk of Magnesia) per os for dilution.
    3) ACTIVATED CHARCOAL/HORSES: Administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube. Neonates: administer 250 grams (one-half pound) activated charcoal in up to 2 quarts water.
    4) ACTIVATED CHARCOAL/RUMINANTS: Administer 2 to 9 grams/ kilogram of activated charcoal in a slurry of 1 gram charcoal/3 to 5 milliliters warm water via stomach tube. Sheep may be given 0.5 kilogram charcoal in slurry.
    5) CATHARTICS/HORSES: Mineral oil is administered 30 minutes after activated charcoal. DOSE: 4 to 6 liters in adult horses and 1 to 4 liters in neonates or foals.
    a) Magnesium sulfate: 0.2 to 0.9 grams/kilogram (500 grams for adults).
    b) The sulfate laxatives are especially effective when given 30 to 45 minutes after mineral oil administration.
    c) Carbachol (lentin): administer 1 milligram to an adult.
    6) CATHARTICS/RUMINANTS & SWINE: Adult cattle: administer 500 grams sodium or magnesium sulfate. Other ruminants and swine: administer 1 to 2 grams/kilogram.
    a) The sulfate laxatives are especially effective when given 30 to 45 minutes after cathartic administration.
    b) Mineral oil: Do not administer within 30 minutes of activated charcoal. DOSE: small ruminants and swine, 60 to 200 milliliters; cattle, 0.5 to 1 gallon.
    c) Magnesium oxide: (Milk of Magnesia) Small ruminants, up to 0.25 gram/kilogram in 1 to 3 gallons warm water; adult cattle up to 1 gram/kilogram in 1 to 3 gallons warm water or 2 to 4 boluses MgOH per os.
    d) Give these solutions via stomach tube and monitor for aspiration.

References

General Bibliography

    1) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    2) Aji DY, Caliskan S, & Nayir A: Haemoperfusion in Amanita phalloides poisoning. J Trop Ped 1995; 41:371-374.
    3) Barbato MP: Poisoning from accidental ingestion of mushrooms. Med J Aust 1993; 158:842-847.
    4) Bedry R, Baudrimont I, Deffieux G, et al: Wild-mushroom intoxication as a cause of rhabdomyolysis.. N Engl J Med 2001; 345:798-802.
    5) Benjamin DR: Mushrooms poisons and panaceas: A handbook for naturalists, mycologists and physicians, W. H. Freeman and Company, New York, NY, 1995.
    6) Beug MW, Shaw M, & Cochran KW: Thirty-plus years of mushroom poisoning: Summary of the approximately 2,000 reports in the NAMA case registry. McIllvainea 2006; 16(2):47-68.
    7) Bringhurst LS, Byrne RN, & Gershon-Cohen J: Respiratory disease of mushroom workers, farmer's lung. JAMA 1959; 171:101-104.
    8) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    9) Bruhn JN & Soderberg MD: Allergic contact dermatitis caused by mushrooms. A case report and literature review. Mycopathologia 1991; 115(3):191-195.
    10) Cappell MS & Hassan T: Gastrointestinal and hepatic effects of Amanita- phalloides ingestion. J Clin Gastroenterol 1992; 15:225-228.
    11) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
    12) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    13) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    14) Chodorowski Z, Waldman W, & Anand JS: Acute poisoning with Tricholoma equestre. Przeglad Lekarski 2002; 59:386-387.
    15) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    16) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    17) Cochran KW: Personal Communication, 1988.
    18) Delaney LT, Schmidt HW, & Stroebel CF: Silo-filler's disease. Proc Staff Meet Mayo Clin 1956; 31:189-187.
    19) Diaz JH: Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med 2005; 33:427-436.
    20) Dickie HA & Rankin J: Farmer's lung: acute granulomatous interstitital pneumonitis occurring in agricultural workers. JAMA 1958; 167:1069-1076.
    21) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    22) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    23) Flammer R & Gallen S: Hemolysis in mushroom poisoning: facts and hypotheses (German). Schweiz Med Wochenschr 1983; 113(42):1555-1561.
    24) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    25) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    26) Grayson RR: Silage gas poisoning: nitrogen dioxide pneumonia, new disease in agricultural workers. Ann Intern Med 1956; 45:393-408.
    27) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    28) Hatfield GM: "Toxic Mushrooms" In: Kinghorn AD (ed.) Toxic Plants, Columbia Univ. Press, New York, NY, 1979, pp 7-58.
    29) Hayes AW: Mycotoxins: a review of biological effects and their role in human diseases. Clin Toxicol 1980; 17:45-83.
    30) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    31) Himmelmann A, Mang G, & Schnorf-Huber S: Lethal ingestion of stored Amanita phalloides mushrooms. Swiss Med Wkly 2001; 131:616-617.
    32) Howland MA: Antidotes in Depth. In: Goldfrank LR, Flomenbaum N, Hoffman RS, et al, eds. Goldfrank's Toxicologic Emergencies. 8th ed., 8th ed. McGraw-Hill, New York, NY, 2006, pp 826-828.
    33) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    34) Iwafuchi Y, Morita T, Kobayashi H, et al: Delayed onset acute renal failure associated with Amanita pseudoporphyria Hongo ingestion. Intern Med 2003; 42(1):78-81.
    35) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    36) Kleyn JG & Wetzler TF: The microbiology of spent mushroom compost and its dust. Microbial 1981; 27:748-753.
    37) Leathem AM, Purssell RA, & Chan VR: Renal failure caused by mushroom poisoning. Clin Tox 1997; 35:67-75.
    38) Lee PT, Wu ML, Tsai WJ, et al: Rhabdomyolysis: an unusual feature with mushroom poisoning. Am J Kid Dis 2001; 38:E17.
    39) Lockey SD: Mushroom worker's pneumonitis. Ann Allergy 1974; 33:282.
    40) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    41) Madaus Inc.: Intravenous Milk Thistle (Silibinin-Legalon) for Hepatic Failure Induced by Amatoxin/Amanita Mushroom Poisoning. ClinicalTrials.gov: a service of the US National Institutes of Health. Bethesda, MD. 2009. Available from URL: http://clinicaltrials.gov/ct2/show/NCT00915681. As accessed 2010-01-13.
    42) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    43) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    44) Omidynia E, Rashidpourai R, & Qaderi MT: Case report - Mycetismus in Hamadan, of West Iran. Southeast Asian J Trop Med Pub 1997; 28:438-439.
    45) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    46) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    47) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    48) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    49) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    50) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    51) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    52) Rietschel RL, Fowler JF, & Fisher AA: Allergic Sensitization to Plants. In: Fisher's Contact Dermatitis, 6th edition, PMPH-USA, Shelton, CT, 2008, pp 405-453.
    53) Rivett MJ & Boon GPG: Mushroom (Amanita phalloides) poisoning in Ciskei. S Afr Med J 1988; 73:317.
    54) Salvaggio J & Aukrust L: Mold-induced asthma. J Allergy Clin Immunol 1981; 68:327-346.
    55) Satora L: Non-specific mushroom poisoning (letter). Vet Human Toxicol 2004; 46(4):224.
    56) Saviuc P & Danel V: New syndromes in mushroom poisoning. Toxicol Rev 2006; 25(3):199-209.
    57) Saviuc PF, Danel VC, Moreau PAM, et al: Erythromelalgia and mushroom poisoning. Clin Toxicol 2001; 39(4):403-407.
    58) Scalzo A, Blume C, & Weber J: Amanita bisporigera - dose related toxicity from intentional abuse (abstract). J Tox-Clin Tox 1998; 36:456.
    59) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    60) Serne EH, Toorians AW, & Gietema JA: Amanita phalloides, a potentially lethal mushroom: its clinical presentation and therapeutic options. Neth J Med 1996; 49:19-23.
    61) Shaw M: Amateur opportunity. In: Rumack BH, Spoerke DG, eds. Handbook of Mushroom Poisoning: Diagnosis and Treatment. 1st ed, 1st. CRC Press Inc., Boca Raton, FL, 1994.
    62) Smith AH: Poisonous mushrooms: their habitats, geographic distributions, and physiological variation within species. In: Rumack BH & Salzman E (eds) Mushroom Poisoning: Diagnosis and Treatment, CRC Press, West Palm Beach, FL, 1978, pp 59-65.
    63) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    64) Tornell E: Thresher's lung: fungoid disease resembling tuberculosis or morbus schaumann. Acta Med Scand 1946; 125:191-219.
    65) Vale JA, Kulig K, American Academy of Clinical Toxicology, et al: Position paper: Gastric lavage. J Toxicol Clin Toxicol 2004; 42:933-943.
    66) Vale JA: Position Statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997; 35:711-719.
    67) Warden CR & Benjamin DR: Acute renal failure associated with suspected Amanita smithiana mushroom ingestions: a case series. Acad Emer Med 1998; 5:808-812.
    68) Yamada EG, Mohle-Boetani J, & Olson KR: Mushroom poisoning due to Amatoxin. West J Med 1998; 169:380-384.
    69) Zettergren L: Thresher's lung (pulmonary moniliasis): experimental investigation. Upsala lakaref forh 1950; 55:257-313.
    70) deHaro L, Jouglard J, Arditti J, et al: [Acute renal insufficiency caused by Amanita proxima poisoning: experience of the Poison Center of Marseille]. Nephrologie 1998; 19(1):21-24.