Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

MUSHROOMS-HALLUCINOGENIC

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The psilocybin-containing mushrooms are commonly referred to as Psilocybin-containing mushrooms.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) Conocybe cyanopus - (no common name)
    2) Copelandia cyanescens - "Panaeolus cyanescens"
    3) Conocybe smithii - "Blue-stemmed Galera"
    4) Gymnopilus aeruginosus - "Green Pholiota"
    5) Gymnopilus luteus - (no common name)
    6) Gymnopilus spectabilis - "Showy Pholiota"
    7) Gymnopilus validipes - (no common name)
    8) Gymnopilus viridans - (no common name)
    9) Panaeolus alter - "Panaeolus fimicola"
    10) Panaeolus cambodginiensis
    11) Panaeolus campanulatus - "Bell-shaped Panaeolus", "Panaeolus papilionaceus"
    12) Panaeolus cyanescens
    13) Panaeolus foenisecii - "Haymaker's Panaeolus or Lawn Mower's mushroom or Mower's mushroom"
    14) Panaeolina foenisecii - "Panaeolus foensecii", "Lawn Mower's mushroom"; "Mower's mushroom"
    15) Panaeolus papilionaceus - "Panaeolus campanulatus", "P. retirugis", "P. sphinctrinus"
    16) Panaeolus sphinctrinus - "Panaeolus papilionaceus"
    17) Panaeolus subbalteatus - "Girdled Panaeolus"
    18) Panaeolus tropicalis
    19) Pluteus salicinus - (no common name)
    20) Psilocybe baeocystis - "Potent Psilocybe"
    21) Psilocybe caerulipes - "Blue-foot Psilocybe"
    22) Psilocybe caerulescens
    23) Psilocybe cubensis
    24) Psilocybe cyanescens - "Bluing Psilocybe"
    25) Psilocybe mexicana
    26) Psilocybe pelliculosa - "Liberty Caps"
    27) Psilocybe semilanceata - "Liberty Caps"
    28) Psilocybe silvatica
    29) Psilocybe strictipes - (no common name)
    30) Psilocybe stunzii - "Stuntz's Blue Legs"
    31) Stropharia semiglobata - "Halfglobe Mushroom"
    32) Psilocybe subaeruginosa
    33) Psilocybe tampanensis
    34) Stropharia coronilla
    35) Stropharia species
    COMMON NAMES
    1) Blue legs
    2) Funny mushrooms
    3) Blue-stemmed Galera - "Common name for Conocybe smithii"
    4) Green Pholiota - " Common name for Gymnopilus aeruginosa "
    5) Showy Pholiota - " Common name for Gymnopilus spectabilis"
    6) Bell-shaped Panaeolus - "Common name for Panaeolus campanulatus "
    7) Haymaker's Panaeolus - "Common name for Panaeolus foenisecii "
    8) Girdled Panaeolus - "Common name for Panaeolus subbalteatus"
    9) Liberty cap
    10) Magic mushrooms
    11) Potent Psilocybe - "Common name for Psilocybe baeocystis"
    12) Blue-foot Psilocybe - "Common name for Psilocybe caerulipes"
    13) Bluing Psilocybe - "Common name for Psilocybe cyanescens"
    14) Liberty Caps - "Common name for Psilocybe pelliculosa"
    15) Liberty Caps - "Common name for Psilocybe semilanceata"
    16) Stuntz's Blue Legs - "Common name for Psilocybe stunzii"
    17) Halfglobe Mushroom - "Common name for Stropharia semiglobata"
    18) Lawn Mower's mushroom - " Common name for Panaeolina foenisecii and Panaeolus foenisecii"
    19) Mower's mushroom - "Common name for Panaeolina foenisecii and Panaeolus foenisecii"
    SYNONYMS FOR THE GROUP
    1) Mushrooms-psilocybe
    2) Psilocybin
    3) Psilocin
    4) 4-hydroxy-N,N-dimethyltryptamine
    5) 4-phosphoryloxy-N,N-dimethyltryptamine

Available Forms Sources

    A) FORMS
    1) The amount of psilocybin and psilocin in collections of Pacific Northwest mushrooms picked for their hallucinogenic effect ranged from 0.1 percent to nearly 2 percent, by dry weight. Psilocybin is most often encountered, but psilocin was usually present as well (though psilocin was NEVER detected in the absence of psilocybin) (Beug & Bigwood, 1982).
    a) One P. cubensis (psilocybe) contains 10 mg of psilocybin/gram of dry mushroom weight. Hallucinations may occur following 4 to 10 mg of psilocybin (Berger & Guss, 2005).
    2) Many of the Psilocybe species are small, brown nondescript mushrooms that may be mistaken for the lethal Galerina species (See Group 1-CYCLOPEPTIDES).
    3) ONSET OF SYMPTOMS - Occurs within 20 to 30 minutes of ingestion (Berger & Guss, 2005).
    4) DURATION OF SYMPTOMS - May continue for an average of 6 to 8 hours (Berger & Guss, 2005).
    B) USES
    1) The abuse of hallucinogenic mushrooms is still prevalent. In a recent report of Danish students, 7.2% had used these mushrooms. Seventy-five percent had used them four or fewer times (Lassen et al, 1993).

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: These mushrooms are most often deliberately used by persons seeking hallucinogenic effects. Inadvertent ingestion of these mushrooms by a person mistaking them for edible mushrooms has rarely been reported. Some "street mushrooms" are treated with synthetic hallucinogens such as d-lysergic acid (LSD) and N,N-dimethyltryptamine (DMT).
    B) TOXICOLOGY: "Street mushrooms" may be adulterated with LSD. Psilocybin and psilocin are structurally similar to LSD and presumed to act at serotonin receptors. Effects are primarily central (hallucinogenic), but there are some peripheral effects. They also produce effects through serotonergic action. Toxins are heat-stable.
    C) EPIDEMIOLOGY: In most communities, mushrooms are less commonly abused than most other recreational drugs. Most users do not come to medical attention and severe toxicity is rare. Psilocybin-containing genera with species known to cause the majority of exposures are Psilocybe, Panaeolus, Copelandia, Gymnopilus, Pluteus, and Conocybe.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: PHYSICAL EFFECTS: Dilated pupils (develops in over 90% of cases), confusion, vertigo, drowsiness, nausea, vomiting, tachycardia, and mild hypertension. PSYCHOTROPIC EFFECTS: Sense of exhilaration, hallucinations including vivid bright colors and shapes, euphoria, distortion of sense of time, dysesthesias, anxiety, perceptual distortions (may result in either a pleasant or apprehensive mood; "good" or "bad" trip), and impaired judgement. Hallucinations: Although hallucinations usually do not persist after 4 to 5 hours, prolonged hallucinations persisting for up to 4 days have rarely been reported. Flashbacks: Flashback phenomena have occurred from 2 weeks to 8 months after ingestion.
    2) SEVERE TOXICITY: PHYSICAL EFFECTS: Muscular weakness, increased deep tendon reflexes, fever (particularly in children), flushing (primarily face and upper trunk), tachycardia, hypertension, ataxia, paresthesias, seizures (more common in children), rhabdomyolysis (very rarely), renal failure, or cardiopulmonary arrest. Intravenous injection of mushroom extract can cause fever, hypoxia, or mild methemoglobinemia. PSYCHOTROPIC EFFECTS: Mood alterations, acute psychosis, panic reactions, and powerful distortions of space and time.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Fever may develop after exposure.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Poisoned patients often present with mydriasis.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Mild and transient hypoxemia has been reported in an adult who used an extract of the mushroom intravenously.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) These mushrooms cause visual hallucinations and perceptual distortions, which may result in either a pleasant or apprehensive mood. Critical judgment is impaired and performance ability is poor. Unmotivated hyperkinetic compulsive movements and laughter may develop. Vertigo, ataxia, and paresthesias may occur. Muscle weakness and drowsiness progressing to sleep may end the episode, which usually lasts 4 to 6 hours. Flashback phenomena have occurred from 2 weeks to 8 months after ingestion. This phenomena, also seen with other hallucinogens, is known as "hallucinogen persisting perception disorder". Seizures, usually intermittent, have occurred in children.

Laboratory Monitoring

    A) Psilocybin is not detected with usual toxicologic screening methods.
    B) Serum electrolytes, CK, and renal function should be assessed with concern for rhabdomyolysis (prolonged agitation, seizures, or coma).

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Treatment is symptomatic and supportive. Treat seizures with benzodiazepines. If seizures persist, administer propofol or barbiturates. Treat agitation by placing the patient in a quiet room with dim lights and talk to the patient in a quiet and reassuring manner. Treat more severe agitation with benzodiazepines using standard doses. Hyperthermia is a severe sign and requires aggressive sedation with benzodiazepines, and rapid cooling with ice water immersion or cool mist sprays.
    B) DECONTAMINATION
    1) Gastrointestinal decontamination is generally not warranted. Patients usually present late and are uncooperative; the risk of aspiration outweighs any potential benefit.
    C) AIRWAY MANAGEMENT
    1) Is rarely indicated, but endotracheal intubation should be performed in patients with persistent seizures and inability to protect airway.
    D) ANTIDOTE
    1) None.
    E) ENHANCED ELIMINATION PROCEDURE
    1) No methods to enhance elimination have been used clinically.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Adults who are minimally symptomatic after recreational use, and are in a safe environment, may be observed at home if a sober, responsible adult is present. Referral for substance abuse counseling should be considered.
    2) OBSERVATION CRITERIA: Patients with more than mild symptoms, those not in a safe environment, any patient with self-harm attempt, and any child should be observed in a medical facility for 6 to 12 hours until free of symptoms.
    3) ADMISSION CRITERIA: Patients exhibiting a behavior that may cause self-harm or harm to others, acute psychosis, seizures, renal failure, rhabdomyolysis, or persistent psychotropic effects should be admitted.
    4) CONSULT CRITERIA: Consult a mycologist for identification of suspected mushroom and a medical toxicologist for assistance with medical management.
    G) PHARMACOKINETICS
    1) Onset of symptoms: 10 to 30 minutes. Average duration of effect: 4 to 5 hours. Patients usually return to normal within 6 to 12 hours of ingestion. "Flashback phenomena" or "Hallucinogen Persisting Perception Disorder" reported to occur 2 weeks to 8 months after ingestion.

Range Of Toxicity

    A) TOXICITY: There is little correlation between the quantity ingested and clinical effects. One to 4 large Psilocybes (10 to 30 grams fresh weight) may yield 5 to 15 mg of psilocybin, and produce hallucinations. A dose of 12 mg or more of psilocybin produces vivid hallucinations. Most cases result in mild or moderate self-limiting effects. Fatality rate is far less than 1% and is probably the result of coningestants or trauma sustained while judgement is impaired.

Clinical Effects

Summary Of Exposure

    A) USES: These mushrooms are most often deliberately used by persons seeking hallucinogenic effects. Inadvertent ingestion of these mushrooms by a person mistaking them for edible mushrooms has rarely been reported. Some "street mushrooms" are treated with synthetic hallucinogens such as d-lysergic acid (LSD) and N,N-dimethyltryptamine (DMT).
    B) TOXICOLOGY: "Street mushrooms" may be adulterated with LSD. Psilocybin and psilocin are structurally similar to LSD and presumed to act at serotonin receptors. Effects are primarily central (hallucinogenic), but there are some peripheral effects. They also produce effects through serotonergic action. Toxins are heat-stable.
    C) EPIDEMIOLOGY: In most communities, mushrooms are less commonly abused than most other recreational drugs. Most users do not come to medical attention and severe toxicity is rare. Psilocybin-containing genera with species known to cause the majority of exposures are Psilocybe, Panaeolus, Copelandia, Gymnopilus, Pluteus, and Conocybe.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: PHYSICAL EFFECTS: Dilated pupils (develops in over 90% of cases), confusion, vertigo, drowsiness, nausea, vomiting, tachycardia, and mild hypertension. PSYCHOTROPIC EFFECTS: Sense of exhilaration, hallucinations including vivid bright colors and shapes, euphoria, distortion of sense of time, dysesthesias, anxiety, perceptual distortions (may result in either a pleasant or apprehensive mood; "good" or "bad" trip), and impaired judgement. Hallucinations: Although hallucinations usually do not persist after 4 to 5 hours, prolonged hallucinations persisting for up to 4 days have rarely been reported. Flashbacks: Flashback phenomena have occurred from 2 weeks to 8 months after ingestion.
    2) SEVERE TOXICITY: PHYSICAL EFFECTS: Muscular weakness, increased deep tendon reflexes, fever (particularly in children), flushing (primarily face and upper trunk), tachycardia, hypertension, ataxia, paresthesias, seizures (more common in children), rhabdomyolysis (very rarely), renal failure, or cardiopulmonary arrest. Intravenous injection of mushroom extract can cause fever, hypoxia, or mild methemoglobinemia. PSYCHOTROPIC EFFECTS: Mood alterations, acute psychosis, panic reactions, and powerful distortions of space and time.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Fever may develop after exposure.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER: May develop in children (102 to 106 degrees F or 39 to 41 degrees C), or in those who use the mushrooms or mushroom extract intravenously (McClintock et al, 2008; Curry & Rose, 1985).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Poisoned patients often present with mydriasis.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MYDRIASIS: is usually present in over 90% of poisoned patients (McClintock et al, 2008; Peden & Pringle, 1982; Benjamin, 1995).
    2) CASE REPORT: A 4-year-old inadvertently exposed to hallucinogenic mushrooms developed marked mydriasis, but the remainder of the physical exam was normal (Goto et al, 2003).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia is commonly observed in patients who seek medical care (McClintock et al, 2008), occurring in 10 of 44 (22.7%) in one series (Peden & Pringle, 1982), in 41 of 318 (13%) in another (Francis & Murray, 1983), and in all of 7 patients in a third series (Mills et al, 1979).
    b) INCIDENCE: Tachycardia occurs in less than half the patients ingesting mushrooms, and has most often been observed in teenagers who were having unpleasant experiences (Benjamin, 1995).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension is common, occurring in 17 of 44 (38.6%) patients in one series (Peden & Pringle, 1982).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Mild and transient hypoxemia has been reported in an adult who used an extract of the mushroom intravenously.
    3.6.2) CLINICAL EFFECTS
    A) CYANOSIS
    1) WITH POISONING/EXPOSURE
    a) Mild transient hypoxemia and perioral cyanosis was reported in one man who injected an unknown amount of extract intravenously (Curry & Rose, 1985; Sivyer & Dorrington, 1984).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) These mushrooms cause visual hallucinations and perceptual distortions, which may result in either a pleasant or apprehensive mood. Critical judgment is impaired and performance ability is poor. Unmotivated hyperkinetic compulsive movements and laughter may develop. Vertigo, ataxia, and paresthesias may occur. Muscle weakness and drowsiness progressing to sleep may end the episode, which usually lasts 4 to 6 hours. Flashback phenomena have occurred from 2 weeks to 8 months after ingestion. This phenomena, also seen with other hallucinogens, is known as "hallucinogen persisting perception disorder". Seizures, usually intermittent, have occurred in children.
    3.7.2) CLINICAL EFFECTS
    A) HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) Visual hallucinations (ie, visual phenomena in which objects take on vivid colors) and perceptual distortions may result in either a pleasant or apprehensive mood ("good" or "bad" trip). The brilliance of colors is enhanced by closing the eyes. Critical judgment is impaired and performance ability is poor, and distortion of time (i.e., slower than real time). Prolonged hallucinations, persisting for up to 4 days, have been reported (Francis & Murray, 1983; Hyde et al, 1978; Benjamin, 1995).
    b) FLASHBACKS - Flashback phenomenon has occurred from 2 weeks to 8 months after ingestion (Espiard et al, 2005; Benjamin, 1979; Francis & Murray, 1983). This phenomena, also seen with other hallucinogens, is known as "hallucinogen persisting perception disorder" (Espiard et al, 2005).
    c) Psychedelic effects include: powerful distortions of space and time, and mood alterations. Higher doses may induce visual hallucinations and dysesthesia. Sensory distortions may be pleasant or frightening and lead to panic reactions or acute psychosis (Schwartz & Smith, 1988).
    d) There appears to be a difference in the psychedelic effects which may be due to a quickly acquired tolerance from regular continued use, or due to the fact that the mushroom material may contain varying concentrations of psychoactive compounds.
    e) CASE REPORT: A 4-year-old boy was inadvertently exposed to a psilocybin-laced chocolate candy bar, which had been intended for adult recreational use. The child developed apparent visual hallucinations (reaching for inanimate objects) and was smiling and laughing. Laboratory analysis confirmed the presence of psilocybin; the remainder of the toxicology screen was negative. Emesis was induced at home and he was given two doses of activated charcoal. The hallucinations resolved within 12 hours and he was discharged (Goto et al, 2003).
    B) CLOUDED CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) Confusion may occur (Benjamin, 1995).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported following use (Benjamin, 1995).
    D) HYPERACTIVE BEHAVIOR
    1) WITH POISONING/EXPOSURE
    a) Unmotivated hyperkinetic compulsive movements and uncontrollable laughter may develop in the early phases of euphoria (Benjamin, 1995).
    E) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Paresthesias and numbness may occur (Harries & Evans, 1981; Peden & Pringle, 1982; Benjamin, 1995).
    F) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Vertigo is common (Lincoff & Mitchel, 1977; Benjamin, 1995).
    G) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Ataxia may occur (Lincoff & Mitchel, 1977).
    H) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Drowsiness progressing to sleep ends the episode which usually lasts only 6 hours.
    b) CASE REPORT: A 28-year-old man developed altered mental status, vomiting, diaphoresis, mydriasis, and agitated euphoria after ingesting psilocybe mushrooms. On presentation, he was unresponsive to command (Glasgow Coma Scale score of 6), intermittently moving all 4 extremities nonpurposefully. The patient became extremely agitated over the next 8 hours with any stimulation despite high dose of propofol infusion. He recovered following supportive care (McClintock et al, 2008).
    I) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Tonic/clonic seizures, usually intermittent, are more likely to occur in children (Benjamin, 1995). Seizures have also been reported in adults (McClintock et al, 2008; McCormick et al, 1979).
    b) PATHOPHYSIOLOGY: Psilocin is a known pyrogen in animals and its not known whether the febrile response observed in children or the direct effects of tryptamine derivatives on the central nervous system play a role in the development of seizures following exposure (Benjamin, 1995).
    J) DISORDER OF BRAIN
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 25-year-old man with a history of hepatitis C developed severe rhabdomyolysis (CK peaked at 500,000 Unit/L on day 1), acute renal failure (serum creatinine peaked at 6.8 mg/dL on day 14), and posterior encephalopathy with cortical blindness after ingesting unknown amounts of magic mushrooms (Psilocybe cubensis). Cranial CT scans revealed the evolution of posterior encephalopathy with bilateral hypodense lesions in the parieto-occipital and frontal region. Following supportive therapy and veno-venous hemodialysis, he recovered completely over several months (Bickel et al, 2005).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting are potential presenting complaints (McClintock et al, 2008), occurring in 20% of cases in two studies (Francis & Murray, 1983; Peden et al, 1981).
    b) Persistent vomiting has been seen with intravenous users (Curry & Rose, 1985).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Mild elevation of aminotransferases was reported in 2 patients after intravenous injection (Sivyer & Dorrington, 1984). Elevated LDH, SGOT, and alkaline phosphatase were reported in 3 cases of Psilocybin-containing mushroom ingestions (McCormick et al, 1979).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) URINARY INCONTINENCE
    1) WITH POISONING/EXPOSURE
    a) Urinary incontinence has been described (Peden & Pringle, 1982; Southcott, 1974).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 25-year-old man with a history of hepatitis C and drug abuse developed severe rhabdomyolysis (CK peaked at 500,000 Unit/L on day 1), acute renal failure (serum creatinine peaked at 6.8 mg/dL on day 14), and posterior encephalopathy with cortical blindness after ingesting unknown amounts of magic mushrooms (Psilocybe cubensis). Following supportive therapy and veno-venous hemodialysis, he recovered completely over several months (Bickel et al, 2005).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH POISONING/EXPOSURE
    a) Mild methemoglobinemia was reported in an intravenous extract user (Curry & Rose, 1985).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis developed in a 28-year-old man who presented with altered mental status, vomiting, and mydriasis after using psilocybe mushrooms (McClintock et al, 2008).
    B) FLUSHING
    1) WITH POISONING/EXPOSURE
    a) Facial and upper trunk flushing was seen in 8 (18%) of 44 cases (Peden & Pringle, 1982).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Severe myalgias and back pain have been reported in intravenous users (Curry & Rose, 1985; Sivyer & Dorrington, 1984).
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) Arthralgias have been reported in intravenous users (Curry & Rose, 1985; Sivyer & Dorrington, 1984).
    C) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness may occur (Lincoff & Mitchel, 1977).
    D) HYPERREFLEXIA
    1) WITH POISONING/EXPOSURE
    a) Hyperreflexia is common (Peden & Pringle, 1982; Peden et al, 1981).
    E) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 25-year-old man with a history of hepatitis C and drug abuse developed severe rhabdomyolysis (CK peaked at 500,000 Unit/L on day 1; ALT 4190 Units/L, AST 866 Units/L), acute renal failure (serum creatinine peaked at 6.8 mg/dL on day 14), and posterior encephalopathy with cortical blindness after ingesting unknown amounts of magic mushrooms (Psilocybe cubensis). Following supportive therapy and veno-venous hemodialysis, he recovered completely over several months (Bickel et al, 2005).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Psilocybin is not detected with usual toxicologic screening methods.
    B) Serum electrolytes, CK, and renal function should be assessed with concern for rhabdomyolysis (prolonged agitation, seizures, or coma).
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) If there is concern the ingestion was part of a mixed mushroom ingestion, monitor for elevated liver function tests. Hallucinogenic mushrooms have been associated with trivial rises in aminotransferases, but are not thought to be hepatotoxic.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulse and blood pressure.

Methods

    A) OTHER
    1) Bluing of the stem with bruising or when painted with metol (a photographic developer) is presumptive evidence for the presence of an indole.
    2) The formation of a blue color when in the presence of brain tissue or mammalian serum is thought to be due to psilocybin reacting with a phosphatase to produce psilocin, which reacts with cytochrome oxidase or Fe3+ (ferric iron) or copper oxidase to produce a blue color. The Ehrlich reaction for indoles using p-dimethylaminobenzaldehyde is a much more sensitive test (Levine, 1967).
    B) CHROMATOGRAPHY
    1) High performance liquid chromatography is used almost exclusively for quantitative analysis of these agents (Kysilka & Wurst, 1990).
    2) Psilocin can be identified by infrared spectroscopy and gas chromatography/mass spectrometry. An aqueous extracting method for the isolation and identification of psilocin from Psilocybe mushrooms has been described (Casale, 1985).

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 exhibiting a behavior that may cause self-harm or harm to others, acute psychosis, seizures, renal failure, rhabdomyolysis, or persistent psychotropic effects should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Adults who are minimally symptomatic after recreational use, and are in a safe environment, may be observed at home if a sober, responsible adult is present. Referral for substance abuse counseling should be considered.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a mycologist for identification of suspected mushroom and a medical toxicologist for assistance with medical management.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with more than mild symptoms, those not in a safe environment, any patient with self-harm attempt, and any child should be observed in a medical facility for 6 to 12 hours until free of symptoms.

Monitoring

    A) Psilocybin is not detected with usual toxicologic screening methods.
    B) Serum electrolytes, CK, and renal function should be assessed with concern for rhabdomyolysis (prolonged agitation, seizures, or coma).

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Gastrointestinal decontamination is generally not warranted. Patients usually present late and are uncooperative; the risk of aspiration outweighs any potential benefit.
    6.5.2) PREVENTION OF ABSORPTION
    A) Gastrointestinal decontamination is generally not warranted. Patients usually present late and are uncooperative; the risk of aspiration outweighs any potential benefit.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Psilocybin is not detected with usual toxicologic screening methods.
    2) Serum electrolytes, CK, and renal function should be assessed with concern for rhabdomyolysis (prolonged agitation, seizures, or coma).
    B) PSYCHOMOTOR AGITATION
    1) INDICATION
    a) If patient is severely agitated, sedate with IV benzodiazepines.
    2) 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).
    3) 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).
    4) 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.
    5) The use of phenothiazines or other antipsychotics is NOT advised; however, chlorpromazine has been used to treat hallucinations with no reported adverse effect (Francis & Murray, 1983).
    C) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Significant hyperthermia is extremely rare following hallucinogenic mushroom ingestions, and probably the result of coingestants or environmental exposure. It requires aggressive sedation with benzodiazepines, and rapid cooling with ice water immersion or cool mist sprays.
    D) SEIZURE
    1) Rare except in children.
    2) 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).
    3) 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 .
    4) 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).
    5) 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).
    6) 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).
    7) 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).

Enhanced Elimination

    A) SUMMARY
    1) No methods to enhance elimination have been used clinically.

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.

Range Of Toxicity

Summary

    A) TOXICITY: There is little correlation between the quantity ingested and clinical effects. One to 4 large Psilocybes (10 to 30 grams fresh weight) may yield 5 to 15 mg of psilocybin, and produce hallucinations. A dose of 12 mg or more of psilocybin produces vivid hallucinations. Most cases result in mild or moderate self-limiting effects. Fatality rate is far less than 1% and is probably the result of coningestants or trauma sustained while judgement is impaired.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) A typical hallucinogenic dose is 20 to 100 mushrooms (Mills et al, 1979).

Minimum Lethal Exposure

    A) FATALITY RATE: Is probably far less than 1%.
    B) PSILOCYBE: One death in a 6-year-old child (due to status epilepticus and hyperthermia) who ate Psilocybe baeocystis has been reported (McCawl et al, 1962).

Maximum Tolerated Exposure

    A) There is little correlation between the history of quantity ingested and clinical effects (Peden & Pringle, 1982). In general, older individuals describe less unpleasant or frightening experiences following use (Benjamin, 1995).
    B) The factors which can influence the effects of the toxins are NOT limited to the dose itself, but can include (Benjamin, 1995):
    1) Circumstances in which ingestion occurs (ie, alone, at home, as part of a ceremony)
    2) Psychological makeup of the individual (includes cultural heritage)
    3) Previous experiences with mushroom ingestion
    4) Dose ingested
    5) Method of preparation
    C) There is great variability in the concentration of various species and even in different collections of the same species from the same mycelium (Beug & Bigwood, 1982).
    D) PSILOCYBIN
    1) It may take as few as 3 to as many as 60 mushrooms to produce the desired effect in the average individual. Approximately, 4 to 8 mg of psilocybin is present in 20 g of fresh mushrooms or 2 g of dried specimens. A dose of 12 mg or more can produce vivid hallucinations (Benjamin, 1995).
    E) PSILOCYBE
    1) One to 4 large Psilocybes (10 to 30 grams fresh weight equals approximately 5 to 15 mg of Psilocybin) produce hallucinations (Benjamin, 1995).
    2) A dose of 12 mg or more of psilocybin produces vivid hallucinations. It is relatively stable and retains its hallucinogenic properties after drying for up to several years and slow loses its effect over time (Benjamin, 1995).
    3) CASE REPORTS
    a) Experienced Shamans consume 6 to 12 caps, and some professionals may consume 26 for a ceremony (Wasson, 1959).
    b) Agitation and hallucinations were reported after ingestion of 10 mushrooms (Francis & Murray, 1983); however, only abdominal pain was noted in another patient who ingested 200 mushrooms. Psychosis and prolonged sympathomimetic effects were noted after ingestion of 50 to 60 mushrooms (Hyde et al, 1978).
    4) CASE SERIES
    a) In a retrospective review of Psilocybe mushroom ingestion, most cases resulted in mild or moderate self-limiting effects of psilocybin intoxication. In this study, concomitant cannabis ingestion was NOT found to increase toxic effects. However, the concomitant use of opiates, ethanol and/or LSD resulted in severe complications (e.g., seizures {one patient}, paraplegia following a fall secondary to hallucinations {one patient}) (Kunz et al, 2000).
    F) PANAEOLUS
    1) Ingestion of 20 to 30 mushrooms each, in 3 teenagers aged 16, 18, and 18, produced euphoria, hallucinations of speed and color, but no anticholinergic effects (Cooles, 1980).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) Serum analysis confirmed the presence of psilocybin metabolite (48 ng/mL) in a 4-year-old that inadvertently ingested a candy bar laced with hallucinogenic mushrooms. The remainder of the toxicology screen was negative (Goto et al, 2003).

Pharmacology Toxicology

Toxicologic Mechanism

    A) HALLUCINOGENIC INDOLES - Psilocybin, psilocin, baeocystin, norbaeocystin, and indoles similar to LSD (d-lysergic acid) are the chief toxins involved (Leung & Paul, 1968).
    B) Their effects are primarily central (hallucinogenic) but there are some peripheral effects, probably through the serotonin-norepinephrine pathways similar to bufotenine.
    C) These indoles are thermostable and are NOT removed by cooking. "Street mushrooms" may be adulterated with LSD, DMT, DET, DPT.

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) CASE REPORT - An 8-year-old, neutered labrador female was reported to be staggering, overtly aggressive, ataxic, salivating, exhibiting nystagmus, hyperthermic, and barking. The animal was difficult to restrain and had to be sedated using intravenous pentobarbitone.
    1) Two hours later, the dog became hypothermic. At the end of the second day the animal was still ataxic, showed nystagmus, and was fearful of approaching people.
    2) By day 3 the patient was normal. A qualitative analysis, revealed the presence of psilocybin (Kirwan, 1990).
    11.1.5) EQUINE/HORSE
    A) Hyde (1990) treated a pony suspected of ingesting Psilocybe species (NOT identified). The animal was fearful, aggressive when stimulated, but motionless when left in a darkened stable. The animal was left in a darkened stable for 2 days and returned to normal.
    B) Hyperexcitability, followed by immobility, muscular tremor, moderate pyrexia, slight but persistent tenesmus, teeth grinding, and fixed dilated pupils were reported in a colt.
    1) The animal was sedated with detomidine and butorphanol, but gradually weakened and developed pressure sores. The colt was euthanized 48 hours later. The suspected poison was Psilocybes species found in the pasture (Jones, 1990).

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) 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.
    2) Treatment should always be done on the advice and with the consultation of a veterinarian.
    3) Additional information regarding treatment of poisoned animals may be obtained from a Veterinary Toxicologist or the National Animal Poison Control Center.
    4) 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) SEIZURES/LARGE ANIMALS: May be controlled with diazepam.
    a) HORSES/DIAZEPAM: Neonates: 0.05 to 0.4 milligrams/kilogram; Adults: 25 to 50 milligrams. Give slowly intravenously to effect; repeat in 30 minutes if necessary.
    b) CATTLE, SHEEP AND SWINE/DIAZEPAM: 0.5 to 1.5 milligrams/kilogram intravenously to effect.
    2) SEIZURES/DOGS & CATS:
    a) DIAZEPAM: 0.5 to 2 milligrams/kilogram intravenous bolus; may repeat dose every ten minutes for four total doses. Give slowly over 1 to 2 minutes to effect.
    b) PHENOBARBITAL: 5 to 30 milligrams/kilogram over 5 to 10 minutes intravenously to effect.
    c) REFRACTORY SEIZURES: Consider anaesthesia or heavy sedation. Administer pentobarbital to DOGS & CATS at a dose of 3 to 15 milligrams/kilogram intravenously slowly to effect. May need to repeat in 4 to 8 hours. Be sure to protect the airway.

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) 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.
    2) Treatment should always be done on the advice and with the consultation of a veterinarian.
    3) Additional information regarding treatment of poisoned animals may be obtained from a Veterinary Toxicologist or the National Animal Poison Control Center.
    4) 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) Ammirati JF, Traquair JA, & Horgen PA: Poisonous Mushrooms of the Northern United States and Canada, University of Minnesota Press, Minneapolis, MN, 1985.
    3) Benjamin C: Persistent psychiatric symptoms after eating psilocybin mushrooms. Br Med J 1979; 1:1319-1320.
    4) Benjamin DR: Mushrooms poisons and panaceas: A handbook for naturalists, mycologists and physicians, W. H. Freeman and Company, New York, NY, 1995.
    5) Berger KJ & Guss DA: Mycotoxins revisited: Part II. J Emerg Med 2005; 28(2):175-183.
    6) Beug MW & Bigwood J: Psilocybin and psilocin levels in twenty species from seven general of wild mushrooms in the Pacific northwest, U.S.A. Journal of Ethnobotany 1982; 5:271-285.
    7) Bickel M, Ditting T, Watz H, et al: Severe rhabdomyolysis, acute renal failure and posterior encephalopathy after 'magic mushroom' abuse. Eur J Emerg Med 2005; 12(6):306-308.
    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) Casale JF: An aqueous-organic extraction method for the isolation and identification of psilocin from hallucinogenic mushrooms. J For Sci 1985; 30:247-250.
    10) 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.
    11) 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.
    12) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    13) Cooles P: Abuse of the mushroom Panaeolus foenisecii. Br Med J 1980; 280:446-447.
    14) Curry SC & Rose MC: Intravenous mushroom poisoning. Ann Emerg Med 1985; 14:900.
    15) Espiard ML, Lecardeur L, Abadie P, et al: Hallucinogen persisting perception disorder after psilocybin consumption: a case study. Eur Psychiatry 2005; 20(5-6):458-460.
    16) Francis J & Murray VSG: Review of inquiries made to the NPIS concerning Psilocybe mushroom ingestion 1973-1981. Human Toxicol 1983; 2:349-352.
    17) Goto CS, Offerman S, Gutglas D, et al: "Happy candy" ingestion: Hallucinations in a four-year-old child caused by a psilocybin-laced chocolate candy bar. J Toxicol - Clin Toxicol 2003; 41(4):542.
    18) Harries AD & Evans V: Sequelae of a 'magic mushroom banquet'. Postgrad Med J 1981; 57:571-572.
    19) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    20) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    21) Hyde C, Glancy G, & Omerod P: Abuse of indigenous psilocybin mushrooms: a new fashion and some psychiatric complications. Br J Psychiat 1978; 132:602-604.
    22) Jones J: 'Magic mushroom' poisoning in a colt. Vet Rec 1990; 127:603.
    23) Kirwan AP: "Magic mushroom" poisoning in a dog. Vet Rec 1990; 126:149.
    24) Kunz MW, Rauber-Luthy CH, & Meier PJ: Acute poisoning with hallucinogenic psilocybe mushrooms in switzerland (abstract), European Assoc of Poisons Centres & Clin Toxicologists, International Congress, Amsterdam, The Netherlands, 2000.
    25) Kysilka R & Wurst M: A novel extraction procedure for psilocybin and psilocin determination in mushroom samples. Planta Medica 1990; 56:327-328.
    26) Lassen JF, Lassen NF, & Skov J: Hallucinogenic mushroom use by Danish students: pattern of consumption. J Int Med 1993; 233:111-112.
    27) Leung P & Paul AG: Baeocystin and norbaeocystin: new analog of psilocybin from Psilocybe baeocystis. J Pharm Sci 1968; 57:1667-1671.
    28) Levine WG: Formation of blue oxidation product from psilocybin. Nature 1967; 215:1292-1293.
    29) Lincoff G & Mitchel DH: Toxic and Hallucinogenic Mushroom Poisoning, Van Nostrand Reinhold Company, New York, NY, 1977.
    30) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    31) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    32) McClintock RL, Watts DJ, & Melanson S: Unrecognized magic mushroom abuse in a 28-year-old man. Am J Emerg Med 2008; 26(8):972-974.
    33) McCormick DJ, Aubel AJ, & Gibbins MC: Nonlethal mushroom poisoning. Ann Intern Med 1979; 90:332-335.
    34) Mills PR, Lesinskas D, & Watkinson G: The danger of hallucinogenic mushrooms. Scot Med J 1979; 24:316-317.
    35) Peden NR & Pringle SD: Hallucinogenic fungi. Lancet 1982; 1:396-397.
    36) Peden NR, Bissett AF, & Macaulay KE: Clinical toxicology of 'magic mushroom' ingestion. Postgrad Med J 1981; 57:543-545.
    37) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    38) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    39) Schwartz RH & Smith BM: Hallucinogenic mushrooms. Clinical Pediatrics 1988; 27(2):70-73.
    40) 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.
    41) Sivyer C & Dorrington L: Intravenous injection of mushrooms (Letter) . Med J Aust 1984; 140:182.
    42) Southcott RV: Notes on some poisonings and other clinical effects following ingestion of Australian fungi. South Australian Clinics 1974; 6:441-478.
    43) 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.
    44) Wasson RG: The hallucinogenic mushrooms of Mexico: an adventure in ethnomycological exploration. Trans Acad Sci, Series II 1959; 21:325-339.