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MUSHROOMS-CHLOROPHYLLUM

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chlorophyllum molybdites is a gastrointestinal irritant mushroom found on lawns, and grasslands during wet periods. It is often mistaken for the edible Agaricus mushrooms (Agaricus guadelupensis).
    B) These mushrooms are often referred to as "green-spored Lepiota", but are frequently confused with two edible Lepiota species known as L. rachodes (parasol mushrooms) and L. procera (shaggy parasol mushroom).
    C) The most significant difference between chlorophyllum molybdites and the Lepiota species is the spore color, with the former having green spores (this may not be easily apparent following a causal inspection).

Specific Substances

    1) Chlorophyllum esculentum - Chlorophyllum molybdites
    2) Chlorophylum molybdites
    3) False Parasol
    4) Green gilled lepiota
    5) Green-Lined Parasol
    6) Green parasol
    7) Green-spored Lepiota
    8) Lepiota esculenta - Volvariella esculenta
    9) Lepiota morganii
    10) Lepiota molybdites
    11) Lepiota naucina
    12) Morgan's Lepiota
    13) Morgan's Mushroom
    14) Smooth Lepiota

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: Chlorophyllum molybdites is a gastrointestinal irritant mushroom found on lawns and grasslands during late summer and early autumn. It is often mistaken for the edible Agaricus mushrooms (Agaricus guadelupensis) or for two edible Lepiota species known as L. rachodes (parasol mushrooms) and L. procera (shaggy parapsol mushroom).
    B) TOXICOLOGY: A purification analysis has identified molybdophyllysin, a small protein, as the potential toxin of C. molybdites. This protein is highly homologous to metalloendopeptidase, which is found in edible mushrooms, such as Grifola frondosa, Pleurotus ostreatus, and Armillaria mellea. Symptoms are typically produced from ingestion of raw mushrooms; well-cooked Chlorophyllum (temperatures more than 70 degrees C for 30 minutes) can usually be eaten without ill effects. Not all consumers will have adverse effects independent of preparation method.
    C) EPIDEMIOLOGY: C. molybdites grow in many areas of North America. Cases have been reported from Ontario, Arizona, Arkansas, California, Colorado, Florida, Hawaii, Iowa, Michigan, Nebraska, New Jersey, New York, North Carolina, Texas, and Wisconsin. Internationally, it inhabits Tahiti, Philippines, New Guinea, Australia, India, Africa, West Indies, South America, Japan, and Israel. Fatalities are very rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: The primary symptoms seen with this mushroom are gastrointestinal irritation. Nausea, vomiting, intense abdominal pain (colicky pain), and diarrhea (which may become bloody) are seen most commonly. Cyanosis of lips, tongue and fingernails may be present. The onset of symptoms varies, but the typical onset for chlorophyllum mushroom poisoning is between 30 minutes and 2 hours. In some cases, symptoms may NOT appear for up to 4 hours. In isolated cases, autonomic nervous system effects can cause the following: altered perception, dilated/pinpoint pupils, dizziness, lacrimation, salivation, and tachycardia. ECG abnormalities and T-wave inversion have occurred infrequently.
    2) SEVERE TOXICITY: One report of CNS depression and seizures led to the death of a 2-year-old girl. Hematologic abnormalities can also be present with bleeding and a condition similar to disseminated intravascular coagulation (DIC). Prolonged dehydration from gastrointestinal symptoms may lead to acute renal insufficiency and electrolyte imbalance.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis, CBC, and coagulation studies in symptomatic patients.
    C) SPORE IDENTIFICATION: If a mycologist is available, stomach contents should be saved for spore identification. This may aid in identifying the offending mushroom and may suggest other mushrooms that may have been ingested concurrently.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Replete fluids and electrolytes. Atropine has been used for presumed symptoms of cholinergic crisis, but one case resulted in urinary retention. No cholinergic toxin has been identified. Insufficient data exists to recommend atropine.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Supportive care with attention to monitoring for respiratory depression. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Treat hypotension with intravenous fluids, add vasopressors if necessary.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended as patients usually do not present until symptoms have developed hours after exposure, and because of the potential for CNS depression and seizures.
    2) HOSPITAL: Gastrointestinal decontamination is generally not recommended as patients usually do not present until symptoms have developed hours after exposure. Consider activated charcoal in patients who present early, who are alert and can protect airway.
    D) AIRWAY MANAGEMENT
    1) Monitor for respiratory depression. Endotracheal intubation may be needed in patients with CNS depression or respiratory failure.
    E) ANTIDOTE
    1) None
    F) ENHANCED ELIMINATION PROCEDURE
    1) No reported use of enhanced elimination in the management of toxicity.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild gastrointestinal symptoms that started before 6 hours can be monitored expectantly from home.
    2) OBSERVATION CRITERIA: Patients with moderate to severe gastrointestinal symptoms or autonomic nervous system effects should be referred to a healthcare facility for evaluation and treatment, and monitored until resolution of symptoms and treated for dehydration.
    3) ADMISSION CRITERIA: Patients with severe dehydration, acute renal insufficiency, bleeding, seizures or respiratory depression should be admitted for further management.
    4) CONSULT CRITERIA: Contact a medical toxicologist or your local poison center for any patient with suspected mushroom toxicity. A mycologist can assist with identification of the mushroom.
    H) PITFALLS
    1) Cooking does not prevent all cases of toxicity. Even small amounts of raw mushroom ingested can cause significant toxicity. Toxicity may vary between individuals consuming the same mushroom, including individuals who have reported no symptoms after ingestion.
    I) DIFFERENT DIAGNOSIS
    1) Any mushroom ingestion that can cause gastrointestinal irritation. Symptoms that begin 6 to 24 hours after ingestion are worrisome for amatoxins with progression to acute liver failure. Mushrooms containing allenic norleucine can cause early gastrointestinal symptoms and late renal and hepatic failure. Mushrooms containing orellanine can have late presenting gastrointestinal symptoms with late systemic toxicity. Also consider structural and infectious causes of nausea, vomiting, and diarrhea.

Range Of Toxicity

    A) TOXICITY: Even one bite of one of these mushrooms taken raw may be sufficient to produce symptoms. Fatalities are extremely rare with appropriate supportive care. A single fatality has been reported in a toddler in 1900.

Clinical Effects

Summary Of Exposure

    A) USES: Chlorophyllum molybdites is a gastrointestinal irritant mushroom found on lawns and grasslands during late summer and early autumn. It is often mistaken for the edible Agaricus mushrooms (Agaricus guadelupensis) or for two edible Lepiota species known as L. rachodes (parasol mushrooms) and L. procera (shaggy parapsol mushroom).
    B) TOXICOLOGY: A purification analysis has identified molybdophyllysin, a small protein, as the potential toxin of C. molybdites. This protein is highly homologous to metalloendopeptidase, which is found in edible mushrooms, such as Grifola frondosa, Pleurotus ostreatus, and Armillaria mellea. Symptoms are typically produced from ingestion of raw mushrooms; well-cooked Chlorophyllum (temperatures more than 70 degrees C for 30 minutes) can usually be eaten without ill effects. Not all consumers will have adverse effects independent of preparation method.
    C) EPIDEMIOLOGY: C. molybdites grow in many areas of North America. Cases have been reported from Ontario, Arizona, Arkansas, California, Colorado, Florida, Hawaii, Iowa, Michigan, Nebraska, New Jersey, New York, North Carolina, Texas, and Wisconsin. Internationally, it inhabits Tahiti, Philippines, New Guinea, Australia, India, Africa, West Indies, South America, Japan, and Israel. Fatalities are very rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: The primary symptoms seen with this mushroom are gastrointestinal irritation. Nausea, vomiting, intense abdominal pain (colicky pain), and diarrhea (which may become bloody) are seen most commonly. Cyanosis of lips, tongue and fingernails may be present. The onset of symptoms varies, but the typical onset for chlorophyllum mushroom poisoning is between 30 minutes and 2 hours. In some cases, symptoms may NOT appear for up to 4 hours. In isolated cases, autonomic nervous system effects can cause the following: altered perception, dilated/pinpoint pupils, dizziness, lacrimation, salivation, and tachycardia. ECG abnormalities and T-wave inversion have occurred infrequently.
    2) SEVERE TOXICITY: One report of CNS depression and seizures led to the death of a 2-year-old girl. Hematologic abnormalities can also be present with bleeding and a condition similar to disseminated intravascular coagulation (DIC). Prolonged dehydration from gastrointestinal symptoms may lead to acute renal insufficiency and electrolyte imbalance.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Elevated body temperature has been observed (Lehmann & Khazan, 1992).

Heent

    3.4.3) EYES
    A) MYDRIASIS has been reported after Chlorophyllum ingestions (Smith, 1980), but pinpoint pupils were reported by others (Whitaker & Box, 1985).
    B) PHOTOPHOBIA and a sensation that lights are bright may occur after ingestions of Chlorophyllum (McCarter, 1959; Graff, 1927).
    3.4.4) EARS
    A) INCREASED SENSITIVITY to sound has been reported in a few of the earlier case reports (Eilers & Nelson, 1974)

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Hypotension has been noted in a few cases (Blayney et al, 1980; Levitan et al, 1981; Stenklyft & Augenstein, 1990; Lehmann & Khazan, 1992).
    B) HYPOTENSIVE EPISODE
    1) Hypovolemic shock has been reported after ingestions.
    C) TACHYCARDIA
    1) Tachycardia has been occasionally mentioned as a sign of poisoning by Chlorophyllum mushrooms (Blayney et al, 1980; Lehmann & Khazan, 1992), but it is unknown if this is a direct or indirect effect (ie, the presence of dehydration secondary to vomiting or diarrhea).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY INSUFFICIENCY
    1) One patient who ingested Chlorophyllum became obtunded and required intubation and mechanical ventilation (Stenklyft & Augenstein, 1990).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) Paresthesias have been described, but may be attributed to fear and hyperventilation (McCarter, 1959; Smith, 1980).
    B) TETANY
    1) Tetany is described, but may be due to fear and hyperventilation (Smith, 1980).
    C) SYNCOPE
    1) Dizziness and fainting may be seen after ingestion of Chlorophyllum (Smith, 1980), possibly as a secondary effect to the extensive vomiting.
    D) DROWSY
    1) Lethargy was noted in a 6-year-old who ingested Chlorophyllum (Stenklyft & Augenstein, 1990). The patient later became obtunded. Lethargy has been a finding in other cases as well (McCarter, 1959; Whitaker & Box, 1985; Young, 1989).
    E) SEIZURE
    1) CASE REPORT: A 2-year-old died of a seizure after ingesting this mushroom (Rumack & Salzman, 1978).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) Acute gastroenteritis with nausea, vomiting, and abdominal cramps may be commonly seen (McCarter, 1959; Bresinsky & Besl, 1990; Natarajan & Kaviyarasan, 1991; Lehmann & Khazan, 1992).
    2) Chlorophyllum produces nausea, vomiting, and diarrhea. Species examined in Argentina also demonstrated cholinergic-like effects in animal tissue studies (Torrelio & Izquierdo, 1970).
    B) DIARRHEA
    1) Diarrhea may be seen after ingestion, often being watery at first, and occasionally bloody in severe cases (Blayney et al, 1980; Levitan et al, 1981; Stenklyft & Augenstein, 1990; Whitaker & Box, 1985).
    2) Diarrhea may persist for days and require hydration therapy (Lehmann & Khazan, 1992).
    C) ABDOMINAL ABSCESS
    1) CASE REPORT - A 45-year-old man ingested a large C. molybdites mushroom and within 30 minutes developed watery diarrhea and violent vomiting along with symptoms of dehydration. The patient was decontaminated. The patient showed slow improvement, but on the fifth hospital day developed a fever and was diagnosed with Bacteroides fragilis bacteremia. A diagnostic exam of the colon was strongly suggestive of pericolic abscess associated with a diverticulum. The patient was placed on extended bowel rest requiring parenteral nutrition and received antibiotic therapy with complete resolution of symptoms by hospital day 22 (Lehmann & Khazan, 1992).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ALBUMINURIA
    1) Protein may be noted in urine (Southcott, 1974; Young, 1989) together with hyaline casts (Young, 1989).
    B) OLIGURIA
    1) Varying degrees of oliguria may be present (Southcott, 1974).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) DISSEMINATED INTRAVASCULAR COAGULATION
    1) A patient described by Levitan et al (1981) developed thrombocytopenia, hypofibrinogenemia, and prolonged partial thromboplastin time associated with acute bleeding. These findings are also associated with disseminated intravascular coagulation (Levitan et al, 1981; Deykin, 1970).
    2) Stenklyft & Augenstein (1990) also saw an elevated partial thromboplastin of 61 seconds (normal 25 to 38 seconds) but the prothrombin time was within normal limits (Stenklyft & Augenstein, 1990).
    B) CYANOSIS
    1) A condition similar to methemoglobinemia has been frequently observed in Australian poisonings. Lips, tongue and fingernails become dusky blue, however no cardiovascular or respiratory dysfunctions have been noted. Patients spontaneously recover without any after effects within 24 hours of commencing intravenous rehydration (Southcott, 1974; Young, 1989).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) Sweating may be seen early in cases of poisoning (Blayney et al, 1980; Lehmann & Khazan, 1992).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis, CBC, and coagulation studies in symptomatic patients.
    C) SPORE IDENTIFICATION: If a mycologist is available, stomach contents should be saved for spore identification. This may aid in identifying the offending mushroom and may suggest other mushrooms that may have been ingested concurrently.
    4.1.2) SERUM/BLOOD
    A) COAGULATION STUDIES
    1) Monitoring various coagulation parameters such as partial thromboplastin time, prothrombin time or INR, and platelet count may be of some benefit.

Methods

    A) OTHER
    1) It is often helpful to identify the mushroom as that may aid in predicting potential toxicity.
    2) SPORE IDENTIFICATION: If a mycologist is available, stomach contents should be saved for spore identification. This may aid in identifying the offending mushroom and may suggest other mushrooms that may have been ingested concurrently (Smith, 1980).
    3) Eilers & Barnard (1973) described a method of diagnosing Chlorophyllum poisoning by identifying the basidiospores in vomitus or stool (Eilers & Barnard, 1973).
    a) The vomitus or stool is filtered through four layers of cheesecloth. The filtrate is centrifuged at 7000 rev/min for 10 minutes to sediment the spores. The supernatant is carefully removed by suction and the pellet is resuspended in a small volume of water.
    b) A drop of this solution is placed on a glass slide and heated to evaporate the liquid and fix the solids on the slide. Several drops of acid fuchsin (1%) is applied to the slide and again heated until dry. Excessive stain is then washed off with water. The basidiospores will appear red and have sufficient contrast to be identified from other particles.

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 with severe dehydration, acute renal insufficiency, bleeding, seizures or respiratory depression should be admitted for further management.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild gastrointestinal symptoms that started before 6 hours can be monitored expectantly from home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Contact a medical toxicologist or your local poison center for any patient with suspected mushroom toxicity. A mycologist can assist with identification of the mushroom.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with moderate to severe gastrointestinal symptoms or autonomic nervous system effects should be referred to a healthcare facility for evaluation and treatment, and monitored until resolution of symptoms and treated for dehydration.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, urinalysis, CBC, and coagulation studies in symptomatic patients.
    C) SPORE IDENTIFICATION: If a mycologist is available, stomach contents should be saved for spore identification. This may aid in identifying the offending mushroom and may suggest other mushrooms that may have been ingested concurrently.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital gastrointestinal decontamination is generally not recommended as patients usually do not present until symptoms have developed hours after exposure, and because of the potential for CNS depression and seizures.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Gastrointestinal decontamination is generally not recommended as patients usually do not present until symptoms have developed hours after exposure. Consider activated charcoal in patients who present early, who are alert and can protect airway.
    B) ACTIVATED CHARCOAL
    1) There are no definitive studies on the effectiveness of activated charcoal (Lehmann & Khazan, 1992), but Floch et al (1966) did find a water-soluble toxin that was adsorbed by charcoal (Floch et al, 1966).
    2) 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.
    3) 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).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Replete fluids and electrolytes. Atropine has been used for presumed symptoms of cholinergic crisis, but one case resulted in urinary retention. No cholinergic toxin has been identified. Insufficient data exists to recommend atropine.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Supportive care with attention to monitoring for respiratory depression. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Treat hypotension with intravenous fluids, add vasopressors if necessary.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor serum electrolytes, renal function, urinalysis, CBC, and coagulation studies in symptomatic patients.
    C) REHYDRATION THERAPY
    1) Fluid and electrolyte balance is especially important in infants, elderly, and debilitated patients. Intravenous fluid replacement may be required (Levitan et al, 1981; Lehmann & Khazan, 1992).
    D) HYPOTENSIVE EPISODE
    1) Vasopressors may be required if patients appear in hypovolemic shock (Stenklyft & Augenstein, 1990; Picchioni, 1965).
    2) 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.
    3) 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).
    4) 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) 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 .
    3) 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).
    4) 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).
    5) 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).
    6) 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) ANTISPASMODIC
    1) Gastrointestinal antispasmodic drugs are not indicated (Stenklyft & Augenstein, 1990).

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) This is one of the most common mushrooms reported each year to the NAMA "Mushroom Poisoning Case Registry".
    B) ADULT
    1) A 20-year-old woman ingested four small brown spade-like mushrooms from a grassy area. Two hours after ingestion, she developed nausea, vomiting, and diarrhea. By five hours postingestion her diarrhea became bloody and she was admitted to the hospital. Vital signs and electrolytes were within normal limits on admission. The patient was given intravenous fluids and the vomiting and diarrhea subsided over the next 12 hours. The patient was discharged 48 hours postadmission (Blayney et al, 1980).
    2) A 22-year-old man ingested a large, "brown spotted" mushroom found in a park. An hour postingestion he developed nausea, vomiting, and yellow colored diarrhea, as well as shaking chills, diaphoresis, diffuse muscle tenderness, and salivation. He did NOT have melena, hematochezia, or hematemesis. Several hours after this, he ingested one "Quaalude" tablet with two glasses of water. He sought medical attention, and on initial examination was shaking and nauseated with a blood pressure of 90/70 mmHg supine and 60 mmHg systolic when sitting. His temperature was 37.7 degrees Centigrade and his pulse rate ranged from 100 to 120 beats per minute. Occult blood was noted in the stool. Electrolytes were within normal limits. He was admitted and treated with symptomatic care and intravenous fluids until all signs resolved 18 hours later. The patient was discharged 48 hours postingestion (Blayney et al, 1980).
    3) A 20-year-old man took one bite of mushroom at 10 am. By 11 am he became thirsty, and by 11:30 nauseous. At 12:10 he started vomiting, which continued at frequent intervals for about 3 hours. At 12:20 he became giddy and had a tingling sensation in both hands. Between 13:30 and 15:15 he experienced considerable diarrhea. He was seen in an emergency room at 13:45. He was weak, had a pulse rate of 108, continuous abdominal pain, and normal pupils. By 18:00 he had recovered (McCarter, 1959).

Range Of Toxicity

Summary

    A) TOXICITY: Even one bite of one of these mushrooms taken raw may be sufficient to produce symptoms. Fatalities are extremely rare with appropriate supportive care. A single fatality has been reported in a toddler in 1900.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Ingestions of this mushroom are almost never fatal unless excessive fluid and electrolyte loss occurs in a debilitated patient.
    2) The toxin(s) is/are thermolabile. Symptoms are typically produced from the ingestion of raw mushrooms; well cooked Chlorophyllum is generally eaten without ill effects (Aberdeen, 1954; Young, 1989). Cooking, however, is considered an unreliable method to remove all of the toxin (Lehmann & Khazan, 1992).
    B) CASE REPORTS
    1) One study reported one fatality in a 2-year-old that died 17 hours postingestion. Seizures developed prior to death (Lehmann & Khazan, 1992).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Eiler & Nelson (1974) found that the highest concentration of the toxin was located in the cap. Uncooked mushrooms also have a higher toxigenic potential (Lehmann & Khazan, 1992).
    2) Even one bite of a mushroom in an adult may cause symptoms (McCarter, 1959). However, extreme individual variability exists with mild to severe illness reported after ingestion (Lehmann & Khazan, 1992). It remains unclear if the differences are based on various stages of mushroom growth or geographic differences resulting in genetically distinct mushrooms.

Pharmacology Toxicology

Toxicologic Mechanism

    A) The toxin found in Chlorophyllum molybdites is different from other mushroom toxins (Buck, 1961). It is thought to be a proteinaceous compound with a molecular weight greater than 40,000 daltons (Eilers & Nelson, 1974). This toxin is acted upon by pepsin and HCl acid, and is heat labile, losing activity after being at 70 degrees Centigrade for 30 minutes (Whitaker & Box, 1985). However, the exact toxic component remains unknown (Lehmann & Khazan, 1992).
    B) Species examined in Argentina also demonstrated cholinergic-like effects in animal tissue studies (Torrelio & Izquierdo, 1970). Lehmann & Khazan (1992), however, reported that mild to moderate cholinergic effects have been reported following human exposure.

Physicochemical

Physical Characteristics

    A) These mushrooms reportedly taste good; therefore, this is NOT a deterrent to ingestion (McCarter, 1959; Young, 1989; Lehmann & Khazan, 1992).

Molecular Weight

    A) Varies

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Chicks given the toxin in Chlorophyllum experienced ataxia, tremors, abdominal contractions, drowsiness, and eventually death (Eilers & Nelson, 1974).
    11.1.12) RODENT
    A) Mice injected with extracts of this mushroom developed psychotropic and sympathetic stimulant reactions (Malone et al, 1967). There was no reaction when the mushroom was given orally (Floch et al, 1966).
    B) Eilers & Nelson (1974) found that mice injected with the Chlorophyllum extracts developed tremors, CNS depression, abdominal contractions, and eventually died.

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