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MUSHROOMS-HAPALOPILUS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Hapalopilus rutilans mushrooms have a high content of polyporic acid, an inhibitor of dihydroorotate dehydrogenase {DHO-DH}, which has cytotoxic properties and can produce neurotoxic effects. The presence of polyporic acid appears to be responsible for the toxic effects observed following ingestion.

Specific Substances

    1) HAPALOPILUS RUTILANS
    a) Boletus rutilans
    b) Hapalopilus nidulans
    c) Polyporus nidulans
    d) Polyporus nidulans f. resupinata
    e) Polyporus rutilans
    f) Polystictus nidulans (former name)
    g) Purple-Dye Polypore

Available Forms Sources

    A) FORMS
    1) CLASSIFICATION
    1) Classification for Hapalopilus Ritulans (Northern Ireland Fungus Group, 2006):
    a) Phylum: Basidiomycota
    b) Class: Basidiomycetes
    c) Order: Polyporales
    d) Family: Hapalopilaceae
    B) USES
    1) Hapalopilus rutilans have rarely been reported as a source of mushroom intoxication, which may be related to its "tough" flesh and poor taste quality. It is considered inedible by most sources (None Listed, 2006; Kraft et al, 1998).

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: Hapalopilus is a group of mushrooms which contain polyporic acid, a secondary metabolite that produces both cytotoxic and neurotoxic effects. Phylum: Basidiomycota, Class: Basidiomycetes, Order: Polyporales, Family: Hapalopilaceae. It is a fleshy, tough and hard mushroom found on hardwood logs and conifer wood in Europe and North America.
    B) TOXICOLOGY: Polyporic acid, a dehydroquinone derivative, is a dihydroorotate dehydrogenase inhibitor which is thought to be responsible for most of the toxic effects of Hapalopilus.
    C) EPIDEMIOLOGY: It is rarely reported as a source of mushroom toxicity, likely due to its texture and poor palatability.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxicity typically consists of nausea, vomiting, anorexia, and abdominal pain and general malaise. Violet colored urine has also been reported.
    2) SEVERE TOXICITY: Severe toxicity includes more neurologic symptoms such as headache, vertigo, ataxia, blurred vision, diplopia, bilateral multidirectional nystagmus, visual hallucinations, unstable gait, weakness and somnolence. These symptoms have occurred 24 hours after ingestion. Electrolyte abnormalities and elevations in serum creatinine and aminotransferases have also been reported.

Laboratory Monitoring

    A) Monitor vital signs and neurologic exam.
    B) Monitor serum electrolytes, renal function, urinalysis and liver enzymes in symptomatic patients.
    C) Assess visual acuity in symptomatic patients.
    D) Urine may appear violet following exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Symptomatic and supportive care is mainstay for Hapalophilus toxicity; including intravenous fluids for volume expansion, and antiemetics for nausea and vomiting.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Support patient with intravenous fluids and pressor support if hemodynamic instability develop. Maintain airway if significant somnolence, encephalopathy or CNS depression develops.
    C) DECONTAMINATION
    1) PREHOSPITAL: Administer activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. However, patients may present for evaluation only after developing symptoms of toxicity 24 hours to several days after ingestion; in these cases charcoal is not helpful.
    2) HOSPITAL: Administer activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. However, patients may present for evaluation only after developing symptoms of toxicity 24 hours to several days after ingestion; in these cases charcoal is not helpful.
    D) AIRWAY MANAGEMENT
    1) Intubation and ventilation may be needed if CNS depression develops, or the patient is unable to protect their airway. However, this is a rare complication.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION PROCEDURE
    1) Short-term hemoperfusion, peritoneal dialysis, or hemodialysis may be beneficial in patients with acute renal insufficiency.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with low dose inadvertent ingestions who are asymptomatic can be watched at home.
    2) OBSERVATION CRITERIA: Any patient who is symptomatic or took a self-harm attempt should be referred to a healthcare facility for evaluation. Patients should be observed until symptoms resolve.
    3) ADMISSION CRITERIA: Patients who have severe toxicity and develop electrolyte abnormality, encephalopathy, hepatic or renal insufficiency, should be admitted for further evaluation.
    4) CONSULT CRITERIA: A mycologist and toxicologist or poison center should be consulted in order to help with identification and guide treatment.
    H) PITFALLS
    1) Pitfalls include not evaluating for other co-ingestants, not recognizing signs and symptoms of toxicity from Hapalopilus, including delayed symptoms, or misidentification of the mushroom.
    I) PHARMACOKINETICS
    1) After ingestion of Hapalopilus, onsets of symptoms have been delayed up to 12 to 24 hours. Polyporic acid is a secondary metabolite in Hapalophilus and is believed to be the cause of the mushroom's toxic effects.
    J) DIFFERENTIAL DIAGNOSIS
    1) Other mushrooms, including Pleurocybella porrigens which can also cause renal insufficiency and encephalopathy.

Range Of Toxicity

    A) TOXICITY: A minimum lethal dose has not been established. A few spoonfuls caused toxicity in a 7-year-old child, including vomiting, nausea, dizziness, abdominal pain, and hepatorenal toxicity 12 hours after exposure which all resolved with supportive care.

Clinical Effects

Summary Of Exposure

    A) USES: Hapalopilus is a group of mushrooms which contain polyporic acid, a secondary metabolite that produces both cytotoxic and neurotoxic effects. Phylum: Basidiomycota, Class: Basidiomycetes, Order: Polyporales, Family: Hapalopilaceae. It is a fleshy, tough and hard mushroom found on hardwood logs and conifer wood in Europe and North America.
    B) TOXICOLOGY: Polyporic acid, a dehydroquinone derivative, is a dihydroorotate dehydrogenase inhibitor which is thought to be responsible for most of the toxic effects of Hapalopilus.
    C) EPIDEMIOLOGY: It is rarely reported as a source of mushroom toxicity, likely due to its texture and poor palatability.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxicity typically consists of nausea, vomiting, anorexia, and abdominal pain and general malaise. Violet colored urine has also been reported.
    2) SEVERE TOXICITY: Severe toxicity includes more neurologic symptoms such as headache, vertigo, ataxia, blurred vision, diplopia, bilateral multidirectional nystagmus, visual hallucinations, unstable gait, weakness and somnolence. These symptoms have occurred 24 hours after ingestion. Electrolyte abnormalities and elevations in serum creatinine and aminotransferases have also been reported.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Decreased visual acuity has been reported in 3 individuals 24 hours after ingesting H. rutilans (Diaz, 2005).
    2) CASE REPORTS: Two patients developed blurred vision, diplopia, and bilateral multidirectional nystagmus after ingesting an unknown quantity of H. rutilans mushrooms (Villa et al, 2013).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported following exposure (Kraft et al, 1998).
    B) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) Based on limited data, 3 individuals developed somnolence, general weakness, reduced motor tone and activity 24 hours after the ingestion of H. rutilans mushroom. Symptoms were similar in rats exposed to polyporic acid, a dihydroorotate dehydrogenase inhibitor, that was identified as the toxic constituent of H. rutilans mushroom (Diaz, 2005).
    b) CASE REPORT: A 7-year-old boy developed EEG abnormalities approximately 3 to 4 days after eating a "few spoonfuls" of fried H. rutilans (mistakenly thought to be 'Fistula hepatica' by his family). Following supportive therapy, somnolence was notably improved one week after exposure, but an EEG still showed evidence of persistent non-specific dysregulation of all brain regions. However, the child continued to improve and had no developmental deficits (Kraft et al, 1998).
    C) VERTIGO
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Vertigo was reported in a child exposed to H. rutilans following the ingestion of a "few spoonfuls" of fried mushroom (Kraft et al, 1998).
    b) CASE REPORT: Vertigo developed in a 13-year-old girl who also developed asthenia, nausea, anorexia, blurred vision, diplopia, bilateral multidirectional nystagmus after ingesting an unknown quantity of Hapalopilus rutilans. The next day, she had a blood pressure of 90/50 mmHg and a pulse of 84 beats/min. Laboratory results revealed elevated serum creatinine, BUN, and serum uric acid, and mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, her condition gradually improved and she was discharged on day 4 (Villa et al, 2013).
    D) ASTHENIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Asthenia developed in a 13-year-old girl who also developed nausea, anorexia, vertigo, blurred vision, diplopia, bilateral multidirectional nystagmus after ingesting an unknown quantity of Hapalopilus rutilans. The next day, she had a blood pressure of 90/50 mmHg and a pulse of 84 beats/min. Laboratory results revealed elevated serum creatinine, BUN, and serum uric acid, and mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, her condition gradually improved and she was discharged on day 4 (Villa et al, 2013).
    b) CASE REPORT: A 41-year-old man with untreated hypertension (BP 160/90 mmHg) developed abdominal pain, nausea, dizziness, visual hallucinations, blurred vision, and diplopia about 12 hours after ingesting an unknown quantity of Hapalopilus rutilans mushrooms. The next day, he had a blood pressure of 110/60 mmHg and a pulse of 70 beats/min. He also had general weakness, anorexia, drowsiness, and violet-colored urine. Bilateral multidirectional nystagmus and unstable gait were observed during physical examination. Laboratory results revealed elevated serum creatinine, BUN, and AST/ALT concentrations, and reduced creatinine clearance, mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, his condition gradually improved and he was discharged 8 days later with only slightly elevated serum creatinine and BUN (Villa et al, 2013).
    E) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness has been reported following the ingestion of H. rutilans mushrooms (Villa et al, 2013).
    F) VISUAL HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 41-year-old man with untreated hypertension (BP 160/90 mmHg) developed abdominal pain, nausea, dizziness, visual hallucinations, blurred vision, and diplopia about 12 hours after ingesting an unknown quantity of Hapalopilus rutilans mushrooms. The next day, he had a blood pressure of 110/60 mmHg and a pulse of 70 beats/min. He also had general weakness, anorexia, drowsiness, and violet-colored urine. Bilateral multidirectional nystagmus and unstable gait were observed during physical examination. Laboratory results revealed elevated serum creatinine, BUN, and AST/ALT concentrations, and reduced creatinine clearance, mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, his condition gradually improved and he was discharged 8 days later with only slightly elevated serum creatinine and BUN (Villa et al, 2013).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been reported at least 12 hours after ingestion (Villa et al, 2013; Kraft et al, 1998).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) An increase in serum aminotransferase was observed in several patients approximately 12 hours after exposure to H. rutilans (Villa et al, 2013; Kraft et al, 1998).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL IMPAIRMENT
    1) WITH POISONING/EXPOSURE
    a) Elevated creatinine along with proteinuria and leukocyturia were reported in a 7-year-old boy several days after exposure (Kraft et al, 1998).
    b) CASE REPORT: A 13-year-old girl developed asthenia, nausea, anorexia, vertigo, blurred vision, and diplopia about 12 hours after ingesting an unknown quantity of Hapalopilus rutilans. The next day, she had a blood pressure of 90/50 mmHg and a pulse of 84 beats/min. Bilateral multidirectional nystagmus was observed during physical examination and she had violet-colored urine. Laboratory results revealed elevated serum creatinine, BUN, and serum uric acid, and mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, her condition improved with urine color returning to normal within 48 hours of presentation, renal function returning to normal within 4 days, and lymphocyte returning to normal within 7 days. She was discharged on day 4 and on follow-up visit a month later, she only had mild proteinuria (Villa et al, 2013).
    c) CASE REPORT: A 41-year-old man with untreated hypertension (BP 160/90 mmHg) developed abdominal pain, nausea, dizziness, visual hallucinations, blurred vision, and diplopia about 12 hours after ingesting an unknown quantity of Hapalopilus rutilans mushrooms. The next day, he had a blood pressure of 110/60 mmHg and a pulse of 70 beats/min. He also had general weakness, anorexia, drowsiness, and violet-colored urine. Bilateral multidirectional nystagmus and unstable gait were observed during physical examination. Laboratory results revealed elevated serum creatinine, BUN, and AST/ALT concentrations, and reduced creatinine clearance, mild proteinuria, lymphopenia, and leukocyturia. Following supportive care, his condition gradually improved and he was discharged 8 days later with only slightly elevated serum creatinine and BUN (Villa et al, 2013).
    B) URINE COLOR ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Violet-colored urine has been reported in patients following exposure to H. rutilans, and is thought to be due to the presence of polyporic acid, a secondary metabolite (Villa et al, 2013; Kraft et al, 1998).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and neurologic exam.
    B) Monitor serum electrolytes, renal function, urinalysis and liver enzymes in symptomatic patients.
    C) Assess visual acuity in symptomatic patients.
    D) Urine may appear violet following exposure.
    4.1.2) SERUM/BLOOD
    A) Monitor serum electrolytes, renal function, urinalysis and liver enzymes in symptomatic patients.
    4.1.3) URINE
    A) Violet Urine
    1) Monitor urine following an exposure. Violet urine has been observed in all cases of H. rutilans mushroom ingestions. The presence of polyporic acid appears to be responsible for the violet color (Kraft et al, 1998).

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 who have severe toxicity and develop electrolyte abnormality, encephalopathy, hepatic or renal insufficiency, should be admitted for further evaluation.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with low dose inadvertent ingestions who are asymptomatic can be watched at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A mycologist and toxicologist or poison center should be consulted in order to help with identification and guide treatment.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any patient who is symptomatic or took a self-harm attempt should be referred to a healthcare facility for evaluation. Patients should be observed until symptoms resolve.

Monitoring

    A) Monitor vital signs and neurologic exam.
    B) Monitor serum electrolytes, renal function, urinalysis and liver enzymes in symptomatic patients.
    C) Assess visual acuity in symptomatic patients.
    D) Urine may appear violet following exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs and neurologic exam.
    2) Monitor serum electrolytes, renal function, urinalysis and liver enzymes in symptomatic patients.
    3) Assess visual acuity in symptomatic patients.
    4) Urine may appear violet following exposure.
    B) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY: Symptomatic and supportive care is mainstay for Hapalophilus toxicity; including intravenous fluids for volume expansion, and antiemetics for nausea and vomiting.
    2) MANAGEMENT OF SEVERE TOXICITY: Support patient with intravenous fluids and pressor support if hemodynamic instability develop. Monitor fluid and electrolyte status. Maintain airway if significant somnolence, encephalopathy or CNS depression develops.
    3) Save all emesis and stools in refrigerator (DO NOT FREEZE) for possible microscopic study and analysis.
    4) HISTORY OF CURRENT ILLNESS
    a) The following questions should be asked in taking the medical history regarding the exposure of the patient to the mushroom:
    1) At what time were the mushrooms eaten?
    2) When was the onset of symptoms after the ingestion?
    3) Was the mushroom eaten at more than one meal?
    4) Were the mushrooms eaten again later and, if so, were they reheated?
    5) Was the mushroom eaten raw or cooked?
    6) Was any alcohol consumed within 24 hours of the meal?
    7) Was more than one kind of mushroom ingested?
    8) How were the mushrooms stored between collection and preparation?
    9) What was the condition of the mushrooms at the time of preparation?
    10) How were the mushrooms prepared (i.e. raw, sauteed, fried, steamed)?
    11) Are ALL persons who ate the mushroom ill?
    12) Are persons in the group who ate NONE of the mushroom ill?
    13) Other important questions regarding the mushroom include:
    a) What kind of substrate was it growing on (eg; wood, soil)?
    b) What kind of tree(s) was it growing near?
    c) What time of year was the mushroom collected?

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis or peritoneal dialysis may be beneficial in patients that develop acute renal insufficiency following H. rutilans exposure (Diaz, 2005).
    B) SHORT-TERM HEMOPERFUSION
    1) Hemoperfusion may be beneficial in patients that develop acute renal insufficiency following H. rutilans exposure (Diaz, 2005).

Range Of Toxicity

Summary

    A) TOXICITY: A minimum lethal dose has not been established. A few spoonfuls caused toxicity in a 7-year-old child, including vomiting, nausea, dizziness, abdominal pain, and hepatorenal toxicity 12 hours after exposure which all resolved with supportive care.

Minimum Lethal Exposure

    A) A minimum lethal dose has not been established.

Maximum Tolerated Exposure

    A) At the time of this review, limited reports of exposure have been found in the literature.
    B) CASE REPORT/PEDIATRIC: A 7-year-old boy ate a "few spoonfuls" of fried H. rutilans (mistakenly thought to be Fistula hepatica) and developed episodes of vomiting, nausea, dizziness and abdominal pain approximately 12 hours after exposure. Clinical effects included hepato-renal failure and neurological symptoms including vertigo, ataxia and somnolence. Following supportive care, no permanent sequelae occurred (Kraft et al, 1998).

Pharmacology Toxicology

Toxicologic Mechanism

    A) Polyporic acid, a secondary metabolite found in H. rutilans mushrooms, is a dihydroorotate dehydrogenase (DHO-DH) inhibitor and is thought to be responsible for the toxic effects observed in both humans and rat model studies (Kraft et al, 1998).

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Bon M: The Mushrooms and Toadstools of Britain and North-Western Europe, Hodder & Stoughton, London, UK, 1988, pp -.
    3) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    4) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    5) Diaz JH: Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med 2005; 33:427-436.
    6) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    7) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    8) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    9) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    10) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    11) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    12) Kraft J, Bauer S, Keilhoff G, et al: Biological effects of the dihydroorotate dehydrogenase inhibitor polyporic acid, a toxic constituent of the mushroom Hapalopilus rutilans, in rats and humans. Arch Toxicol 1998; 72(11):711-721.
    13) Kuo, M: Hapalopilus nidulans. MushroomExpert.Com. Charleston, IL. 2003. Available from URL: http://www.mushroomexpert.com/hapalopilus_nidulans.html.
    14) None Listed: Hapalopilus nidulans. Rogers Plants Ltd. London, UK. 2006. Available from URL: http://www.rogersmushrooms.com/gallery/DisplayBlock~bid~5990.asp.
    15) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    16) Northern Ireland Fungus Group: Hapalopilus nidulans from the Online Atlas of Fungi in Northern Ireland. Northern Ireland Fungus Group. Belfast, UK. 2006. Available from URL: www.nifg.org.uk/foldertree/BMSSYS0000007626.htm .
    17) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    18) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    19) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    20) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    21) Villa AF, Saviuc P, Langrand J, et al: Tender Nesting Polypore (Hapalopilus rutilans) poisoning: report of two cases. Clin Toxicol (Phila) 2013; 51(8):798-800.