IDENTIFICATION
Correct identification of the mushroom/s is imperative for optimal risk assessment. Consider and enquire about the possibility that more than one type of mushroom was ingested. If the identity is uncertain, or the patient’s signs and symptoms differ from those listed or are delayed in onset, seek advice from a reliable source such as your local Poisons Information Center. Further information on unidentified mushrooms can also be found by following the below link: |
IMAGE
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HABITAT
Amanita phalloides occurs mainly in deciduous and mixed deciduous forests, especially under oak trees but also near hornbeam or beech. The fungus avoids colder localities.  |
USES
This mushroom is poisonous, however it may be mistaken for other edible mushrooms.
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INTERVENTION CRITERIA
Medical assessment, observation, and, if appropriate, decontamination, is recommended for: - Any ingestion of a cyclopeptide mushroom - Exposures with intent to self-harm |
All patients require medical attention. |
Any patient known to have ingested this type of mushroom must be admitted for monitoring and treatment, certainly those with symptoms or deranged biochemistry. |
If it is suspected that the patient has ingested cyclopeptide mushrooms, every effort should be made to get the mushroom identified by a mycologist.
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When possible, a sample of the mushroom should be collected for identification. A whole mushroom, including the stalk and its base is preferable. The sample should be placed in a paper (not plastic) bag and then put in a sturdy container to protect the mushroom from damage. If the mushroom needs to be stored, it should be placed in the refrigerator, not the freezer. |
Wieland (Meixner) Test:  Determines presence of amatoxin Methods - Perform indoors away from sunlight and excessive heat - Squeeze a small drop of fungus juice onto a piece of pulp paper i.e. newspaper, phone book page - Encircle wet stop with pencil to mark location - Dry the spot with warm air - Add a drop of concentrated hydrochloric acid to the dry spot The presence of amatoxins is indicated by the formation of a blue color False positives - Use a control without amatoxins so false positives can be identified - A false positive reaction can occur at high temperatures or exposure to sunlight - Psilocybin, bufotenine, and certain terpines can give false positives   This test is limited but can be helpful in the rapid testing in cases of suspected cyclopeptide poisoning. |
Any patient who has ingested cyclopeptide mushrooms must be admitted. Furthermore, any patient who has ingested an unknown mushroom but has features or biochemical changes indicative of cyclopeptide poisoning must be admitted. The admission hospital will require the following resources: Advanced care/ICU Enhanced elimination |
TREATMENT
TREATMENT SUMMARY
Any patient suspected of ingesting cyclopeptide-containing mushrooms should be admitted to hospital. Initial management consists of vigorous monitoring and replacement of expected fluid losses, which may be several liters per day.  Along with fluid replacement correction of metabolic disturbances such as acidosis, hypoglycemia, and electrolyte imbalances should be undertaken. The patient should be hemodynamically monitored and biochemical parameters followed closely. Due to the low oral bioavailability of cyclopeptide mushrooms and the difficulty humans have in digesting large amounts of mushrooms, single dose activated charcoal may be given up to 12 hours following ingestion.   The use of multiple dose activated charcoal in the enhanced elimination of amatoxins is indicated up to 48 hours post-ingestion due to the extensive enterohepatic circulation of these toxins.  It is important that a good renal output is established during the first 48 hours following ingestion. Use of sedating drugs is not recommended due to their impact on the assessment of mental function/encephalopathy. Acute hepatic failure is a well-recognized concern and transplantation may be required.   Advice should be sought from a specialist liver transplant unit if: The International Normalized Ratio (INR) is greater or equal to 2 at 24 hours or, 3 at any time or Creatinine is greater or equal to 200 umol/L (2.2 mg/dL) or pH is less than or equal to 7.3 or bicarbonate less than or equal to 18 mmol/L (18 mEq/L) or Blood pressure is low after volume loading (mean arterial pressure less than or equal to 60 mmHg) or The patient becomes encephalopathic Early discussion of patients with a liver transplant unit is essential. Advice may be given and a decision to transport dependent upon results. In general it is considered desirable to transport patients prior to development of grade 2 encephalopathy. |
EMERGENCY STABILIZATION
Ensure Adequate Cardiopulmonary Function |
Immediately establish secure intravenous access. |
Profound hypotension may occur requiring volume replacement.
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CHILD Hypotension in children is determined by age and systolic blood pressure Age | Hypotension if Systolic Blood Pressure (mm Hg) is: | 0 to 28 days | < 60 | 1 to 12 months | < 70 | 1 to 10 years | < 70 + (age in years x 2) | > 10 years | < 90 |
Administer an isotonic crystalloid fluid 10 mL/kg IV over 5 to 10 minutes If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight of the isotonic crystalloid over 5 to 10 minutes. The intraosseous route can be used if IV access is difficult or delayed. ADULT Administer a bolus of isotonic crystalloid fluid if systolic blood pressure is less than 100 mmHg. Isotonic crystalloid fluid dose: 20 mL/kg IV over 5 to 10 minutes If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes. The intraosseous route can be used if IV access is difficult or delayed. |
Seizure activity Blood pressure Heart rate ECG Fluid balance Serum electrolytes Renal function Liver function |
DECONTAMINATION
Single Dose Activated Charcoal |
Administer activated charcoal up to 12 hours following a potentially toxic ingestion. |
Single dose activated charcoal CHILD 1 to 2 g/kg orally ADULT 50 to 100 g orally |
ANTIDOTE(S)
Animal studies have shown that silibinin (Milk thistle) prevents the uptake of amatoxins by hepatocytes, reducing enterohepatic circulation and therefore enhancing renal elimination. Furthermore, silibinin stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.  However, controlled human studies are still pending. Unfortunately, silibinin is not widely available. |
Silibinin is indicated in:  All patients presenting with cyclopeptide mushroom ingestion |
Silibinin dose:   CHILD IV Initial dose 5 mg/kg IV over 1 hour Maintenance dose of 20 mg/kg as a continuous infusion ADULT IV Initial dose 5 mg/kg IV over 1 hour Maintenance dose of 20 mg/kg as a continuous infusion Treatment should be continued for up to 72 hours, or until significant declines in INR and liver function tests are apparent. |
Documented hypersensitivity to silibinin.
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Recommended doses could be administered during pregnancy without being harmful to the fetus.  |
Silibinin appears to be well tolerated. However the following adverse effects have been reported following administration:   Gastrointestinal upset (nausea, vomiting, diarrhea, abdominal pain) Intermittent episodes of sweating Arthralgia Pruritus Headache Urticaria Weakness |
Animal studies indicate that sublethal doses of amatoxins deplete hepatic glutathione content.  N-acetylcysteine is thought to serve as a glutathione precursor and consequently, the administration of N-acetylcysteine in cyclopeptide mushroom poisoning may prevent reduced glutathione levels and subsequent hepatocellular damage.   Additionally N-acetylcysteine has been shown to reduce morbidity and mortally in severe hepatic failure irrespective of origin.  It is therefore recommended in cyclopeptide mushroom poisoning. |
N-acetylcysteine should be administered in:  All patients presenting with cyclopeptide mushroom ingestion |
While acetylcysteine is recommended to be administered intravenously in 5% dextrose in water, 1/2 normal (0.45%) saline or normal saline (0.9%) may be substituted if necessary.  In children there is a risk of hyponatremia with 5% dextrose alone  and therefore normal (0.9%) saline should be used. CHILD  It is recommended that acetylcysteine dose for children be calculated for actual body weight. Children < 14 years old: 200 mg/kg in 7 mL/kg (up to 500 mL) of normal saline over 4 hours Followed by 100 mg/kg in 14 mL/kg (up to 1,000 mL) of normal saline over 16 hours Children 14 years and older: As per adults Closely monitor fluid and electrolyte balance. It is recommended that acetylcysteine dose for adults be calculated for actual body weight rounded up to the nearest 10 kg with a ceiling weight of 110 kg. Administer: 200 mg/kg in 500 mL of 5% dextrose over 4 hours Followed by 100 mg/kg in 1,000 mL of 5% dextrose over 16 hours |
Acetylcysteine should be administered to pregnant patients following the standard adult regimen. Transplacental transport of acetylcysteine is not thought to be clinically significant,  however, delay in initiation of acetylcysteine treatment is associated with increased incidence of spontaneous abortion and fetal death.  Acetylcysteine is not considered teratogenic.  |
Six to 23% of patients receiving IV acetylcysteine develop an anaphylactoid reaction.   These do not represent an immunological (allergic) reaction; rather, they are thought due to a direct dose-dependent effect on histamine release and generally occur within the first two hours of an infusion. History of previous anaphylactoid reaction to acetylcysteine does not contraindicate use. If there is concern of recurrence of the reaction the patient may be pre-treated 15 minutes before commencement of the infusion with an antihistamine.  Effects range from mild flushing to urticaria, angioedema, or bronchospasm. Hypotension may occasionally occur. Asthmatics appear more at risk. However, effects are usually easily managed and there is no reason to withhold acetylcysteine from any patient when indicated.  |
Hyponatremia has been reported in children if administered acetylcysteine in 5% dextrose following adult protocols for dilution of infused dose.  |
SIGNS AND SYMPTOMS
Cyclopeptide mushroom ingestion produces the Phalloides syndrome, which typically exhibits a quadriphasic course, and appears to be dose related. Phase 1 and 3 are latent periods where the patient generally feels relatively well. Phase 2 begins approximately 12 hours after mushroom ingestion and consists predominantly of severe gastrointestinal symptoms, which leads to significant water and electrolyte loss. The final phase is hepatorenal, where severe hepatotoxicity may occur and hepatic and renal failure can ensue. In fatal cases, death may occur six to 16 days following ingestion.  |
Cyclopeptide mushrooms are usually ingested in fresh condition. Poisoning typically occurs as a result of amateur mushroom gatherers mistaking the mushrooms for various edible varieties. The toxins remain stable when boiled, thus poisoning is possible whether the mushrooms are eaten raw or cooked.  |
Onset/Duration of Symptoms |
Symptoms following the ingestion of amatoxin-containing mushrooms occur in four phases. NOTE: Time frames may vary considerably to those listed below. Latent asymptomatic phase (< 24 hours and usually up to 12 hours post-ingestion) No symptoms Gastrointestinal phase (6 to 24 hours post-ingestion) Abdominal pain Vomiting Severe diarrhea Hypovolemia Electrolyte disturbances Acid-base disturbance Period of well-being (24 to 48 hours post-ingestion) Hepatic and renal function deteriorates Hepatic phase (3 to 5 days post-ingestion) LFT increases Acute hepatic failure Acute renal failure In fatal cases, death may occur 6 to 16 days following ingestion due to hepatic and/or renal failure.  |
Mild Cyclopeptide Toxicity | Moderate Cyclopeptide Toxicity | Severe Cyclopeptide Toxicity | Nausea Vomiting Diarrhea Abdominal pain | Electorlyte imbalances Hypoglycemia Right upper quadrant tenderness Hepatitis Renal dysfunction Metabolic acidosis | Coagulopathy Fulminant hepatic failure Acute renal failure Hepatic encephalopathy Death |
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Do Not Archive. This document is current on day of issue,
NZ: 21.Jan.2021 |
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