AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Of more than 5000 species of mushrooms in the United States, approximately 100 are poisonous, and less than a dozen are deadly.

Most fatalities resulting from mushroom ingestion are associated with amatoxins within the mushrooms. Amatoxins (cyclic octapeptides) represent 1 of 3 groups of cyclopeptides and are heat-stable, insoluble in water, and not destroyed by drying. At least 5 subtypes of amatoxins exist; alpha and beta amatoxins are the most significant subtypes.

Alpha amatoxin inhibits RNA polymerase II, which ultimately leads to cell death. Amanita toxins are found in several Amanita species and some members of the genera Galerina and Lepiota. Even experienced mushroom pickers may mistake death cap (Amanita phalloides) for one of its benign cousins.

Pathophysiology

Amatoxin poisoning can be divided into 3 stages.

• Amatoxin poisoning has a characteristic latent period of 6-12 hours postingestion before onset of clinical symptoms. After this asymptomatic period, abdominal cramping, vomiting, and profuse watery diarrhea (rice water, choleralike) occur. Fluid losses may be severe enough to cause profound dehydration and even circulatory collapse.
• Once this acute gastrointestinal phase is over (usually after 24 h), the second stage begins. Although the patient appears to have improved clinically, ongoing liver damage is occurring as indicated by laboratory abnormalities (elevation of serum aminotransferase levels, prothrombin time). This stage may last as long as 2-3 days.
• Hepatic and renal injury become clinically apparent and may progress to fulminant hepatic failure in the third phase. Death may occur in 3-7 days.

Frequency

United States

In 1996, 10,584 mushroom exposures were reported to the American Association of Poison Control Centers.¹

• Eighty-eight percent of reported mushroom exposures were unidentified.
• Only 54 were identified as amatoxin exposures; however, this number is undoubtedly an underestimation given the number of unknown mushroom exposures.
• One author estimates incidence of mushroom exposures at 5 exposures per 100,000 population per year.

International

No adequate database exists to estimate worldwide exposures.

• Mushroom foraging is more common in parts of Europe and Russia than in other parts of the world.
• From mid-July to September of 1998, 9 people died and 180 were poisoned from mushrooms in Russia.
• In July and August of 1997, 34 people died of mushroom poisoning across Russia.

Mortality/Morbidity

Ninety-five percent of all mushroom fatalities in North America are associated with cyclopeptide-containing species (amatoxins). Worldwide, most mushroom fatalities are ascribed to amatoxins. Amatoxins are associated with mortality rates ranging from 10-60%.

Ingestion of a single Amanita phalloides mushroom can be lethal.

Age

• Most accidental mushroom exposures occur in children younger than 6 years.
• Mortality is higher in children because they absorb a larger dose of toxins per body weight.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

With amatoxin ingestion, onset of GI symptoms typically is delayed 6-12 hours or more. An earlier onset of symptoms suggests that another mushroom is responsible for symptomatology. However, if the patient's meal included several different mushrooms, an earlier onset of symptomatology does not rule out concomitant amatoxin ingestion.

• Presenting complaints include severe abdominal pain, cramping, nausea and vomiting, profuse diarrhea, and weakness.
• With delayed presentation, complaints may include symptoms attributable to hepatic dysfunction, such as jaundice, lethargy, or bruising.
• If a mushroom sample is available, place it in a dry paper bag (do not moisten or refrigerate).

Physical

Assessing the patient's volume status is an important component of the initial evaluation. With delayed presentations, look for signs of hepatic or CNS dysfunction.

• Vital signs
• • Tachycardia

  • Hypotension

• Skin
• • Poor turgor

  • Jaundice, bruising (with hepatic failure)

• Abdomen
• • Mild tenderness

  • Diarrhea, may have a positive result on a Hemoccult test (guaiac positive)

• Neurologic (if hepatic failure or hypoglycemia)
• • Confusion

  • Lethargy

  • Coma

Causes

• Accidental childhood ingestions
• Misidentification of mushroom by forager
• Deliberate seeking of psychotropic mushrooms

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Obtain liver function tests because hepatic damage is the main concern with amatoxin poisoning.
  
  
  • Prothrombin time (PT) (most reliable indicator for severity of poisoning)
  • Aminotransferase levels
  • Bilirubin level
  • Alkaline phosphatase level
• Complete blood count (CBC)
• Electrolytes, BUN, and creatinine levels (dehydration from vomiting and diarrhea)
• Glucose level (monitor very closely with hepatic failure)
• Urinalysis (hematuria and proteinuria signifying renal involvement)
• Amylase/lipase level (pancreatitis)

• Urinary amanitin analysis (a pilot study suggests high specificity and positive predictive value)

Imaging Studies

• Abdominal radiographs may be obtained if bowel obstruction or ileus appears in the differential diagnosis. Mushrooms are not radiopaque and, therefore, will not be seen on abdominal radiographs.

Other Tests

• Perform a Maixner test if a specimen of the ingested mushroom is available for analysis.
• • Place a drop of liquid expressed from the mushroom on lignin-containing paper (ie, paper derived from wood pulp, such as newspaper but not filter paper).

  • After the drop has dried, place a drop of 10-12 N HCl on the spot.

  • The appearance of a blue color within several minutes suggests the presence of amatoxins.

  • A delayed appearance of a blue color suggests that amatoxin is present but in lower concentrations.

  • Presence of psilocybin can lead to a false-positive result.

  • Gastric contents are not suitable for this test.

• An experienced mycologist may analyze and identify spores in gastric contents.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

Institute supportive measures if needed, such as intravenous access and oxygen.

Emergency Department Care

Aggressively treat a patient with suspected ingestion because the mortality rate of ingested amatoxin is as high as 60%.

• Reduction of amatoxin absorption
  
  
  • Consider gastric lavage if the patient has not already vomited. In general, lavage should be attempted within 1 hour of ingestion. Given the delayed presentation of these intoxications, efficacy of this procedure is uncertain.
  • Administer activated charcoal. Amatoxins appear to undergo enterohepatic circulation and repeat dose activated charcoal may interrupt this cycle and reduce toxicity.
• The mainstays of treatment include aggressive intravenous fluids and electrolytes to correct and maintain adequate hydration. Serum electrolyte and glucose levels should be closely monitored.
• Several drugs have been postulated to reduce uptake of amatoxin into hepatocytes. Animal data support the use of some of these drugs, but only anecdotal support is available for humans.
  
  
  
  • High-dose penicillin G along with silibinin (not approved for use in the United States) appears to be the most promising treatment.
  • Silibinin (water-soluble milk thistle extract, not available in the United States) along with high-dose penicillin G appears to be the most promising treatment.
  • Vitamin K (if coagulopathy is present)
  • N-acetylcysteine
  • Cimetidine

Consultations

• Consult a regional poison center or toxicologist for assistance in case management.
• Contacting a mycologist for possible mushroom identification may be helpful. Possible sources for mushroom identification include the following:
• • North American Mycological Association

  • Local botanical garden

  • Local mycology club

  • Regional poison control center

• Consult a gastroenterologist if hepatic dysfunction is present. If hepatic failure is present, medical personnel who work with a liver transplant program should be consulted to facilitate a preoperative evaluation should spontaneous recovery not occur.

• For fulminant hepatic failure, consult a liver transplant service.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Management of amatoxin poisoning is primarily supportive.

Drug Category: GI decontaminants

These agents bind toxin in the GI tract and limit systemic adsorption. Repeat doses may effectively interrupt enterohepatic circulation.

Drug Category: Pharmacologic antidotes - experimental

Medications documented in case reports and literature reviews without solid clinical evidence for use.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Admission criteria: Admit all patients with amatoxin poisoning for aggressive supportive care and monitoring of hepatic function.

Transfer

• Consider transfer of any patient with amatoxin poisoning to a facility with a medical toxicologist.
• Consider transfer of any patient with progressive hepatic dysfunction to a facility that has a liver transplant service.

Deterrence/Prevention

• No single test can be used to determine the edibility of wild mushrooms.
• Foragers should abide by the following: "No rule is the only rule."
• Immigrants, even if very experienced in their countries of origin, may not be able to distinguish poisonous mushrooms from edible mushrooms in the United States.

Complications

• Liver failure is the most serious complication of amatoxin ingestion.
• Hepatic coma and hypoglycemia can complicate liver failure.
• Progressive hepatic failure can lead to hepatorenal syndrome.
• A recent retrospective study concluded that the prothrombin index in combination with the serum creatinine level from day 3 to day 10 after ingestion may help predict those patients needing liver transplantation. In this study, an international normalized ratio (INR) of 2.5 or higher along with a serum creatinine level greater than 106 µmol/L was predictive of fatal outcome.²

Prognosis

• Mortality rates of 10-60% have been reported. With good supportive care, mortality rates are now lower than in the past.
• Liver transplant can save the life of a patient with the most severe amatoxin poisoning.

Patient Education

• For excellent patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Activated Charcoal.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to consider mushroom ingestion with acute gastroenteritis or signs of hepatic injury
• Failure to consider an amatoxin mushroom poisoning when a patient presents with symptoms early (meal may have included several different mushrooms)

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Litovitz TL, Smilkstein M, Felberg L, Klein-Schwartz W, Berlin R, Morgan JL. 1996 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1997;15(5):447-500. [Medline].
2. Ganzert M, Felgenhauer N, Zilker T. Indication of liver transplantation following amatoxin intoxication. J Hepatol. Feb 2005;42(2):202-9. [Medline].
3. Butera R, Locatelli C, Coccini T, Manzo L. Diagnostic accuracy of urinary amanitin in suspected mushroom poisoning: a pilot study. J Toxicol Clin Toxicol. 2004;42(6):901-12. [Medline].
4. Feinfeld DA, Mofenson HC, Caraccio T, Kee M. Poisoning by amatoxin-containing mushrooms in suburban New York--report of four cases. J Toxicol Clin Toxicol. 1994;32(6):715-21. [Medline].
5. Floersheim GL. Treatment of human amatoxin mushroom poisoning. Myths and advances in therapy. Med Toxicol. Jan-Feb 1987;2(1):1-9. [Medline].
6. Giannini L, Vannacci A, Missanelli A, Mastroianni R, Mannaioni PF, Moroni F. Amatoxin poisoning: A 15-year retrospective analysis and follow-up evaluation of 105 patients. Clin Toxicol (Phila). 2007;45(5):539-42. [Medline].
7. Goldfrank LR. Mushrooms: toxic and hallucinogenic. In: Goldfrank's Toxicologic Emergencies. 5^th ed. Appleton & Lange; 1994:951-961.
8. Olesen LL. Amatoxin intoxication. Scand J Urol Nephrol. 1990;24(3):231-4. [Medline].
9. Paydas S, Kocak R, Erturk F, Erken E, Zaksu HS, Gurcay A. Poisoning due to amatoxin-containing Lepiota species. Br J Clin Pract. Nov 1990;44(11):450-3. [Medline].
10. Pond SM, Olson KR, Woo OF, et al. Amatoxin poisoning in northern California, 1982-1983. West J Med. Aug 1986;145(2):204-9. [Medline].
11. Warden CR, Benjamin DR. Acute renal failure associated with suspected Amanita smithiana mushroom ingestions: a case series. Acad Emerg Med. Aug 1998;5(8):808-12. [Medline].
12. Yamada EG, Mohle-Boetani J, Olson KR, Werner SB. Mushroom poisoning due to amatoxin. Northern California, Winter 1996-1997. West J Med. Dec 1998;169(6):380-4. [Medline].

Article Last Updated: Jul 19, 2007