1) TOXICITY: Ingestions of these mushrooms have caused nervousness, anxiety, dizziness, diaphoresis, blurred vision, gastrointestinal distress, elevated hepatic enzymes, moderate cytolytic hepatitis, and acute renal failure (characterized by acute tubulointerstitial nephropathy).
2) ONSET OF GASTROINTESTINAL SYMPTOMS (nausea, vomiting, diarrhea, and abdominal pain): varies, but has been reported as soon as 30 minutes (when eaten raw) and as late as 14 hours after ingestion.
3) ONSET OF HEPATORENAL IMPAIRMENT: 1 to 4 days. In one study, all patients with Amanita proxima poisoning recovered completely within 3 weeks without evidence of chronic hepatic or renal damage.

1) Treatment is symptomatic and supportive.

1) Treatment is symptomatic and supportive. Correct any electrolyte abnormalities in patients with severe diarrhea and/or vomiting. Administer antiemetics. Benzodiazepines may be given for agitated behavior though this is rarely necessary. Hyperkalemia may develop in patients with renal failure secondary to Amanita smithiana ingestion. Monitor serum electrolytes and correct if necessary. Hemodialysis may be necessary if renal failure develops.

1) PREHOSPITAL: Severe vomiting may occur with ingestions; therefore, decontamination may NOT be necessary. Administer activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. However, patients usually 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: Severe vomiting may occur with ingestions; therefore, decontamination may NOT be necessary. Administer activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. However, patients usually present for evaluation only after developing symptoms of toxicity 24 hours to several days after ingestion; in these cases charcoal is not helpful.

1) None.

1) HOME CRITERIA: Home management is not appropriate for suspected or confirmed cases of ingestion of these mushrooms.
2) OBSERVATION CRITERIA: All patients with suspected ingestion of these mushrooms should be referred to a healthcare facility for evaluation. Outpatient followup for testing of renal function and liver enzymes should be arranged in patients who are discharged.
3) ADMISSION CRITERIA: Patients who have severe toxicity and develop electrolyte abnormality and 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. A nephrologist should be consulted for any patient with renal failure.

1) Pitfalls include not evaluating for other co-ingestants, not recognizing signs and symptoms of toxicity from these mushrooms, including delayed symptoms, or misidentification of the mushroom. Onset of renal and hepatic toxicity may be delayed by several days.

1) Other mushrooms that can also cause renal failure or hepatotoxicity.

1) AMANITA SMITHIANA: Blurred vision was reported in a 73-year-old man 5 hours after ingesting one large cooked mushroom that was later identified as Amanita smithiana (Leathem, 1996).
2) AMANITA ECHINOCEPHALA: Visual disturbances developed in a 55-year-old woman who also developed gastrointestinal distress and acute renal failure after eating about 500 g of a mushroom believed to be Amanita echinocephala mushroom. She underwent 4 sessions of hemodialysis until her renal function recovered; however, her visual disturbances did not improve. An ophthalmologic examination revealed a regular ocular fundus and regular anterior chamber, a total loss of color vision and defects in the upper visual fields in both eyes, fitting for a toxic atrophy of the optic nerve (Kirchmair et al, 2012).

1) Nervousness and anxiety were reported after ingesting Amanita smithiana mushrooms (Tulloss & Lindgren, 1992).

1) Dizziness was reported in three patients 2 to 11 hours after ingestion of mushrooms subsequently determined to be Amanita smithiana (Leathem, 1996; Tulloss & Lindgren, 1992; Warden & Benjamin, 1998).

1) Severe nausea, vomiting, and diarrhea may commonly occur following Amanita smithiana mushroom ingestions (West et al, 2009; Tulloss & Lindgren, 1992; Leathem, 1996; Leathem et al, 1997; Warden & Benjamin, 1998).
2) CASE REPORT: Nausea and vomiting occurred in a man, 4 hours after ingesting what he believed to be a matsutake mushroom, and continued for three days. The mushroom was later determined to be Amanita smithiana (Tulloss & Lindgren, 1992).
3) CASE REPORT: A 31-year-old woman developed severe nausea, vomiting, and diarrhea 8 hours after ingesting wild mushrooms. The vomiting and diarrhea persisted for 7 days; both fluids showed evidence of blood. The nausea, vomiting, and diarrhea gradually resolved (Leathem et al, 1997)
4) ONSET OF GASTROINTESTINAL SYMPTOMS (nausea, vomiting and diarrhea): Varies, but has been reported as soon as 30 minutes (when eaten raw) and as late as 14 hours after ingestion (Saviuc & Danel, 2006; Warden & Benjamin, 1998).
5) AMANITA PROXIMA: Five patients developed gastrointestinal symptoms, cytolytic hepatitis, and acute renal failure 8 to 24 hours after the ingestion of Amanita proxima mushrooms. Four patients required temporary dialysis. Following symptomatic treatment, all patients recovered completely within 3 weeks of ingestion (Leray et al, 1994).
6) AMANITA PROXIMA: In one study, 31 cases of amanita proxima poisoning were reported. Twenty-six cases (83%) resulted from confusion with edible Amanita ovoidea mushrooms. All patients developed gastrointestinal symptoms following mushroom ingestion (mean onset 13 hours and 12 minutes postingestion). Following supportive treatment, all patients recovered completely without further sequelae (deHaro et al, 1998).
7) AMANITA BOUDIERI/GEMMATA: Two patients developed nausea, vomiting, acute renal failure, and mild hepatitis after ingesting about 500 g of mushrooms. Initially, orellanine mushroom poisoning was suspected. Following supportive therapy, including hemodialysis (in one patient), and prednisone and oral n-acetylcysteine therapy, both patients recovered completely. Mushroom specimens collected by the patients were tested after discharge and were found to be A. boudieri and A. gemmata mushrooms (Kirchmair et al, 2012).
8) AMANITA ECHINOCEPHALA: A 55-year-old woman developed nausea, vomiting, and diarrhea within 10 hours of ingesting about 500 g of mushrooms she collected in a public park. Her symptoms persisted and she presented a day later with vomiting and visual disturbances. Laboratory results revealed normal liver enzymes, except for bilirubin of 2.3 mg/dL, but an acute renal failure with serum creatinine of 5.2 mg/dL, BUN of 48 mg/dL, lactate dehydrogenase 326 Units/L (normal less than 240), C-reactive protein 2.3 mg/dL (normal less than 0.5), potassium 2.01 mmol/L (normal 3.5 to 5), and leucocytes 12,500/mcL (normal 400 to 9000). On day 4, a renal biopsy revealed massive tubular necrosis with eosinophil casts in the tubular lumina a minimal lymphocytic infiltration of the interstitium. A kidney biopsy specimen did not reveal the presence of orellanine. She underwent 4 sessions of hemodialysis until her renal function recovered; however, her visual disturbances did not improve. Mushroom poisoning with Amanita echinocephala was suspected (Kirchmair et al, 2012).

1) Abdominal pain is a common occurrence following Amanita smithiana mushroom ingestions and may be severe at times (Leathem, 1996; Tulloss & Lindgren, 1992; Leathem et al, 1997; Warden & Benjamin, 1998).

1) Elevated ALT, AST and LDH levels were reported following mushroom ingestions suspected to be Amanita smithiana (Leathem et al, 1997; Warden & Benjamin, 1998). Moderate cytolytic hepatitis has also been reported. Elevated enzymes were limited to 15 times the upper limit of normal (Saviuc & Danel, 2006).
2) AMANITA SMITHIANA: A 55-year-old man developed mild elevation of hepatic transaminases (peaked 24 hours post-ingestion) and renal insufficiency after ingesting raw amanita smithiana mushrooms. His liver enzymes returned to normal 7 days after presentation. Following 39 days of hemodialysis, he recovered completely (West et al, 2009).
3) AMANITA PROXIMA: Five patients developed gastrointestinal symptoms, cytolytic hepatitis, and acute renal failure 8 to 24 hours after the ingestion of Amanita proxima mushrooms. Four patients required temporary dialysis. Following symptomatic treatment, all patients recovered completely within 3 weeks of ingestion (Leray et al, 1994).
4) AMANITA PROXIMA: In one study, 31 cases of amanita proxima poisoning were reported. Twenty-six cases (83%) resulted from confusion with edible Amanita ovoidea mushrooms. All patients developed gastrointestinal symptoms following mushroom ingestion (mean onset 13 hours and 12 minutes postingestion). Moderate cytolytic hepatitis was observed in 10 cases. Following supportive treatment, all patients recovered completely without further sequelae (deHaro et al, 1998).
5) AMANITA BOUDIERI/GEMMATA: A 51-year-old woman developed anorexia, nausea, and vomiting a day after ingesting 2 consecutive mushroom meals (total about 500 g). Her symptoms persisted and she presented 5 days later with weakness and hypouresis. Laboratory results showed severe acute renal failure with serum creatinine 11.7 mg/dL (normal: less than 1.2), BUN 68.18 mg/dL (normal: less than 18), and a mild hepatic cytolysis with elevation of ALT (64 Units/L (normal: 10 to 35). At this time, orellanine mushroom poisoning was suspected. Following treatment with hemodialysis and prednisolone 60 mg once daily and oral n-acetylcysteine 600 mg every 6 hours, her renal function improved gradually. Her BUN was 15.9 mg/dL and serum creatinine 1 mg/dL on 2-month followup. Her husband, a 47-year-old man, developed mild dyspepsia, anorexia, and severe renal impairment (BUN: 50 mg/dL; serum creatinine 8.6 mg/dL) and mild elevations of ALT (69 Units/L) and AST (32 Units/L). He was also treated with prednisone and oral n-acetylcysteine. A kidney biopsy on day 4 revealed marked focal interstitial lymphocytic infiltrate with areas of tubular necrosis, and one ischemic glomerulus. The glomeruli and arterioles were normal. His renal function gradually improved and his serum creatinine was 0.8 mg/dL on 2-month followup. Mushroom specimens collected by the patients were tested after discharge and were found to be A. boudieri and A. gemmata mushrooms (Kirchmair et al, 2012).

1) Acute renal failure, usually with oliguria or anuria, has been reported as the primary toxicity following Amanita smithiana mushroom ingestions (West et al, 2009; Leathem, 1996; Tulloss & Lindgren, 1992; Warden & Benjamin, 1998; Leathem et al, 1997). Renal impairment which is characterized as acute tubulointerstitial nephropathy, appears earlier and does not have the same poor prognosis as the orellanine-induced syndrome (Saviuc & Danel, 2006).
2) AMANITA BOUDIERI/GEMMATA: A 51-year-old woman developed anorexia, nausea, and vomiting a day after ingesting 2 consecutive mushroom meals (total about 500 g). Her symptoms persisted and she presented 5 days later with weakness and hypouresis. Laboratory results showed severe acute renal failure with serum creatinine 11.7 mg/dL (normal: less than 1.2), BUN 68.18 mg/dL (normal: less than 18), and a mild hepatic cytolysis with elevation of ALT (64 Units/L (normal: 10 to 35). At this time, orellanine mushroom poisoning was suspected. Following treatment with hemodialysis and prednisolone 60 mg once daily and oral n-acetylcysteine 600 mg every 6 hours, her renal function improved gradually. Her BUN was 15.9 mg/dL and serum creatinine 1 mg/dL on 2-month followup. Her husband, a 47-year-old man, developed mild dyspepsia, anorexia, and severe renal impairment (BUN: 50 mg/dL; serum creatinine 8.6 mg/dL) and mild elevations of ALT (69 Units/L) and AST (32 Units/L). He was also treated with prednisone and oral n-acetylcysteine. A kidney biopsy on day 4 revealed marked focal interstitial lymphocytic infiltrate with areas of tubular necrosis, and one ischemic glomerulus. The glomeruli and arterioles were normal. His renal function gradually improved and his serum creatinine was 0.8 mg/dL on 2-month followup. Mushroom specimens collected by the patients were tested after discharge and were found to be A. boudieri and A. gemmata mushrooms (Kirchmair et al, 2012).
3) AMANITA ECHINOCEPHALA: A 55-year-old woman developed nausea, vomiting, and diarrhea within 10 hours of ingesting about 500 g of mushrooms she collected in a public park. Her symptoms persisted and she presented a day later with vomiting and visual disturbances. Laboratory results revealed normal liver enzymes, except for bilirubin of 2.3 mg/dL, but an acute renal failure with serum creatinine of 5.2 mg/dL, BUN of 48 mg/dL, lactate dehydrogenase 326 Units/L (normal less than 240), C-reactive protein 2.3 mg/dL (normal less than 0.5), potassium 2.01 mmol/L (normal 3.5 to 5), and leucocytes 12,500/mcL (normal 400 to 9000). On day 4, a renal biopsy revealed massive tubular necrosis with eosinophil casts in the tubular lumina a minimal lymphocytic infiltration of the interstitium. A kidney biopsy specimen did not reveal the presence of orellanine. She underwent 4 sessions of hemodialysis until her renal function recovered; however, her visual disturbances did not improve. An ophthalmologic examination revealed a regular ocular fundus and regular anterior chamber, a total loss of color vision and defects in the upper visual fields in both eyes, fitting for a toxic atrophy of the optic nerve. Mushroom poisoning with Amanita echinocephala was suspected (Kirchmair et al, 2012).
4) AMANITA SMITHIANA: A 63-year-old man with a medical history of hypertension and coronary artery disease developed fatigue and malaise about 4 hours after ingesting a soup containing Amanita smithiana mushrooms. A day later, he developed nausea, vomiting, chills, abdominal pain, and non-bloody diarrhea. He presented to the ED with anuria 2 days after ingesting the mushroom soup. Laboratory analysis revealed elevated serum creatinine (12.3 mg/dL), urea (70 mg/dL), AST (119 Units/L), ALT (160 Units/L), and LDH (1843 Units/L). Despite supportive care, he remained anuric. On day 4, he underwent hemodialysis daily for 3 days and then every second day (total 6 sessions). He continued to improve and was discharged on day 16 with a serum creatinine of 7.4 mg/dL. Thin-layer chromatography was used to identify the presence of Amanita smithiana toxin in a sample of mushroom soap (Apperley et al, 2013).
5) AMANITA PSEUDOPORPHYRIA: A 66-year-old man presented to the hospital with fatigue, facial edema, and loss of appetite. Laboratory analysis showed proteinuria, glucosuria, hematuria, and a serum creatinine of 16.48 mg/dL. CT scan showed slight swelling of the kidneys. Renal biopsy revealed tubulointerstitial lesions, confirming a diagnosis of acute renal failure due to acute tubular necrosis. The patient admitted eating amanita pseudoporphyria hongo mushrooms along with other edible mushrooms two weeks prior to hospital admission. Because other causes, such as dehydration and drug use, could not be found, it is suspected that the acute renal failure was caused by ingestion of amanita pseudoporphyria hongo. The patient gradually recovered after receiving hemodialysis three times per week for three weeks (Iwafuchi et al, 2003).
6) AMANITA PROXIMA: Five patients developed gastrointestinal symptoms, cytolytic hepatitis, and acute renal failure 8 to 24 hours after the ingestion of Amanita proxima mushrooms. Four patients required temporary dialysis. Following symptomatic treatment, all patients recovered completely within 3 weeks of ingestion (Leray et al, 1994).
7) AMANITA PROXIMA: In one study, 31 cases of amanita proxima poisoning were reported. Twenty-six cases (83%) resulted from confusion with edible Amanita ovoidea mushrooms. All patients developed gastrointestinal symptoms following mushroom ingestion (mean onset 13 hours and 12 minutes postingestion). Oliguria or anuria developed in 14 of cases within a few days of ingestion; 11 patients required hemodialysis. Following supportive treatment, all patients recovered completely without further sequelae (deHaro et al, 1998).

1) Metabolic acidosis may develop in patients with acute renal failure (Leathem et al, 1997; Warden & Benjamin, 1998).
2) Renal tubular acidosis has been reported after recovery from Amanita smithiana-induced acute tubular necrosis (Leathem et al, 1997).
3) CASE REPORT: A 31-year-old female ingested wild mushrooms thought to be pine mushrooms and experienced oliguria four days later (Leathem et al, 1997). Laboratory values six days post-ingestion included chloride 73 mmol/L, urea 47.6 mmol/L, creatinine 1175 mcmol/L, and arterial blood gas measurements showed an initial serum pH of 7.27 and a bicarbonate level of 7 mmol/L.

1) CASE REPORT: A 30-year-old woman ingested mushrooms misidentified as matsutake mushrooms and developed intense diffuse pruritus 4 days later. The patient also developed a nonspecific erythematous macular rash (Warden & Benjamin, 1998).

1) Increased sweating was reported as a result of ingestion of Amanita smithiana mushrooms (Tulloss & Lindgren, 1992; Leathem et al, 1997; Warden & Benjamin, 1998).

1) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
2) Monitor renal function and liver enzymes in symptomatic patients.

1) Monitor arterial blood gases in patients with metabolic acidosis.

1) Monitor for acute renal failure following exposure. Obtain urinalysis and monitor urinary output.

1) Urinary amanitin levels may be useful in the early diagnosis of amanita mushroom poisoning or in cases where ingestion is suspected. An amanitin level of 5 ng/mL has high sensitivity and specificity if samples are collected within 36 hours of mushroom exposure (Butera et al, 2006). This test is not widely available in clinical practice.

1) ECG

A) Patients who have severe toxicity and develop electrolyte abnormality and hepatic or renal insufficiency, should be admitted for further evaluation.

A) Home management is not appropriate for suspected or confirmed cases of ingestion of these mushrooms.

A) A mycologist and toxicologist or poison center should be consulted in order to help with identification and guide treatment. A nephrologist should be consulted for any patient with renal failure.

A) All patients with suspected ingestion of these mushrooms should be referred to a healthcare facility for evaluation. Outpatient followup for testing of renal function and liver enzymes should be arranged in patients who are discharged.

1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) Severe vomiting may occur with ingestions; therefore, decontamination may NOT be necessary. Administer activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. However, patients usually present for evaluation only after developing symptoms of toxicity 24 hours to several days after ingestion; in these cases charcoal is not helpful.
2) CHARCOAL ADMINISTRATION
3) CHARCOAL DOSE

1) MANAGEMENT OF MILD TO MODERATE TOXICITY: Treatment is symptomatic and supportive.
2) MANAGEMENT OF SEVERE TOXICITY: Treatment is symptomatic and supportive. Correct any electrolyte abnormalities in patients with severe diarrhea and/or vomiting. Administer antiemetics. Benzodiazepines may be given for agitated behavior though this is rarely necessary. Hyperkalemia may develop in patients with renal failure secondary to Amanita smithiana ingestion. Monitor serum electrolytes and correct if necessary.

1) Monitor vital signs and mental status.
2) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
3) Monitor renal function and liver enzymes in symptomatic patients.
4) Monitor arterial blood gases in patients with metabolic acidosis.
5) Obtain an ECG, and institute continuous cardiac monitoring in patients with hyperkalemia.

1) In cases of severe vomiting or diarrhea, monitor fluid and electrolyte levels and correct if necessary.

1) Hyperkalemia may develop in patients with renal failure secondary to Amanita smithiana ingestion (Leathem et al, 1997). Institute continuous cardiac monitoring and obtain an ECG. Progressive ECG changes occur with increasing serum potassium levels.
2) ECG manifestations of hyperkalemia and/or a serum potassium concentration of 7.5 milliequivalents/liter or greater indicates a medical emergency and requires aggressive therapy.