Mushroom poisoning: Difference between revisions

(Created page with "Mushroom poisoning encompasses a spectrum of clinical syndromes caused by ingestion of toxic mushroom species. The key distinction for the emergency physician is between '''early-onset''' (<6 hours) and '''delayed-onset''' (>6 hours) symptoms, as delayed presentations are far more likely to be life-threatening.<ref name="Diaz2018">Diaz JH. Amatoxin-Containing Mushroom Poisonings: Species, Toxidromes, Treatments, and Outcomes. ''Wilderness Environ Med''. 2018;29(1):111-11...")
 
(Moved intro into Background as bullets; removed excessive bold from bullet lead-ins; added Mushroom toxicity DDX template)
Line 1: Line 1:
Mushroom poisoning encompasses a spectrum of clinical syndromes caused by ingestion of toxic mushroom species. The key distinction for the emergency physician is between '''early-onset''' (<6 hours) and '''delayed-onset''' (>6 hours) symptoms, as delayed presentations are far more likely to be life-threatening.<ref name="Diaz2018">Diaz JH. Amatoxin-Containing Mushroom Poisonings: Species, Toxidromes, Treatments, and Outcomes. ''Wilderness Environ Med''. 2018;29(1):111-118. doi:10.1016/j.wem.2017.10.002</ref>
==Background==
==Background==
*Mushroom poisoning encompasses a spectrum of clinical syndromes caused by ingestion of toxic mushroom species.
*The key distinction for the emergency physician is between early-onset (<6 hours) and delayed-onset (>6 hours) symptoms, as delayed presentations are far more likely to be life-threatening.<ref name="Diaz2018">Diaz JH. Amatoxin-Containing Mushroom Poisonings: Species, Toxidromes, Treatments, and Outcomes. ''Wilderness Environ Med''. 2018;29(1):111-118. doi:10.1016/j.wem.2017.10.002</ref>
*There are over 5,000 species of mushrooms; approximately 50-100 are toxic to humans<ref name="StatPearls">Amatoxin Mushroom Toxicity. ''StatPearls''. 2023. PMID: 28613706</ref>
*There are over 5,000 species of mushrooms; approximately 50-100 are toxic to humans<ref name="StatPearls">Amatoxin Mushroom Toxicity. ''StatPearls''. 2023. PMID: 28613706</ref>
*'''95% of mushroom-related deaths worldwide''' are caused by amatoxin-containing mushrooms (''Amanita'', ''Galerina'', ''Lepiota'' species)<ref name="Diaz2018"/>
* 95% of mushroom-related deaths worldwide are caused by amatoxin-containing mushrooms (''Amanita'', ''Galerina'', ''Lepiota'' species)<ref name="Diaz2018"/>
*Most poisonings occur in foragers who misidentify wild mushrooms as edible species
*Most poisonings occur in foragers who misidentify wild mushrooms as edible species
**Immigrants may mistake toxic local species for edible ones from their home country
**Immigrants may mistake toxic local species for edible ones from their home country
**Recreational users may confuse toxic species for hallucinogenic ''Psilocybe'' mushrooms
**Recreational users may confuse toxic species for hallucinogenic ''Psilocybe'' mushrooms
*'''Children''' and '''elderly''' are more susceptible to volume depletion and toxicity
* Children and '''elderly''' are more susceptible to volume depletion and toxicity
*Amatoxins are '''heat-stable''' — cooking does not eliminate the toxin<ref name="StatPearls"/>
*Amatoxins are '''heat-stable''' — cooking does not eliminate the toxin<ref name="StatPearls"/>
*Most mushroom ingestions are benign GI irritants; the challenge is identifying the dangerous minority
*Most mushroom ingestions are benign GI irritants; the challenge is identifying the dangerous minority
Line 30: Line 30:
*Caused by ''Inocybe'' and ''Clitocybe'' species
*Caused by ''Inocybe'' and ''Clitocybe'' species
*Onset 15-30 minutes
*Onset 15-30 minutes
*'''SLUDGE/DUMBELS:''' salivation, lacrimation, urination, diarrhea, GI cramping, emesis; diaphoresis, urination, miosis, bronchospasm/bronchorrhea, emesis, lacrimation, salivation
* SLUDGE/DUMBELS: salivation, lacrimation, urination, diarrhea, GI cramping, emesis; diaphoresis, urination, miosis, bronchospasm/bronchorrhea, emesis, lacrimation, salivation
*[[Bradycardia]], [[Hypotension|hypotension]]
*[[Bradycardia]], [[Hypotension|hypotension]]
*Treatment: '''[[Atropine|atropine]]'''
*Treatment: '''[[Atropine|atropine]]'''
Line 38: Line 38:
*Onset 30 min - 2 hours
*Onset 30 min - 2 hours
*Confusion, agitation, hallucinations, [[Ataxia|ataxia]], myoclonus, [[Seizure|seizures]]
*Confusion, agitation, hallucinations, [[Ataxia|ataxia]], myoclonus, [[Seizure|seizures]]
*'''Mydriasis''', tachycardia, dry skin
* Mydriasis, tachycardia, dry skin
*Alternating sedation and excitation
*Alternating sedation and excitation
*No hepatic or renal injury
*No hepatic or renal injury
Line 65: Line 65:
====Amatoxin syndrome (most dangerous)====
====Amatoxin syndrome (most dangerous)====
*Caused by ''Amanita phalloides'' (death cap), ''A. virosa'' (destroying angel), ''A. verna'', ''A. bisporigera'', ''Galerina'' spp., ''Lepiota'' spp.
*Caused by ''Amanita phalloides'' (death cap), ''A. virosa'' (destroying angel), ''A. verna'', ''A. bisporigera'', ''Galerina'' spp., ''Lepiota'' spp.
*'''Phase 1 (6-24 hours):''' severe cholera-like vomiting and watery diarrhea → dehydration, electrolyte derangement
* Phase 1 (6-24 hours): severe cholera-like vomiting and watery diarrhea → dehydration, electrolyte derangement
*'''Phase 2 (24-48 hours):''' apparent clinical improvement ('''"false recovery"''' or "quiescent phase") — transaminases begin rising
* Phase 2 (24-48 hours): apparent clinical improvement ('''"false recovery"''' or "quiescent phase") — transaminases begin rising
*'''Phase 3 (48-96 hours):''' fulminant [[Acute liver failure|hepatic failure]] — markedly elevated AST/ALT, coagulopathy, hypoglycemia, [[Hepatic encephalopathy|encephalopathy]], [[Hepatorenal syndrome|hepatorenal syndrome]], [[DIC]], multiorgan failure, death<ref name="Diaz2018"/>
* Phase 3 (48-96 hours): fulminant [[Acute liver failure|hepatic failure]] — markedly elevated AST/ALT, coagulopathy, hypoglycemia, [[Hepatic encephalopathy|encephalopathy]], [[Hepatorenal syndrome|hepatorenal syndrome]], [[DIC]], multiorgan failure, death<ref name="Diaz2018"/>
*Mortality 10-30% overall; higher in children and delayed presentations<ref name="StatPearls"/>
*Mortality 10-30% overall; higher in children and delayed presentations<ref name="StatPearls"/>
*Mechanism: alpha-amanitin inhibits RNA polymerase II → arrests protein synthesis → hepatocellular necrosis
*Mechanism: alpha-amanitin inhibits RNA polymerase II → arrests protein synthesis → hepatocellular necrosis
Line 109: Line 109:
*[[Caustic ingestion]]
*[[Caustic ingestion]]
*[[Organophosphate toxicity]] (for muscarinic symptoms)
*[[Organophosphate toxicity]] (for muscarinic symptoms)
{{Mushroom toxicity DDX}}


==Evaluation==
==Evaluation==
===Workup===
===Workup===
*'''Detailed history is the most critical diagnostic tool:'''
* Detailed history is the most critical diagnostic tool:
**Timing of symptom onset relative to ingestion (early vs. delayed)
**Timing of symptom onset relative to ingestion (early vs. delayed)
**Type of mushroom (save specimens if available; photograph; consult mycologist)
**Type of mushroom (save specimens if available; photograph; consult mycologist)
Line 119: Line 122:
**Number of people who shared the meal and their symptoms
**Number of people who shared the meal and their symptoms
**Co-ingestion (especially alcohol for coprine syndrome)
**Co-ingestion (especially alcohol for coprine syndrome)
*'''Attempt mushroom identification:'''
* Attempt mushroom identification:
**Save any remaining mushroom specimens (including spore prints)
**Save any remaining mushroom specimens (including spore prints)
**Contact local [[Poison control]] center — may have access to mycologists
**Contact local [[Poison control]] center — may have access to mycologists
**Telemedicine/photograph-based identification resources
**Telemedicine/photograph-based identification resources
*'''Labs (for all symptomatic patients):'''
* Labs (for all symptomatic patients):
**CBC, BMP, hepatic function panel (AST, ALT, total bilirubin, albumin), coagulation studies (PT/INR), lipase
**CBC, BMP, hepatic function panel (AST, ALT, total bilirubin, albumin), coagulation studies (PT/INR), lipase
**Blood glucose (hypoglycemia may signal hepatic failure)
**Blood glucose (hypoglycemia may signal hepatic failure)
**Urinalysis
**Urinalysis
**Lactate
**Lactate
*'''Additional labs for suspected amatoxin or serious poisoning:'''
* Additional labs for suspected amatoxin or serious poisoning:
**Serial LFTs and coagulation studies every 6-12 hours for at least 48-72 hours (transaminases may be initially normal during Phase 1)
**Serial LFTs and coagulation studies every 6-12 hours for at least 48-72 hours (transaminases may be initially normal during Phase 1)
**Ammonia (for hepatic encephalopathy)
**Ammonia (for hepatic encephalopathy)
**Blood type and screen (anticipate possible liver transplant)
**Blood type and screen (anticipate possible liver transplant)
**Urine amatoxin assay — available at some specialty/reference labs; may be positive within 24-48 hours of ingestion; not widely available or rapid enough to guide acute management<ref name="StatPearls"/>
**Urine amatoxin assay — available at some specialty/reference labs; may be positive within 24-48 hours of ingestion; not widely available or rapid enough to guide acute management<ref name="StatPearls"/>
*'''Additional labs for specific syndromes:'''
* Additional labs for specific syndromes:
**Methemoglobin level (gyromitrin poisoning)
**Methemoglobin level (gyromitrin poisoning)
**CK (rhabdomyolysis)
**CK (rhabdomyolysis)
**Serial creatinine (orellanine, norleucine syndromes)
**Serial creatinine (orellanine, norleucine syndromes)
*'''Salicylate, acetaminophen, ethanol levels''' — if intentional ingestion suspected
* Salicylate, acetaminophen, ethanol levels — if intentional ingestion suspected


===Diagnosis===
===Diagnosis===
*Primarily clinical, based on timing of symptom onset and symptom constellation
*Primarily clinical, based on timing of symptom onset and symptom constellation
*'''Key diagnostic rule:''' GI symptoms >6 hours post-ingestion = assume amatoxin poisoning until proven otherwise
* Key diagnostic rule: GI symptoms >6 hours post-ingestion = assume amatoxin poisoning until proven otherwise
*Rising AST/ALT after initial GI illness is highly concerning for amatoxin or gyromitrin hepatotoxicity
*Rising AST/ALT after initial GI illness is highly concerning for amatoxin or gyromitrin hepatotoxicity
*The '''"false recovery"''' period in amatoxin poisoning (GI symptoms improve before liver failure manifests) is a dangerous diagnostic trap — do not discharge patients during this window
*The '''"false recovery"''' period in amatoxin poisoning (GI symptoms improve before liver failure manifests) is a dangerous diagnostic trap — do not discharge patients during this window
Line 153: Line 156:


===GI decontamination===
===GI decontamination===
*'''Activated charcoal''' (1 g/kg, max 50 g) if presenting within 1-2 hours of ingestion<ref name="Medscape"/>
* Activated charcoal (1 g/kg, max 50 g) if presenting within 1-2 hours of ingestion<ref name="Medscape"/>
*For suspected '''amatoxin poisoning:''' give '''multi-dose activated charcoal''' (even if presenting late) to interrupt enterohepatic recirculation<ref name="StatPearls"/>
*For suspected '''amatoxin poisoning:''' give '''multi-dose activated charcoal''' (even if presenting late) to interrupt enterohepatic recirculation<ref name="StatPearls"/>
**Repeat dosing every 2-4 hours
**Repeat dosing every 2-4 hours
Line 161: Line 164:
===Amatoxin-specific management===
===Amatoxin-specific management===
No proven antidote exists; all therapies are supportive and based on limited evidence:<ref name="StatPearls"/><ref name="Diaz2018"/>
No proven antidote exists; all therapies are supportive and based on limited evidence:<ref name="StatPearls"/><ref name="Diaz2018"/>
*'''N-acetylcysteine (NAC):''' IV per [[Acetaminophen toxicity|acetaminophen]] protocol — provides glutathione, hepatoprotective; widely recommended
* N-acetylcysteine (NAC): IV per [[Acetaminophen toxicity|acetaminophen]] protocol — provides glutathione, hepatoprotective; widely recommended
*'''Silibinin (IV):''' 5 mg/kg IV over 1 hour, then 20 mg/kg/day as continuous infusion — thought to block hepatic amatoxin uptake; used in Europe; not FDA-approved in the US
* Silibinin (IV): 5 mg/kg IV over 1 hour, then 20 mg/kg/day as continuous infusion — thought to block hepatic amatoxin uptake; used in Europe; not FDA-approved in the US
**'''Silymarin (oral):''' milk thistle extract, 1 g PO QID — available over-the-counter in North America as surrogate for IV silibinin
** Silymarin (oral): milk thistle extract, 1 g PO QID — available over-the-counter in North America as surrogate for IV silibinin
*'''High-dose penicillin G:''' 300,000-1,000,000 units/kg/day IV (commonly 4 million units q4h) — may compete with hepatic uptake of amatoxin; evidence is limited
* High-dose penicillin G: 300,000-1,000,000 units/kg/day IV (commonly 4 million units q4h) — may compete with hepatic uptake of amatoxin; evidence is limited
*'''Multi-dose activated charcoal''' — interrupts enterohepatic recirculation (see above)
* Multi-dose activated charcoal — interrupts enterohepatic recirculation (see above)
*'''Aggressive fluid resuscitation''' — maintain urine output to enhance renal amatoxin clearance
* Aggressive fluid resuscitation — maintain urine output to enhance renal amatoxin clearance
*'''Liver transplant evaluation:''' early referral to a transplant center for patients with progressive hepatic failure
* Liver transplant evaluation: early referral to a transplant center for patients with progressive hepatic failure
**King's College criteria or Clichy criteria may guide transplant listing
**King's College criteria or Clichy criteria may guide transplant listing
**Approximately 50% of patients who develop fulminant hepatic failure will require transplantation<ref name="Diaz2018"/>
**Approximately 50% of patients who develop fulminant hepatic failure will require transplantation<ref name="Diaz2018"/>


===Gyromitrin-specific management===
===Gyromitrin-specific management===
*'''Pyridoxine (vitamin B6):''' 25 mg/kg IV — for seizures refractory to benzodiazepines (gyromitrin depletes pyridoxal phosphate/GABA)<ref name="Medscape"/>
* Pyridoxine (vitamin B6): 25 mg/kg IV — for seizures refractory to benzodiazepines (gyromitrin depletes pyridoxal phosphate/GABA)<ref name="Medscape"/>
*'''Folinic acid''' — adjunctive (hydrazines inhibit folic acid conversion)
* Folinic acid — adjunctive (hydrazines inhibit folic acid conversion)
*'''Methylene blue''' 1-2 mg/kg IV — for [[Methemoglobinemia|methemoglobinemia]]
* Methylene blue 1-2 mg/kg IV — for [[Methemoglobinemia|methemoglobinemia]]
*Supportive care for hepatic failure similar to amatoxin poisoning
*Supportive care for hepatic failure similar to amatoxin poisoning


===Muscarinic syndrome management===
===Muscarinic syndrome management===
*'''[[Atropine]]''' 0.5-1 mg IV (adults), 0.01-0.02 mg/kg IV (children); titrate to effect (drying of secretions, resolution of bradycardia)
* [[Atropine]] 0.5-1 mg IV (adults), 0.01-0.02 mg/kg IV (children); titrate to effect (drying of secretions, resolution of bradycardia)
*May need repeated dosing
*May need repeated dosing


===Isoxazole/psilocybin syndrome management===
===Isoxazole/psilocybin syndrome management===
*Supportive care
*Supportive care
*'''[[Benzodiazepines]]''' for agitation, anxiety, or seizures
* [[Benzodiazepines]] for agitation, anxiety, or seizures
*Reassurance and calm environment (especially psilocybin)
*Reassurance and calm environment (especially psilocybin)
*Avoid restraints if possible (risk of rhabdomyolysis with agitation)
*Avoid restraints if possible (risk of rhabdomyolysis with agitation)
Line 193: Line 196:


==Disposition==
==Disposition==
*'''Early-onset GI symptoms only (<6 hours), known non-toxic species, mild symptoms:'''
* Early-onset GI symptoms only (<6 hours), known non-toxic species, mild symptoms:
**Observe 4-6 hours; if tolerating PO and clinically well, may discharge with return precautions
**Observe 4-6 hours; if tolerating PO and clinically well, may discharge with return precautions
*'''Symptom onset >6 hours post-ingestion, unknown mushroom species, or suspected amatoxin:'''
* Symptom onset >6 hours post-ingestion, unknown mushroom species, or suspected amatoxin:
**'''Admit all patients''' — ICU if hemodynamically unstable or evidence of organ injury
** Admit all patients — ICU if hemodynamically unstable or evidence of organ injury
**Serial labs (LFTs, coagulation, renal function, glucose) every 6-12 hours for minimum 48-72 hours
**Serial labs (LFTs, coagulation, renal function, glucose) every 6-12 hours for minimum 48-72 hours
**'''Do NOT discharge during the "false recovery" phase''' (24-48 hours post-ingestion when GI symptoms improve but hepatic injury is evolving)
**'''Do NOT discharge during the "false recovery" phase''' (24-48 hours post-ingestion when GI symptoms improve but hepatic injury is evolving)
**Early contact with liver transplant center for amatoxin poisoning<ref name="Diaz2018"/>
**Early contact with liver transplant center for amatoxin poisoning<ref name="Diaz2018"/>
*'''Patients with isoxazole/psilocybin syndromes:'''
* Patients with isoxazole/psilocybin syndromes:
**Observe until symptoms resolve (typically 4-8 hours); discharge if stable and safe
**Observe until symptoms resolve (typically 4-8 hours); discharge if stable and safe
**Psychiatric evaluation if intentional ingestion
**Psychiatric evaluation if intentional ingestion
*'''Orellanine suspected:'''
* Orellanine suspected:
**Admit; serial renal function monitoring; nephrology consultation
**Admit; serial renal function monitoring; nephrology consultation
*'''All intentional ingestions:''' psychiatric evaluation mandatory prior to discharge
* All intentional ingestions: psychiatric evaluation mandatory prior to discharge
*'''All patients:''' contact [[Poison control]] (1-800-222-1222 in the US)
* All patients: contact [[Poison control]] (1-800-222-1222 in the US)


==See Also==
==See Also==

Revision as of 15:33, 19 March 2026

Background

  • Mushroom poisoning encompasses a spectrum of clinical syndromes caused by ingestion of toxic mushroom species.
  • The key distinction for the emergency physician is between early-onset (<6 hours) and delayed-onset (>6 hours) symptoms, as delayed presentations are far more likely to be life-threatening.[1]
  • There are over 5,000 species of mushrooms; approximately 50-100 are toxic to humans[2]
  • 95% of mushroom-related deaths worldwide are caused by amatoxin-containing mushrooms (Amanita, Galerina, Lepiota species)[1]
  • Most poisonings occur in foragers who misidentify wild mushrooms as edible species
    • Immigrants may mistake toxic local species for edible ones from their home country
    • Recreational users may confuse toxic species for hallucinogenic Psilocybe mushrooms
  • Children and elderly are more susceptible to volume depletion and toxicity
  • Amatoxins are heat-stable — cooking does not eliminate the toxin[2]
  • Most mushroom ingestions are benign GI irritants; the challenge is identifying the dangerous minority

Critical clinical pearl

  • Symptom onset >6 hours after ingestion should be considered potentially lethal until proven otherwise[1]
  • Early-onset GI symptoms (<6 hours) are generally self-limited
  • Delayed-onset GI symptoms (6-24+ hours) suggest amatoxin, gyromitrin, or orellanine poisoning and carry significant morbidity and mortality

Clinical features

Classified by onset and predominant toxidrome:[3]

Early-onset syndromes (<6 hours)

GI irritant syndrome (most common)

  • Caused by many species (e.g. Chlorophyllum molybdites, Entoloma, Boletus)
  • Nausea, vomiting, abdominal cramps, diarrhea within 1-3 hours
  • Self-limited; resolves with supportive care
  • Rarely life-threatening unless severe dehydration

Muscarinic (cholinergic) syndrome

  • Caused by Inocybe and Clitocybe species
  • Onset 15-30 minutes
  • SLUDGE/DUMBELS: salivation, lacrimation, urination, diarrhea, GI cramping, emesis; diaphoresis, urination, miosis, bronchospasm/bronchorrhea, emesis, lacrimation, salivation
  • Bradycardia, hypotension
  • Treatment: atropine

Isoxazole (anticholinergic/GABAergic) syndrome

  • Caused by Amanita muscaria (fly agaric), A. pantherina
  • Onset 30 min - 2 hours
  • Confusion, agitation, hallucinations, ataxia, myoclonus, seizures
  • Mydriasis, tachycardia, dry skin
  • Alternating sedation and excitation
  • No hepatic or renal injury
  • Treatment: supportive; benzodiazepines for agitation/seizures

Psilocybin syndrome

  • Caused by Psilocybe, Panaeolus, Gymnopilus species
  • Onset 30 min - 1 hour
  • Hallucinations (visual), euphoria, anxiety, agitation, tachycardia, mydriasis, hyperthermia
  • Self-limited (4-6 hours)
  • Treatment: supportive; benzodiazepines for agitation; reassurance

Coprine (disulfiram-like) syndrome

  • Caused by Coprinus atramentarius (inky cap)
  • Symptoms occur only when mushroom ingestion is combined with alcohol (within 2-72 hours of mushroom ingestion)
  • Flushing, tachycardia, headache, nausea, vomiting, hypotension
  • Treatment: supportive; IV fluids; avoid alcohol; fomepizole may be considered in severe cases[3]

GI with early renal toxicity

  • Caused by Amanita smithiana
  • GI symptoms as early as 2-4 hours; renal injury follows
  • May present earlier than other serious syndromes — do not assume safety based on early onset alone

Delayed-onset syndromes (>6 hours) — potentially life-threatening

Amatoxin syndrome (most dangerous)

  • Caused by Amanita phalloides (death cap), A. virosa (destroying angel), A. verna, A. bisporigera, Galerina spp., Lepiota spp.
  • Phase 1 (6-24 hours): severe cholera-like vomiting and watery diarrhea → dehydration, electrolyte derangement
  • Phase 2 (24-48 hours): apparent clinical improvement ("false recovery" or "quiescent phase") — transaminases begin rising
  • Phase 3 (48-96 hours): fulminant hepatic failure — markedly elevated AST/ALT, coagulopathy, hypoglycemia, encephalopathy, hepatorenal syndrome, DIC, multiorgan failure, death[1]
  • Mortality 10-30% overall; higher in children and delayed presentations[2]
  • Mechanism: alpha-amanitin inhibits RNA polymerase II → arrests protein synthesis → hepatocellular necrosis
  • Amatoxin undergoes enterohepatic recirculation, which is the rationale for multi-dose activated charcoal

Gyromitrin syndrome

  • Caused by Gyromitra esculenta (false morel) and related species
  • Onset 6-12 hours
  • GI symptoms followed by hepatic failure (similar to amatoxin)
  • Also causes methemoglobinemia, hemolysis, seizures (via GABA inhibition)
  • Mechanism: gyromitrin metabolized to monomethylhydrazine (rocket fuel analog)
  • Treatment: pyridoxine (vitamin B6) 25 mg/kg IV for seizures refractory to benzodiazepines; folinic acid; methylene blue for methemoglobinemia[3]

Orellanine syndrome

  • Caused by Cortinarius species
  • Onset delayed 1-3 days, sometimes up to 2 weeks
  • GI symptoms followed by progressive renal failure
  • Renal injury may be irreversible, requiring long-term hemodialysis or transplant
  • No specific antidote; supportive care

Norleucine (allenic norleucine) syndrome

  • Caused by Amanita smithiana, A. proxima
  • Onset 4-12 hours (may overlap with early-onset range)
  • GI symptoms followed by renal failure (typically reversible)
  • Mild hepatotoxicity may accompany

Differential diagnosis

Other causes of acute gastroenteritis

Other causes of acute liver failure

Other toxic ingestions


Mushroom toxicity by Type

Mushroom Toxin Pathologic Effect
Amanita Amatoxin Hepatotoxicity
Coprine Disulfiram-like
Crotinarius Orellanine Delayed renal failure
Gyromitra Gyromitrin Seizures
Ibotenic Acid Anticholinergic
Muscarine Cholinergic
Orellanin Nephrotoxicity
Psilocybin Hallucinations

Evaluation

Workup

  • Detailed history is the most critical diagnostic tool:
    • Timing of symptom onset relative to ingestion (early vs. delayed)
    • Type of mushroom (save specimens if available; photograph; consult mycologist)
    • Geographic location and season of foraging
    • Preparation method (raw, cooked)
    • Number of people who shared the meal and their symptoms
    • Co-ingestion (especially alcohol for coprine syndrome)
  • Attempt mushroom identification:
    • Save any remaining mushroom specimens (including spore prints)
    • Contact local Poison control center — may have access to mycologists
    • Telemedicine/photograph-based identification resources
  • Labs (for all symptomatic patients):
    • CBC, BMP, hepatic function panel (AST, ALT, total bilirubin, albumin), coagulation studies (PT/INR), lipase
    • Blood glucose (hypoglycemia may signal hepatic failure)
    • Urinalysis
    • Lactate
  • Additional labs for suspected amatoxin or serious poisoning:
    • Serial LFTs and coagulation studies every 6-12 hours for at least 48-72 hours (transaminases may be initially normal during Phase 1)
    • Ammonia (for hepatic encephalopathy)
    • Blood type and screen (anticipate possible liver transplant)
    • Urine amatoxin assay — available at some specialty/reference labs; may be positive within 24-48 hours of ingestion; not widely available or rapid enough to guide acute management[2]
  • Additional labs for specific syndromes:
    • Methemoglobin level (gyromitrin poisoning)
    • CK (rhabdomyolysis)
    • Serial creatinine (orellanine, norleucine syndromes)
  • Salicylate, acetaminophen, ethanol levels — if intentional ingestion suspected

Diagnosis

  • Primarily clinical, based on timing of symptom onset and symptom constellation
  • Key diagnostic rule: GI symptoms >6 hours post-ingestion = assume amatoxin poisoning until proven otherwise
  • Rising AST/ALT after initial GI illness is highly concerning for amatoxin or gyromitrin hepatotoxicity
  • The "false recovery" period in amatoxin poisoning (GI symptoms improve before liver failure manifests) is a dangerous diagnostic trap — do not discharge patients during this window

Management

All patients

  • IV fluid resuscitation; correct electrolyte abnormalities and hypoglycemia
  • Continuous cardiac monitoring
  • Contact Poison control and attempt mushroom identification
  • Anti-emetics (ondansetron) for persistent vomiting

GI decontamination

  • Activated charcoal (1 g/kg, max 50 g) if presenting within 1-2 hours of ingestion[3]
  • For suspected amatoxin poisoning: give multi-dose activated charcoal (even if presenting late) to interrupt enterohepatic recirculation[2]
    • Repeat dosing every 2-4 hours
  • Gastric lavage generally not recommended beyond 1 hour post-ingestion
  • Whole-bowel irrigation may be considered for amatoxin ingestion

Amatoxin-specific management

No proven antidote exists; all therapies are supportive and based on limited evidence:[2][1]

  • N-acetylcysteine (NAC): IV per acetaminophen protocol — provides glutathione, hepatoprotective; widely recommended
  • Silibinin (IV): 5 mg/kg IV over 1 hour, then 20 mg/kg/day as continuous infusion — thought to block hepatic amatoxin uptake; used in Europe; not FDA-approved in the US
    • Silymarin (oral): milk thistle extract, 1 g PO QID — available over-the-counter in North America as surrogate for IV silibinin
  • High-dose penicillin G: 300,000-1,000,000 units/kg/day IV (commonly 4 million units q4h) — may compete with hepatic uptake of amatoxin; evidence is limited
  • Multi-dose activated charcoal — interrupts enterohepatic recirculation (see above)
  • Aggressive fluid resuscitation — maintain urine output to enhance renal amatoxin clearance
  • Liver transplant evaluation: early referral to a transplant center for patients with progressive hepatic failure
    • King's College criteria or Clichy criteria may guide transplant listing
    • Approximately 50% of patients who develop fulminant hepatic failure will require transplantation[1]

Gyromitrin-specific management

  • Pyridoxine (vitamin B6): 25 mg/kg IV — for seizures refractory to benzodiazepines (gyromitrin depletes pyridoxal phosphate/GABA)[3]
  • Folinic acid — adjunctive (hydrazines inhibit folic acid conversion)
  • Methylene blue 1-2 mg/kg IV — for methemoglobinemia
  • Supportive care for hepatic failure similar to amatoxin poisoning

Muscarinic syndrome management

  • Atropine 0.5-1 mg IV (adults), 0.01-0.02 mg/kg IV (children); titrate to effect (drying of secretions, resolution of bradycardia)
  • May need repeated dosing

Isoxazole/psilocybin syndrome management

  • Supportive care
  • Benzodiazepines for agitation, anxiety, or seizures
  • Reassurance and calm environment (especially psilocybin)
  • Avoid restraints if possible (risk of rhabdomyolysis with agitation)

Orellanine syndrome management

  • No specific antidote
  • Supportive care with nephrology consultation
  • Hemodialysis for renal failure; renal transplant if no recovery

Disposition

  • Early-onset GI symptoms only (<6 hours), known non-toxic species, mild symptoms:
    • Observe 4-6 hours; if tolerating PO and clinically well, may discharge with return precautions
  • Symptom onset >6 hours post-ingestion, unknown mushroom species, or suspected amatoxin:
    • Admit all patients — ICU if hemodynamically unstable or evidence of organ injury
    • Serial labs (LFTs, coagulation, renal function, glucose) every 6-12 hours for minimum 48-72 hours
    • Do NOT discharge during the "false recovery" phase (24-48 hours post-ingestion when GI symptoms improve but hepatic injury is evolving)
    • Early contact with liver transplant center for amatoxin poisoning[1]
  • Patients with isoxazole/psilocybin syndromes:
    • Observe until symptoms resolve (typically 4-8 hours); discharge if stable and safe
    • Psychiatric evaluation if intentional ingestion
  • Orellanine suspected:
    • Admit; serial renal function monitoring; nephrology consultation
  • All intentional ingestions: psychiatric evaluation mandatory prior to discharge
  • All patients: contact Poison control (1-800-222-1222 in the US)

See Also

External Links

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Diaz JH. Amatoxin-Containing Mushroom Poisonings: Species, Toxidromes, Treatments, and Outcomes. Wilderness Environ Med. 2018;29(1):111-118. doi:10.1016/j.wem.2017.10.002
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Amatoxin Mushroom Toxicity. StatPearls. 2023. PMID: 28613706
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Mushroom Toxicity. Medscape. 2024.
Retrieved from "https://www.wikem.org/w/index.php?title=Mushroom_poisoning&oldid=386225"