MUSHROOM POISONING
EARLY ONSET GI SYMPTOMS
• Chlorophyllum molybdites , Omphalotus, Boletus, Entoloma,
Gomphus, Hebeloma, Lactarius, and Verpa genera.
CLINICAL FEATURES
• Vomiting and diarrhea <2 hours after ingesting the mushroom.
• Intestinal cramping,
• Chills,
• Headache,
• Myalgias.
• Diarrhea usually watery, but occasionally bloody with fecal leukocytes.
• Most commonly, symptoms are mild and self-limited.
• Symptoms usually resolve within 24 hours but may last up to several days.
TREATMENT
• Treat symptomatic toxic mushroom ingestion with activated charcoal
0.5 to 1.0 gram/kg, PO or by nasogastric tube.
• There is no role for prophylactic decontamination therapy of
asymptomatic patients.
• Supportive treatment and includes IV fluid and electrolyte replacement
when necessary.
• Antiemetics can be given, but do not give antidiarrheal agents, because
they may prolong exposure to the toxin.
• In most cases, symptoms are self-limited, resolving within 12 to 24
hours.
EARLY-ONSET NEUROLOGIC SYMPTOMS
• Symptoms typically develop within 2 hours of ingestion of hallucinogenic
mushrooms.
• Euphoria,
• A heightened imagination,
• A loss of the sense of time,
• Visual distortions or hallucinations are common.
• Tachycardia and hypertension may be noted because of the presence of
phenylethylamine in psilocybin-containing mushrooms.
• Fever and seizures in rare cases.
• Symptoms generally last 4 to 6 hours but can persist up to 12 hours.
• There are infrequent reports of flashbacks for up to 4 months after
ingestion, particularly in association with other substances that alter
cognition such as alcohol or marijuana.
• Patients ingesting isoxazole-containing mushrooms usually present
with symptoms within 30 minutes of ingestion.
• Signs of muscarinic poisoning are the first apparent (nausea, vomiting,
diarrhea, vasodilation, diaphoresis, salivation).
• These are replaced by an atropine-like symptom complex about 30 minutes after
ingestion along with drowsiness, amentia, dizziness, photosensitivity, euphoria,
motor hyperactivity, ataxia, muscle jerking, hallucinations, and delirium with
difficulty with perception of size, time, and place.
• Seizures have been reported in children.
• Symptoms are typically self-limited, resolving within 4 to 6 hours after ingestion.
• Headache and fatigue occur the day following ingestion, with headache lasting up
to a few weeks.
Treatment
• Supportive.
• Place the patient in a darkened, quiet room, devoid of visual stimuli, and
provide reassurance.
• If sedation is required, benzodiazepines such as diazepam or lorazepam
are preferred.
• Do not give anticholinergic agents because they may aggravate delirium.
• Treat symptomatic ingestion of isoxazole-containing mushrooms with
activated charcoal.
• In patients with severe vomiting and diarrhea, replace fluids and
electrolytes.
• Treat seizures with benzodiazepines.
• Consider treatment with physostigmine only for patients with severe
anticholinergic symptoms.
• Dose: 1 to 2 milligrams IV in adults and 0.5 milligram IV in
children, administered slowly.
• Monitor continuous cardiorespiratory effects and blood pressure
during administration.
• Base the decision to discharge from the ED on duration of symptoms
and need for ongoing pharmacologic sedation or intubation.
EARLY ONSET MUSCARINIC SYMPTOMS
• Mushrooms of the Inocybe and
Clitocybe genera are common causes
of muscarinic poisoning.
• The Inocybe mushrooms are small
brown mushrooms with conical caps,
typically found under hardwoods and
conifers.
CLINICAL FEATURES
• Salivation,
• Lacrimation,
• Urination,
• Defecation,
• GI hypermotility and
• emesis).
• Diaphoresis,
• Muscle fasciculations,
• Miosis,
• Bradycardia and
• Bronchorrhea.
Symptoms typically present within 30 minutes of ingestion and spontaneously resolve in 4 to 12 hours.
TREATMENT
• In most cases, muscarinic symptoms are mild and self-limited. Supportive care is sufficient.
• Patients with severe vomiting may require IV fluid and electrolyte replacement.
• Antidote: Atropine
• Dose is 0.5 to 1.0 milligram IV for adults and 0.01 milligram/kg IV for children (minimum dose, 0.1
milligram; maximum does, 1 milligram).
• The dose can be repeated as necessary to control bronchorrhea, bradycardia, or hypotension.
• Oxygen and inhaled β agonists (albuterol) are recommended for the treatment of patients with increased
pulmonary secretions and bronchospasm.
• Muscarinic poisoning frequently resolve within 12 hours of ingestion.
DELAYED-ONSET GI SYMPTOMS
• Mushrooms of two different genera,
Gyromitra and Amanita, cause
significant toxicity, which
characteristically presents several hours
after ingestion.
CLINICAL FEATURES
• The initial GI symptoms resolve within 2 to 5 days.
• In a mild ingestion, the neurologic symptoms persist for several days and resolve
without sequelae.
• Patients who ingest amatoxin-containing mushrooms also have delayed onset of GI
symptoms (6 to 24 hours).
• There are four stages in amatoxin poisoning.
• The first (latent) stage : Absence of any signs or symptoms and lasts up to 24 hours after
ingestion.
• Second Stage: During the 12 to 24 hours of the second stage, intense cramping abdominal
pain, nausea, vomiting, and diarrhea dominate the clinical picture. Both stools and
vomitus may become bloody. Although right upper quadrant tenderness and
hepatomegaly may be noted, results of liver function tests are usually normal. Patients
who present during this stage are frequently misdiagnosed with gastroenteritis.
• Third or convalescent phase : lasts 12 to 24 hours. Patient seem
better. Liver enzymes begin to rise, heralding the onset of liver
damage. Renal function may also deteriorate.
• In the fourth and final stage : 2 to 4 days after ingestion, transaminase
levels rise dramatically, and liver and renal function deteriorate.
Hyperbilirubinemia, coagulopathy, hypoglycemia, acidosis, hepatic
encephalopathy, and hepatorenal syndrome are noted.
• In both Gyromitra and Amanita toxicity, prothrombin time may be
elevated and unresponsive to administration of vitamin K or fresh
frozen plasma.
• Amylase and lipase elevation suggests pancreatic damage, although
symptomatic pancreatitis is rare.
• Abnormal laboratory findings in amatoxin poisoning include a decrease in
neutrophils, lymphocytes, and platelets, and abnormal thyroid function results.
Hypophosphatemia (primarily noted in children), hypocalcemia, and elevated
insulin levels occur.
• None of these laboratory abnormalities correlates with clinical disease, and their
cause is unknown.
• The mortality from Gyromitra ingestion is estimated at 15% to 35% and is
generally attributed to hepatic failure, renal failure, or fluid and electrolyte
disorders.
• Patients who survive severe hepatic failure from amatoxin may
develop signs of chronic active hepatitis with persistent elevation in
liver transaminase levels, development of anti–smooth muscle
antibodies, and presence of cryoglobulins.
• No prolonged effects from gyromitrin toxicity have been reported.
Treatment
• Activated Charcoal administration. Repeated doses of charcoal for at
least the first 24 hours may be effective, particularly in the presence
of amatoxin (because it undergoes enterohepatic circulation).
• Fluid and electrolyte replacement is mandatory.
• Glucose level monitoring as hypoglycemia is one of the most common
causes of death in early mushroom toxicity.
• Low-protein diet
• Fresh frozen plasma and vitamin K for prolonged prothrombin time,
but in many cases, coagulopathy does not respond to treatment.
• Liver transplantation.
• Auxiliary liver transplantation has also been used.
• Gyromitrin-Specific Treatment : For neurological symptoms provides the cofactor
required for the regeneration of γ-aminobutyric acid.
• Dose: 25 milligrams/kg IV over 30 minutes up to a maximum of 25 grams/d, are
recommended, but doses of pyridoxine in excess of 40 grams are associated with
severe peripheral neuropathy.
• Pyridoxine does not affect the development or course of hepatic failure, and there
is no specific therapy for gyromitrin induced hepatic failure.
Amatoxin-Specific Treatment
• Activated charcoal, silybinum marianum, and N-acetylcysteine are emerging as
the best-supported treatment modalities.
• Silybinum marianum,
• Dose: loading dose of 5 milligrams/kg over 1 hour followed by 20 milligrams/kg/d for 6
days.
• N-Acetylcysteine
• Dose: IV three sequential doses of 150 milligrams/kg over 1 hour, 50 milligrams/kg over
4 hours, and 100 milligrams/kg over 16 hours.
• In cases of amatoxin-induced liver failure, the amatoxin itself is rapidly absorbed
and excreted, which limits the utility of hemoperfusion and/or hemodialysis.
• Orthotopic liver transplantation and auxiliary partial orthotopic liver
transplantation.
• Penicillin G and ceftazidime have both demonstrated a capacity for decreasing
the uptake of amanitin by hepatocytes.
• However, these therapies appear to be less effective than using silybinum alone.
• Thioctic acid is a free radical scavenger and has been used for many years but
has not yet gained support in the literature.
DELAYED ONSET RENAL FAILURE
• Seen after ingestion of Cortinarius (Cortinarius orellanus, Cortinarius
speciosissimus, and Cortinarius gentilis and A. smithiana mushrooms.
• Found mainly in North America.
• Toxins: Orellanine and ortinarin A and B , heat stable, inhibits protein synthesis in
the kidneys.
• Histopathologic examination indicates interstitial nephritis with edema and
leukocyte infiltration, tubular necrosis, basal membrane rupture, and fibrosis
without glomerular injury.
CLINICAL FEATURES
• Initially with GI symptoms, including nausea, vomiting, and nonbloody diarrhea.
• Symptoms begin several hours to days after ingestion and may persist for 3
days.
• Occasionally, paresthesias, abnormal taste, and cognitive dysfunction are
reported.
• Symptoms of renal failure, including lumbar and flank pain, oliguria, or more
rarely polyuria, begin between 3 and 20 days after ingestion.
TREATMENT
• No specific treatment.
• Monitor urine output and electrolyte, calcium, magnesium, BUN, and
creatinine levels.
• Hemodialysis is indicated for refractory hyperkalemia, refractory
acidosis, uremic symptoms, or severe renal dysfunction.
• Supportive hemodialysis may be required, but many patients
experience a spontaneous return of normal renal function.
• Because spontaneous improvement is reported, renal transplantation
should be withheld for several months to monitor patient response.
DELAYED ONSET DISULFIRAM LIKE REACTION
• Coprinus genus.
• Very common in North America.
• The mushroom contains coprine, which is chemically related to
disulfiram.
• Coprine causes inhibition of alcohol dehydrogenase within 2 hours of
ingestion, and activity may last up to 72 hours.
• If alcohol is consumed during this sensitive period, patients develop a
typical disulfiram reaction.
• Mushrooms ingested at the same time as alcohol produce no toxicity.
CLINICAL FEATURES
• headache,
• paresthesias of distal extremities,
• metallic taste,
• flushing,
• palpitations,
• chest pain,
• nausea,
• vomiting,
• and diaphoresis and generally occur within minutes to several hours after alcohol consumption.
• Symptoms generally last for 2 to 4 hours but may last up to 2 days.
• Most symptoms are mild.
• Diagnosis is made based on presence of the symptom complex and its association with alcohol
consumption.
TREATMENT
• GI decontamination has no role and charcoal administration is not beneficial.
Patients
• Occasionally become hypotensive and respond to administration of IV fluids
or, in refractory cases, norepinephrine.
• Excessive sympathetic activity can be inhibited by β-blockers.
• Most cases are self-limited, and patients can be discharged once they
• can tolerate oral fluids.
THANK YOU

Approach to Mushroom Poisoning Explained.pptx

  • 1.
  • 3.
    EARLY ONSET GISYMPTOMS • Chlorophyllum molybdites , Omphalotus, Boletus, Entoloma, Gomphus, Hebeloma, Lactarius, and Verpa genera.
  • 4.
    CLINICAL FEATURES • Vomitingand diarrhea <2 hours after ingesting the mushroom. • Intestinal cramping, • Chills, • Headache, • Myalgias. • Diarrhea usually watery, but occasionally bloody with fecal leukocytes. • Most commonly, symptoms are mild and self-limited. • Symptoms usually resolve within 24 hours but may last up to several days.
  • 5.
    TREATMENT • Treat symptomatictoxic mushroom ingestion with activated charcoal 0.5 to 1.0 gram/kg, PO or by nasogastric tube. • There is no role for prophylactic decontamination therapy of asymptomatic patients. • Supportive treatment and includes IV fluid and electrolyte replacement when necessary. • Antiemetics can be given, but do not give antidiarrheal agents, because they may prolong exposure to the toxin. • In most cases, symptoms are self-limited, resolving within 12 to 24 hours.
  • 6.
    EARLY-ONSET NEUROLOGIC SYMPTOMS •Symptoms typically develop within 2 hours of ingestion of hallucinogenic mushrooms. • Euphoria, • A heightened imagination, • A loss of the sense of time, • Visual distortions or hallucinations are common. • Tachycardia and hypertension may be noted because of the presence of phenylethylamine in psilocybin-containing mushrooms. • Fever and seizures in rare cases. • Symptoms generally last 4 to 6 hours but can persist up to 12 hours.
  • 7.
    • There areinfrequent reports of flashbacks for up to 4 months after ingestion, particularly in association with other substances that alter cognition such as alcohol or marijuana. • Patients ingesting isoxazole-containing mushrooms usually present with symptoms within 30 minutes of ingestion. • Signs of muscarinic poisoning are the first apparent (nausea, vomiting, diarrhea, vasodilation, diaphoresis, salivation).
  • 8.
    • These arereplaced by an atropine-like symptom complex about 30 minutes after ingestion along with drowsiness, amentia, dizziness, photosensitivity, euphoria, motor hyperactivity, ataxia, muscle jerking, hallucinations, and delirium with difficulty with perception of size, time, and place. • Seizures have been reported in children. • Symptoms are typically self-limited, resolving within 4 to 6 hours after ingestion. • Headache and fatigue occur the day following ingestion, with headache lasting up to a few weeks.
  • 9.
    Treatment • Supportive. • Placethe patient in a darkened, quiet room, devoid of visual stimuli, and provide reassurance. • If sedation is required, benzodiazepines such as diazepam or lorazepam are preferred. • Do not give anticholinergic agents because they may aggravate delirium. • Treat symptomatic ingestion of isoxazole-containing mushrooms with activated charcoal. • In patients with severe vomiting and diarrhea, replace fluids and electrolytes.
  • 10.
    • Treat seizureswith benzodiazepines. • Consider treatment with physostigmine only for patients with severe anticholinergic symptoms. • Dose: 1 to 2 milligrams IV in adults and 0.5 milligram IV in children, administered slowly. • Monitor continuous cardiorespiratory effects and blood pressure during administration. • Base the decision to discharge from the ED on duration of symptoms and need for ongoing pharmacologic sedation or intubation.
  • 11.
    EARLY ONSET MUSCARINICSYMPTOMS • Mushrooms of the Inocybe and Clitocybe genera are common causes of muscarinic poisoning. • The Inocybe mushrooms are small brown mushrooms with conical caps, typically found under hardwoods and conifers.
  • 12.
    CLINICAL FEATURES • Salivation, •Lacrimation, • Urination, • Defecation, • GI hypermotility and • emesis). • Diaphoresis, • Muscle fasciculations, • Miosis, • Bradycardia and • Bronchorrhea. Symptoms typically present within 30 minutes of ingestion and spontaneously resolve in 4 to 12 hours.
  • 13.
    TREATMENT • In mostcases, muscarinic symptoms are mild and self-limited. Supportive care is sufficient. • Patients with severe vomiting may require IV fluid and electrolyte replacement. • Antidote: Atropine • Dose is 0.5 to 1.0 milligram IV for adults and 0.01 milligram/kg IV for children (minimum dose, 0.1 milligram; maximum does, 1 milligram). • The dose can be repeated as necessary to control bronchorrhea, bradycardia, or hypotension. • Oxygen and inhaled β agonists (albuterol) are recommended for the treatment of patients with increased pulmonary secretions and bronchospasm. • Muscarinic poisoning frequently resolve within 12 hours of ingestion.
  • 14.
    DELAYED-ONSET GI SYMPTOMS •Mushrooms of two different genera, Gyromitra and Amanita, cause significant toxicity, which characteristically presents several hours after ingestion.
  • 15.
    CLINICAL FEATURES • Theinitial GI symptoms resolve within 2 to 5 days. • In a mild ingestion, the neurologic symptoms persist for several days and resolve without sequelae. • Patients who ingest amatoxin-containing mushrooms also have delayed onset of GI symptoms (6 to 24 hours). • There are four stages in amatoxin poisoning. • The first (latent) stage : Absence of any signs or symptoms and lasts up to 24 hours after ingestion. • Second Stage: During the 12 to 24 hours of the second stage, intense cramping abdominal pain, nausea, vomiting, and diarrhea dominate the clinical picture. Both stools and vomitus may become bloody. Although right upper quadrant tenderness and hepatomegaly may be noted, results of liver function tests are usually normal. Patients who present during this stage are frequently misdiagnosed with gastroenteritis.
  • 16.
    • Third orconvalescent phase : lasts 12 to 24 hours. Patient seem better. Liver enzymes begin to rise, heralding the onset of liver damage. Renal function may also deteriorate. • In the fourth and final stage : 2 to 4 days after ingestion, transaminase levels rise dramatically, and liver and renal function deteriorate. Hyperbilirubinemia, coagulopathy, hypoglycemia, acidosis, hepatic encephalopathy, and hepatorenal syndrome are noted. • In both Gyromitra and Amanita toxicity, prothrombin time may be elevated and unresponsive to administration of vitamin K or fresh frozen plasma.
  • 17.
    • Amylase andlipase elevation suggests pancreatic damage, although symptomatic pancreatitis is rare. • Abnormal laboratory findings in amatoxin poisoning include a decrease in neutrophils, lymphocytes, and platelets, and abnormal thyroid function results. Hypophosphatemia (primarily noted in children), hypocalcemia, and elevated insulin levels occur. • None of these laboratory abnormalities correlates with clinical disease, and their cause is unknown. • The mortality from Gyromitra ingestion is estimated at 15% to 35% and is generally attributed to hepatic failure, renal failure, or fluid and electrolyte disorders.
  • 18.
    • Patients whosurvive severe hepatic failure from amatoxin may develop signs of chronic active hepatitis with persistent elevation in liver transaminase levels, development of anti–smooth muscle antibodies, and presence of cryoglobulins. • No prolonged effects from gyromitrin toxicity have been reported.
  • 19.
    Treatment • Activated Charcoaladministration. Repeated doses of charcoal for at least the first 24 hours may be effective, particularly in the presence of amatoxin (because it undergoes enterohepatic circulation). • Fluid and electrolyte replacement is mandatory. • Glucose level monitoring as hypoglycemia is one of the most common causes of death in early mushroom toxicity. • Low-protein diet • Fresh frozen plasma and vitamin K for prolonged prothrombin time, but in many cases, coagulopathy does not respond to treatment. • Liver transplantation.
  • 20.
    • Auxiliary livertransplantation has also been used. • Gyromitrin-Specific Treatment : For neurological symptoms provides the cofactor required for the regeneration of γ-aminobutyric acid. • Dose: 25 milligrams/kg IV over 30 minutes up to a maximum of 25 grams/d, are recommended, but doses of pyridoxine in excess of 40 grams are associated with severe peripheral neuropathy. • Pyridoxine does not affect the development or course of hepatic failure, and there is no specific therapy for gyromitrin induced hepatic failure.
  • 21.
    Amatoxin-Specific Treatment • Activatedcharcoal, silybinum marianum, and N-acetylcysteine are emerging as the best-supported treatment modalities. • Silybinum marianum, • Dose: loading dose of 5 milligrams/kg over 1 hour followed by 20 milligrams/kg/d for 6 days. • N-Acetylcysteine • Dose: IV three sequential doses of 150 milligrams/kg over 1 hour, 50 milligrams/kg over 4 hours, and 100 milligrams/kg over 16 hours.
  • 22.
    • In casesof amatoxin-induced liver failure, the amatoxin itself is rapidly absorbed and excreted, which limits the utility of hemoperfusion and/or hemodialysis. • Orthotopic liver transplantation and auxiliary partial orthotopic liver transplantation. • Penicillin G and ceftazidime have both demonstrated a capacity for decreasing the uptake of amanitin by hepatocytes. • However, these therapies appear to be less effective than using silybinum alone. • Thioctic acid is a free radical scavenger and has been used for many years but has not yet gained support in the literature.
  • 23.
    DELAYED ONSET RENALFAILURE • Seen after ingestion of Cortinarius (Cortinarius orellanus, Cortinarius speciosissimus, and Cortinarius gentilis and A. smithiana mushrooms. • Found mainly in North America. • Toxins: Orellanine and ortinarin A and B , heat stable, inhibits protein synthesis in the kidneys. • Histopathologic examination indicates interstitial nephritis with edema and leukocyte infiltration, tubular necrosis, basal membrane rupture, and fibrosis without glomerular injury.
  • 24.
    CLINICAL FEATURES • Initiallywith GI symptoms, including nausea, vomiting, and nonbloody diarrhea. • Symptoms begin several hours to days after ingestion and may persist for 3 days. • Occasionally, paresthesias, abnormal taste, and cognitive dysfunction are reported. • Symptoms of renal failure, including lumbar and flank pain, oliguria, or more rarely polyuria, begin between 3 and 20 days after ingestion.
  • 25.
    TREATMENT • No specifictreatment. • Monitor urine output and electrolyte, calcium, magnesium, BUN, and creatinine levels. • Hemodialysis is indicated for refractory hyperkalemia, refractory acidosis, uremic symptoms, or severe renal dysfunction. • Supportive hemodialysis may be required, but many patients experience a spontaneous return of normal renal function. • Because spontaneous improvement is reported, renal transplantation should be withheld for several months to monitor patient response.
  • 26.
    DELAYED ONSET DISULFIRAMLIKE REACTION • Coprinus genus. • Very common in North America. • The mushroom contains coprine, which is chemically related to disulfiram. • Coprine causes inhibition of alcohol dehydrogenase within 2 hours of ingestion, and activity may last up to 72 hours. • If alcohol is consumed during this sensitive period, patients develop a typical disulfiram reaction. • Mushrooms ingested at the same time as alcohol produce no toxicity.
  • 27.
    CLINICAL FEATURES • headache, •paresthesias of distal extremities, • metallic taste, • flushing, • palpitations, • chest pain, • nausea, • vomiting, • and diaphoresis and generally occur within minutes to several hours after alcohol consumption. • Symptoms generally last for 2 to 4 hours but may last up to 2 days. • Most symptoms are mild. • Diagnosis is made based on presence of the symptom complex and its association with alcohol consumption.
  • 28.
    TREATMENT • GI decontaminationhas no role and charcoal administration is not beneficial. Patients • Occasionally become hypotensive and respond to administration of IV fluids or, in refractory cases, norepinephrine. • Excessive sympathetic activity can be inhibited by β-blockers. • Most cases are self-limited, and patients can be discharged once they • can tolerate oral fluids.
  • 29.

Editor's Notes

  • #2 Depending on the type of mushroom, adverse effects from ingestion range from mild GI symptoms to major cytotoxic effects resulting in organ failure and death. Toxicity varies based on the amount ingested, the age of the mushroom, the season, the geographic location, and the way in which the mushroom was prepared prior to ingestion
  • #9 Physostigmine can produce bradycardia, hypotension, and seizures, so administration should be reserved for severely symptomatic patients
  • #11 Muscarine was the first mushroom toxin to be identified.
  • #21 Silybinum : a milk thistle isolate, is also thought to prevent toxicity by interfering with transmembrane transport during enterohepatic circulation and inhibiting the binding of α-amanitin to hepatocytes.