AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

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

INTRODUCTION

Section 2 of 9  

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

Background

Muscarine was first extracted from Amanita muscaria (fly agaric) in 1869. It played an important part in delineating the role of acetylcholine (ACh) in neurohumoral physiology. In fact, since the late 1800s, pharmacologists have referred to the effects of stimulation of postganglionic choline receptors as the muscarinic effects of ACh.

An ironic note is that A muscaria provided the first source of muscarine (hence its name) but actually contains miniscule amounts of muscarine (0.005%). To produce a toxic effect, mushrooms must contain at least 0.01% of muscarine (as described in the Poisindex).¹ Mushrooms from the genera Inocybe and Clitocybe reliably contain sufficient amounts of this toxin. In fact, one species, Clitocybe dealbata, is so well known for its reliably high muscarine content that it is commonly referred to as the sweating mushroom. Mushrooms in the genera Boletus, Omphalotus, or Amanita may also contain some muscarine. Bear in mind that the muscarine content may vary from plant to plant, depending on where they are grown, on how they are prepared, or on how they are stored.

Mushrooms, which are classified as fungi, differ from other plants because they do not have chlorophyll. They have been a part of the human diet for years because they are a source of protein and essential amino acids. The edible varieties satisfy gustatory pleasures while providing nutritional value. They are generally low in calories and cholesterol and can improve the immune system and blood pressure. Because they are promoted for their nutrient values, many grocery stores now carry various commercially grown mushrooms, including shiitake, portabella, morels, chanterelle, oyster, and other mushrooms. The commercially grown, cultured mushrooms are the safest to enjoy.

Increased awareness and interest in the large variety of mushrooms found around the world has led to growing interest in foraging for wild mushrooms. Although finding mushroom delicacies in the wild may be satisfying, caution is required because many mushrooms contain deadly toxins. The challenge to all who forage for mushrooms is that they must be able to distinguish truffles (edible varieties) from toadstools (from the German todesstuhl,  which means "death stool").

Mistaking a toxic mushroom for an edible one is the most common cause of poisoning. This problem might be especially important among immigrant populations if they mistake a toxic variety indigenous to their new country for a nontoxic variety they were used to eating in their homeland.

Fortunately, mushroom poisoning is rare. Of the roughly 5000 known mushroom species, approximately 200-300 are edible, and only 50-100 are poisonous. The odds are clearly favorable when one ingests an unidentified mushroom. However, approximately 7000 mushroom ingestions are reported every year to the American Association of Poison Control Centers (AAPCC) Poison Exposure Database.²

Children and adolescents younger than 19 years account for 78% of all reported ingestions. Many ingestions in children younger than 6 years are unintentional and consist of a child simply tasting a mushroom found growing in their yard or play area. This is not the case for ingestions in older children. Adolescents are most likely to engage in a misguided attempt to experience hallucinogenic effects of magic mushrooms or to intentionally ingest toxic mushrooms to commit suicide. Of note, poisonings can also occur when otherwise edible mushrooms are improperly stored, prepared, or cooked. Some unintentional ingestions might result from the purchase of misidentified or adulterated mushroom products through unregulated marketers on the Internet or other illicit sources.

Classes of mushroom toxins

Muscarine is one of the commonly accepted classes of mushroom toxins. Toxin groups include the following:

• Cyclopeptide (eg, Amanita phalloides) and cyclopeptide and/or orellanine (Cortinarius mushrooms)
• Ibotenic acid and/or muscimol (Amanita muscaria, Amanita pantherina)
• Gyromitrin or monomethylhydrazine (genus Gyromitra)
• Muscarine (Inocybe and Clitocybe mushrooms)
• Coprine (Coprinus atramentarius) (ie, inky cap)
• Psilocybin (Psilocybe and Paneolus mushrooms, magic mushrooms)
• GI irritants
• Miscellaneous

Distribution and recognition of mushrooms

Mushrooms that contain muscarine are commonly found in yards and public parks. Their prevalence and enticing appearance may pose a challenge to parents as they try to keep their children from sampling these potentially toxic plants. Clitocybe, Inocybe, and Amanita species are among those most commonly involved in muscarinic poisoning. Being able to recognizing these mushrooms and to educate parents and children about their dangers is important.

Clitocybe mushrooms are found as single specimens on lawns in the summer and fall. The mushrooms are whitish tan-to-gray and have 15- to 33-mm caps. Their stalks are hairless and are 1- to 5-cm long. Their gills are decurrent (running down the stalk), and the spores are white.

Inocybe mushrooms are typically found in or under hardwoods and conifers in the summer and fall. The mushrooms are small and brown and have conical caps as large as 6 cm in diameter. Stalks are 2-10 cm and have fine, brown-to-white hairs. The gills are notches, and the spores are brown.

A muscaria can occur singly or in groups, and it is found on the ground of forests, grassy areas, and lawns, especially under trees. The mushroom has a scarlet cap 5-30 cm in diameter, with warts. The stalk is white, frequently hollow, and often as long as 15-20 cm. A prominent cup (volva) is found at the bottom of the stalk with numerous rings extending superiorly. The gills are free and white. The spores are also white. The appearance varies depending on the geographic location. The scarlet red cap is found predominantly in western parts of North America. In eastern North America, the cap is orange to yellow-orange.

Classification systems

Because of the large numbers of mushroom species and difficulties in their identification, toxicologists have struggled with developing a system to facilitate the recognition of mushrooms and the treatment of mushroom ingestion.

In 1987, a group started in Germany proposed classifying mushroom poisonings on the basis of (1) a description of the mushroom, (2) toxicologic analysis, and (3) the patient's presenting signs and symptoms.

Because the lag time to toxicity appears to be an important factor, any system of classification should incorporate this lag. According to several observers, latent periods of >12 hours differentiate the lethal amatoxin poisonings from less serious, early-onset poisonings involving other toxins. People working with mushroom poisonings have known that notable mushroom toxicity can occur before 12 hours and suggest use of a lag time of >6 hours to separate the clinically significant ingestions of amanitin and gyromitrin from less toxic ingestions. Of course, serious ingestions may be neglected if they have a short onset time to GI irritation followed by serious problems, such as seizures, renal failure, liver failure, or hemolytic anemia.

To refine the current classification scheme, a toxin-directed system was developed. Mushroom ingestions may be classified on the basis of evidence of poisoning from the following toxins: amanitin, orellanine, gyromitrin, muscarine, pantherine, psilocybin, coprine, Paxillus toxin, and miscellaneous GI irritants. This system, which was originally proposed in Europe, was adapted for use in the United States. Table 1 below shows this toxin-based scheme.

US and European Classes of Mushroom Toxins

An unfortunate feature is that all of the systems of nomenclature fail to recognize newly discovered toxic effects, such as those causing acute renal failure, delayed renal failure, rhabdomyolysis, and delayed CNS failure. To address these shortcomings, some have proposed simplifying the classification system by basing it on whether the toxins are hepatotoxic, nephrotoxic, neurotoxic, psychotropic, myotoxic, or gastroenteric.

Old taxonomy clearly fails to consider the lag times of various poisons. Although the 6-hour cutoff works well for amatoxin and gyromitrin toxicity, it causes some early onset toxicities to be missed and underestimates the need for the prolonged care needed in patients with delayed-onset toxicities.

When one combines the type of toxin and the onset of its effects, a new, time-to-onset–stratified, syndromic system emerges. This approach may enable early detection and enable application specific therapies, including transplantation.

A classification of 14 syndromic categories of mushroom poisoning has been proposed. This classification system includes an improved definition of the miscellaneous category but has yet to be widely adopted.³ Muscarine is designated as an early-onset (<6 h) cholinergic neurotoxin in this new system.

• Early onset (<6 h)
• • Neurotoxic
  • • Cholinergic (muscarine type, eg, from Clitocybe and Inocybe mushrooms)
    • Glutamatergic (isoxazoles, eg, muscimol, ibotenic acid from A muscaria or A pantherina)
    • Epileptogenic (monomethylhydrazines from Gyromitra species)
    • Hallucinogenic (eg, from Psilocybe mushrooms)
  • Allergic
  • • Immunohemolytic (from Paxillus, or poison pax; not included in old taxonomy)
    • Pneumonic (puffballs, not included in old classifications)
  • GI
  • • Disulfiram reaction (old coprine toxin group)
    • Miscellaneous toxins causing GI distress
• Late onset (6-24 h)
• • Hepatotoxic (with amatoxic [cyclopeptide] subgroup)
  • Nephrotoxic (previously unclassified)
  • Erythromelalgic (previously unclassified)
• Delayed (³24 h): Orellanine is now considered a late-onset nephrotoxin. Toxins derived from Tricholoma equestre (yellow Trich) and Russula subnigricans (blackening Russula) are the rhabdomyolytic late-onset toxins. The purple-dye toxin (from Hapalopilus rutilans) is a late-onset neurotoxin.
• • Nephrotoxic
  • Rhabdomyolytic
  • Neurotoxic

Perhaps clinicians will use this new syndromic classification system in the near future to quickly recognize possible mushroom poisonings and to make appropriate decisions regarding intervention, observation, and follow-up.

Pathophysiology

Mechanism of action

As noted above, muscarine is one of the 8 major mushroom toxins. It exerts its effects by means of the autonomic nervous system. The autonomic nervous system is composed of the sympathetic and parasympathetic systems and uses ACh as the chemical transmitter at both preganglionic and postganglionic synapses in the parasympathetic system. ACh is also the neurotransmitter at sympathetic preganglionic synapses, at some sympathetic postganglionic synapses, at the neuromuscular junction (somatic nervous system), and at some sites in the CNS. Nerve fibers that release ACh from their endings are described as cholinergic fibers.

ACh receptors are ligand-gated cation channels composed of 4 polypeptide subunits arranged in the form (a₂)(b)(g)(d). Two main classes of ACh receptors are recognized and are differentiated by their response to nicotine or muscarine.

When ACh stimulates preganglionic synapses, it produces sympathetic effects at various end organs of the autonomic system. These effects can be reproduced with the administration of nicotine as therefore are known as the nicotinic effects of ACh. ACh may also stimulate postganglionic receptors to produce effects such as salivation, lacrimation, defecation, micturition, sweating, miosis, bradycardia, and bronchospasm. Muscarine produces these effects, and hence they are referred to as muscarinic effects, and the postganglionic receptors are called muscarine receptors. Muscarinic receptors are the most diffuse receptors and are G-protein coupled. Two subgroups have been identified: M1 and M2. M1 receptors are excitatory, and M2 receptors are inhibitory. By convention, the muscarinic effects of various drugs are also referred to as cholinergic effects.

Muscarine is a quaternary trimethyl ammonium salt of 2-methyl-3-oxy-5-(amino)-tetrahydrofuran. It can stimulate both the M1 and M2 types of postganglionic cholinergic receptors (muscarinic receptors). When it does, it results in parasympathetic stimulation similar to that caused by the release of endogenous ACh. Because it is a quaternary salt, muscarine does not readily cross the blood-brain barrier. As a result, it causes few, if any, CNS symptoms. Muscarine is not metabolized by cholinesterase and therefore has a long biologic half-life.

Toxicity

The lethal dose is estimated to be 40-180 mg.

Frequency

United States

In 2005, 7146 mushroom ingestions were reported by US poison control centers.² Nineteen (0.3%) were attributed to the muscarine-containing group of toadstools. Four (21%) of the 19 patients were children younger than 19 years of age. The 15 others (79%) were over 19 years.

International

In Europe, the incidence of all types of toxic mushroom ingestions is higher than that of the United States. An average of 70 cases per year occurs in Japan. Other countries, such as China and South Africa, also report mushroom toxicities. Whether these toxicities are due to mushrooms containing muscarine is not known.

Mortality/Morbidity

Fatalities from mushroom poisoning are rare but do occur.

• In Japan, 3-4 fatal cases due to mushrooms are reported per year, but whether muscarine is involved is unknown.
• Deaths due to Inocybe patouillardii have been reported in Europe.
• In 2005, 6 deaths were reported to US poison control centers, but none were due to muscarine-containing mushrooms.² No deaths in the United States have been attributed to muscarine toxicity in the last 20 years.

Age

• Adults often forage for morels or truffles. Because toxin-containing mushrooms may appear similar to edible mushrooms and because they grow in the same areas because of their similar nutrient requirements, erroneous identification and ingestion may occur. Immigrant groups unfortunately mistake toxic, mushrooms in their new countries for edible mushrooms that grow in their native countries.
• Children are primarily poisoned by sampling wild mushrooms on their own or when an adult feeds them a poison mushroom, intentionally or not.
• Teens may ingest toxic mushrooms in a quest for a drug-toxin induced hallucinogenic experience. Lay information and misinformation are certainly factors with the widespread growth of Internet sites that promote the ingestion of wild mushrooms for their effects.

CLINICAL

Section 3 of 9  

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

History

Assess the following:

• Quantity of mushrooms ingested
• Preparation of the mushroom
• Time of the ingestion
• Symptoms
• Timing of symptom onset
• Treatment before the patient's arrival
• Other medications, coingestants
• Past medical history
• • Heart block
  • Asthma
  • Prostate hypertrophy
  • Gastric disorders
  • Gastric outlet obstruction
• Possibility of adulterants, such as pesticides

Physical

Signs and symptoms related to the ingestion of a muscarine-containing mushroom typically appear after 0.5-2 hours and may last 6-24 hours. Muscarinic effects, such as sweating, salivation, lacrimation, urination, defecation, gastric cramping, miosis, emesis, bronchospasm, and bradycardia are seen. Profuse sweating is a prominent feature and should alert the provider to the possibility of a cholinergic poisoning.

The acronyms SLUDGE (salivation, urination, diarrhea, gastric upset, and emesis) and DUMBBELS (diarrhea, urination, miosis, bradycardia, bronchospasm, emesis, lacrimation, and salivation) may be useful memory aids.

• Vital signs
• • Pulse - Reflex tachycardia or bradycardia
  • Respiration - Unaffected to labored with bronchospasm
  • Blood pressure - Hypotension
• Integumentary findings
• • Flushing
  • Sweating
• Head, ears, eyes, nose, and throat findings
• • Pupillary constriction
  • Blurred vision
  • Copious secretions
  • Watery eyes
  • Tearing
• Cardiovascular symptoms
• • Reflex tachycardia
  • Bradycardia (more commonly)
• Respiratory signs
• • Copious bronchial secretion
  • Wheezing
  • Shortness of breath
• GI symptoms
• • Cramping
  • Vomiting
  • Increased bowel activity
  • Diarrhea
• Urinary tract symptoms
• • Bladder spasms
  • Ureteral spasms
  • Increased urination
• Neurologic signs
• • Headache
  • Ataxia
  • Seizures (uncommon)

Causes

• Erroneous identification and ingestion of a wild mushroom containing the muscarine toxin is one cause.
• Reliance on various urban myths regarding the ability to detect a poisonous mushroom from an edible one is another cause. Myths include the following:
• • Staining of silver is an indicator or lack of safety.
  • The person can peel the mushroom cap or rely on the presence of bugs and slugs. These are unreliable safety markers.
  • The person can evaluate the particular habitat where a mushroom grows to predict the safety of the plant. This thought is erroneous.
• Children fed mushrooms that were incorrectly identified.
• Children may sample or taste toxic mushrooms they find in yards or picnic areas.
• Inadvertent poisoning can occur after a person ingests dried mushrooms purchased on the Internet or from other sources where the composition of the mushroom may be unreliable or where the mushrooms may be contaminated with unknown toxic compounds.

DIFFERENTIALS

Section 4 of 9  

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

Other Problems to be Considered

Poisoning with cholinergic agents

Poisoning with plants containing muscarine: Examples include A muscaria, Clitocybe cerrusata, C dealbata, Clitocybe nubulosa, Inocybe fastigiata, Inocybe geophylla, Inocybe rimosus, and Omphalotus illudens (jack-o'-lantern plant).

Organophosphates poisoning: Patients may present with the same symptoms as those of muscarine poisonings. However, they should also have muscle fasciculations and weakness. These are nicotinic effects and can help in differentiating organophosphate poisoning from muscarinic poisoning.

Poisoning with other drugs

Acetylcholine
Bethanechol (Urecholine)
Carbachol (Miostat intraocular solution, Isopto Carbachol)
Cevimeline
Methacholine (Amechol eye drops, Provocholine)
Pilocarpine
Physostigmine
Neostigmine
Pyridostigmine

WORKUP

Section 5 of 9  

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

Lab Studies

• In symptomatic patients, a mycologist should identify the mushroom (see Procedures).
• Specialized reference laboratories can detect muscarine in the patient's urine to confirm the diagnosis, but this confirmation is generally not performed because of limited availability of testing facilities.
• A CBC count is indicated. Various mushroom toxins (eg, gyromitrin) can cause hemolytic anemia.
• Liver function studies are indicated. The ingestion of toxic mushrooms (eg, cyclopeptide-type mushrooms) may involve hepatotoxins.
• Evaluate the basic metabolic profile, including potassium, chlorine, carbon dioxide, creatinine, glucose, and calcium levels.

Imaging Studies

• Chest radiography may be helpful in evaluating bronchospasm and cardiac effects.

Other Tests

• Gastric contents may be examined. A mycologist may be able to microscopically identify the spores recovered from the patient's gastric contents or feces.
• Obtain an electrocardiogram to look evaluate for atrioventricular (AV) nodal disease and heart block.

Procedures

• Amatoxin detection
• • Rule out poisoning by amatoxin or coingestion of amatoxin.
  • An amanitin detection kit (Amanitin Enzyme-Linked Immunosorbent Assay [ELISA]) has been developed for research use but is not intended for diagnostic use.⁴
• Identifying unknown mushrooms
• • In general, identifying unknown mushrooms or testing for amanitin toxins is unrealistic for most emergency physicians.
  • However, if symptoms such as vomiting, diarrhea, and abdominal pain begin 6 hours or longer after the ingestion, consider poisoning with potentially life-threatening cyclopeptide-type mushroom (eg, A phalloides) and begin stabilization and management to preserve the liver.
  • Send images to a mycologist. Advances in technology have created the possibility for remote viewing by means of digital photography and Internet transmission. These tools may help in the identification of many unknown mushrooms.⁵
  • Identifying the offending mushroom may prove helpful in diagnosis and management. However, identification of the offending mushroom is usually not successful. A 1991 analysis of mushroom ingestions showed that only 3.4% of ingestions were identified.⁶ However, from 1979-1995, the AAPCC reported that the exact species was identified in more than 95% of suspected mushroom ingestions.²
  • When a patient presents with suspected mushroom ingestion and when no specimen is available, send a volunteer or investigator to the site to collect the suspect mushroom and any others that might be growing in the same environment. The entire mushroom should be dug up to preserve the architecture of the bulb, stem, and cap. Collect any specimens lying around the patient's campsite or home.
  • Collecting gastric contents by means of lavage or emesis might yield identifiable spores.
  • Contact a mycologist. Helpful resources include the local poison center, a mycology club, the North American Mycological Association, a botanical garden, or a local university.
  • Contact the Poison Control Center in your area (in the United States, call 800-222-1222) because many centers have mycologists on call or know who to contact for assistance with identification.
  • If a specimen of the plant is available, a mycologist might be able to identify it on the basis of the pileus (cap), stipe (stalk), lamellae (gills), and volva.
  • A spore print can be made by placing the pileus facedown on a piece of filter paper for at least 4-6 hours. The sample should be covered or left in a windless area.

TREATMENT

Section 6 of 9  

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

Medical Care

• Symptomatic patients may be treated with supportive measures.
• Start an intravenous (IV) infusion with Ringer lactate or normal sodium chloride solution. The initial rate should be a maintenance rate. Adjust the rate or give bolus infusions to treat dehydration or hemodynamic instability.
• Begin cardiopulmonary monitoring.
• Begin monitoring pulse oximetry.
• Start bronchodilator therapy if the patient is wheezing.
• Start atropine or glycopyrrolate therapy to manage copious secretions or wheezing.
• Consider placing a nasogastric (NG) or orogastric (OG) tube to minimize vomiting.

Consultations

• Consultation with a mycologist is recommended to identify the mushroom.
• Psychiatric evaluation may be helpful if the ingestion was intentional or if suicidal intentions are suspected.

MEDICATION

Section 7 of 9  

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

Medications that have been useful in treating cholinergic excess include atropine sulfate and glycopyrrolate. For bronchospasm, albuterol may be helpful.

Drug Category: Anticholinergic agents

These agents elicit the competitive inhibition of ACh. They relieve the muscarinic effects, especially bronchorrhea.

Drug Name	Glycopyrrolate (Robinul)
Description	Acts in smooth muscle, CNS, and secretory glands, where it blocks action of ACh at parasympathetic sites.
Adult Dose	0.1-0.2 mg IV; repeat q20-30min prn to control bronchial secretions
Pediatric Dose	0.008 mg/kg (8 mcg/kg) IV; repeat prn to control secretions; not to exceed 0.2 mg/dose
Contraindications	Documented hypersensitivity; narrow-angle glaucoma, tachycardia, ulcerative colitis, paralytic ileus, acute hemorrhage, obstructive uropathy, toxic megacolon, asthma, myasthenia gravis
Interactions	Drugs with anticholinergic effects (eg, antihistamines, clozapine, digoxin, haloperidol, loxapine, metoclopramide, tricyclic antidepressants) have additive effects; levodopa decreases effects; amantadine and cyclopropane increase toxicity
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	May increase risk of megacolon, hyperthyroidism, CHF, coronary heart disease (CAD), hiatal hernia, and benign prostatic hyperplasia (BPH); may cause hyperactive response in Down syndrome

Drug Category: Beta2-adrenergic agonists

These provide reasonable reversal of the bronchospastic actions of the toxins.

Drug Category: Anticonvulsants

These are used to stop or control seizures that may occur.

Drug Name	Lorazepam (Ativan)
Description	Useful to treat delirium, seizures, or agitation. May depress all levels of CNS (eg, limbic and reticular formations) by increasing action of GABA (major inhibitory neurotransmitter in brain).
Adult Dose	4-8 mg IV infused over 2-5 min; administer 4 mg initially; may repeat in 10-15 min
Pediatric Dose	0.05-0.1 mg/kg IV infused over 2-5 min; may repeat in 10-15 min prn; not to exceed 2 mg/dose
Contraindications	Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma
Interactions	CNS toxicity increases with concurrent use of alcohol, phenothiazines, barbiturates, and MAOIs
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; monitor blood pressure after administration (adjust dose prn)

Drug Name	Midazolam (Versed)
Description	Useful to treat delirium, seizures, or agitation. Alternative in termination of refractory status epilepticus. Because water soluble, requires approximately 3 times longer than diazepam to achieve peak EEG effects. Therefore, wait 2-3 min to fully evaluate sedative effects before starting procedure or repeating dose.
Adult Dose	2.5-5 mg IV; may repeat in 10-15 min
Pediatric Dose	0.05-0.1 mg/kg IV, not to exceed 2 mg or the adult dose, or intranasally
Contraindications	Documented hypersensitivity; preexisting hypotension, narrow-angle glaucoma, and sensitivity to propylene glycol (diluent)
Interactions	Theophyllines may antagonize sedative effects; narcotics and erythromycin may accentuate sedative effects because of decreased clearance
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution in CHF, pulmonary disease, renal impairment, and hepatic failure

Drug Name	Phenobarbital (Luminal)
Description	In status epilepticus, achieves therapeutic levels as quickly as possible. IV dose may require approximately 15 min to attain peak levels in brain. If injected continuously until convulsions stop, brain concentrations may continue to increase and exceed those required to control seizures. Use minimal amount required and wait for anticonvulsant effect to develop before administering second dose.
Adult Dose	600-1200 mg IV loading dose; may follow with maintenance dose after12 h prn
Pediatric Dose	15-20 mg/kg IV loading dose; may follow with maintenance dose after 12 h prn
Contraindications	Documented hypersensitivity; severe respiratory disease, marked impairment of liver function, and nephritis
Interactions	May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients taking anticoagulants may require dose adjustments if drug added to or withdrawn from regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects; induction of microsomal enzymes may decrease effects of PO contraceptives in women (must use additional contraception to prevent unwanted pregnancy; menstrual irregularities may occur)
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Monitor respirations, especially if used with or shortly after benzodiazepines, observe for hypotension; in prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema

FOLLOW-UP

Section 8 of 9  

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

Further Inpatient Care

• Inpatient care with IV fluids may be required if vomiting is prominent.
• Provide psychiatric inpatient care in cases involving intentional ingestions with a suicidal intent.

Deterrence/Prevention

• Differentiating a poisonous mushroom from an edible one is difficult, and one cannot rely on traditional beliefs, color, odor, or taste to discern the differences.
• People should eat only commercially grown, cultivated mushrooms.
• Regard pure white, little brown, large brown, and red or pink mushrooms without lamellae growing in the wild as poisonous.
• People should have a mycologist or another expert identify any wild mushroom before eating it.
• If individuals do eat wild mushrooms, they should always keep a few mushroom specimens (eg, whole plant, bulb, stem, cap) for later identification.
• • They should place individual mushrooms in a dry paper bag and not a plastic or cloth bag.
  • Transporting the mushrooms in a careful, dry manner minimizes destruction of the natural architecture of the mushrooms, discoloration of the cap or gills, or premature release of the spores.
  • They should not refrigerate or crush the mushrooms.
• Remove all mushrooms from the scene of ingestion to prevent children from having further contact with them.

Prognosis

• The prognosis is excellent because most intoxications by muscarine-containing mushrooms are self-limited.
• Be sure to evaluate the patient for other toxins, such as amatoxin or gyromitrin. Many times, patients have eaten several varieties of toxic plants.

REFERENCES

Section 9 of 9

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

1. Poisindex managements, mushrooms – muscarine. In: Poisindex System, internet version [database online]. Greenwood Village (CO): Thomson Micromedex; May 31, 2007.
2. Lai MW, Klein-Schwartz W, Rodgers GC, et al. 2005 Annual Report of the American Association of Poison Control Centers' National Poisoning and Exposure Database. Clin Toxicol (Phila). 2006;44:803–932. [Full Text].
3. Diaz JH. Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med. Feb 2005;33(2):427-36. [Medline].
4. American Laboratory Products Company. Amanitin ELISA product information. ALPCO Diagnostics. Available at http://www.alpco.com/pdfs/01/01-EK-AM1.pdf. Accessed June 4, 2007.
5. Fischbein CB, Mueller GM, Leacock PR, et al. Digital imaging: a promising tool for mushroom identification. Acad Emerg Med. Jul 2003;10(7):808-11. [Medline].
6. Turner NJ, Szczawinski AF. The amanita group. In: Common Poisonous Plants and Mushrooms of North America. Portland, Or: Timber; 1991:35.
7. Benjamin DR. Mushrooms: Poisons and Panaceas. New York, NY: WH Freeman; 1995.
8. Berger KJ, Guss DA. Mycotoxins revisited: Part I. J Emerg Med. Jan 2005;28(1):53-62. [Medline].
9. Berger KJ, Guss DA. Mycotoxins revisited: Part II. J Emerg Med. Feb 2005;28(2):175-83. [Medline].
10. Brent J, Kulig K. Mushrooms. In: Haddad LM, Shannon MW, Winchester JF, eds. Clinical Management of Poisoning and Drug Overdose. 3^rd ed. Philadelphia, PA: WB Saunders; 1998:365-74.
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Article Last Updated: Feb 12, 2008