eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Mushroom - Muscarine

Peter A Chyka, PharmD, FAACT, DABAT, Professor and Executive Associate Dean, College of Pharmacy, University of Tennessee Health Science Center
William Banner Jr, MD, PhD,, Medical Director, Oklahoma Poison Control Center; Clinical Professor of Pharmacy, Oklahoma University College of Pharmacy-Tulsa; Adjunct Clinical Professor of Pediatrics, Oklahoma State University College of Osteopathic Medicine

Updated: Oct 14, 2009

Introduction

Background

Although many mushrooms may contain cholinergic toxins like muscarine in small amounts, it is the mushrooms of the Inocybe and Clitocybe genera that contain sufficient amounts to produce a muscarinic cholinergic poisoning. In particular, Amanita muscaria is named for trace amounts of muscarine present but it does not cause clinical cholinergic toxicity.

<em>Inocybe geophylla</em>.

Inocybe geophylla.



<em>Inocybe lacera</em>.

Inocybe lacera.



Mushrooms that contain muscarine are commonly found in yards, parks, and wooded areas throughout the United States, Europe, and Asia. Clitocybe and Inocybe genera are most commonly responsible for muscarinic mushroom poisoning in the United States. Many other species contain muscarine including Boletus, Mycena, and Omphalotus. Muscarine-containing mushrooms typically produce cholinergic symptoms such as sweating; facial flushing; salivation; lacrimation; vomiting; abdominal cramps; diarrhea; urination; miosis; and occasionally bradycardia, hypotension, and dizziness. Symptoms typically occur within 1 hour of ingestion, last for 4-24 hours, and resolve in most cases without drug therapy or with a dose of atropine.[1,2 ]
 

<em>Clitocybe dealbata</em>.

Clitocybe dealbata.


Muscarine was first extracted from Amanita muscaria in 1869, but this mushroom does not contain significant amounts of muscarine to cause toxicity . Ibotenic acid and muscimol are the major toxins in this mushroom and cause ethanol-like intoxication and jerking movements.

Mushroom poisoning in children is an infrequent but perennial problem for parents and clinicians. Parental anxiety is generally high because of fears of unknown or untoward effects. Clinicians are challenged to identify such poisonings, to discern whether poisoning has taken place, to order appropriate diagnostic studies, and to prescribe reasonable therapy. The varied nature of mushroom toxicities, their ubiquitous distribution, and the relative infrequency of the ingestions make the task difficult.

Several general types of mushrooms can cause poisoning:[3,4,5 ]

  • Cyclopeptides (eg, Amanita phalloides) - Hepatotoxic
  • Orellanine and orelline (Cortinarius mushrooms) - Nephrotoxic
  • Ibotenic acid and muscimol (A muscaria, A pantherina), also termed isoxazoles - Intoxication and jerking movements
  • Gyromitrin or monomethylhydrazine (Gyromitra mushroom) - Hemolytic
  • Muscarine (Inocybe and Clitocybe mushrooms) - Cholinergic
  • Coprine (Coprinus atramentarius, inky cap) - Disulfiramlike reaction
  • Psilocybin (Psilocybe and Paneolus mushrooms, magic mushrooms) - Hallucinogenic
  • GI irritants
  • Allenic norleucine (Amanita smithiana) - Nephrotoxic
  • Myotoxic (Tricholoma equestre) - Rhabdomyolysis

A classification of 14 syndromic categories of mushroom poisoning has been also proposed, but this classification system has yet to be widely adopted.[6,7 ]

Pathophysiology

Muscarine stimulates M1 and M2 types of postganglionic cholinergic receptors (muscarinic receptors) in the autonomic nervous system. This action results in parasympathetic stimulation similar to that caused by the release of endogenous acetylcholine at postganglionic receptors of smooth muscle and the exocrine glands, such as sweat, bronchial, lacrimal, salivary, and gastrointestinal. The action on muscarinic receptors produces a cholinergic syndrome that is characterized by sweating, bronchorrhea with shortness of breath, salivation, lacrimation, diarrhea, miosis, abdominal cramps, and bradycardia. There is negligible activity on nicotinic receptors; hence, muscle weakness, fasciculations, and paralysis are not present. Because muscarine is a quaternary amine, it does not readily cross the blood-brain barrier and does not directly cause CNS effects. Muscarine is not metabolized by cholinesterase and has a longer biologic half-life than acetylcholine.

Frequency

United States

In 2007, 7351 mushroom ingestions were reported to the National Poison Data System of the American Association of Poison Control Centers (AAPCC).[8 ]Of these cases, 86% of cases involved mushrooms of unknown type. Mushrooms containing muscarine accounted for 27 cases, with 4 (15%) involving children younger than 6 years. About 15% of all cases involving muscarine were intentional ingestions and 70% were treated at a healthcare facility. No deaths from muscarine-containing mushrooms were reported in 25 years of data collection by AAPCC.

International

The incidence of all types of toxic mushroom poisonings, including those from the muscarine group, appears to be increasing in Europe and Asia. Estimates of the actual incidence are not available.[6,7 ]

Mortality/Morbidity

Fatalities from muscarine mushroom poisoning are very rare, and symptoms typically are mild to moderate in severity and self-limiting.

  • From 1999-2007, 28 deaths due to mushrooms were reported to US poison control centers through the AAPCC, but none were attributed to muscarine mushroom poisoning.
  • For the 27 exposures to muscarine-containing mushrooms reported by US poison control centers through the AAPCC, 63% of cases had no or minor effects, 7% had moderate effects, 4% suffered severe effects, and the outcome was unknown in 26% during 2007.[8 ]
  • Most toxic effects of mushrooms containing muscarine are temporary and self-limiting, lasting 6-24 hours.[1,2 ]
  • In Australia, a 53-year-old woman ate 2 large mushrooms (leftovers later identified as a Bolete mushroom, Rubinoboletus sensu lato pro tempe) and came to a hospital with a 2-hour history of headache, chest and abdominal pain, vomiting, and profuse sweating. At 3 hours, she also developed diarrhea and her condition deteriorated rapidly with hypotension, bradycardia, coma, and respiratory distress. At 7 hours, she remained in shock and did not respond to resuscitative measures. During the first hour of hemodialysis, she developed asystole and died 10 hours after ingestion. The patient's partner had eaten some of the mushrooms, but promptly vomited and did not exhibit any toxic effects.[9 ]Whether this mushroom grows in North America is unknown.

Descriptions of cases reported to the North American Mycological Association, toxicology section illustrate the typical course of many mushroom poisonings; however, these cases were not necessarily observed by health care professionals.[10 ]

Age

Adults are frequently involved as foragers for edible mushrooms. Because of errors in identification, they may ingest toxin-containing look-alike mushrooms. Adults and adolescents may also be inadvertently poisoned when they intentionally consume mushrooms, picked from the ground or purchased dried, to achieve intoxication. Young children may be poisoned by mushrooms when they unintentionally eat mushrooms found outside, typically in yards or outdoor play areas.

Clinical

History

Ask the patient about how many mushrooms were consumed, how they were prepared, and when the mushrooms were eaten. The concentration of active substances is low in any one mushroom. The effects of mushrooms vary greatly, and cooking may not alter toxicity. Typically, the amount consumed at a meal or a single whole mushroom is sufficient to cause symptoms.[1 ]

  • Obtain a history of the exposure that includes the following:
    • Quantity of mushrooms ingested
    • Preparation of the mushroom (eg, raw, cooked)
    • Source of the mushroom (eg, outdoors, the Internet)
    • Time of the ingestion
    • Symptoms and time of onset after ingestion
    • Prehospital treatment including home remedies
    • Medications regularly taken and any coingestants
    • Past medical history with a focus on arrhythmias, asthma, prostatic hypertrophy, and gastric outlet obstruction
  • The timing of symptom onset is a crucial element of the history in differentiating life-threatening or severe mushroom poisonings from those that are less serious and typically have an onset of symptoms well within 5 hours of ingestion such as the muscarine-containing mushrooms.[6,7,3,4,5 ]
    • Mushrooms from the cyclopeptide (Amanita phalloides) or orellanine (Cortinarius mushrooms) groups, which can produce hepatic or renal failure, respectively, typically produce symptoms 6-24 hours after ingestion.
    • Amanita smithiana (allenic norleucine group) found in the Northwestern states can also be nephrotoxic, but it has an onset of gastrointestinal distress within 1-12 hours.[11 ]These mushrooms are often confused with edible pine mushrooms.
    • For mushroom ingestions in the Pacific Northwest region of the United States, patients who have early-onset symptoms and remain symptomatic should be fully evaluated in a hospital until the mushroom identity is confirmed to be nontoxic or the patient’s condition improves.[5 ]
  • Identification of the actual mushroom consumed is important but is typically impossible because the mushroom in question has already been digested.
    • 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 notched, and the spores are brown.
    • Different types of mushrooms can be found in the same location, and a single sample can lead to false identification of the mushroom that was ingested. Consider all possible mushrooms in the immediate vicinity of where the ingestion occurred.
    • When no specimen is brought in by a patient with a suspected mushroom ingestion, sending an experienced forager to the site to collect any mushrooms growing in the area might be helpful.
    • When mushrooms are obtained for identification, the entire mushroom should be dug up to preserve the architecture of the bulb, stem, and cap. Place individual mushrooms in a dry, paper bag, 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, and premature release of the spores. Do not refrigerate or crush the mushrooms.
    • Collecting the patient's gastric contents by means of gastric lavage or after emesis might yield identifiable spores.
    • Remote viewing of the mushroom by digital photography and Internet transmission may aid the identification of unknown mushrooms by mycologists.[12 ]

Physical

Signs and symptoms related to the ingestion of a muscarine-containing mushroom typically appear after 0.5-2 hours and may last for 6-24 hours. Muscarinic effects, such as sweating, salivation, lacrimation, urination, defecation, abdominal cramps, miosis, emesis, bronchorrhea with shortness of breath, and bradycardia are seen. Profuse sweating and facial flushing are prominent features and should raise the suspicion of a muscarinic poisoning.[1,2 ]

The acronyms SLUDGE (salivation, lacrimation, urination, diarrhea, gastric distress, and emesis) and DUMBBELS (diarrhea, urination, miosis, bradycardia, bronchorrhea, emesis, lacrimation, and salivation) may be useful memory aids for the cholinergic syndrome affecting muscarinic receptors.

Muscarine does not directly cause CNS symptoms because it does not cross the blood-brain barrier due to its chemical nature as an ionized quaternary amine. The dizziness and headache occasionally experienced by patients poisoned with muscarine are the consequence of the peripheral cardiovascular and respiratory effects.

If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 hours or more after ingestion, poisoning with the potentially life-threatening or severe mushrooms such as the cyclopeptide (Amanita phalloides) or orellanine (Cortinarius mushrooms) groups, which can produce hepatic or renal failure, respectively, should be considered.[6,7,3,4,5 ] Amanita smithiana (allenic norleucine group) found in the Northwestern US can also be nephrotoxic but has an onset of gastrointestinal distress within 1-12 12 hours after ingestion.[11 ]For mushroom ingestions in the Pacific Northwest region of the United States, patients who have early-onset symptoms and remain symptomatic should be fully evaluated in a hospital until the mushroom identity is confirmed or the patient’s condition improves.[5 ]

  • Vital signs
  • Pulse - Bradycardia or reflex tachycardia
    • Respiration - Unaffected to labored with shortness of breath
    • Blood pressure - Hypotension in severe cases
    • Temperature - No changes expected
  • Integumentary findings
    • Facial flushing
    • Sweating
  • Head, ears, eyes, nose, and throat findings
    • Pupillary constriction
    • Blurred vision
    • Excessive salivation
    • Watery eyes
  • Cardiovascular symptoms
    • Bradycardia (more common)
    • Reflex tachycardia
  • Respiratory signs
    • Copious bronchial secretions
    • Wheezing
    • Shortness of breath
  • GI symptoms
    • Cramps
    • Vomiting
    • Increased bowel activity
    • Diarrhea
  • Urinary tract symptoms
    • Increased urination
    • Bladder spasms
  • Neurologic signs
    • Dizziness and headache from hypotension

Causes

  • Incorrect mushroom identification by a naive forager, such as an immigrant who mistakes one of the local poisonous varieties for an edible mushroom native to his or her homeland or a novice mushroom harvester
  • Intentional ingestion by a suicidal person or person attempting substance abuse
  • Unintentional ingestion by a child who found mushrooms growing in yards or outdoor play areas
  • Foul play in which an individual is poisoned by someone else
  • Inadvertent poisoning from dried mushrooms purchased on the Internet or from other sources where the composition of the mushroom is unreliable or where the mushroom might contaminated with unknown toxic compounds

Differential Diagnoses

Asthma
Gastroenteritis
Heart Failure, Congestive
Hypoglycemia
Toxicity, Organophosphate

Other Problems to Be Considered

Poisoning with cholinergic agents

Poisoning with mushrooms containing muscarine such as Clitocybe cerrusata, C dealbata, Clitocybe nubulosa, Inocybe fastigiata, Inocybe geophylla, Inocybe rimosus, and Omphalotus olearius (jack-o'lantern mushroom).

<em>Omphalotus olearius</em> (jack o'lantern mush...

Omphalotus olearius (jack o'lantern mushroom).



Organophosphate insecticides: Patients may exhibit similar cholinergic symptoms as those of muscarine poisonings, but muscle fasciculations and weakness, respiratory paralysis, decreased level consciousness, and an insecticide odor are usually also present.

Poisoning with cholinergic and anticholinesterase drugs

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

Workup

Laboratory Studies

  • Several texts, such as Goldfrank's Toxicological Emergencies,[5 ]describe how to determine if the suspect botanical contains amatoxin, a potent toxin found in some of the Amanita species. However, for symptomatic patients, identification of the mushroom by a mycologist is desirable. (See Consultations.)
  • Obtain a complete blood count because some mushroom toxins (eg, gyromitrin) can cause hemolytic anemia.
  • Baseline liver function studies are indicated because possible ingestion of other toxic mushrooms, such as cyclopeptide-type mushrooms, can cause hepatotoxicity.
  • Baseline renal function studies are indicated because some mushrooms are nephrotoxic, such as Amanita smithiana ( in Northwestern US) and orelline mushrooms.
  • Consider evaluation for rhabdomyolysis if signs and symptoms warrant because some mushrooms, Tricholoma equestre, may cause muscle toxicity.
  • Obtain a basic serum metabolic profile (sodium, potassium, chlorine, carbon dioxide, creatinine, glucose, and calcium) to evaluate fluid and electrolyte disturbances.
  • Urine drug screening should be considered, especially if the patient has unexplained behavioral changes; if suicidal intent, substance abuse, or foul play is suspected; or if ingestion of unknown toxins is suspected.
  • Chromatographic techniques (eg, thin-layer chromatography [TLC], gas-liquid chromatography [GLC], high-pressure liquid chromatography [HPLC]) are available to detect amanitins, orellanine, muscimol and ibotenic acid, psilocybin, muscarine, and the gyromitrins. However, these techniques are typically unavailable to the general practitioner because they are limited to laboratories conducting research on these compounds.

Imaging Studies

  • Chest radiography may be helpful in evaluating pulmonary edema.

Other Tests

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

Procedures

No particular diagnostic procedures are available or needed for most patients with toxicity from mushrooms containing muscarine.

Treatment

Medical Care

  • Symptomatic patients may be treated with supportive measures.
  • The entire episode usually subsides in 6-8 hours; some symptoms may take up 24 hours to fully resolve.
  • Consider using atropine when excessive bronchial secretions compromise breathing and cause shortness of breath.
  • Monitor with pulse oximetry.
  • Be prepared to support the airway and perform orotracheal suctioning if needed.[2 ]

Consultations

  • Consult a mycologist to assist with mushroom identification. A mycologist can be contacted through the local poison center (in the United States, call 800-222-1222), a mycology club, the North American Mycological Association, a botanical garden, or local university.
  • Consultation with a medical toxicologist may be helpful, if available.
  • Consult a psychiatrist when the ingestion may have been a suicidal gesture.

Medication

Most patients with poisoning due to mushrooms containing muscarine can be treated without medications. If patients exhibit excessive bronchial secretions or other symptoms of cholinergic excess (bradycardia) that are of significant concern, atropine may decrease these symptoms. If the patient presents within 1 hour of ingestion oral administration of activated charcoal may be considered,[13 ]but adsorption to activated charcoal has not been demonstrated for these constituents.[14 ]No evidence suggests that routine administration of multiple doses of activated charcoal is useful. Ipecac syrup should generally be avoided because vomiting often occurs spontaneously and evidence for effectiveness is lacking.

Anticholinergic agents

Atropine is a competitive inhibitor of acetylcholine and muscarine in the autonomic nervous systems and relieves the muscarinic effects, especially bronchorrhea. Inhaled anticholinergic agents (eg, ipratropium) may also be considered.


Ipratropium (Atrovent)

Chemically related to atropine. Has antisecretory properties and, when applied locally, inhibits secretions from serous, and seromucous glands lining the nasal mucosa.

Dosing

Adult

Nebulizer: 1 vial (500 mcg) inhaled via nebulizer tid/qid
MDI: 2 actuations PO qid; not to exceed 12 inhalations/24 h

Pediatric

Nebulizer: 250 mcg inhaled via nebulizer tid
Metered dose inhaler: 1-2 actuations PO tid; not to exceed 6 inhalations/24 h

Interactions

Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects of ipratropium

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction


Atropine sulfate injection

Acts at parasympathetic receptor sites to block the actions of acetylcholine and muscarine.

Dosing

Adult

0.4-1 mg IV/IM; repeat q20-30min prn to control bronchial secretions and titrate the dose to response

Pediatric

0.02 mg/kg IV/IM; minimal dose is 0.1 mg; repeat q10-20min prn to control secretions and titrate the dose to response

Interactions

Additive effects in the presence of other anticholinergics; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects

Contraindications

Documented hypersensitivity; benefits may outweigh risks if cholinergic symptoms life-threatening toxicity; thyrotoxicosis, narrow-angle glaucoma, tachycardia, obstructive uropathy, paralytic ileus, toxic megacolon, asthma, and myasthenia gravis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid prophylactic use and only when significant symptoms are present; avoid in Down syndrome and brain damage to prevent hyperreactive response; avoid in coronary heart disease, tachycardia, congestive heart failure (CHF), cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can cause dysuria (catheterization may be required)

Follow-up

Further Inpatient Care

  • Administer intravenous fluids if vomiting becomes prominent, although this is rare.
  • Provide psychiatric care to patients with intentional ingestions and suicidal thinking.

Deterrence/Prevention

  • Avoid eating mushrooms that are not commercially cultivated for human consumption.
  • Cautious mushroom hunters eat only one type of mushroom and save a sample in a dry, paper bag for later identification, if needed.
    • Identification of mushrooms is best left to experts.
    • Prevention is best achieved by eating only commercially cultivated mushrooms.
  • Regularly remove mushrooms from sites where children are routinely present.

Prognosis

  • The prognosis is excellent because many patients who ingest these mushrooms exhibit minor or no symptoms. Symptoms are typically self-limited, and patients recover without drug therapy. If needed, atropine relives most significant muscarinic symptoms.

Multimedia

<em>Inocybe geophylla</em>.

Media file 1: Inocybe geophylla.

<em>Inocybe lacera</em>.

Media file 2: Inocybe lacera.

<em>Clitocybe dealbata</em>.

Media file 3: Clitocybe dealbata.

<em>Omphalotus olearius</em> (jack o'lantern mush...

Media file 4: Omphalotus olearius (jack o'lantern mushroom).

References

  1. Benjamin DR. Muscarine poisoning. In: Mushrooms: Poisons and Panaceas. New York, NY: WH Freeman; 1995:340-50.

  2. Poisindex managements, mushrooms – muscarine / histamine. In: Poisindex System, internet database online [database online]. Greenwood Village (CO): Thomson Reuters (Healthcare); February 27, 2009.

  3. Berger KJ, Guss DA. Mycotoxins revisited: Part I. J Emerg Med. Jan 2005;28(1):53-62. [Medline].

  4. Berger KJ, Guss DA. Mycotoxins revisited: Part II. J Emerg Med. Feb 2005;28(2):175-83. [Medline].

  5. Goldfrank LR. Mushrooms. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies. 8th. New York: McGraw-Hill; 2006:1564-76.

  6. Diaz JH. Evolving global epidemiology, syndromic classification, general management, and prevention of unknown mushroom poisonings. Crit Care Med. Feb 2005;33(2):419-26. [Medline].

  7. Diaz JH. Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med. Feb 2005;33(2):427-36. [Medline].

  8. Bronstein AC, Spyker DA, Cantilena Jr LR, Green JL, Rumack BH, Heard SE. 2007 Annual report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th annual report. Clin Toxicol. 2008;46:927-1057.

  9. Pauli JL, Foot CL. Fatal muscarinic syndrome after eating wild mushrooms. Med J Aust. Mar 21 2005;182(6):294-5. [Medline].

  10. NAMA (North American Mycological Association). Annual reports. North American Mycological Association, Toxicology Section. Available at http://www.namyco.org/toxicology. Accessed March 4, 2009.

  11. West PL, Lindgren J, Horowitz BZ. Amanita smithiana mushroom ingestion: a case of delayed renal failure and literature review. J Med Toxicol. Mar 2009;5(1):32-8. [Medline].

  12. Fischbein CB, Mueller GM, Leacock PR, Wahl MS, Aks SE. Digital imaging: a promising tool for mushroom identification. Acad Emerg Med. Jul 2003;10(7):808-11. [Medline].

  13. Beuhler MC, Sasser HC, Watson WA. The outcome of North American pediatric unintentional mushroom ingestions with various decontamination treatments: an analysis of 14 years of TESS data. Toxicon. 2009;53:437-43.

  14. Chyka PA, Seger D, Krenzelok EP, Vale JA, ,. Position paper: Single-dose activated charcoal. Clin Toxicol (Phila). 2005;43(2):61-87. [Medline].

Keywords

muscarine, mushroom poisoning, mushroom poisoning symptoms, cholinergic syndrome, Inocybe, Clitocybe, Boletus, Mycena, Omphalotus, jack o'lantern mushroom, sweating mushroom

Contributor Information and Disclosures

Author

Peter A Chyka, PharmD, FAACT, DABAT, Professor and Executive Associate Dean, College of Pharmacy, University of Tennessee Health Science Center
Peter A Chyka, PharmD, FAACT, DABAT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Clinical Pharmacy, and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Coauthor(s)

William Banner Jr, MD, PhD,, Medical Director, Oklahoma Poison Control Center; Clinical Professor of Pharmacy, Oklahoma University College of Pharmacy-Tulsa; Adjunct Clinical Professor of Pediatrics, Oklahoma State University College of Osteopathic Medicine
William Banner Jr, MD, PhD, is a member of the following medical societies: American College of Medical Toxicology
Disclosure: Nothing to disclose.

Medical Editor

Michael E Mullins, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine
Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians
Disclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Merck Salary Employment

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Martin I Herman, MD, to the development and writing of this article.

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