eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Mushroom - Gyromitra Toxin

Reed Brozen, MD, Director of Air Transport, Associate Professor, Department of Emergency Medicine, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center
Marcus J Hampers, MD, MBA, Instructor, Department of Medicine, Dartmouth Medical School; Consulting Staff, Department of Internal Medicine, Section of Hospital Medicine, Department of Anesthesiology, Section of Critical Care Medicine, and Department of Emergency Medicine, Dartmouth Hitchcock Medical Center

Updated: Feb 29, 2008

Introduction

Background

Thousands of mushroom species are studied and collected by amateur mushroom hunters, but only a handful cause death. False morel mushrooms (eg, Gyromitra esculenta, Gyromitra ambigua, Gyromitra infula) can cause fatal poisonings. These mushrooms are found on the ground or on rotten wood, are orange-brown to brown, have no gills, and have convoluted brainlike caps that are occasionally saddle-shaped. Gyromitra species fruit in the spring, and most poisonings occur during spring or early summer.

Pathophysiology

Some Gyromitra mushrooms contain hydrazones, including the toxin gyromitrin (N -methyl-N-formylhydrazone). Gyromitrin rapidly decomposes in the stomach to form acetaldehyde and N -methyl-N-formylhydrazine, which is converted to monomethylhydrazine (MMH) by slow hydrolysis. MMH is a water-soluble toxin that causes gastroenteritis, hemolysis, methemoglobinemia, hepatorenal failure, seizures, and coma. MMH is employed in rocket fuel and causes similar toxicity in aerospace industry workers. Cooking can render these mushrooms less toxic, although not reliably so. MMH is volatile and the fumes from cooking may cause toxicity.

Neurotoxicity

MMH exposure is similar to that of isoniazid in that it generates functional pyridoxine deficiency by inhibition of pyridoxine kinase. Pyridoxine kinase inhibition interferes with production of pyridoxal phosphate, an essential cofactor for a number of enzymatic steps, including glutamic acid decarboxylase (GAD).

Gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter of the brain, is produced from glutamate (an excitatory neurotransmitter) by the enzyme GAD. MMH also may inhibit GAD directly. The resultant GABA deficiency, with loss of inhibitory neurotransmission, may lead to seizures.

Gastrointestinal toxicity

Inhibition of diamine oxidase in intestinal mucosa may be responsible for GI effects. Association of individual variability in acetylation rates (eg, slow vs fast acetylators) in hepatotoxicity is not well established.

Hematopoietic toxicity

Hemolysis and methemoglobinemia can occur. Resultant hemoglobinuria may cause renal failure.

Frequency

United States

In 2004, a total of 2,438,644 toxic substance exposures and 1,183 deaths were reported to the American Association of Poison Control Centers (AAPCC) Toxic Exposure Surveillance System. Mushroom exposures accounted for 8,601 cases and 5 fatalities.¹

• In the same 2004 report, known gyromitrin-containing mushrooms accounted for 52 exposures and no fatalities. Only 1 fatality was in an unknown mushroom type.¹
• Unknown mushroom type makes up the majority of exposures each year, usually accounting for well over 80% of mushroom exposures, but deaths in this group remain remarkably low (0-2 per year since 1996).
• In 2003, known gyromitrin-containing mushrooms accounted for 71 exposures and only 1 fatality.²
• In 2002, gyromitrin-containing mushrooms accounted for 66 exposures and 1 death.³
• In 2001, gyromitrin-containing mushrooms accounted for 44 exposures and no deaths.⁴
• In 2000, gyromitrin-containing mushrooms accounted for 36 exposures and no deaths.⁵
• In 1999, gyromitrin-containing mushrooms accounted for 36 exposures but no recognized fatalities.⁶
• In 1998, gyromitrin-containing mushrooms accounted for 77 exposures but no deaths.⁷
• In 1997, gyromitrin-containing mushrooms accounted for 86 exposures, 3 with major outcomes, but no deaths.⁸
• In 1996, gyromitrin-containing mushrooms accounted for 62 exposures but no deaths.⁹
• Another study published in May 2000 used data from the National Center for Health Statistics and found no difference from the AAPCC annual report in numbers of deaths caused by mushroom exposures.¹⁰

International

No adequate international database exists. In the past, gyromitrin-containing mushrooms have been associated with significant mortality in Eastern Europe.

Mortality/Morbidity

• Mortality rates from 10-40% have been reported; however, death from gyromitrin-containing mushrooms in North America is exceedingly rare.
• Toxicity of gyromitrin-containing mushrooms varies by region and season.

Age

• Children are more sensitive to gyromitrin toxicity than adults.
• Overall about 60% of mushroom exposures are in children younger than 6 years. Although with Gyromitra species specifically, children younger than 6 years account for only 3% of exposures.

Clinical

History

Determining history of mushroom exposure is helpful. Query patients presenting with gastroenteritis about mushroom collecting, cooking, and ingestion.

• Onset of symptoms typically is delayed with gyromitrin poisoning.
  • GI symptoms typically occur 6-10 hours after ingestion; however, symptoms may begin earlier with severe poisonings.
  • Symptoms may be delayed 48 hours with mild poisonings.
  • Inhalation exposure characteristically produces symptoms within 2 hours of exposure.
  • GI phase of toxicity may be followed by neurologic and hepatorenal toxicity.
• Details of ingestion and progression of symptoms are helpful in differentiating ingestions of different mushroom types. Ask the following questions to ascertain specific history:
  • When were the mushrooms ingested (or when was patient exposed to vapors of cooking mushrooms)?
  • When did each symptom begin?
  • Where were the mushrooms found?
  • Were other species ingested?
  • Did others become ill after eating the mushrooms?
• Clinical history includes the following:
  • GI symptoms are prominent, with complaints of abdominal pain, bloating, vomiting, and diarrhea.
  • Other complaints (eg, weakness, dizziness, headache, confusion, seizures) may be caused by volume depletion, anemia, and renal, hepatic, or neurologic toxicity.
  • Typical duration of symptoms is 1-2 days but may be as long as 5 days.

Physical

• Vital signs
  • Tachycardia
  • Hypotension
  • Tachypnea (secondary to methemoglobinemia and/or hemolysis)
  • Fever
• General appearance
  • Dry skin with poor turgor (from vomiting and fluid losses)
  • Pale skin (from hemolysis)
  • Cyanosis unresponsive to oxygen (from methemoglobinemia)
  • Jaundice (from liver damage and hemolysis)
• Neurologic findings
  • Tremor, muscle spasms
  • Seizures, delirium
  • Stupor and encephalopathy
• Abdominal and rectal findings
  • Hyperactive bowel sounds, bloating, mild tenderness to palpation
  • Hepatomegaly
  • Liquid or heme-positive stool
• Hematologic findings
  • Muddy-colored urine from hemoglobinuria (due to hemolysis)
  • Chocolate-colored brown blood (from methemoglobinemia)

Causes

MMH poisoning may occur after ingestion of fresh, dried, or raw gyromitrin-containing mushrooms or with inhalation of vapors while cooking gyromitrin-containing mushrooms.

• Severity depends on amount of toxin ingested. Amount of toxin greatly varies among mushrooms, and significant variation in individual susceptibility exists.
  • Raw mushrooms have more toxin than cooked mushrooms.
  • Fresh mushrooms have more toxin than dry mushrooms.
  • Environmental factors appear to influence the amount of toxin, which varies regionally in these mushrooms. Michigan has a large number of Gyromitra mushrooms.

Differential Diagnoses

Other Problems to Be Considered

Shigellosis

Workup

Laboratory Studies

• Electrolytes, BUN, creatinine, and glucose
  • Patients often are dehydrated.
  • Assess renal function of patients with hemolysis.
  • Hyperglycemia may be present as an acute stress reaction; however, sudden hypoglycemia is a greater concern than hyperglycemia with hepatic injury.
• Complete blood count and/or peripheral blood smear: Assess for anemia from hemolysis or blood loss.
• Hepatic transaminases and serum bilirubin
  • Findings may be normal at presentation; however, if hepatic injury exists it becomes abnormal within days of exposure.
  • Bilirubin may be elevated from hemolysis or liver toxicity.
• Methemoglobin levels: Measure by co-oximetry (determine need for methylene blue treatment).
• Tests for hemolysis
  • Urinalysis: Positive dip test for blood without RBCs on microscopic analysis suggests either hemolyzed blood (hemoglobinuria) or myoglobin.
  • Free plasma hemoglobin increases with hemolysis.
  • Serum haptoglobin decreases with hemolysis.
  • Blood smears: Heinz body formation is observed with special stains, and bite cells are observed with Wright stain.

Other Tests

• Determination of mushroom type
  • If a specimen of the ingested mushroom is available, save it in a paper bag for potential identification. An experienced mycologist may identify the mushroom.
  • Save any food specimen or gastric contents (from emesis); further testing for gyromitrin toxin occasionally may be performed.
• Gas-liquid chromatography, gas mass spectrometry, and thin-layer chromatography can be used to identify hydrazone and hydrazine compounds.

Treatment

Prehospital Care

Initiate supportive care, including intravenous (IV) fluids and seizure control with pyridoxine and benzodiazepines.

Emergency Department Care

• Initiate supportive care and decontamination as follows:
  • ABCs and coma protocols
  • Correction of fluid and electrolyte imbalances
  • Antiemetics (if needed)
  • Dextrose (if needed)
  • Consideration of activated charcoal (although with typical delayed presentation of poisoning by Gyromitra species, value from this intervention is unlikely)
• Administer IV fluids to maintain brisk urine output and prevent renal damage from hemolysis.
• Treat seizures with both pyridoxine (vitamin B-6) and benzodiazepines.
  • Although limited cases exist in which pyridoxine was used as an antidote for gyromitrin-containing mushroom poisoning, pyridoxine is the antidote of choice for isoniazid-induced seizures, which are due to hydrazine and hydrazone metabolites of isoniazid interfering with GABA synthesis.
  • Phenobarbital has been demonstrated to increase metabolism of hydrazines to toxic metabolites and should be avoided. Phenobarbital metabolism may be decreased if liver failure from gyromitrin toxicity has occurred.
• Methemoglobinemia involves oxygen and methylene blue.
  • Methemoglobin cannot transport oxygen; functional anemia results.
  • Modest levels of methemoglobinemia may be tolerated with supportive care. With higher levels (eg, >20%) and associated symptoms, such as mental status changes, dyspnea, ischemic chest pain, or acidosis, consider treatment with methylene blue.
• Anemia due to hemolysis may require blood transfusion.
• Theoretically, folinic acid may be beneficial. Hydrazines inhibit metabolism of folic acid to tetrahydrofolate.

Consultations

• Consultation with a regional poison control center and toxicologist may be helpful. They may assist in contacting a mycologist for mushroom identification.
• Obtain a gastroenterology consultation if evidence of liver dysfunction is present.

Medication

The goals of pharmacotherapy are to reduce morbidity, prevent complications, and neutralize the effects of the toxin.

GI decontaminants

Empirically used to minimize systemic adsorption of toxin. May benefit only if administered within 1-2 hours of ingestion.

Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water. For maximum effect, administer within 30 min of ingesting poison.

Dosing

Adult

1 g/kg PO (usual dose 30-100 g)

Pediatric

1 g/kg PO (typical dose 12.5-25 g)
<2 years: Use aqueous charcoal without cathartic

Interactions

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties)

Contraindications

Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies; aspiration risk (consider nasogastric tube and endotracheal intubation)

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

Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administering activated charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; protect airway in patients with depressed level of consciousness; if using multiple doses of charcoal, monitor for presence of bowel sounds to minimize risk of charcoal ileus and vomiting with subsequent pulmonary aspiration

Pharmacologic antidotes

Prevents seizure recurrence and terminates clinical and electrical seizure activity. May be used in conjunction with benzodiazepines.

Pyridoxine (Nestrex)

Involved in synthesis of GABA within CNS. Administer with benzodiazepines.

Dosing

Adult

25 mg/kg IV over 15-30 min to 5 g IV initial; may be repeated for recurring seizures; not to exceed 15-20 g/d

Pediatric

25 mg/kg IV over 15-30 min to 5 g IV initial; initial doses of >70 mg/kg may be associated with greater toxicity

Interactions

May decrease levodopa, phenytoin, and phenobarbital serum levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

>200 mg/d may precipitate withdrawal effects when medication is discontinued; risk of peripheral neuropathy increases with increasing dose; ataxia, incoordination, and seizures reported

Benzodiazepines

Prevents seizure recurrence and terminates clinical and electrical seizure activity. May be used in conjunction with pyridoxine (vitamin B-6).

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Dosing

Adult

5-10 mg IV q10-15min until symptoms resolve; not to exceed 30 mg

Pediatric

30 days to 5 years: 0.2-0.5 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 5 mg
>5 years: 1 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 10 mg

Interactions

Increased CNS depression if coadministered with phenothiazines, barbiturates, alcohols, or other sedative medications

Contraindications

Documented hypersensitivity; hypotension; acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Even though classified as Category D in pregnancy, remains DOC along with pyridoxine for initial treatment of status seizures in this specific case; caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); intubation may be necessary

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. May depress all levels of CNS, including limbic and reticular formation, by increasing action of GABA, which is a major inhibitory neurotransmitter in the brain. Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Dosing

Adult

2-8 mg slow IVP; not to exceed 2 mg/min; may repeat prn

Pediatric

0.05-0.1 mg/kg IV over 1-2 min; may repeat prn

Interactions

Increased CNS depression when used with alcohol, phenothiazines, or barbiturates

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

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; intubation may be necessary

Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

Dosing

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, not to exceed 10 mg) IV given slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg followed by continuous infusion of 1 mcg/kg/min, titrating dose upward q5min until seizures controlled

Interactions

Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when using together

Contraindications

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and in patients >60 y; monitor for respiratory depression with high or repeated doses; consider lower dosages in patients with organic brain syndrome and those who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Methemoglobin treatments

In reduced form, leukomethylene blue is an electron donor to reduce methemoglobin. Reduction of methylene blue is by NADPH generated by G-6-PD.

Methylene blue (Urolene blue)

Used to convert ferrous iron of reduced hemoglobin to ferric form that is the basis for antidotal action.

Dosing

Adult

1-2 mg/kg (0.1-0.2 mL/kg of 1% solution) IV over 5 min; may repeat q4h prn; not to exceed 7 mg/kg total IV dose

Pediatric

1-2 mg/kg IV over 5 min; not to exceed 7 mg/kg total IV dose

Interactions

None reported

Contraindications

Documented hypersensitivity; renal insufficiency

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

Can cause profound hemolytic anemia in G-6-PD deficiency; do not inject into CNS; high doses can induce methemoglobinemia; IV infiltration can cause tissue necrosis

Follow-up

Further Inpatient Care

• Admit all symptomatic patients in whom gyromitrin poisoning is suspected for further management and monitoring.
• Monitor patients for dehydration, neurologic toxicity, and liver or renal failure.

Further Outpatient Care

• Patients with gyromitrin ingestion who seek medical care, are asymptomatic 8 hours after ingestion, and are without clinical or laboratory signs of toxicity may be considered for discharge.
  • Early follow-up care for reevaluation must be in place at the time of discharge. Instruct patients to return immediately if they become symptomatic.
  • Instruct patients to keep themselves well hydrated.

Transfer

• Consider patients who have developed seizures, coma, severe methemoglobinemia, or hemolysis for intensive care unit admission.

Complications

• Aspiration pneumonia
• Rhabdomyolysis
• Renal failure secondary to hemolysis and rhabdomyolysis
• Liver failure
• Anoxic and hepatic encephalopathy

Prognosis

• Most patients fully recover after 2-5 days of a gastric illness.
• Death from Gyromitra species is rare in North America.

Patient Education

• Inform patients that Gyromitra mushrooms are toxic and potentially lethal.
• For excellent patient education resources, visit eMedicine's Poisoning Center and Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Activated Charcoal.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider diagnosis
• Failure to elicit history
• Assuming that everyone who ingests mushrooms becomes ill or suffers same severity of illness
• Discharging asymptomatic patients prematurely or without good follow-up instructions and planned follow-up care
• Failure to consider ingestion of several species of mushrooms, including more toxic species (eg, Amanita phalloides), when patient presents within hours of mushroom ingestion

References

1. Watson WA, Litovitz TL, Rodgers GC, et al. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2005;23(5):589-666. [Medline].

2. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline].

3. Watson WA, Litovitz TL, Rodgers GC, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2003;21(5):353-421. [Medline].

4. Litovitz TL, Klein-Schwartz W, Rodgers GC, et al. 2001 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2002;20(5):391-452. [Medline].

5. Litovitz TL, Klein-Schwartz W, White S, et al. 2000 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2001;19(5):337-95. [Medline].

6. Litovitz TL, Klein-Schwartz W, White S, et al. 1999 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2000;18(5):517-74. [Medline].

7. Litovitz TL, Klein-Schwartz W, Caravati EM, et al. 1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1999;17(5):435-87. [Medline].

8. Litovitz TL, Klein-Schwartz W, Dyer KS, et al. 1997 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1998;16(5):443-97. [Medline].

9. Litovitz TL, Smilkstein M, Felberg L, et al. 1996 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1997;15(5):447-500. [Medline].

10. Hoppe-Roberts JM, Lloyd LM, Chyka PA. Poisoning mortality in the United States: comparison of national mortality statistics and poison control center reports. Ann Emerg Med. May 2000;35(5):440-8. [Medline].

11. Braun R, Greeff U, Netter KJ. Liver injury by the false morel poison gyromitrin. Toxicology. Feb 1979;12(2):155-63. [Medline].

12. Brent J, Kulig K. Mushrooms. In: Haddad LM, et al, eds. Clinical Management of Poisoning and Drug Overdose. 3^rd ed. WB Saunders; 1998:365-74.

13. Karlson-Stiber C, Persson H. Cytotoxic fungi--an overview. Toxicon. Sep 15 2003;42(4):339-49. [Medline].

14. Leathem AM, Dorran TJ. Poisoning due to raw Gyromitra esculenta (false morels) west of the Rockies. CJEM. Mar 2007;9(2):127-30. [Medline].

15. Michelot D, Toth B. Poisoning by Gyromitra esculenta--a review. J Appl Toxicol. Aug 1991;11(4):235-43. [Medline].

16. Schneider A, Attaran M, Meier PN, Strassburg C, Manns MP, Ott M. Hepatocyte transplantation in an acute liver failure due to mushroom poisoning. Transplantation. Oct 27 2006;82(8):1115-6. [Medline].

17. Trestrail JH. Monomethylhydrazine-containing mushrooms. In: Spoerke DG, Rumack BH, eds. Handbook of Mushroom Poisoning: Diagnosis and Treatment. CRC Press LLC; 1994:279-87.

18. Yildirim C, Bayraktaroglu Z, Gunay N, Bozkurt S, Köse A, Yilmaz M. The use of therapeutic plasmapheresis in the treatment of poisoned and snake bite victims: an academic emergency department's experiences. J Clin Apher. Dec 2006;21(4):219-23. [Medline].

Keywords

mushroom poisoning, false morel mushrooms, Gyromitra esculenta, Gyromitra ambigua, Gyromitra infula, mushroom toxicity, gyromitra toxin, gyromitra poisoning, hydrazones, N -methyl-N-formylhydrazone, mushroom exposure, gyromitrin-containing mushrooms, poisonous mushrooms

Contributor Information and Disclosures

Author

Reed Brozen, MD, Director of Air Transport, Associate Professor, Department of Emergency Medicine, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center
Reed Brozen, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, New Hampshire Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Marcus J Hampers, MD, MBA, Instructor, Department of Medicine, Dartmouth Medical School; Consulting Staff, Department of Internal Medicine, Section of Hospital Medicine, Department of Anesthesiology, Section of Critical Care Medicine, and Department of Emergency Medicine, Dartmouth Hitchcock Medical Center
Marcus J Hampers, MD, MBA is a member of the following medical societies: American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Medical Association, New Hampshire Medical Society, Society of Critical Care Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Medical Editor

B Zane Horowitz, MD, FACMT, Professor, Fellowship Director, Department of Emergency Medicine, Oregon Health and Sciences University; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System
B Zane Horowitz, MD, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Michael Hodgman, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare
Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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