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Toxicity, Monoamine Oxidase Inhibitor

Updated: Sep 22, 2009

Introduction

Background

Neurotransmitters are generally monoamines. They are "manufactured," stored in vesicles in the nerve terminals, and then released through the plasma membrane into the synaptic cleft. When released into the synaptic space, neurotransmitters are either reabsorbed into the proximal nerve and metabolized by monoamine oxidase (MAO) or destroyed by catechol-o-methyl transferase (COMT) in the synaptic cleft. It is hypothesized that clinical depression is related to decreases in concentration of the neurotransmitters. For this reason, pharmaceutical research has produced drugs that can either block the reuptake of neurotransmitters (eg, cyclic antidepressants, newer selective serotonin reuptake inhibitors) or interfere with the breakdown of the reabsorbed monoamines within the nerve terminal (monoamine oxidase inhibitors [MAOIs]).¹

The 2 types of MAO are MAO-A and MAO-B. MAO-A is found primarily in the liver and gastrointestinal tract with some found in the monoaminergic neurons. MAO-A present in the liver is involved in the elimination of ingested monoamines such as dietary tyramine. Circulating monoamines, such as epinephrine, norepinephrine, and dopamine, are inactivated when they pass through a liver rich in MAO-A. MAO-B, on the other hand, is found primarily in the brain and in platelets.

The older MAOIs, such as phenelzine (Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate), are considered nonselective inhibitors, while the newer MAOIs tend to be more specific inhibitors of either MAO-A or MAO-B. However, the selectivity is primarily dose related. Additionally, the older MAOIs bind irreversibly to the enzyme, while the newer products are bound reversibly in a competitive equilibrium.

Pathophysiology

Monoamine oxidase is responsible for the deactivation of active monoamines such as epinephrine, norepinephrine, dopamine, and serotonin. Such oxidases are present in a wide variety of body tissues. They control the concentration of monoamines in the nerve terminal.

Two categories of MAOs exist: MAO-A and MAO-B. MAOIs are said to be specific for the two types, but such specificity seems to be somewhat dose dependent.

The widely prescribed monoamine oxidase inhibitors (MAOIs) are rather unique in the fact that they bind irreversibly (moclobemide [Aurorix, Manerix] is an exception, since it is a reversible inhibitor) at their sites of action, are eliminated from circulation by such binding and, since they do not recirculate after such binding, their effects are not, strictly speaking, related to their blood levels. Additionally, MAOs are located in many tissues, including the gut wall. MAOIs absorbed through the gastrointestinal tract bind significantly to MAO in the gut mucosa and liver producing significant first pass effect.

To be effective in the CNS, their location of clinically significant effect, they must be given in high enough concentration to reach plasma levels and thus brain levels, sufficient to produce binding centrally to MAO. MAO-A in the gut acts as a barrier to the absorption of tyramine, and thus ingestion of substances containing tyramine may produce significant toxicity.

Recently, a transdermal preparation of a "selective" MAO-B drug, selegiline, has appeared on the market, which by by-passing the first pass effect of gut and hepatic MAOI effects, appears to produce antidepressant effects with significantly reduced risk for dietary-induced toxicity.^2,3

MAOI poisoning is classified into the following 3 subtypes:

Actual poisoning from an overdose (uncommon)
Drug-food interaction
Drug-drug interaction

The symptoms and signs of all 3 categories are quite similar and represent the effects of excessive catecholamine neurotransmitters. MAOIs inhibit breakdown of the neurotransmitters norepinephrine, dopamine, and serotonin, resulting in hypertension, tachycardia, tremors, seizures, and hyperthermia.

Remembering that symptomatology of intentional overdose may be delayed for 6-12 hours post ingestion is extremely important. These patients require prolonged close monitoring to prevent significant morbidity.

Frequency

United States

In 2003, the American Association of Poison Control Centers' Toxic Exposure Surveillance System (AAPCC-TESS) reported 285 MAOI exposures in the United States.⁴ This is compared with 463 MAOI exposures in 1997, which was an increase from the 451 exposures reported in 1996 but a significant drop compared with the 618 cases reported in 1990.^5,6,7

Of the toxic exposures reported in 2003, 32 occurred in children younger than 6 years and 244 occurred in those older than 19 years. The data from 2003 also showed that 157 of the toxic exposures were unintentional and 74 were intentional. In 2003, of those who ingested MAOIs, 2 died and 20 had severe clinical manifestations.⁴

In 2005, the same database reported 275 exposures with 2 deaths. Thus, the rate of exposures seems to be steady.⁸

In 2007, 302 exposures were reported to the AAPCC's new National Poison Data System.⁹

Mortality/Morbidity

Severe toxicity is manifested by hyperthermia, seizures, respiratory depression, and CNS depression. Hypotension, cardiovascular collapse, and death may ensue.

Race

No scientific data have found that outcomes of toxic MAOI exposure are dependent on race.

Sex

No scientific data have found that outcomes of toxic MAOI exposure are dependent on sex.

Clinical

History

The monoamine oxidase inhibitor (MAOI) agents currently available in the United States include phenelzine sulfate (Nardil), tranylcypromine sulfate (Parnate), isocarboxazid (Marplan), and selegiline (Eldepryl [specific for the MAO-B enzyme]), all of which irreversibly bind to MAO. Reversible inhibitors of MAO are available in Europe (eg, brofaromine, cimoxatone, clorgyline, lazabemide, moclobemide). Substances, such as St. John's wort, that may have MAOI-like activity are frequently used for self-treatment of depression.

According to recent reviews of the experience with one of the newer selective MAOIs, moclobemide (Aurorix, Manerix), little is expected in the way of symptoms and signs from a simple overdose, except in the circumstance of the co-ingestion of another serotonin-active substance.

For food and drug interactions, the history must include a careful search for potential offending agents, including over-the-counter preparations.

Often, a significant lag or so-called latent period occurs between exposure and manifestation of clinical effects. Often, the initial effects are that of progressively severe catecholamine excess, hyperthermia, tachycardia, sweating, hypertension, and agitation followed after a lag of many hours with hypotension, seizures, and coma.

Ingestion of an MAOI can induce a complex array of hypermetabolic signs that include the following:
- Fever
- Tachycardia
- Generalized muscle rigidity
- Tachypnea
- Metabolic acidosis
- Hypoxemia
- Hypercapnia
Acute overdose usually does not produce a hypertensive crisis unless the patient provokes the interaction.
Early mild symptoms
- Irritability
- Anxiety
- Flushing
- Sweating
Moderate symptoms
- Anxiousness
- Restlessness
- Fever
Severe symptoms
- Severe fever
- Seizures
- Sleepiness

Physical

Monoamine oxidase inhibitor (MAOI) overdoses or interactions present with excessive catecholamine stimulation toxidromes. Late in the course, the patient may become hypotensive and comatose. Symptoms can be classified into mild, moderate, and severe.

A peculiar nystagmus has been reported in cases of overdose. Rapid jerking movement of the eyes as if watching a tennis or ping pong match termed "ping pong gaze"¹⁰ has been reported in severe MAOI intoxication.

Mild symptoms
- Agitation
- Confusion
- Flushing
- Diaphoresis
Moderate symptoms
- Altered mental status
- Fever
- Diplopia
- Hypertension
- Tachycardia
- Tachypnea
Severe symptoms
- Severe hyperpyrexia
- Seizures
- CNS depression
- Coma
- Cardiorespiratory depression
- Malignant hyperthermia
- Muscle rigidity

Causes

Monoamine oxidase inhibitors (MAOIs) may have drug interactions with serotonin reuptake inhibitors, several analgesics (particularly meperidine [Demerol]), and tyramine-containing foods. Any drug that releases catecholamines may precipitate life-threatening events in individuals also using MAOIs.

Tyramine-containing foods
- Aged cheeses
- Aged, pickled, or smoked meats (eg, salami)
- Yeast extracts
- Beer (dark more than light, on tap more than in bottles because tyramine is adsorbed to glass)
- Red wine more than white wine
- Avocado
- Sauerkraut
Potential drug interactions
- Meperidine
- Dextromethorphan
- Selective serotonin reuptake inhibitors (SSRIs) – Fluoxetine, paroxetine
- Sertraline
- Sumatriptan
- All serotonergic agents
- Linezolid, an antibiotic used to treat certain drug-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA), has been determined to be a reversible, nonselective MAOI and has been implicated in acute serotonin syndrome, so it may be a risk.¹¹

Differential Diagnoses

Acute Respiratory Distress Syndrome	Toxicity, Cocaine
Hypertensive Emergencies	Toxicity, Methamphetamine
Hyperthyroidism, Thyroid Storm, and Graves Disease	Toxicity, Monoamine Oxidase Inhibitor
Neuroleptic Malignant Syndrome	Withdrawal Syndromes
Toxicity, Amphetamine
Toxicity, Anticholinergic
Toxicity, Antidepressant

Workup

Laboratory Studies

Standard laboratory tests for poisoned patients are indicated if the patient has significant symptoms.
Quantitative levels of MAOIs are not clinically useful.
Electrolytes with lactic acid to evaluate for acidosis due to hypoperfusion
Toxicology screens are primarily useful in ruling out other toxins.
- Acetaminophen level should be ordered in every patient with intentional overdose.
Obtain pregnancy tests in women of childbearing age.

Treatment

Prehospital Care

Stabilization of vital signs
- IV fluids
Treatment of seizure activity
- Benzodiazepines
Attention to airway maintenance
Attention to temperature control

Emergency Department Care

Decontamination
- Because of the potential for severe toxicity and lack of antidotes, an aggressive decontamination is very important.
- Consider gastric lavage, particularly in patients with recent ingestion (within an hour).
- Administer charcoal: Secure unprotected airway prior to lavage and charcoal administration if needed.
If the patient is hyperthermic, rapidly (within 20-30 min) decreasing the temperature is imperative.
- Antipyretics and use of a cooling blanket are generally inadequate.
- The best methods for cooling patients include increasing evaporative losses by wetting their skin with warm water and maintaining airflow over them with fans.
- Removing the patient's clothing and exposing the patient to room air may help. In extreme cases, packing the individual in ice or in a bath of ice water may prove life saving.
Fluid therapy is of paramount importance. Patients may be significantly dehydrated from hyperthermia.
Treating the associated hypertension is usually not necessary.
- It may actually be dangerous because of the eventual hypotensive phase (avoid beta-blockers because they leave unopposed alpha-stimulation), which may exacerbate the clinical picture.
- If antihypertensive therapy is deemed necessary, use of a short-acting antihypertensive agent, such as nitroprusside, is advisable.
Intravenous benzodiazepines are useful for agitation and seizure control; they also may help control the hypertension.

Consultations

Consult the regional poison control center or a local medical toxicologist (certified through the American Board of Medical Toxicology and/or the American Board of Emergency Medicine) to obtain additional information and patient care recommendations.
Critical care management may be required for cardiovascular complications.

Medication

Pharmaceutical agents should be used after the patient is adequately hydrated. Choose medications that have a short half-life and are easily titratable because of the rapid changes in cardiovascular status that may occur from a toxic exposure to the MAOIs, or from a drug-drug, or drug-food interaction.

GI decontaminants

Useful for limiting systemic burden of the ingested substance, especially if administered within 1-4 h 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.
Alternate use of cathartic and monitor for active bowel sounds.

Dosing

Adult

1 g/kg PO; may repeat in 2-4 h at one-half original dose

Pediatric

1 g/kg PO (typical 12.5-25 g)
<2 years: Cathartic not recommended

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 adsorption)

Contraindications

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

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 giving 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 dose charcoal, monitor for presence of bowel sounds to minimize risk of charcoal ileus and vomiting with subsequent pulmonary aspiration

Cardiovascular agents

Used to lower blood pressure during hypertensive crisis.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher doses, may exacerbate myocardial ischemia by increasing the heart rate.

Dosing

Adult

0.1-8 mcg/kg/min IV; titrate to effect

Pediatric

Administer as in adults

Interactions

Aspirin and indomethacin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary); concurrent use with DHE may increase toxicity of both agents

Contraindications

Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter; sildenafil (Viagra) use in previous 24 h

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

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; monitor for thiocyanate and cyanide if used for >24 h; risk of cyanide toxicity is increased with infusions >2 mcg/kg/min; has ability to lower blood pressure and, thus, should be used only in patients with mean arterial pressures >70 mm Hg; not first-line in pregnancy unless hypertensive emergency

Nitroglycerin (Deponit, Nitrostat)

Relaxes vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production, resulting in a decreased blood pressure.
May administer bolus of 12.5-25 mcg before continuous infusion.
Initial infusion rate of 10-20 mcg/min may be increased 5-10 mcg/min, q5-10min until desired clinical or hemodynamic response is achieved.
Infusion rates of 500 mcg/min have occasionally been required.

Dosing

Adult

400 mcg SL or 5 mcg/min IV; titrate to effect

Pediatric

Not established

Interactions

Contraindications

Documented hypersensitivity; severe anemia, hypovolemia, constrictive pericarditis or pericardial effusion, hypertrophic cardiomyopathy, shock, postural hypotension, head trauma, closed-angle glaucoma, cerebral hemorrhage, and sildenafil (Viagra) use in previous 24 h

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

Caution in coronary artery disease, low systolic blood pressure, glaucoma, hepatic disease, and hyperthyroidism

Benzodiazepines

Useful to control agitation and for treatment of drug-induced seizures.

Diazepam (Valium)

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

Dosing

Adult

2-5 mg IV/IM q15-20min; not to exceed 30 mg

Pediatric

0.1-0.3 mg/kg IV/IM

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of ethanol, phenothiazines, barbiturates, alcohols, and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

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

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); monitor for respiratory depression with high doses

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.
By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.

Dosing

Adult

0.044 mg/kg (2-4 mg) IV; titrate to effect
Status epilepticus: 4 mg IV over 2-5 min; may repeat second dose in 10-15 min if needed; not to exceed 8 mg

Pediatric

Infants and children: 0.02-0.1 mg/kg IV slowly over 2-5 min; repeat in 10-15 min at 0.05 mg/kg prn; not to exceed 4 mg/dose
Adolescents: 0.7 mg/kg IV slowly over 2-5 min; repeat in 10-15 min at 0.05 mg/kg prn; not to exceed 4 mg/dose

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with ethanol, phenothiazines, barbiturates, and MAOIs

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and 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; monitor for respiratory depression with high or repeated doses; contains benzyl alcohol, which may be toxic to infants in high doses

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, up to 10 mg) IV 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, and 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 patients >60 y; monitor for respiratory depression with high or repeated doses; consider lower dosages in organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Follow-up

Further Inpatient Care

Maintain vigilance regarding recrudescence of fever and fluid requirements.
Because toxicity may be delayed in onset of overdose, admit the patient and observe in a monitored setting.

Prognosis

Patients should recover without sequelae if no adverse reactions occur, such as renal failure, stroke, or refractory hypotension.

Patient Education

All patients medicated with MAOIs should receive extensive education regarding drug and food interaction problems. Encourage them to have all of their prescriptive and nonprescriptive drugs dispensed from one pharmacy so that an accurate medication profile can be maintained.

Miscellaneous

Medicolegal Pitfalls

Failure to recognize toxicity, particularly the potential for drug/drug interaction
Failure to early and aggressively decontaminate the patient with monoamine oxidase inhibitor (MAOI) exposure
Failure to admit and observe patients with MAOI overdose
Administering contraindicated drugs, especially meperidine, to patients taking MAOIs

References

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Preskorn SH. Why the transdermal delivery of selegiline (6 mg/24 hr) obviates the need for a dietary restriction on tyramine. J Psychiatr Pract. May 2006;12(3):168-72. [Medline].
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Keywords

monoamine oxidase inhibitor toxicity, monoamine oxidase inhibitor poisoning, antidepressant overdose, MAOI, MAO, MAO-A, MAO-B, MAOI poisoning, phenelzine sulfate, Nardil, tranylcypromine sulfate, Parnate, isocarboxazid, Marplan, selegiline, serotonin reuptake inhibitors, analgesics, tyramine-containing foods, catecholamines, excessive catecholamine neurotransmitters, MAOI overdose

Contributor Information and Disclosures

Author

Steven Marcus, MD, Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital, University of Medicine and Dentistry of New Jersey; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center
Steven Marcus, MD is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Clinical Toxicology, American Academy of Pediatrics, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Medical Editor

Richard Lavely, MD, JD, MS, MPH, Lecturer in Health Policy and Administration, Department of Public Health, Yale University School of Medicine
Richard Lavely, MD, JD, MS, MPH is a member of the following medical societies: American College of Emergency Physicians, American College of Legal Medicine, and American Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Chair, Department of Emergency Medicine, Director of Medical Toxicology - Allegheny General Hospital, Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
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, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

Further Reading