Methamphetamine Toxicity


Practice Essentials

Methamphetamine is a highly addictive psychostimulant drug that is chemically related to amphetamine. Methamphetamine can produce euphoria and stimulant effects like those from other stimulants such as cocaine. In addition, methamphetamine is easily synthesized from inexpensive and readily obtainable chemicals. Those qualities have led to the widespread and rampant abuse of this dangerous drug.

Methamphetamine use has increased rapidly throughout the world, with more than 30 million users worldwide.[1] Over the past decade, all regions of the United States experienced a significant increase in the number of persons using the drug, and a corresponding increase in the number of patients with medical complications seen in emergency departments (EDs).[1, 2]  Fortunately, this trend seems to have reached a plateau in some areas, with the National Institute on Drug Abuse reporting that  from 2015 to 2016, methamphetamine use in the past year by those 12 years of age and older decreased from 0.6% to 0.5% of the population.[3]  

Methamphetamine is available in powder and crystalline forms. It may be taken orally or intravenously, or be snorted or smoked. The smokable form of methamphetamine (“ice”) produces an immediate euphoria similar to that of crack cocaine, but the effects may last much longer.[4, 5]

Inadvertent absorption of methamphetamine may occur in “body packers”, who swallow packages of the drug for transportation purposes, or “body stuffers”, who insert bags of methamphetamine rectally or vaginally in an attempt to elude drug enforcement. There are also users who indulge in "parachuting", in which the drug is loosely wrapped to delay absorption and prolong effect. These persons, and body stuffers, are at high risk for toxicity as the drug wrapping may be compromised and allow complete drug absorption.[6]

North American methamphetamine abusers are predominantly white males in their 30s and 40s.[7, 8] Epidemic abuse has been described in adolescents; they cite availability, low cost, and a longer duration of action than cocaine as reasons for their drug preference.[9]

Most cases of methamphetamine toxicity can be managed supportively. In severe overdoses, termination of methamphetamine-induced seizure activity and arrhythmias are of immediate importance. Correction of hypertension, hypotension, hyperthermia, metabolic and electrolyte abnormalities, and control of severe psychiatric agitation are indicated. See Treatment and Medication.


The medical history of amphetamine-like compounds extends back nearly 100 years.[4, 5] A Japanese pharmacologist first synthesized methamphetamine in 1919. A more detailed analysis of the pharmacology of amphetamine derived from the basic phenylethylamine structure was reported in 1930. In the 1930s, amphetamine was introduced in the form of inhalers for rhinitis and asthma treatment. The stimulant, euphoric, and anorectic effects of amphetamine were quickly recognized, leading to its abuse.

In 1937, a report that amphetamine enhanced intellectual performance and wakefulness further contributed to its popularity. Amphetamines were used extensively by Allied and Axis armed forces during World War II and during the recent Iraq and Afghanistan conflicts to increase wakefulness and attention.[4, 10]

In the late 1950s, initial federal controls were enacted; however, in spite of additional regulation and increased enforcement, amphetamines continued to be used by students, athletes, shift workers, long haul drivers, and for weight loss.[4, 5] The Controlled Substance Act of 1970 stringently regulated the manufacture of amphetamine.


Amphetamines stimulate the central nervous system (CNS), which results in clinical effects that include the following[4, 11] :

In the CNS, amphetamines block presynaptic reuptake of catecholamines (ie, dopamine, norepinephrine), causing hyperstimulation at selected postsynaptic neuron receptors. Indirect sympathomimetic effects result from blockade of presynaptic vesicular storage and by reduction in cytoplasmic destruction of catecholamines by inhibition of mitochondrial monoamine oxidase.[12, 13]

Indirectly, these hyperstimulated neurons can stimulate various other noncatecholaminergic central and peripheral nervous pathways. Changes in mood, excitation, motor movements, sensory perception, and appetite appear to be mediated more directly by CNS dopaminergic alterations. It has been postulated that serotonin alterations also contribute to mood changes, psychotic behavior, and aggressiveness.[14]

Long-term exposure to methamphetamine results in significant down-regulation of both presynaptic and postsynaptic aspects of the dopamine system in the striatum. Dysregulation of the dopamine system has been proposed as a mechanism of addiction.[15]  Oxidative stress and neuroinflammation appear to play a role in the psychosis and cognitive deficits induced by repeated low doses of methamphetamine.[16]

In humans, the half-life of methamphetamine ranges from 10-20 hours, depending on the urine pH, history of recent use, and dosage.[12] Metabolism occurs faster in acidic urine. Methamphetamine has greater CNS effects compared with D-amphetamine of equal milligram quantity. The majority of methamphetamine is metabolized to amphetamine, which provides further CNS stimulation.

Methamphetamine is absorbed readily from the gut, airway, nasopharynx, muscle, placenta, and vagina.[17, 18] Peak plasma levels are observed approximately 30 minutes after intravenous or intramuscular routes and 2-3 hours after ingestion.[13] Rapid tissue redistribution occurs with steady-state cerebrospinal fluid levels at 80% of plasma levels. Hepatic conjugation pathways with glucuronide and glycine addition result in inactivation and urinary excretion of metabolites.

When methamphetamine is used with ethanol, increased psychological and cardiac effects are observed.[19] This is presumed to be the result of pharmacodynamic rather than pharmacokinetic interactions. Similarly, the increased toxicity of concomitant opioids and amphetamines ("speedballing"), appear to result from pharmacodynamic interactions.

The euphoric effects produced by methamphetamine, cocaine, and various designer amphetamines are similar and may be difficult to clinically differentiate.[5] A distinguishing clinical feature is the longer pharmacokinetic and pharmacodynamic half-life of methamphetamine, which may be as much as 10 times longer than that of cocaine. Because of the variability in quality and concentration of illicitly purchased methamphetamines, the clinical observation of toxic effects is more relevant than estimated total ingested dose.[20]



United States

Methamphetamine use is widespread in the United States but varies regionally, with higher use in Hawaii, the West, and parts of the Midwest.[21] The Drug Abuse Warning Network estimates that methamphetamine was involved in 102,961 emergency department visits in 2011.[2]

According to the 2016 National Survey on Drug Use and Health (NSDUH), approximately 667,000 people were current methamphetamine users. Approximate numbers of users by age group and percentages of that age group were as follows[22] :


 The United Nations Office on Drugs and Crime estimates that worldwide in 2015 there were 37 million users of amphetamine-type stimulants, which includes methamphetamine. Methamphetamine is a feature of amphetamine-type stimulant markets worldwide, but is particularly dominant in East and Southeast Asia and North America  In East and Southeast Asia, the market for both tablet and crystalline methamphetamine is large and growing.[1]

An Australian study that used liquid chromatography–mass spectrometry to analyze wastewater (an increasingly popular method for monitoring trends of illicit drug use) reported that from 2009-2015, methamphetamine consumption increased fivefold. In the study, which involved wastewater from wastewater treatment plants in South East Queensland, methamphetamine residues were consistently detected in both urban and rural catchments.[23]


Acute methamphetamine overdose may result in sympathetic overdrive, intracranial hemorrhage,[24] cardiovascular collapse, rhabdomyolysis, ventricular tachyarrhythmia, and death. Injuries from blunt and penetrating trauma are common.[4, 11, 25, 26]

Long-term methamphetamine use may result in the following[27] :

In a study of 590 patients between 18 and 50 years old with cardiomyopathy or heart failure who were seen at a single medical center from 2008-2012, the 223 patients with a history of methamphetamine use were more likely to have a moderately or severely reduced ejection fraction ≤40%). In addition, male patients were more likely to have worse left ventricular systolic dysfunction.[28]

Methamphetamine abuse has severe adverse effects on oral health, colloquially termed "meth mouth". As a result of its sympathomimetic effects, methamphetamine results in significantly reduced saliva production and pH, and increased bruxism. Consequently, long-term abusers are at increased risk for caries, dental erosion, periodontal lesions, and temporomandibular joint pain.[29]

Use of methamphetamine during pregnancy has been associated with intrauterine growth restriction and preterm birth. Neonates have an increased incidence of poor cardiorespiratory adaptation, cardiac defects, and floppy muscle tone.[30]  Prenatal exposure may have a long-term impact on cognitive skills that becomes more pronounced with age.[31]

Race-, Sex-, and Age-related Demographics

Demographic variations include the following[7, 8] :


Cardiovascular signs and symptoms of methamphetamine use are as follows[32, 33, 34, 35, 36, 37] :

Central nervous system manifestations of methamphetamine use are as follows[38, 39, 40, 41] :

Respiratory manifestations of methamphetamine use are as follows[42, 43, 44] :

Skin manifestations of methamphetamine use are as follows[45] :

Gastrointestinal manifestations of methamphetamine use are as follows[17, 46] :

Dental manifestations of methamphetamine use are as follows[47, 48] :


Acute and long-term methamphetamine use may lead to abnormal findings on examination of the following organ systems:

Cardiovascular findings are as follows:

Central nervous system findings are as follows:

Respiratory findings are as follows:

Gastrointestinal findings are as follows:

Renal failure associated with amphetamines has been related to the following[54] :

Skin findings include the following:

On dental examination, severe caries, especially of the maxillary teeth, is commonly seen in chronic methamphetamine users ("meth mouth"). This results from maxillary artery vasoconstriction, xerostomia, and poor hygiene.[47, 48]

Pregnancy and lactation

Methamphetamine use during pregnancy can be fatal to the mother and fetus.[56, 57] Methamphetamine has been shown to cause placental vasoconstriction and interfere with placental monoamine transporters resulting in spontaneous abortion.[58]

Methamphetamine is secreted in breast milk. A case of infant death from ingestion of methamphetamine-toxic breast milk has been reported.[59]


Methamphetamine is a derivative of phenylethylamine. The substances differ structurally in that a methyl group attaches to the terminal nitrogen to form methamphetamine.

Most of the methamphetamine abused in the United States is produced in so-called superlabs, many of which are located in Mexico.[21] However, methamphetamine is relatively easy and inexpensive to synthesize, and small-scale illicit production occurs in home kitchens, workshops, recreational vehicles, and rural cabins.[5, 55, 60] Instructions for synthesis can be found on the Internet and the precursors are not difficult to obtain.

A common method of synthesis begins with ephedrine, which is reduced to methamphetamine using hydriodic acid and red phosphorus. Alternative approaches include using a different acid, a different catalyst, or a substituted ephedrine (eg, chloroephedrine, methylephedrine). The federal government and some states have enacted laws decreasing the availability of necessary precursor chemicals such as ephedrine, but many of these agents can still be obtained in other countries.

The methamphetamine produced by ephedrine reduction is a lipid-soluble pure base form, which is fairly volatile and can evaporate if left exposed to room air temperature. This product is converted to the water-soluble form, methamphetamine hydrochloride (HCl) salt. The manufacture of "ice", the smokable form of methamphetamine, from standard quality methamphetamine HCl is essentially a purification process.

Illicitly synthesized methamphetamine is frequently contaminated by nonstimulant organic or inorganic impurities. Poisoning from heavy metals, such as lead and mercury, or from carcinogenic solvents used in the synthesis process, has been reported.[61, 62] Street methamphetamine may be mixed with other drugs, including cocaine and phencyclidine.

Laboratory Studies

Laboratory studies should be selected on the basis of the patient's symptoms. Although hair and saliva analysis may be obtained, most toxicological monitoring or testing is performed with urine and blood samples. Studies to obtain may include the following:

Imaging Studies

See the list below:

Other Tests

Obtain an electrocardiogram for patients with chest pain, altered mental status, and tachycardia.


Lumbar puncture may be indicated in patients with altered mental status to rule out meningitis or subarachnoid hemorrhage.

Prehospital Care

Patients with acute methamphetamine intoxication may be highly agitated and present a serious safety risk to themselves and prehospital personnel. Seek additional help from police or other emergency medical services (EMS) providers before the patient is transported, if possible.

Patients' mental function may be sufficiently impaired that they are unable to make an informed decision to refuse treatment and transport. Prehospital intravenous access is warranted with or without patient consent, allowing for treatment of seizures and agitation using intravenous sedatives according to medical direction or protocol.

Emergency Department Care

Most cases of methamphetamine toxicity can be managed supportively. In the case of a severe overdose, immediate supportive care, including airway control, oxygenation and ventilation support, and appropriate monitoring is required. Specific treatments for heavy metal toxicity caused by contaminants in some methamphetamine preparations may be needed.

For suspected toxic oral ingestions, polyethylene glycol (PEG) solution should be initiated if possible. Animal studies suggest that orally ingested amphetamine-like compounds can be decontaminated with oral activated charcoal.[64]  In body packers, whole-bowel irrigation can be considered for removal of the ingested packets, although controlled data documenting improvement in clinical outcome with this technique are lacking.[65]

In severe overdoses, termination of methamphetamine-induced seizure activity and arrhythmias are of immediate importance. Correction of hypertension, hypotension, hyperthermia, metabolic and electrolyte abnormalities, and control of severe psychiatric agitation are indicated. Consider health maintenance activities, such as testing for viral hepatitis and HIV disease and rehabilitation follow-up.

Treatment of agitation

Because of the ability of methamphetamine to cause significant central nervous system (CNS) and psychiatric activation, patients who present to emergency departments (EDs) for acute intoxication often require physical restraint and pharmacologic intervention.

Treat hyperactive or agitated patients with droperidol or haloperidol, which are butyrophenones that antagonize CNS dopamine receptors and mitigate the excess dopamine produced from methamphetamine toxicity.[66] These medications should be administered intravenously (IV), with doses titrated to the symptoms (see Medication).

Multiple human and animal studies attest to the efficacy of droperidol and haloperidol in acute methamphetamine toxicity.[67, 68, 52] However, droperidol has been subject to a Black Box warning by the US Food and Drug Administration (FDA), based on concerns of QT prolongation and the potential for torsades de pointes. As a result, some institutions restrict its use. It is important to note that the Black Box warning specifies dementia-related psychosis and is not supported by the literature for doses below 2.5 mg.[69]

Benzodiazepines diminish methamphetamine-induced behavioral and psychiatric intoxication.[66] This class of drug is also used to terminate methamphetamine-induced seizures.[67, 70] However, benzodiazepines may cause respiratory depression and often require repeated dosing to achieve adequate sedation.

In a study of 146 patients presenting to the ED agitated, violent, or psychotic from methamphetamine, droperidol produced more rapid and profound sedation than lorazepam. Both droperidol and lorazepam produced clinically significant reductions in pulse, systolic blood pressure, respiration rate, and temperature over a 60-minute period.[52]

Newer antipsychotics such as olanzapine and risperidone have been used to treat amphetamine psychosis.[71, 72, 73] A study of 58 patients comparing haloperidol to olanzapine demonstrated that both were effective, but olanzapine had fewer adverse side effects such as extrapyramidal symptoms.[71] To date, no large studies in the setting of the ED have been performed.[74]

Dexmedetomidine, a sedative with analgesic, sympatholytic, and anxiolytic effects, has been used to control agitation in several case series involving amphetamine toxicity and may be useful if available in the ED. This drug has an added advantage of causing minimal respiratory depression.[75, 76, 66]

Lipid-soluble beta-blockers (eg, metoprolol), which cross the blood-brain barrier, may also mitigate agitation as well as sympathomimetic symptoms.[77, 66]

After chemical restraint has been successfully implemented, physical restraints should be loosened or removed altogether. If physical and chemical restraint is unsuccessful, rapid sequence induction, paralysis, and intubation may be required in extreme cases.

Treatment of hypertension and tachycardia

If sedation fails to reduce blood pressure, antihypertensive agents such as beta-blockers and vasodilators are effective in reversing methamphetamine-induced hypertension and tachycardia.

With regard to choice of beta-blockers, labetalol is preferred because of combined anti–alpha-adrenergic and anti–beta-adrenergic effects. Labetalol has been shown to safely lower mean arterial pressure in cocaine-positive patients.[78] Carvedilol, which like labetalol is a nonselective beta-blocker with alpha-blocking activity, may also be effective for this indication.[79, 80] Esmolol is advantageous because of its short half-life but must be administered via IV drip. Metoprolol has excellent CNS penetration characteristics and may also ameliorate agitation, as previously mentioned.

These drugs should be given IV in smaller than usual doses and titrated to effect. The concern for "unopposed alpha stimulation," with sudden rise in blood pressure or coronary artery vasoaspasm after beta-blocker therapy, is theoretical and has never been demonstrated in patients with methamphetamine toxicity.[66] An extensive evidence-based systematic review of this topic demonstrated the safety and efficacy of beta-blockers for this indication.[66] At our institution, we routinely use beta-blockers for methamphetamine-induced tachycardia and hypertension with good results.

In rare instances, afterload reduction with agents such as hydralazine, nitroprusside, or fenoldopam may be necessary.[66]

Treatment of acute coronary syndrome

The approach to the patient with methamphetamine-induced cardiac ischemia should be no different than standard of care treatment for acute coronary syndrome (ACS). Nitrates, beta-blockers, aspirin, heparin, and morphine should be administered if indicated.

Based on the latest American College of Cardiology Foundation/American Heart Association guidelines, methamphetamine- and cocaine-using patients with chest pain and suspected ACS should also receive sublingual nitroglycerin if labetalol is used to treat hypertension (systolic blood pressure >150 mm Hg) or sinus tachycardia (pulse >100 beats per min).[81]

Patients with ST-segment elevation should be triaged to thrombolytic treatment and/or catheterization with cardiology consultation.

Treatment of seizures

Treat methamphetamine-induced seizures like other seizures of unknown etiology, as follows:

Treatment of rhabdomyolysis

Suspect rhabdomyolysis and follow creatine kinase (CK) levels in patients who present to the ED with severe agitation from methamphetamine or have had prolonged periods of immobilization. Management of rhabdomyolysis is as follows:


For body-packers, body-stuffers, or "parachuters," consultation with surgery or gastroenterology specialists may be warranted. Consult with a 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. Cardiology, nephrology, and psychiatry consultation may be indicated in certain cases.

Medication Summary

The goals of pharmacotherapy are to reduce the toxic effects of the drug, reduce morbidity, and prevent complications. Treatment measures may include gastrointestinal decontamination, sedation, seizure control, and control of catecholamine-induced hypertension and tachycardia.

Polyethylene glycol (PEG) solution

Clinical Context:  Laxative with strong electrolyte and osmotic effects. Cathartic actions in GI tract. May be indicated in treatment of methamphetamine ingestion in people who carry methamphetamine packages in their body. Must administer after activated charcoal. Liquid reconstituted per package instructions.

Activated charcoal (Liqui-Char)

Clinical Context:  A form of carbon processed to be riddled with small, low-volume pores that increase the surface area available for adsorption or chemical reactions. Due to its high degree of microporosity, one gram of activated charcoal has a surface area in excess of 500 square meters, and further chemical treatment often enhances adsorption properties.

Class Summary

Empirically used to minimize systemic absorption of the toxin.

Lorazepam (Ativan)

Clinical Context:  Benzodiazepine. GABA receptor agonist.

Diazepam (Valium)

Clinical Context:  Benzodiazepine. GABA receptor agonist.

Midazolam (Versed)

Clinical Context:  Benzodiazepine. GABA receptor agonist.

Haloperidol (Haldol)

Clinical Context:  CNS dopamine D2 receptor antagonist.

Droperidol (Inapsine)

Clinical Context:  CNS dopamine D2 receptor antagonist.

Olanzapine (Zyprexa, Zydis)

Clinical Context:  The exact mechanism of action of olanzapine is not known. It binds to alpha-1, dopamine, histamine H-1, muscarinic, and serotonin type 2 (5-HT2) receptors.

Ziprasidone (Geodon)

Clinical Context:  Dopamine and serotonin receptor antagonist. It also inhibits the re-uptake of serotonin and norepinephrine in the CNS.

Class Summary

Neuroleptic agents are CNS dopamine antagonists that are useful for control of agitated patients. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, benzodiazepines depress all levels of CNS, including limbic and reticular formation. Haloperidol and droperidol are D2 receptor antagonists that interfere with dopaminergic neurotransmission in the limbic system and the cerebral cortex.

Labetalol (Normodyne, Trandate)

Clinical Context:  Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure. When given IV, acts primarily as a beta-receptor antagonist.

Metoprolol (Lopressor, Toprol)

Clinical Context:  Blocks beta1-adrenergic receptor sites, decreasing heart rate.

Class Summary

Used to control catecholamine-induced hypertension and tachycardia.

Further Outpatient Care

Referral to a drug treatment center and/or psychiatrist may be indicated. Studies of methamphetamine-dependent patients have found that methamphetamine withdrawal is marked by sleep disruption. Withdrawal symptoms typically resolve over 2 to 3 weeks, and particularly in the first week. Depression typically improves during that time, but anxiety may not.[82, 83]  

To date, phase II trials have yet to identify a pharmacologic agent that is strongly effective in helping patients achieve abstinence from methamphetamine. However, agents with novel therapeutic targets appear promising.[84]

Further Inpatient Care

Critical care management may be needed for patients with any of the following:


Methamphetamine addiction is notoriously difficult to treat successfully, as it is difficult to remove the patient from the subculture involved in the production, distribution, and abuse of the drug.

A study by McKetin et al attempted to evaluate the impact of community-based drug treatment on methamphetamine use. Participants were methamphetamine users entering community-based detoxification (n = 112) or residential rehabilitation (n = 248) services and a quasi-control group of methamphetamine users (n = 101) recruited from the community. Compared to the quasi-control group, detoxification did not reduce methamphetamine use at follow-up. Residential rehabilitation showed some efficacy in reducing methamphetamine use, but the decrease was time-limited.[85]


Complications of methamphetamine use include the following:

Patient Education

For patient education information, see the Mental Health and Behavior Center, and Substance Abuse Center, as well as Drug Dependence & Abuse, Substance Abuse, Club Drugs, and  Poisoning.


What is methamphetamine toxicity?What is the historical background of methamphetamine?What is the pathophysiology of methamphetamine toxicity?What is the prevalence of methamphetamine toxicity in the US?What is the approximate number of methamphetamine users by age group?What is the global prevalence of methamphetamine toxicity?What is the mortality and morbidity in methamphetamine toxicity?What are effects of long-term methamphetamine use?What are severe adverse effects of methamphetamine abuse?What are the demographic predilections in the prevalence of methamphetamine toxicity?What are cardiovascular signs and symptoms of methamphetamine toxicity?What are CNS manifestations of methamphetamine toxicity?What are respiratory symptoms of methamphetamine toxicity?What are cutaneous symptoms of methamphetamine toxicity?What are GI symptoms of methamphetamine toxicity?What are oral symptoms of methamphetamine toxicity?Which organ systems are affected by methamphetamine toxicity?Which cardiovascular findings suggest methamphetamine toxicity?Which CNS findings suggest methamphetamine toxicity?Which respiratory findings suggest methamphetamine toxicity?Which GI findings suggest methamphetamine toxicity?Which renal findings suggest methamphetamine toxicity?Which cutaneous findings suggest methamphetamine toxicity?Which dental findings suggest methamphetamine toxicity?How does methamphetamine toxicity affect pregnancy and lactation?What cause methamphetamine toxicity?What are the differential diagnoses for Methamphetamine Toxicity?What is the role of lab studies in the workup of methamphetamine toxicity?What is the role of imaging studies in the workup of methamphetamine toxicity?What is the role of electrocardiogram in the workup of methamphetamine toxicity?What is the role of lumbar puncture in the workup of methamphetamine toxicity?What is included in prehospital care for methamphetamine toxicity?What is the focus of treatment for methamphetamine toxicity?How is agitation managed in methamphetamine toxicity?What are other modalities used for treatment of agitation in patients affected by methamphetamine toxicity?How are hypertension and tachycardia managed in methamphetamine toxicity?How is acute coronary syndrome (ACS) managed in methamphetamine toxicity?How are seizures managed in methamphetamine toxicity?How is rhabdomyolysis managed in methamphetamine toxicity?Which specialists should be consulted in the treatment of methamphetamine toxicity?What are the goals of drug treatment for methamphetamine toxicity?Which medications in the drug class Cardiovascular Agents are used in the treatment of Methamphetamine Toxicity?Which medications in the drug class Sedatives are used in the treatment of Methamphetamine Toxicity?Which medications in the drug class GI decontaminant are used in the treatment of Methamphetamine Toxicity?What is included in follow-up care for methamphetamine toxicity?When is critical care management indicated in the treatment of methamphetamine toxicity?How is methamphetamine toxicity prevented?What are complications of methamphetamine toxicity?Where can patient education information about methamphetamine toxicity be found?


John R Richards, MD, FAAEM, Professor, Department of Emergency Medicine, University of California, Davis, Medical Center

Disclosure: Nothing to disclose.


Robert W Derlet, MD, Professor of Emergency Medicine, University of California at Davis School of Medicine; Chief Emeritus, Emergency Department, University of California at Davis Health System

Disclosure: Nothing to disclose.

Timothy E Albertson, MD, PhD, MPH, Professor of Pharmacology and Toxicology, Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Chair, Department of Internal Medicine, University of California, Davis, School of Medicine; Professor of Anesthesiology, Professor of Emergency Medicine and Clinical Toxicology, Davis Medical Center; Chief of Pulmonary and Critical Care, Veterans Affairs, Northern California Health Care System; Medical Director of Poison Control System, University of California, San Francisco, School of Pharmacy

Disclosure: Nothing to disclose.

Specialty Editors

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

Disclosure: Nothing to disclose.

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Attending Physician in Emergency Medicine and Medical Toxicology, Excela Health System

Disclosure: Nothing to disclose.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD, Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor - Chief Editor for Medscape.

Additional Contributors

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.

Edward A Michelson, MD, Associate Professor, Program Director, Department of Emergency Medicine, University Hospital Health Systems of Cleveland

Disclosure: Nothing to disclose.


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