Amphetamine Toxicity

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Practice Essentials

Amphetamines are a class of compounds that are abused in many regions of the world, including the United States, Australasia, and Europe. Synthetic amphetamine compounds commonly are produced in clandestine laboratories and vary in purity and potency. Other potentials for amphetamine abuse include prescription medications often used for attention deficit disorder and various over-the-counter diet pills.

Clinical effects of amphetamine abuse are significant and commonly observed in emergency departments (EDs).[1] Hendrickson et al found that about 2.4% of visits at their institution were related to methamphetamine use and generated annual estimated hospital costs of $6.9 million.[2]  Although that rate is probaby much higher than at most institutions, methamphetamine nonetheless remains a major source of morbidity and a driver of cost to the healthcare system. Patients may present with a range of psychiatric and medical problems, including agitation, psychosis, and seizures, in addition to potentially life-threatening cardiac dysrhythmias; see Presentation, Workup, and Treatment.

See also Methamphetamine Toxicity and MDMA Toxicity.

Pathophysiology

Amphetamines are a group of structurally related compounds that produce central nervous system (CNS) and peripheral nervous system (PNS) stimulation. The phenylethylamine structure of amphetamines (see the image below) is similar to catecholaminergic, dopaminergic, and serotonergic agonists (biogenic amines), which may explain their actions.



View Image

Amphetamine and epinephrine.

The degree to which an amphetamine can stimulate the receptors of these biogenic amines depends on the chemical substituents on the amphetamine molecule; thus, the clinical presentation depends on the type of amphetamine used. For example, methamphetamine lacks much of the peripheral stimulant properties of amphetamine while still offering euphoric and hallucinogenic properties. These actions are similar to those of cocaine; however, while effects of cocaine last for 10-20 minutes, duration of amphetamine action is much longer—as long as 10-12 hours.

The routes of amphetamine administration may be oral (ingestion), inhalation (smoke), or injection (intravenous). Oral use is associated with an approximate 1-hour lag time before onset of symptoms, whereas inhaled and intravenous methods yield effects within a few minutes. Peak plasma concentrations occur in 5 minutes with intravenous use, 30 minutes with nasal or intramuscular use, and 2-3 hours postingestion.

Use appears to vary with gender and race. Research has found correlations between personality traits (risk taking and reward sensitivity) and responses to amphetamine use.[3]

Central nervous system

Amphetamine compounds cause a general efflux of biogenic amines from neuronal synaptic terminals (indirect sympathomimetics). They inhibit specific transporters responsible for reuptake of biogenic amines from the synaptic nerve ending and presynaptic vesicles. Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. The net effect is an increase of neurotransmitter release into the synapse. Physiologic adaptation occurs through receptor or coupling down-regulation; this tolerance and an accompanying psychological tolerance[4] can lead to escalating use of the drug and increased toxicity.[5] Long-term use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug—a washout.

Elevated catecholamine levels usually lead to a state of increased arousal and decreased fatigue. Increased dopamine levels at synapses in the CNS may be responsible for movement disorders,[6] schizophrenia, and euphoria. Serotonergic signals may play a role in the hallucinogenic and anorexic aspects of these drugs.

Other serotonergic and dopaminergic effects may include resetting the thermal regulatory circuits upward in the hypothalamus and causing hyperthermia.[7] The hyperthermia produced by amphetamines is similar to that of the serotonin syndrome.

Laboratory studies reveal that amphetamines interfere with the normal control of the neurohumoral (hypothalamopituitary) axis, affecting secretion of such factors as adrenocorticotropic hormone (ACTH). Amphetamines may alter other neural functions such as complex behavioral and learning patternings; this may be important for understanding effects of amphetamine use on the fetus during pregnancy.

Animal studies indicate that amphetamines interact with N-methyl-D-aspartate (NMDA) receptors on serotonergic neurons, leading to neuronal destruction. This interaction may contribute to seizure activity.

In vitro, amphetamines have been found to stimulate regulatory molecules, such as the oncogenes c-fos and ras and cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein. Amphetamines have been found to act on ras-mediated striatal motor control.[8] These proteins are responsible for signaling long-term changes at the transcriptional level.

Cardiovascular

Catecholaminergic (sympathomimetic) effects of amphetamines include inotropic and chronotropic effects on the heart, which can lead to tachycardia and other dysrhythmias. The vasoconstrictive properties of the drugs can lead to hypertension and/or coronary vasospasm.[9]

Serotonergic action of amphetamines on peripheral vasculature can lead to vasoconstriction, which is especially problematic in placental vessels. Animal studies have shown that serotonergic actions of amphetamines effect changes in plasma levels of oxytocin, somatostatin, gastrin, and cholecystokinin.[10]

Long-term use of the drugs can lead to myonecrosis and dilated cardiomyopathy.[11, 12] Amphetamine use is also associated with myocardial infarction[13]

Etiology

Marked tolerance develops after amphetamine use and leads to rapid escalation of drug doses. Increasing the dose produces increasing toxicity and complications from acute and chronic amphetamine use.

Epidemiology

Frequency

United States

Accurate estimation of illicit amphetamine use is difficult. An estimated 13 million Americans use these compounds without medical supervision. Random toxicologic screens performed in the ED indicate amphetamine presence in about 2% of patients. The 2022 Annual Report of the American Association of Poison Control Centers' National Poison Data System noted 9931 single exposures with 1640 moderate outcomes, 140 major outcomes, and one death.[14]

According to National Institute on Drug Abuse estimates for 2020, including prescriptions for attention deficit disorder (ADD) or attention deficit hyperactivity disorder (ADHD), 6% of 8th graders, 5.4% of 10th graders, and 5.3% of 12th graders reported using amphetamines during the past year.[15] Self-reporting among college students indicates an approximate 4% prevalence. An age-matched survey of fourth-year medical students revealed that about 1.2% use amphetamines. It is unclear how many of these uses are of amphetamine-containing prescriptions for attention deficit disorder (ADD) or attention deficit hyperactivity disorder (ADHD). 

International

The United Nations Office on Drugs and Crime (UNODC) estimates that worldwide, there were 36 million users of amphetamines and prescription stimulants in 2021.[16]  According to the UNODC World Drug Report, global confiscations of amphetamines reached a record high in 2019, with 49% of confiscations in the Near and Middle East/South and West Asia. Western and Central Europe accounted for 26% of confiscations.[17]  

Race- and sex-related demographics

Amphetamine use in the US characteristically occurs in single White men aged 20-35 years who are typically unemployed.[18] Data from rural populations reveal that Whites use amphetamines significantly more than Blacks.[19] However, among 12th grade students, the annual prevalence of amphetamine use is highest in Blacks (3%), followed by Hispanics (2%). White 12th grade students had the lowest prevalence, at 1%, but again it is unclear how many of these uses are of amphetamine-containing prescriptions for ADD or ADHD.[15]

According to the National Institute on Drug Abuse, the prevalence of amphetamine use is higher among girls than among boys in 8th grade, but nearly equal by 12th grade. This is thought to be due to higher use in 8th-grade girls to aid in weight loss.[15]

One study suggests that the action of estrogen within the CNS might explain why fewer women than men use amphetamines. Women in their late follicular phase (when estrogen levels are high and progesterone levels are low) were more likely to report "unpleasant stimulation" when exposed to amphetamine. This effect was not observed in the early follicular phase, when both hormone levels are low.[20]

Prognosis

Patients without signs or symptoms of end-organ failure or complications may do well with sedation and reassurance. No established modalities exist for treatment of amphetamine addiction, and most treatment focuses on behavioral aspects. Recently, there has been considerable interest in ketamine-assisted therapy for addiction disorders,[21]  as well as psychedelic-assisted therapy (eg, with psilocybin) for the treatment of methamphetamine use disorder.[22]  However, such modalities are still investigational and not widely available, and there are legal, political, and cultural barriers to conducting scientifically rigorous studies.

Hyperthermia accompanies and complicates significant amphetamine intoxication. Liver damage apparently is linked to elevated body temperature and consumption of reduced glutathione in metabolism of amphetamines. Because amphetamines often are synthesized in poorly controlled settings, individuals with amphetamine intoxication may experience concomitant toxic exposures. Lead, other metals, organic solvents, and precursor molecules all have been found in amphetamine samples and blood of individuals with amphetamine toxicity.

Acute overdose of amphetamines can result in the following:

Habitual amphetamine use produces toxic psychosis resembling paranoid schizophrenia. Hallucinations, delusions, and bizarre violent behavior are common. In a few patients, amphetamine use produces long-term paranoid schizophrenia; whether this results from unmasking underlying disease is unclear. Severe psychological depression and prolonged sleep follow chronic use and binges.

Amphetamine abuse during pregnancy has been linked with adverse outcomes in offspring.[25, 26] However, use of prescribed medication for ADHD during pregnancy appears to be safe.[27]

 

Patient Education

Educate patients on the toxic effects of amphetamines and that amphetamines are not a safe alternative to cocaine use. For patient education information, see the following:

History

Many patients with amphetamine intoxication are identified by a change of mental status alone. In other cases, the mental status change is associated with another injury and/or illness. Trauma often accompanies amphetamine intoxication and should be sought in the evaluation of the patient.

Central nervous system manifestations are as follows:

Cardiovascular manifestations are as follows:

Gastrointestinal manifestations are as follows:

Skin/cutaneous manifestations are as follows:

Genitourinary (GU) manifestations include difficult micturition. Ocular manifestations include mydriasis.

Physical Examination

Physical examination findings may demonstrate the strong central nervous system and peripheral nervous system stimulation produced by amphetamine compounds. Hyperthermia accompanies and complicates significant amphetamine intoxication.[28]  Modification of the basic amphetamine molecule produces compounds with variable effects on target organs. Methamphetamine produces prominent central nervous system effects with minimal cardiovascular stimulation.

Long-term users of intravenous amphetamines are at risk of infection and vascular injury.

General findings are as follows:

Cardiovascular findings are as follows:

Central nervous system findings are as follows:

Cutaneous findings are as follows:

Other organ system findings are as follows:

Laboratory Studies

Patients with amphetamine intoxication who present with no life-threatening signs or symptoms may be treated with sedation and observation and may require no laboratory workup.

Patients who are experiencing seizures or prolonged mental status changes require rapid serum glucose determination (eg, fingerstick) and sometimes other testing, such as electrolyte assays.

Patients with suicidal ideations may need additional testing, such as measurement of serum acetaminophen levels.

In patients with significant or prolonged hyperthermia, additional testing includes evaluating kidney and liver function, and for potential infectious causes. When appropriate, evaluation may also include the following:

Because hyperthermia may induce disseminated intravascular coagulation (DIC), monitor for DIC and treat appropriately if it occurs.

Obtain urine and serum creatinine kinase levels to monitor for rhabdomyolysis. If the dipstick result is positive for blood but shows few or no red blood cells on microscopic examination, rhabdomyolysis may be present.

Urine specimens for drug and toxicologic screens may be collected after Foley catheter placement if the physician believes that these tests will help guide therapy.

Usually, the presence of a pure sympathomimetic toxidrome precludes the need for drug screening. However, with methamphetamine and other designer amphetamines, significant peripheral effects may not be observed.

Imaging Studies

Patients who are demonstrating only mild symptoms from amphetamine intoxication often respond to sedation and recover rapidly under observation. Such patients require no imaging studies unless trauma is suspected.

Obtain a chest radiograph for patients complaining of chest pain or respiratory distress. Obtain a CT scan of the head for patients with recurrent seizures or prolonged mental status changes if no metabolic cause can be quickly found and corrected.

Look for infectious causes in patients who are demonstrating significant or prolonged hyperthermia; this may include chest radiography, echocardiography, CT of the head and abdomen, and extremity ultrasonography of suspected abscesses.

Other Tests

Perform electrocardiographic testing and monitor patients complaining of chest pain. Obtain appropriate cardiac enzyme testing if pain is prolonged or cardiac injury is suspected.

Procedures

A lumbar puncture (LP) should be performed in hyperthermic patients with altered mental status when CNS infection is suspected

Prehospital Care

Prehospital care of patients with amphetamine intoxication often requires physical or chemical restraint of the patient and treatment of complications of intoxication, including seizures, loss of competent airway, cardiac dysrhythmias, and trauma.

Amphetamine intoxication may cause sleep deprivation or paranoia, resulting in behaviors that appear aggressive: these patients can find it impossible to keep still or stop talking and may be temporarily incapable of responding to commands. It is important to bear in mind that failure to follow orders from law enforcement or cooperate with EMTs is not necessarily a sign of aggression or willful noncompliance. These behavioral disturbances can be managed through rehydration and cooling, which reduce the effects of stimulant use.[36]   Unfortunately, the disturbances place these patients at high risk of lethal use of force by police officers.[36]   

Emergency Department Care

Patients with amphetamine intoxication who present with no life-threatening signs or symptoms may be treated with sedation and observation. Those who present with complications may require airway management, fluid resuscitation, or vigorous cooling measures.

In patients who present shortly after oral ingestion of amphetamines, gastrointestinal (GI) decontamination with activated charcoal can be performed, provided their airway is secure. Orogastric lavage often is not necessary but may be performed when the patient presents with immediately life-threatening intoxication shortly after ingestion. Whole-bowel irrigation may be indicated in suspected cases of body stuffing or body packing (large quantities of drugs in wrapping for international transport or drug hiding, respectively).

Foley catheter placement may be useful to monitor urine output, particularly in situations in which diuretics are administered to manage pulmonary edema. Patients often have decreased urination due to the effects on bladder sphincter muscles. Other individuals may be dehydrated after recreational use in raves and club events. Quick assessment of bladder fullness can be performed with bedside ultrasonography or bladder palpation.

Agitation or persisting seizures in patients with amphetamine toxicity requires generous titration of benzodiazepines and a calm soothing environment. Avoid physical restraints, if possible.

Significant cardiac dysrhythmias may require cardioversion, defibrillation, and antidysrhythmics. Prolonged hypertension may present a cardiovascular risk. Use benzodiazepine sedation (nonspecific sympatholysis) to initially manage hypertension. Refractory cases or cases associated with significant end-organ toxicity (eg, cardiovascular accident [CVA], myocardial ischemia) can be managed with intravenous phentolamine, nitroprusside, or nitroglycerin.

Avoid use of beta-blockers in order to prevent unopposed alpha effect (vasoconstriction). Note that combination alpha-adrenergic and beta-adrenergic antagonists may play a valuable role in managing tachycardias; this recommendation is based on class IIb evidence in the revision of unstable angina/non-ST segment elevation myocardial infarction guidelines by the American Heart Association (based on similarities of amphetamine and cocaine toxicities).[37]

Cardiogenic pulmonary edema can be managed with nitroglycerin and diuretics.

Aggressively cool hyperthermic patients with evaporative cooling, ice packs to the groin and axilla, and use of "ice-bath" (total body immersion in ice). Patients with severe hyperthermia (temperature > 104°F) associated with psychomotor agitation may require immediate neuromuscular paralysis to rapidly decrease temperature. Temperature control should be achieved within 15-20 minutes upon presentation in order to prevent multiorgan failure and death.

Use of haloperidol is controversial in the treatment of agitation in any patient with the potential to seize or develop hyperthermia, because this drug has been associated with a lowered seizure threshold and altered thermoregulation.[38] Of all neuroleptic drugs, however, haloperidol rarely is associated with seizures (minimal effects on seizure threshold). In addition, animal studies suggest that haloperidol can antagonize amphetamine-induced hyperthermia. Haloperidol can be considered as an adjunct to benzodiazepines for afebrile patients with normal vital signs and psychomotor agitation that requires chemical restraint.

Treat rhabdomyolysis with generous intravenous fluids alkalinized with sodium bicarbonate, control of agitation, and temperature normalization.

Look for and treat traumatic injuries in patients with amphetamine intoxication.

Admission is appropriate for monitoring and treatment of the following severe sequelae of amphetamine use:

A patient with stable vital signs who exhibits paranoid psychosis and has no evidence of cardiac, cerebral, renal, hepatic, or pulmonary complications of amphetamine use may need to be transferred to a psychiatric hospital for observation and treatment.

 

Consultations

A medical toxicologist may be consulted for assistance in the management of amphetamine toxicity cases. Patients who demonstrate focal neural deficits or whose imaging studies indicate intracranial bleeding may need neurologic or neurosurgical consultations. Patients who show significant cardiac injury may require cardiologic consultation.

Patients may need referral for outpatient detoxification centers or for management of addictive behaviors.

Prevention

No established modalities exist for treatment of amphetamine addiction, and most treatment focuses on behavioral aspects.  Research is in progress on ketamine-assisted therapy for addiction disorders,[21]  as well as psychedelic-assisted therapy (eg, with psilocybin) for the treatment of methamphetamine use disorder.[22]  However, such modalities are still investigational and not widely available, and there are legal, political, and cultural barriers to conducting scientifically rigorous studies.

Medication Summary

Medications that may be used for amphetamine toxicity include the following:

Activated charcoal

Clinical Context:  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 ingestion of poison. May administer as aqueous suspension or combine with cathartic (usually sorbitol 70%) in the presence of active bowel sounds.

Repeat dose, if necessary (without cathartic), to adsorb large pill masses or drug packages.

With superactivated forms, use of doses of 0.5 g/kg PO may be possible.

Class Summary

These agents are used to adsorb amphetamine after acute ingestion and to limit absorption into systemic circulation. Limited utility beyond 4 h of ingestion, unless the patient ingested sustained-release formulation or is suspected of being a body packer (ie, ingestion of a large amount of drug in a plastic bag or condom to smuggle or avoid arrest). Charcoal is not beneficial for other routes of exposure (eg, IV, inhalation or injection). Clinician should be aware of potential risk of charcoal aspiration and death due to aspiration pneumonia, especially in patients with altered mental status and/or having seizures. Prudent airway control is recommended in such population.

Lorazepam (Ativan)

Clinical Context:  Beneficial for sedative and anticonvulsant effects. In addition, the calming effects may prove beneficial for the adverse cardiovascular effects (eg, hypertension, tachycardia) of amphetamines.

Diazepam (Valium)

Clinical Context:  Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Third-line agent for agitation or seizures because of shorter duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.

Midazolam (Versed)

Clinical Context:  An alternative for termination of refractory status epilepticus. Has twice the affinity for benzodiazepine receptors than diazepam but because it is water soluble, takes approximately 3 times longer than diazepam to reach peak effects. Thus, clinicians must wait 2-3 min to evaluate sedative efficacy before taking further action (eg, repeating dose). May be administered IM if vascular access cannot be obtained.

Class Summary

These agents are important for counteracting the central and peripheral nervous system excitation from amphetamines. A benzodiazepine is generally considered the first agent of choice for hypertension and agitation, in addition to its utility for treating seizures.

Haloperidol (Haldol)

Clinical Context:  DOC for patients with acute psychosis when no contraindications exist. Noted for high potency and low potential for causing orthostasis. Downside is the high potential for EPS (dystonia) and lowering the seizure threshold.

Use in acute amphetamine toxicity is controversial. If haloperidol is being considered, administer a benzodiazepine first. May then be used as adjunctive therapy to control agitation in afebrile patients with normal vital signs.

Parenteral dosage form may be admixed in syringe with 2 mg lorazepam for better anxiolytic effects.

Class Summary

Antipsychotics are used to manage psychosis, agitation, and hyperthermia that may result from amphetamine use.

Dantrolene (Dantrium)

Clinical Context:  Has been used successfully in isolated case reports to control hyperthermia; however, efficacy has not been established for amphetamine-associated hyperthermia. Reverse of hyperthermic effects may take several hours. Because morbidity and mortality from hyperthermia is closely correlated with severity and duration of hyperthermia, aggressive cooling (eg, ice bath) and agents that work more readily to reverse hyperthermia are preferred over dantrolene.

Class Summary

These agents are used to control or reverse hyperthermic effects. Most hyperthermia is mediated by neuromuscular agitation.

Labetalol

Clinical Context:  Blocks beta1-, alpha-, and beta2-adrenergic receptor sites decreasing blood pressure.

Phentolamine (Regitine)

Clinical Context:  Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha-adrenergic receptors.

Nitroprusside (Nitropress)

Clinical Context:  Produces vasodilation and increases inotropic activity of the heart. May exacerbate myocardial ischemia at higher doses by increasing heart rate.

Nitroglycerin IV (Deponit, Nitro-bid, Nitrostat)

Clinical Context:  Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in blood pressure. Valuable for controlling cardiac pain and pulmonary edema.

May administer bolus of 12.5-25 mcg or give a 400-mcg tab SL as a bolus 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 occasionally have been required.

Class Summary

Alpha- and beta-adrenergic antagonists control peripheral vasoconstriction that results from sympathetic stimulation due to amphetamines. Treating with a beta-blocker to control the heart rate will leave unopposed alpha activity that can cause vasoconstriction. Combination alpha- and beta-adrenergic antagonists, such as labetalol, may have therapeutic value. Alpha-adrenergic antagonists specifically may be used to treat severe headache, SAH, cardiac ischemia, and hypertension associated with amphetamines. Use nitrates to control vasoconstriction and hypertensive emergency.

Furosemide (Lasix)

Clinical Context:  Increases excretion of water by interfering with chloride-binding cotransport system that, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Class Summary

These agents are used to control and treat pulmonary edema and could be beneficial in a hypertensive crisis.

What is amphetamine toxicity?What is the pathophysiology of amphetamine toxicity?What are the pathophysiologic effects of amphetamine toxicity on the central nervous system?What are the pathophysiologic effects of amphetamine toxicity on the cardiovascular system?What causes amphetamine toxicity?What is the US prevalence of amphetamine toxicity?What is the global prevalence of amphetamine toxicity?Which patient groups have the highest prevalence of amphetamine toxicity?What is the prognosis for amphetamine toxicity?What is included in patient education about amphetamine toxicity?Which clinical history findings are characteristic of amphetamine toxicity?What are the signs and symptoms of amphetamine toxicity?Which physical exam findings are characteristic of amphetamine toxicity?Which conditions are included in the differential diagnoses of amphetamine toxicity?What are the differential diagnoses for Amphetamine Toxicity?What is the role of lab tests in the workup for amphetamine toxicity?What is the role of imaging studies in the workup for amphetamine toxicity?What is the role of cardiac tests in the workup for amphetamine toxicity?When is lumbar puncture indicated in the workup for amphetamine toxicity?What is included in prehospital care for amphetamine toxicity?When is inpatient care indicated for the treatment of amphetamine toxicity?What is included in emergency department (ED) care for amphetamine toxicity?Which specialist consultations are beneficial to patients with amphetamine toxicity?What is the role of medications in the treatment of amphetamine toxicity?Which medications in the drug class Diuretics are used in the treatment of Amphetamine Toxicity?Which medications in the drug class Cardiovascular agents are used in the treatment of Amphetamine Toxicity?Which medications in the drug class Skeletal muscle relaxants are used in the treatment of Amphetamine Toxicity?Which medications in the drug class Neuroleptics are used in the treatment of Amphetamine Toxicity?Which medications in the drug class Benzodiazepines are used in the treatment of Amphetamine Toxicity?Which medications in the drug class GI decontaminant are used in the treatment of Amphetamine Toxicity?

Author

Jesse Borke, MD, FACEP, FAAEM, Associate Medical Director, Department of Emergency Medicine, Los Alamitos Medical Center

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.

Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

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, Prisma Health Richland Hospital

Disclosure: Nothing to disclose.

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.

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT, Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Disclosure: Nothing to disclose.

Neal Handly, MD, MS, MSc, Attending Physician, Department of Emergency Medicine, Hahnemann Hospital; Adjunct Associate Professor of Emergency Medicine, Drexel University College of Medicine

Disclosure: Nothing to disclose.

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Amphetamine and epinephrine.

Amphetamine and epinephrine.