eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Sympathomimetic

Paul Kolecki, MD, FACEP, Associate Professor, Department of Emergency Medicine, Thomas Jefferson University Hospital, Director of Undergraduate Emergency Medicine Student Education, Jefferson Medical College, Philadelphia, PA, Consultant, Philadelphia Poison Control Center, Philadelphia, PA

Updated: Mar 24, 2009

Introduction

Background

Poisoning from sympathomimetic agents occurs secondary to the use of prescription and nonprescription agents. The public commonly uses prescription sympathomimetic agents, especially for treating diseases such as asthma and narcolepsy. Examples of nonprescription sympathomimetic agents include the over-the-counter cold agents (containing ephedrine), illegal street drugs (eg, cocaine, amphetamines, methamphetamine), dietary supplements (eg, ephedra alkaloids), and the very popular illicit designer drugs (eg, 3,4-methylenedioxy methamphetamine [MDMA, "ecstasy"]).

Cocaine is one of the most commonly abused drugs in the United States, especially in urban areas. Methamphetamine is frequently made and abused throughout the United States. Recent reports state that methamphetamine use has been linked to a rise in HIV transmission. In 2007, approximately 46,000 cases of sympathomimetic and street drug exposures were reported to the American Association of Poison Control Centers.¹ Even more alarming are the number of out-of-hospital cardiac arrests secondary to sympathomimetic toxicity reported in the Seattle area and the number of deaths nationally secondary to sympathomimetics. Cocaine, methamphetamine, and ecstasy are 3 of the most common drug-related causes of emergency department visits in the United States. Methamphetamine use in trauma patients has increased significantly and has been associated with a financial burden on trauma centers.²

The many different sympathomimetic agents produce their physiologic and toxicologic properties through several different mechanisms. Toxicity secondary to these agents typically presents with classic sympathomimetic signs and symptoms that include tachycardia, hypertension, diaphoresis, hyperthermia, agitation, and combativeness.

The general treatment for preventing the potentially significant end-organ damage that is possible after overdose is similar for the sympathomimetic agents because their clinical presentation of toxicity is similar. Most sympathomimetic agents produce central stimulation following overdose. When central stimulation occurs in patients, the most important treatment involves physical and, more importantly, pharmacological control of their agitation.

Pathophysiology

Sympathomimetic agents produce their physiologic and toxic effects by 5 different mechanisms, as follows:

• The first mechanism involves direct stimulation of the alpha- and beta-adrenergic receptors. Albuterol is a very commonly used direct-acting beta2-agonist.
• The second mechanism involves the indirect release of norepinephrine from the presynaptic cytoplasm through a process that bypasses exocytosis. Amphetamine and its derivatives work through this mechanism.
• The third mechanism involves direct stimulation of adrenergic receptors and an indirect release of presynaptic norepinephrine. Dopamine is the classic example of a mixed-acting agent.
• The fourth mechanism involves the prevention of presynaptic uptake of norepinephrine. By preventing uptake, norepinephrine concentration rises in the synapse, leading to excessive stimulation of adrenergic receptors. Cocaine and the tricyclic antidepressants produce their sympathomimetic effects mainly by inhibiting presynaptic norepinephrine uptake.
• The final mechanism involves the prevention of norepinephrine metabolism. As norepinephrine is mainly metabolized by the enzyme monoamine oxidase, the monoamine oxidase inhibitors (MAOIs) are the class of drugs that produce their sympathomimetic effects through this final mechanism.

The pathophysiology of sympathomimetic toxicity is much more involved than what was just listed. To explore these mechanisms in more detail, references for further reading are provided in the reference section. An important clinical point is that the signs and symptoms produced by these 5 different mechanisms are very similar. In most cases, clinical poisoning by one sympathomimetic agent is indistinguishable from that of a second sympathomimetic agent with a different mechanism of action.

Frequency

United States

Sympathomimetic poisoning continues to be a very common toxicologic emergency. The 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported approximately 46,000 sympathomimetic and street drug exposures and approximately 180 fatalities.¹ This category includes exposures to amphetamines, cocaine, and methamphetamine.

Mortality/Morbidity

In 2007, the AAPCC reported approximately 180 deaths from stimulants and street drugs.¹
 
The exact number of stimulant deaths in 2006 is unknown but is expected to be greater than the number reported by the AAPCC.

Race

No scientific data have demonstrated that outcomes of sympathomimetic exposure are dependent on race.

Sex

No scientific data have demonstrated that outcomes of sympathomimetic exposure are dependent on sex.

Clinical

History

• Knowing that a sympathomimetic agent was ingested is helpful for treating a poisoned patient. Query patients about the use of cocaine, methamphetamine, and ecstasy. In addition, patients should be asked about their use of over-the-counter cold medications (containing ephedrine) and herbal preparations (eg, ephedra, Ma-Huang). Phenylpropanolamine used to be a very popular amphetamine sold over-the-counter; however, it was taken off the market by the Food and Drug Administration (FDA) because of the risk of intracranial hemorrhage associated with its use. The FDA banned the sale of ephedra and ephedra-containing products.
• Maintain a high index of suspicion of sympathomimetic poisoning when treating an unknown overdose, especially in patients that present with the sympathomimetic toxidrome.
• Another aid in the history of sympathomimetic poisoning is that the onset of symptoms usually occurs within 2 hours postexposure.
• Life-threatening complications typically occur within 2-6 hours postexposure.

Physical

Adult sympathomimetic toxicity produces typical adrenergic signs and symptoms, some of which can be deadly.

• Bronchospasm and wheezing can occur in patients who smoke crack cocaine. In addition, crack cocaine use can cause asthma exacerbations, pneumothorax, and lung injury.
• Hyperthermia associated with sympathomimetic toxicity may result secondary to the destructive behavior and extreme agitation experienced by these patients. The abuse of sympathomimetic agents in hot, humid environments (eg, dance clubs, summer evenings) can further exacerbate hyperthermia. Seizures resulting from overdose can also produce hyperthermia. Sympathomimetic-induced hyperthermia can produce significant morbidity (from end-organ damage) and death.
• Extreme hypertension can result in headache, hypertensive encephalopathy, and intracranial hemorrhage.
• Sympathomimetic toxicity also can result in asymptomatic hypertension, which may require an urgent reduction in blood pressure.
• The following cardiac arrhythmias may result from sympathomimetic toxicity:
  • Sinus and supraventricular tachycardia (including atrial fibrillation and atrial flutter)
  • Premature ventricular beats
  • Accelerated idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
  • Second-degree and third-degree heart block (as a reflex response to hypertension)
• Sympathomimetic-induced chest pain, myocardial ischemia, myocardial infarction, and cardiomyopathy (eg, cocaine) also can occur.
• Seizures, strokes, and intracerebral bleeds are well-documented complications of sympathomimetic toxicity.
• Dissecting thoracic aneurysms and mesenteric ischemia are rare but deadly consequences of sympathomimetic poisoning.
• Sympathomimetic toxic adult patients may also experience some nonlethal signs and symptoms, as follows:
  • Mydriasis
  • Tachycardia
  • Diaphoresis
  • Acute psychosis
  • Paranoia
  • Delirium Bruxism (amphetamines)
• Although adult poisoning is well documented, pediatric sympathomimetic toxicity is not. Pediatric patients with sympathomimetic toxicity present with the same signs and symptoms observed in adults.
  • One study noted that some pediatric patients with sympathomimetic toxicity initially presented with inconsolable crying, vomiting, and abdominal pain.
  • These signs and symptoms are also the presenting features of many serious pediatric diseases (eg, sepsis, intussusception, intracranial lesion), and several of these pediatric patients received expensive ancillary tests to rule out significant disease.

Causes

• Poisoning from sympathomimetic agents occurs secondary to the use of prescription agents, nonprescription agents, and illegal agents.
• Typically, prescription and over-the-counter sympathomimetic agents are inhaled or orally administered.
• In general, the inhalational agents (eg, albuterol, crack cocaine) have a quicker onset of action than the oral agents and a shorter duration of action.
• Sympathomimetic toxicity following ingestion typically peaks 1-4 hours postingestion and last 4-8 hours, but sustained-release preparations may alter this time course.
• The onset of toxicity following intravenous use of a sympathomimetic agent occurs within minutes.
• Presently, many illegal sympathomimetic agents are commonly abused.
  • On the streets, some of these illegal agents have interesting names that, for the most part, are based on the psychological effects produced by the specific drug.
  • In general, all sympathomimetic agents are rapidly absorbed when ingested.
  • The popular designer amphetamines (eg, ecstasy) and ephedrine are abused mainly by the oral route.
  • Abuse of sympathomimetic agents often occurs at contemporary disco or rave party scenes, where adolescents use them before and during hours of rigorous dancing in crowded rooms with a hot and humid atmosphere.
  • Many reports of adolescent morbidity (eg, dehydration, hyperthermia, cardiac dysrhythmias) and mortality are associated with the use of illegal sympathomimetic agents at discos and rave parties. Other recreational drugs used at rave parties include marijuana, ketamine, gamma-hydroxybutyrate (GHB), and gamma-butyrolactone (GBL).
  • Some of the illegal sympathomimetic agents are more commonly abused by the inhalational route (eg, crack cocaine, methamphetamine) or the IV route (eg, cocaine, methamphetamine, methcathinone) than by the oral route.
• The duration of action of illegal sympathomimetic agents differ based on their chemical structure. Methamphetamine has the chemical structure of amphetamine with an additional methyl group. The half-life of methamphetamine, however, is much longer (2-24 h) than that of amphetamine, thus partially accounting for methamphetamine's present popularity.
• The route of abuse also contributes to the duration of action of some of these illegal sympathomimetic agents. The duration of action of cocaine is more than 3 hours if ingested. However, the duration of action is much shorter after nasal snorting (1-2 h), inhalation (15-30 min), or IV injection (15-30 min).

Differential Diagnoses

Other Problems to Be Considered

Alcohol-sedative withdrawal presents in a manner similar to that of sympathomimetic poisoning. In addition to the above listed differential, sympathomimetic poisoning can present in a manner similar to sedative-hypnotic withdrawal and monoamine oxidase inhibitor poisoning.

Workup

Laboratory Studies

• Drugs levels generally are not helpful.
• Routine screening for other potentially treatable toxins is recommended (eg, acetaminophen, salicylate).
• Obtaining electrolytes, BUN, creatinine, bedside (eg, Accu-Chek) and laboratory blood sugar, and an anion gap measurement is recommended. Special attention should be given to the sodium level, as there are reports of hyponatremia associated with the use of ecstasy. Significant free-water intake along with sodium loss from excessive dancing (eg, rave dancing) may contribute to the development of hyponatremia.
• Measure total creatinine kinase (CK) levels to check for rhabdomyolysis. Risk factors for developing rhabdomyolysis include delirium, seizures, coma, hypotension, cardiac dysrhythmia, and cardiac arrest.
• Performing a urine drug screen is recommended. Urine drug screening for cocaine is fairly sensitive and specific and typically can detect the presence of cocaine if used in the past 1-3 days. Drug screening for amphetamines, however, is not as specific.

Imaging Studies

• Consider a CT scan of the head to rule out intracerebral bleeds in unresponsive patients or those with focal neurologic deficits.

Other Tests

• Obtain an electrocardiogram (ECG) to check for evidence of myocardial ischemia and dysrhythmias. Cardiac markers (eg, CPK-MB, troponin) are also appropriate to screen for cardiac injury.

Treatment

Prehospital Care

• Managing the airway and controlling agitation are the two main prehospital treatment concerns. Many patients with sympathomimetic poisoning present in an agitated state. In these cases, physical and/or chemical restraint may be required.
• A rapid bedside blood sugar test (eg, Accu-Chek) should be performed to rule out hypoglycemia. Hypoglycemia should be treated if detected.

Emergency Department Care

• General supportive care is the main treatment measure for sympathomimetic toxicity because no antidote exists. Assessment of the airway, breathing, and circulation immediately is recommended. In addition, close monitoring of the vital signs is recommended.
• Sympathomimetic toxicity is frequently associated with significant agitation, thus necessitating the use of physical restraints and chemical sedation. However, physically restrained patients with sympathomimetic-associated agitation or hyperthermia have an associated significant risk of sudden death. The liberal use of chemical sedation in such instances is strongly recommended.
  • Benzodiazepines (eg, Valium) are the safest first approach in calming sympathomimetic-poisoned patients. They should be administered frequently in titrated doses.
• Consider gastric decontamination for oral ingestions of sympathomimetic agents. Gastric decontamination is associated with subsequent vomiting and aspiration. Thus, airway control is strongly recommended prior to any gastric decontamination.
  • In addition, the patient's airway, breathing, circulation, and agitation should be stabilized before performing GI decontamination.
• It is imperative to measure the core temperature of sympathomimetic poisoned patients. If hyperthermia is present, standard cooling measures should be initiated. Controlling agitation significantly helps in cooling a hyperthermic patient.
• Hypertension unresponsive to sedation should be treated with a rapidly acting and easily titrated agent (eg, sodium nitroprusside).
• Seizures should be rapidly controlled with benzodiazepines and/or barbiturates. Obtaining a CT scan of the brain for all sympathomimetic toxic patients who seize, develop a focal neurologic deficit, or experience a severe headache with or without accompanying hypertension is recommended.

Consultations

• Consultation from the regional poison control center or a local medical toxicologist (certified by the American Board of Medical Toxicology and/or the American Board of Emergency Medicine) for additional information and patient care recommendations is recommended.
• Prolonged critical care management often is required for the numerous complications that may occur with the severe overdose (eg, hyperthermia, seizures, advanced respiratory distress syndrome [ARDS], renal failure, rhabdomyolysis, CNS dysfunction).

Medication

Treatment of sympathomimetic toxicity is focused on controlling agitation, managing seizure activity, and treating hypertension unresponsive to sedation. The most accepted pharmacologic option for controlling agitation is the use of benzodiazepines. Butyrophenones lower the seizure threshold, increase the risk of hyperthermia, and may prolong the QT interval (eg, droperidol); the use of butyrophenones is NOT recommended. Sympathomimetic-induced seizures should be treated with benzodiazepines or barbiturates (eg, phenobarbital). Hypertension should be managed with a short-acting, easily titrated agent (eg, nitroprusside) if it is not controlled with benzodiazepine-induced sedation.

Benzodiazepines and other sedatives

Used for controlling sympathomimetic-induced agitation.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Individualize dosage and increase cautiously to avoid adverse effects. Easily titrated with a long half-life.

Dosing

Adult

0.2 mg/kg IV at 2 mg/min; not to exceed 20 mg (as a single dose); may repeat

Pediatric

0.2-0.5 mg/kg IV
<5 years: not to exceed 5 mg
>5 years: not to exceed 10 mg

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, cimetidine, 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 and hypotension

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.
Excellent when patient requires sedation for more than 24 h.

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 prn; not to exceed 8 mg/dose

Pediatric

Infants and children: 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: 0.07 mg/kg IV slowly over 2-5 min; repeat in 10-15 min prn; not to exceed 4 mg/dose

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, 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 IV, followed by continuous infusion of 1 mcg/kg/min IV; titrate 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 with organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Phenobarbital (Barbita, Luminal)

Interferes with transmission of impulses from thalamus to cortex of brain. Used for sympathomimetic-induced seizure unresponsive to diazepam.

Dosing

Adult

15-20 mg/kg IV load

Pediatric

Administer as in adults

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and fatality; chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy); menstrual irregularities also may occur

Contraindications

Documented hypersensitivity; severe respiratory disease, marked impairment of liver function, and nephritic patients

Precautions

Pregnancy

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

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema; monitor for respiratory depression and hypotension

Cardiovascular agents

Control sympathomimetic-induced hypertension.

Nitroprusside (Nitropress)

Rapidly acting, easily titrated antihypertensive. Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Dosing

Adult

0.3 mcg/kg/min IV; titrate to effect

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter; sildenafil (Viagra) use within 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, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has the ability to lower blood pressure and, thus, should be used only in patients with mean arterial pressures >70 mm Hg

Nitroglycerin (Deponit, Nitrostat)

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production, resulting in a decrease in 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

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

Follow-up

Further Inpatient Care

• Excluding long-acting preparations, patients with sympathomimetic toxicity who remain asymptomatic after 6 hours postingestion may be medically discharged.
• Patients with ingestion of long-acting preparations typically should be monitored for 24 hours. Most of these patients are admitted to a telemetry floor or an intensive care unit.
• Consider psychiatric evaluation before discharging patients from the hospital.
• If inpatient care is required, it should be under the direction of a medical toxicologist or a physician with expertise in critical care.

Inpatient & Outpatient Medications

• Benzodiazepines remain the initial agent of choice to treat sympathomimetic-induced tachycardia, agitation, seizures, hypertension, and hyperthermia.

Complications

• Lethal complications of sympathomimetic toxicity include hyperthermia, hypertension emergency, cardiac arrhythmias, myocardial infarction, CNS disasters, and thoracic and mesenteric vascular disasters.

Prognosis

• Patients who present with hyperthermia and cardiovascular collapse have poor long-term prognosis.

Patient Education

• For excellent patient education resources, visit eMedicine's Sleep Disorders Center. Also, see eMedicine's patient education article Narcolepsy.

Miscellaneous

Medicolegal Pitfalls

• Failure to aggressively treat hyperthermia
• Failure to aggressively treat rhabdomyolysis to prevent renal failure
• Failure to recognize that the ingestion was that of a long-acting designer amphetamine, thus discharging the patient prematurely
• Failure to rule out hypoglycemia and hyponatremia as causes for change in mental status for a sympathomimetic poisoned patient.

References

1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline].

2. Swanson SM, Sise CB, Sise MJ, Sack DI, Holbrook TL, Paci GM. The scourge of methamphetamine: impact on a level I trauma center. J Trauma. Sep 2007;63(3):531-7. [Medline].

3. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). Dec 2007;45(8):815-917. [Medline].

4. Budisavljevic MN, Stewart L, Sahn SA. Hyponatremia associated with 3,4-methylenedioxymethylamphetamine ("Ecstasy") abuse. Am J Med Sci. Aug 2003;326(2):89-93. [Medline].

5. Chiang WK. Amphetamines. In: Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. 2002. 7^th ed. New York: McGraw-Hill; 2002:1020-1033.

6. Curry SC, Mills KC, Graeme KA. Neurotransmitters. In: Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. 7^th ed. New York, NY: McGraw-Hill; 2002:133-165.

7. Duffy MR, Ferguson C. Role of dantrolene in treatment of heat stroke associated with Ecstasy ingestion. Br J Anaesth. Jan 2007;98(1):148-9. [Medline].

8. Hollander JE, Henry TD. Evaluation and management of the patient who has cocaine-associated chest pain. Cardiol Clin. Feb 2006;24(1):103-14. [Medline].

9. Hollander JE, Hoffman RS. Cocaine. In: Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. 7^th ed. New York, NY: McGraw-Hill; 2002:1004-1019.

10. Kolecki P. Inadvertent methamphetamine poisoning in pediatric patients. Pediatr Emerg Care. Dec 1998;14(6):385-7. [Medline].

11. Lineberry TW, Bostwick JM. Methamphetamine abuse: a perfect storm of complications. Mayo Clin Proc. Jan 2006;81(1):77-84. [Medline].

12. Paredes VL, Rea TD, Eisenberg MS. Out-of-hospital care of critical drug overdoses involving cardiac arrest. Acad Emerg Med. Jan 2004;11(1):71-4. [Medline].

13. Sue YM, Lee YL, Huang JJ. Acute hyponatremia, seizure, and rhabdomyolysis after ecstasy use. J Toxicol Clin Toxicol. 2002;40(7):931-2. [Medline].

Keywords

sympathomimetic agents, sympathomimetics toxicity, ephedrine, asthma, narcolepsy, over-the-counter agent, over-the-counter medication, over-the-counter drug, OTC, OTC agent, OTC medication, OTC drug, pseudoephedrine, illegal street drug, cocaine, amphetamines, methamphetamine, meth, dietary supplement, ephedra alkaloids, ephedra, designer drug, 3, 4-methylenedioxy methamphetamine, MDMA, ecstasy, cardiac arrest

Contributor Information and Disclosures

Author

Paul Kolecki, MD, FACEP, Associate Professor, Department of Emergency Medicine, Thomas Jefferson University Hospital, Director of Undergraduate Emergency Medicine Student Education, Jefferson Medical College, Philadelphia, PA, Consultant, Philadelphia Poison Control Center, Philadelphia, PA
Paul Kolecki, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Mark S Slabinski, MD, FACEP, FAAEM, Vice President, EMP Medical Group
Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State 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, 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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