MDMA Toxicity Medication

  • Author: In-Hei Hahn, MD, FACEP; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Mar 9, 2011
 

Medication Summary

Objectives in pharmacotherapeutic intervention of MDMA toxicity include the following: (1) decontamination with activated charcoal/sorbitol; (2) sedation with benzodiazepines in agitated and anxious patients; (3) treatment of hyperthermia with rapid convection cooling, spraying water onto the body and using an electric fan to circulate the air, attempting to cool the core temperature to 101°F within 30-45 minutes; (4) relief of muscle spasms and/or cramping with benzodiazepines, (5) prevention of rhabdomyolysis with IV fluids (benefit of furosemide or sodium bicarbonate remains controversial); (6) seizure control with benzodiazepines; and (7) stabilization of hemodynamic and/or cardiovascular disturbances with nitroprusside or nitroglycerin.

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Benzodiazepines

Class Summary

These agents are important for sedation, muscle relaxation, and seizure management.

Lorazepam (Ativan)

 

Beneficial for sedative and anticonvulsant effects. Sedation also can lower amphetamine-induced hypertension. DOC for initial treatment of status epilepticus.

Diazepam (Valium, Diazemuls, Diastat)

 

Depresses all levels of CNS, possibly by increasing activity of GABA; individualize dosage and increase cautiously to avoid adverse effects.

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Barbiturates

Class Summary

Class of anticonvulsants useful when phenytoin and benzodiazepines fail.

Phenobarbital (Luminal, Barbita, Solfoton)

 

Exhibits anticonvulsant activity in anesthetic doses. In status epilepticus, important to achieve therapeutic levels as quickly as possible. IV dose may require approximately 15 min to attain peak levels in brain.

If IM route is chosen, administer into areas such as one of the large muscles (eg, gluteus maximus, vastus lateralis, other areas with little risk of encountering a nerve trunk or major artery); permanent neurologic deficit may result from injection into or near peripheral nerves.

Restrict IV use to conditions in which other routes are not possible, either because patient is unconscious or because prompt action is required; if used to terminate generalized convulsive status epilepticus, administer up to 15-20 mg/kg.

Ventilation and intubation may be necessary; hypotension may require treatment; a trend exists in recommendations to use agents other than phenobarbital (propofol, midazolam, other barbiturates) for refractory status epilepticus.

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Alkalinizing agent

Class Summary

These agents are used to facilitate treatment of rhabdomyolysis.

Sodium bicarbonate (Neut)

 

Useful in alkalization of urine to prevent acute myoglobinuric renal failure; titrate dose to increase pH to 7.45-7.55; onset of action is within minutes and lasts approximately 15-30 min; monitor blood pH to avoid excess alkalosis. Maintain normal serum potassium level because urinary alkalinization impossible if patient is hypokalemic.

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Osmotic diuretics

Class Summary

These agents increase osmolarity of glomerular filtrate and induce diuresis. They hinder tubular reabsorption of water, causing sodium and chloride excretion to increase.

Mannitol (Osmitrol)

 

Alternative diuretic used when urine output is inadequate despite aggressive fluid therapy.

Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg IV over 3-5 min; should produce urine flow of at least 30-50 mL/h of urine over 2-3 h.

In children, assess for adequate renal function by administering test dose of 200 mg/kg IV over 3-5 min; should produce urine flow of at least 1 mL/h over 1-3 h.

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Antihypertensives

Class Summary

Design treatment of hypertension to reduce the blood pressure and other risk factors of coronary heart disease. Individualize pharmacologic therapy based on a patient's age, race, known pathophysiologic variables, and concurrent conditions. Design treatment not only to lower blood pressure safely and effectively but also to avoid or reverse hyperlipidemia, glucose intolerance, and left ventricular hypertrophy.

Phentolamine (Regitine)

 

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

Sodium nitroprusside (Nitropress)

 

Produces vasodilation and increases inotropic activity of heart; at higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Nitroglycerin (Nitro-Bid, Nitrostat, Deponit)

 

Decreases coronary vasospasm, which increases coronary blood flow; in addition, induces vessel dilatation, decreasing cardiac workload.

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Diuretic

Class Summary

Diuretics facilitate diuresis during treatment of rhabdomyolysis.

Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule; potent vasodilator of medullary vessels serving to wash out concentration gradient of countercurrent system, resulting in marked diuresis.

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GI decontamination

Class Summary

Activated charcoal adsorbs MDMA after acute ingestions and limits absorption into systemic circulation. Most beneficial if administered within 4 hours of ingestion.

Activated charcoal (Liqui-Char, Actidose-Aqua)

 

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 poison ingestion; may administer as aqueous suspension or combined with cathartic (usually sorbitol 70%) and with presence of active bowel sounds; may need to be repeated (without cathartic) to adsorb large pill masses or drug packages.

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Glucose supplement

Class Summary

This agent is used to raise the patient's serum glucose level.

Dextrose (Glucose-D)

 

Monosaccharide, absorbed from intestine and distributed, stored, and used by tissues. Parenterally injected dextrose is used in patients unable to obtain adequate oral intake; direct oral absorption results in rapid increase of blood glucose concentrations. Effective in small doses; no evidence indicates that it may cause toxicity; concentrated infusions provide higher amounts of glucose and increased caloric intake with minimum fluid volume.

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Vitamin supplementation

Class Summary

Vitamins are indicated to correct thiamine deficiency and prevent Wernicke-Korsakoff encephalopathy.

Thiamine (Vitamin B-1)

 

Supplementation ensures adequate cofactor for maintenance of cellular aerobic respiration. CNS depletion of thiamine may result in Wernicke encephalopathy.

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Contributor Information and Disclosures
Author

In-Hei Hahn, MD, FACEP  Attending Physician, Department of Emergency Medicine, Danbury Hospital Center, Assistant Professor, Department of Surgery, University of Vermont; St Lukes-Roosevelt Hospital Center; and Danbury Hospital Center; Assistant Clinical Professor, Department of Medicine, Columbia University College of Physicians and Surgeons.

In-Hei Hahn, MD, FACEP is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Specialty Editor Board

Peter MC DeBlieux, MD  Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John G Benitez, MD, MPH  Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author David Yew, MD, to the original writing and development of this article.

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