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Acute amphetamine and synthetic cathinone (“bath salt”) intoxication

Thomas C Arnold, MD, FAAEM, FACMT
Mark L Ryan, PharmD
Section Editor
Stephen J Traub, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Amphetamines first appeared as a nasal decongestant in the form of a Benzedrine inhaler and were then used by the military as agents to promote alertness in battle-fatigued troops. In the 1950s, they gained popularity as weight-loss drugs and shortly thereafter became popular substances of abuse. Amphetamine sulfate and other stimulants like ephedra have a long history of abuse in the United States. Cathinones are beta-ketone amphetamine analogs. Abuse of the new synthetic cathinones (bath salts) emerged in Europe in 2009 and spread to the United States in 2010 [1,2]; these drugs were initially marketed in the United States as “bath salts” or “plant food” to avoid restrictions under the United States Controlled Substances Act.

This topic will discuss the basic pharmacology, clinical presentation, and management of acute intoxication with traditional amphetamines (eg, ephedrine, ma-huang, khat, propylhexedrine) and synthetic cathinones. Intoxication with other stimulants, such as methamphetamine, cocaine, and methylenedioxymethamphetamine, is reviewed separately. (See "Methamphetamine intoxication" and "Cocaine: Acute intoxication" and "MDMA (ecstasy) intoxication" and "General approach to drug poisoning in adults".)


Phenethylamines, including traditional amphetamines and the newer synthetic compounds, share multiple pharmacodynamic properties. Stimulation of alpha and beta adrenergic receptors is primarily responsible for the acute effects of amphetamines, which include hyper-alertness, hypertension, tachycardia, mydriasis, and diaphoresis. Together, these symptoms are part of the sympathomimetic toxic syndrome (or toxidrome) (table 1). Adrenergic receptors are reviewed separately. (See "Use of vasopressors and inotropes", section on 'Receptor physiology'.)

Phenylethylamines cause the release of neurotransmitters, such as dopamine, serotonin, and norepinephrine and may also inhibit their reuptake. Some cause the release of serotonin from central axons, and some are serotonin receptor agonists [1,3].

Psychotic symptoms in overdose occur from excess dopamine and serotonin. Ring substitutions and other “designer” modifications have produced various psychoactive properties. Hallucinogenic properties appear to be enhanced by greater 5HT-2a receptor agonism.


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Literature review current through: Sep 2016. | This topic last updated: Nov 5, 2014.
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