Imaging of Emergency Department Patients With Cocaine Intoxication

Abstract

Cocaine is the second most abused illicit drug in the United States with 2.4 million users in 2006 (Cannabis is the leading offender). Cocaine is also the most common recreational drug resulting in emergency department visits. According to the Drug Abuse Warning Network, a public health surveillance system, there were 2.1 million drug-abuse-related emergency department visits in the United States in 2008, and more than 400,000 of these visits directly involved cocaine use. Based on the 2010 National Survey on Drug Use and Health report, the 18-to 25-year-old population accounted for nearly 45% of illicit drug use during 2010, with those aged 26 to 34 years accounting for an additional 30%. These statistics are important because cocaine use can result in acute and chronic pathology involving almost every body organ system and often more than a single organ system at a time. Commonly involved organ systems include the central nervous, cardiovascular, pulmonary, gastrointestinal, and musculoskeletal. The most dramatic complication of cocaine use is sudden death, which can occur after a single-use episode. After completing this CME activity, the radiologist will be able to recognize the emergency department presentations that may be associated with cocaine use, thus leading to a higher level of suspicion of cocaine abuse when a young, relatively healthy patient presents to the emergency department. BackgroundCocaine, an alkaloid derived from the Erythroxylum coca plant, was first introduced in 1884 for its pharmacologic effect of local anesthesia. Cocaine is primarily available as a hydrochloride salt (powder) or free base ("crack") and can be inhaled (snorted/sniffed or smoked), injected, ingested, and chewed.Locally, cocaine blocks electrical impulse transmission by preventing rapid depolarization of the cell membrane via sodium ion influx. Systemically, cocaine exerts action by preventing presynaptic reuptake of norepinephrine, serotonin, and dopamine, which (via norepinephrine) can lead to sympathetic nervous system activation, resulting in arterial and venous vasoconstriction and elevation of blood pressure. Cocaine also increases endothelin-1 (a potent vasoconstrictor) while decreasing nitric oxide (a vasodilator). 1 Cocaine modulates cardiac inotropism (myocyte contractility), dromotropism (atrioventricular node conduction), and chronotropism (heart rate, tachycardia) mainly through ␤-1-receptors. Alphaadrenergic effects are controversial, with some studies demonstrating block of vasospasm with phentolamine or prazosin, and other studies demonstrating block only by diltiazem, the 1 After participating in this activity, the diagnostic radiologist should be better able to evaluate the varied imaging manifestations of cocaine use, particularly those relevant to the emergency department setting.