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Cocaine: Acute intoxication

INTRODUCTION

Cocaine, purported to be the most potent stimulant of natural origin, is extracted from the leaves of the coca plant (Erythroxylum coca), which is indigenous to the Andean highlands of South America. Natives in this region chew or brew coca leaves into a tea for refreshment and to relieve fatigue, similar to the customs of chewing tobacco and drinking tea or coffee in other cultures.

Pure cocaine was first isolated in the 1880s and was first used as a local anesthetic in eye surgery. It was particularly useful in surgery of the nose and throat because of its ability to provide anesthesia and constrict blood vessels, thereby limiting bleeding. Cocaine was legal and widely used in the United States during the second half of the 19th Century and was a main ingredient of the original Coca-Cola®. Despite legislative attempts dating from the early 20th century to eradicate its use, cocaine remains a common and dangerous drug of abuse.

This topic review will discuss the basic pharmacology, clinical presentation, and management of acute cocaine intoxication. Treatment for chronic cocaine abuse, general management of acute drug overdose, and other aspects of drug abuse are discussed elsewhere. A summary table to facilitate emergent management is provided (table 1). (See "Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations, medical consequences, and diagnosis" and "Evaluation and management of the cardiovascular complications of cocaine abuse" and "Pulmonary complications of cocaine abuse" and "General approach to drug poisoning in adults".)

EPIDEMIOLOGY

Other than alcohol, cocaine is the most common cause of acute drug-related emergency department (ED) visits in the United States. It accounts for more reports to the Drug Abuse Warning Network (DAWN) than marijuana, synthetic marijuana, or hashish the next leading causes [1]. Death from unintentional cocaine overdose and cocaine-related violence occurs throughout the world [2-5]

PHARMACOLOGY

Cocaine is well-absorbed following contact with the oral, nasal, gastrointestinal, rectal, and vaginal mucosa, or via the pulmonary alveoli following inhalation. Cocaine's vasoconstrictive properties prolong the rate of absorption and delay its peak effect when absorbed from mucosal surfaces. The bioavailability of cocaine is approximately 90 percent when smoked and about 80 percent after intranasal use. Bioavailability is decreased when cocaine is ingested, though this is not well studied [6].

                                 

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Literature review current through: Nov 2014. | This topic last updated: Jun 16, 2014.
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