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Cocaine is a tropane ester alkaloid found in leaves of the Erythroxylum coca plant, a bush that grows in the Andes Mountain region of South America. Its stimulant properties have been known to the indigenous population for at least 2000 years. Oral use of the coca leaf continues to this day and is not associated with significant abuse.

Little attention was paid to coca outside South America until its active ingredient, cocaine, was isolated from the leaf in 1860 by a German graduate student, Albert Niemann. This spawned the widespread popularity of cocaine-containing consumer products, including patent medicines, wine, and other beverages. One of the most popular was a non-alcoholic drink containing about 0.75 mg of cocaine per ounce: Coca-Cola®. Increasing reports of adverse effects, such as stroke and cardiac arrest, led to strict government controls. Cocaine was removed from Coca-Cola in 1903. It received little public or medical attention for the next 70 years, until the “crack” cocaine epidemic of the 1980s.

The 1914 Harrison Narcotic Act limited cocaine to prescription drug status in the United States (US). Cocaine hydrochloride is still legally available in the US as a 4 or 10 percent solution for use as a local or topical anesthetic, although it has largely been replaced in clinical practice by synthetic local anesthetics. Cocaine is classified as a Schedule II medication under the Controlled Substances Act.

Cocaine use is most prevalent in North and South America, and increasingly in Western Europe, especially among urban men aged 15 to 35 years. It is the illegal drug most often associated with emergency department visits in the US.

Up to one in six persons who use cocaine will become dependent; abuse liability is greater with intravenous and smoked cocaine, compared to intranasal and oral use. Cocaine base has a low melting point and can be smoked; cocaine salt is water soluble and can be injected or absorbed across mucous membranes.

Cocaine is largely metabolized to inactive hydrolytic products in the liver and plasma. Use of alcohol with cocaine produces a new metabolite, cocaethylene, which has actions similar to cocaine but a longer half-life. Concurrent alcohol use with cocaine may cause more severe and longer lasting toxic effects.

Acute intoxication — Treatment of acute intoxication is presented separately.

Withdrawal — Cocaine withdrawal is treated by allowing the patient to sleep and eat ad lib in a supportive environment. No medication has been proven effective in treating the withdrawal syndrome, although bromocriptine and amantadine have been used on the theoretical basis that dopaminergic agents may ameliorate the hypothesized dopamine deficiency state of cocaine withdrawal. Propranolol has been used to manage severe cocaine withdrawal symptoms but can aggravate coronary vasoconstriction. Hospitalization is rarely indicated on medical grounds, and has not been shown to improve the short-term outcome for cocaine addiction.

A short-acting benzodiazepine such as lorazepam may be helpful in selected patients who develop severe agitation or sleep disturbance. Persistent (more than two to three weeks) depression or suicidal ideation may require antidepressant treatment. The risk of relapse is high during the early withdrawal period, in part because drug craving is easily triggered by stress or encounters with drug-associated stimuli. Patients should be referred to an addiction treatment program for ongoing care.

Screening — There are no broadly validated brief screening tests for cocaine abuse. Best studied are two tests modified from those used to screen for alcoholism: the 4-question CAGE and 2-question TICS. Both tests have sensitivities and specificities of 80 percent or greater in primary care settings for populations including women, pregnant women, the elderly, and patients with HIV infection.

Drug testing — Drug testing detects cocaine use, but is not diagnostic of cocaine abuse, which implies adverse consequences from use. Conversely, a negative drug screen may only indicate lack of recent use. Cocaine and its metabolites can be measured in urine, blood, oral fluid, sweat, and hair. The window of detection is shorter for cocaine than for its major metabolite, benzoylecgonine, and varies with the sensitivity of the assay method.

Urine testing (which measures benzoylecgonine, not cocaine) is common in clinical settings because the sample can be collected non-invasively. It has a detection window of about two to three days after cocaine use, but may be positive up to two weeks after chronic heavy use.

Central nervous system — Cocaine euphoria is associated with transient increases in EEG activity followed by longer-lasting increases in activity. Seizures may occur in persons without a seizure history, even with first time use of cocaine. These are usually single, generalized tonic-clonic seizures occurring within 90 minutes of cocaine use.

Craving for cocaine is associated with increased activity in the so-called mesocorticolimbic reward circuit in the brain. This includes the inferior frontal-orbitofrontal gyrus, amygdala (thought to mediate stimulus-reward association), anterior cingulate (mediating anticipation of reward), and nucleus accumbens/subcalllosal gyrus (mediating incentive motivation).

Cerebral vasoconstriction, cerebrovascular disease, and hemorrhagic and ischemic stroke are increased in cocaine users, even in patients with no other risk factors. Etiologic mechanisms include tachycardia and increased blood pressure from sympathetic activation, vasoconstriction, vasospasm, and intravascular thrombosis due to increased platelet aggregation.

Acute intoxication — Typical cocaine doses are 12 to 15 g orally (coca leaf), 20 to 100 mg intranasally, 10 to 50 mg intravenously, and 50 to 200 mg smoked. The intended effects include increased energy, alertness, and sociability; elation or euphoria; and decreased fatigue, need for sleep, and appetite. The intense pleasurable feeling has been described as a “total body orgasm”.

There is wide variability in the acute response to cocaine and poor correlation between cocaine plasma concentrations and toxic effects . Fatal cases of cocaine intoxication may present with 100-fold differences in plasma cocaine concentration.

Unintended adverse effects occur with increasing dose, duration of use, or a more efficient route of administration (eg, intravenous or smoked versus intranasal). These effects include dysphoric mood (anxiety, irritability), panic attacks, suspiciousness, paranoia, grandiosity, impaired judgment, and psychotic symptoms such as delusions and hallucinations. Up to 40 percent of non-treatment-seeking cocaine users may experience sleep disturbance, weight loss (due to appetite suppression), paranoia, or hallucinations. Concurrent behavioral effects include restlessness, agitation, tremor, dyskinesia, and repetitive or stereotyped behaviors such as picking at the skin or foraging for drugs (”punding,” “hung-up activity”). Associated physiological effects include tachycardia, pupil dilation, diaphoresis, and nausea, reflecting stimulation of the sympathetic nervous system.