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Cocaine is one of the most popular drugs of abuse. It may be sniffed into the nose (snorted), smoked, or injected IV. Occasionally, it is combined with heroin and injected (“speedball”). Cocaine purchased on the street may contain adulterant drugs such as lidocaine or benzocaine (See Anesthetics, Local) or stimulants such as caffeine (See Caffeine), methamphetamine [See Amphetamines], ephedrine (See Pseudoephedrine, Phenylephrine, and Other Decongestants), and phencyclidine (See Phencyclidine (PCP) and Ketamine). Most illicit cocaine in the United States is adulterated with levamisole, an antiparasitic drug that can cause agranulocytosis.

The “free base” form of cocaine is preferred for smoking because it volatilizes at a lower temperature and is not as easily destroyed by heat as the crystalline hydrochloride salt. Free base is made by dissolving cocaine salt in an aqueous alkaline solution and then extracting the free base form with a solvent such as ether. Heat sometimes is applied to hasten solvent evaporation, creating a fire hazard. “Crack” is a free base form of cocaine produced by using sodium bicarbonate to create the alkaline aqueous solution, which is then dried.

  1. Mechanism of toxicity. The primary actions of cocaine are local anesthetic effects (See Anesthetics, Local), CNS stimulation, and inhibition of neuronal uptake of catecholamines.

    1. Central nervous system stimulation and inhibition of catecholamine uptake result in a state of generalized sympathetic stimulation very similar to that of amphetamine intoxication [See Amphetamines].

    2. Cardiovascular effects of high doses of cocaine, presumably related to blockade of cardiac cell sodium channels, include depression of conduction (QRS prolongation) and contractility. Cocaine-induced QT prolongation also has been described.

    3. Pharmacokinetics. Cocaine is well absorbed from all routes, and toxicity has been described after mucosal application as a local anesthetic. Smoking and IV injection produce maximum effects within 1–2 minutes, whereas oral or mucosal absorption may take up to 20–30 minutes. Once absorbed, cocaine is eliminated by metabolism and hydrolysis, with a half-life of about 60 minutes. In the presence of ethanol, cocaine is transesterified to cocaethylene, which has similar pharmacologic effects and a longer half-life than cocaine (see also Table II–61.)

  2. Toxic dose. The toxic dose is highly variable and depends on individual tolerance, the route of administration, and the presence of other drugs, as well as other factors. Rapid IV injection or smoking may produce transiently high brain and heart levels, resulting in convulsions or cardiac arrhythmias, whereas the same dose swallowed or snorted may produce only euphoria.

    1. The usual maximum recommended dose for intranasal local anesthesia is 100–200 mg (1–2 mL of 10% solution).

    2. A typical “line” of cocaine to be snorted contains 20–30 mg or more. Crack usually is sold in pellets or “rocks” containing 100–150 mg.

    3. Ingestion of 1 g or more of cocaine is likely to be fatal.

  3. Clinical presentation

    1. Central nervous system manifestations of toxicity may occur within minutes after smoking or IV injection or may be delayed for 30–60 ...

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