Tuesday, February 7, 2023

Pediatric Cocaine Abuse

Background

According to the 2014 National Survey on Drug Use and Health, there were 39,000 adolescents aged 12 to 17 who were current users of cocaine in 2014, including 8,000 who used crack. These numbers represent 0.2 percent of adolescents who used cocaine and less than 0.1 percent who used crack.

The National Institute on Drug Abuse (NIDA) estimates that 10% of people who begin to use cocaine graduate to heavy use.
Adolescent drug use typically develops out of curiosity about available substances. Use begins in a social environment with drugs that are legal for adults and available to minors (eg, alcohol, cigarettes). Children and adolescents rarely experiment with an illicit drug such as cocaine prior to trying alcohol and cigarettes.

Academic and psychosocial impairments are particularly important in pediatric substance abuse. Role impairment at home, school, work, close relationships, and in social life are clues to either a psychiatric disorder, substance abuse, or both. The most common psychiatric conditions associated with substance abuse disorders are mood and anxiety disorders, attention deficit hyperactivity disorder, and antisocial personality disorders. Persons with a major depressive episode were more likely than those without a major depressive episode to abuse or have dependence on illicit drugs. In 2004, 22% of those surveyed in the 12- to 17-year-old age group received treatment or counseling within the past year for emotional or behavioral problems.
This number underestimates the actual percentage of youths with depression and other psychiatric illness.

A family history of substance abuse may be a risk factor for early cocaine use and for rapid dependence on cocaine. The following discussion on pediatric cocaine abuse almost exclusively applies to adolescents.
However, accidental ingestion of cocaine, passive inhalation of crack cocaine smoke, and transmission through breast milk have been reported as means of cocaine exposure in infants.

Cocaine is obtained from the leaves of the Erythroxylon coca and other Erythroxylon trees indigenous to Colombia, Bolivia, Peru, Indonesia, and the West Indies. For centuries, Amerindian workers who traveled in mountainous South American countries have chewed coca leaves, a practice they believe improves their stamina and suppresses hunger.

Deliberate extraction of cocaine from coca leaves began in the second half of the 19th century. Several uses of cocaine were marketed and advocated. Sigmund Freud wrote of cocaine’s potential to treat asthma, syphilis, and wasting diseases. Halstead used cocaine’s anesthetic effects to perform nerve blocks. Curiously, both these prominent advocates of the medicinal values of cocaine became addicted to the substance.

Cocaine ingestion increased with use of several preparations, including beverages such as early 20th century Coca Cola. Recreational and fashionable use brought increasing reports of cocaine-related morbidities and several fatalities. The Harrison Narcotics Act of 1914 made unprescribed use of cocaine illegal. Elaborate levels of cocaine production, smuggling, and distribution have challenged efforts to diminish supply. Despite extensive drug control policies, cocaine’s popularity surged in the 1970s and 1980s. The high potency and relatively cheap cost of crack cocaine created another US cocaine epidemic.

By the late 1970s, modifications in cocaine processing led to the development of freebase and crack cocaine. Cocaine (C17 H21 NO4), when treated with hydrochloric acid, becomes a water-soluble hydrochloride salt, which can be absorbed through the nasal mucosa and can be taken intravenously (IV).

Freebase is formed when aqueous hydrochloride salt is added to ammonia to form a base, which then is dissolved in ether. The ether then evaporates. Residual ether is flammable and can pose a danger when heated.

Crack cocaine is formed when the aqueous hydrochloride salt is mixed with baking soda and then heated. The soft mass that forms is left to harden into a rock or slab of crack cocaine. This form of cocaine is the cheapest and most potent. Smoked crack is rapidly absorbed by the pulmonary vasculature and reaches the brain’s circulation in 6-8 seconds. Other drugs (eg, alcohol, nicotine, heroin) frequently are used either in parallel or as a direct mixture with cocaine.

Cocaine powder can be absorbed across any mucous membrane of the body; the nasal route is most common. Snorting or insufflation is usually performed through a straw-like apparatus or from a spoon. Effect onset typically occurs in 3 minutes, peaks in 15 minutes, and lasts 45-90 minutes. The intranasal (IN) route has slower absorption because of cocaine’s vasoconstrictive effects on the nasal mucosa. The IV route of self-administered cocaine yields an onset of action in 15 seconds, peaks in 3-5 minutes, and lasts 40-60 minutes.

Cocaine is primarily metabolized by plasma cholinesterases. A small portion is metabolized in the liver by carboxylesterase and less than 10% is metabolized by N -methylation in the liver to norcocaine. In pregnancy, cocaine diminishes maternal and fetal plasma cholinesterase activity, leading to prolonged presence and effect in pregnant women. Approximately 1-5% of cocaine is not metabolized and is excreted unchanged in the urine. Immunoassays can detect benzoylecgonine 3-6 hours after use.

Alcohol used with cocaine increases the drug’s bioavailability. In addition, alcohol allows carboxylesterase to transfer an ethyl group to cocaine to form cocaethylene. Cocaethylene, as is true with cocaine, eventually is metabolized to benzoylecgonine. With a half-life of 2.5 hours (compared with cocaine’s 40 min), cocaethylene has fewer dysphoric effects than cocaine, but its other toxic effects are more potent.

Chronic nicotine use can damage blood vessels and, just as cocaine, can increase atherosclerotic development or coronary spasm and its consequences.

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