Pediatric Cocaine Abuse

No Results

No Results


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. [1]

The National Institute on Drug Abuse (NIDA) estimates that 10% of people who begin to use cocaine graduate to heavy use. [2] 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. [3] 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. [4] 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. [5, 6, 7]

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.

Cocaine causes a significant release of catecholamines and blocks their presynaptic reuptake. The state of elevated catecholamines leads to tachycardia, hypertension, and increased myocardial oxygen consumption. Enhanced alpha-adrenergic stimulation provokes arterial vasospasm, including the coronary arteries. Cocaine also promotes platelet aggregation, decreases prostacyclin production and release, and increases thromboxane A production.

Local increased levels of platelet-derived serotonin may lead to vasospasm sufficient to provoke distal myocardial ischemia or myocardial infarction (MI). [8] Chronic cocaine use leads to accelerated atherosclerosis. The dopamine depletion that accompanies chronic cocaine use can lead to coronary vasoconstriction. Thus, cocaine-related myocardial insults could be caused by coronary atherosclerosis, coronary spasm, or both; tachycardia and hypertension may increase myocardial work.

Direct toxic effects on the cardiac muscle include focal myocarditis, fibrosis, and hypertrophy. These histologic changes provide anatomical substrates for dysrhythmias (ie, may be an area of slower conduction and may lead to reentry tachycardia) during a catecholamine surge. Cocaine has sodium channel blockade effects. Resultant intraventricular conduction delays can lead to cardiac output corrected for heart rate, electrocardiographic wave (QRS) complex widening, and possible (QTc) prolongation. Large cocaine doses may even induce a state of severe myocardial dysfunction (myocardial stunning) that may lead to bradycardia and even death.

Chronic depletion of dopamine from long-term cocaine use can impair functioning of the extrapyramidal motor system; consequences include dystonic reactions, bradykinesias, and parkinsonian movements. Cocaine use increases the risk of dystonic reactions when used with medications that antagonize nigrostriatal dopamine function (eg, neuroleptics). Unusual motor activity (“crack dancing”) may also be observed.

Cocaine lowers the seizure threshold. Most patients with subarachnoid and intracerebral hemorrhages after cocaine use have underlying vascular abnormalities that rupture as a result of cocaine’s acute hypertensive effect. Hemorrhagic and ischemic strokes may develop as a result of atherosclerosis and acute and chronic hypertensive states. Vasospasm and increased platelet aggregation may also play a role in CNS infarctions.

Cocaine also blocks sodium channels, thus lessening the membrane potential and the action potential while lengthening the duration of the action potential. This action causes local anesthetic effects. Cocaine, in the form of tetracaine, adrenalin, and cocaine (TAC), continues to be used in medicine, primarily for its topical anesthetic effects in laceration repair. Cocaine is used widely as a local anesthetic in ear, nose, and throat (ENT) and ophthalmologic procedures.

Wider use of crack cocaine has increased the incidence of pulmonary hemorrhage, pneumonitis, pneumomediastinum, pneumothorax, asthma, and pulmonary edema. Barotrauma and immunologic reactions to cocaine adulterants and foreign bodies are responsible for most pulmonary effects.

Cocaine toxicity and resultant hyperactivity may lead to hyperthermia.

Cocaine-induced vasospasm can cause intestinal or splenic ischemia following all routes of cocaine use. Of particular note are “body packers” and “body stuffers.” Cocaine body packers ingest usually well-sealed packages of cocaine to avoid detection as they smuggle the drugs across borders. Body stuffers, in contrast, attempt to avoid detection during an impending arrest by hastily ingesting poorly constructed packets of drug.

Cocaine can cause renal failure by rhabdomyolysis or direct renal infarction. Hyperthermia, seizures, or prolonged unconsciousness can lead to rhabdomyolysis.

Cocaine use has well-known negative effects on pregnancy, including an increased risk of preterm labor, abruptio placentae, spontaneous abortions, and intrauterine growth retardation. [9, 10] Newborns can be born addicted to cocaine and go through withdrawal within 48 hours of birth. The following effects may also occur:

Increased spotting or vaginal bleeding

Precipitous labor

Placental insufficiency

Premature rupture of membranes


Intrauterine fetal demise

Breech presentation

Low birth weight

What makes cocaine so addictive? The drug causes a significant release of catecholamines and blocks their presynaptic reuptake. Catecholamine excess causes a physiologically and behaviorally excited state.

A similar but more moderate effect on dopamine and serotonin occurs. Elevated dopamine may be the root of positive reinforcement and addiction, according to current hypotheses. Dopamine has been implicated in the incentive motivational effects of food, sex, and several abused drugs.

All commonly abused drugs stimulate the brain’s limbic system. The limbic system is a group of well-defined structures that communicate with each other to regulate memory, learning, and emotions. The limbic system networks with the hypothalamus, which coordinates the interaction between many brain structures. The limbic system also communicates with the frontal lobe, which is the central area for perceptions, feelings, and speech. Indeed, the structural center for pleasure perceptions is located in the nucleus accumbens of the limbic system. Localized dopamine elevations support this theory. All psychoactive drugs affect sleep, level of alertness, perceptions, emotions, movement, judgment, and attention.

Use of cocaine, a psychoactive drug, can lead to significant and socially unacceptable behavioral and psychological changes that are destructive to the user or others. Cocaine-associated environments, people, and thoughts become etched into the memory of the cocaine user.

Cocaine’s effects are biphasic; the pleasurable “rush” or “high” is temporary and is followed by a “crash” as binding sites release cocaine and dopamine and other neurotransmitters resume reuptake. The user slips into a state of physical exhaustion and diminished alertness and emotion. The symptoms in some individuals may include agitation, anxiety, and psychosis.

Cocaine’s dopamine-driven rush serves as a positive reinforcement for repeated cocaine use. With continued use, the nervous system adapts to the drug’s effects. Up-regulation of presynaptic binding sites results in less intense pleasure from a given amount of the drug, promoting increased cocaine use.

Patients may be exhausted and can sleep for long hours after intense or prolonged cocaine binges due to dopamine depletion. This is called the “washout phase”.

Intense and unpleasant withdrawal symptoms contribute to eventual dependence on the drug. Psychiatric symptoms are evident in most substance users during intoxicated and withdrawal states. About 60% of cocaine users say they have experienced psychiatric problems related to drug use. Almost 20% of patients report tactile or visual hallucinations. Their most common hallucination is formication, the sensation of bugs crawling on the skin. Persistent or worsening symptoms suggest a comorbid psychiatric disorder that requires treatment.

United States

In 2014, there were 1.5 million current cocaine users aged 12 or older, or 0.6 percent of the population. Of these users, 39,000 were adolescents aged 12 to 17, including 8,000 who used crack. [1]


Cocaine continues to be a major drug of abuse internationally. In Mexico, for example, patients in drug abuse treatment programs in 16 cities report cocaine as the primary drug of choice.

Regarding emergency department (ED) visits in 2011, the Drug Abuse Warning Network (DAWN) reports that cocaine and marijuana were the most commonly involved drugs, with 505,224 ED visits (40.3%) and 455,668 ED visits (36.4%), respectively. [11]

In the 2013 Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among Hispanic (9.5%) than white (4.8%) and black (2.1%) students. [12]

In a study of racial and ethnic variations in substance-related disorders in the US, Wu et al concluded that substance use is widespread among Native American, white, Hispanic, and multiple race/ethnicity adolescents. [13]

In the 2013 National Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among male (6.6%) than female (4.5%) students. [12]

According to the 2013 National Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among 11th-grade (6.8%) and 12th-grade (7.1%) than 9th-grade (4.4%) and 10th-grade (4.0%) students, higher among 11th-grade female (5.8%) than 10th-grade female (3.1%) students, and higher among 11th-grade male (7.9%) and 12th-grade male (9.5%) than 9th-grade male (4.6%) and 10th-grade male (5.0%) students. [12]

Data from the 2014 Monitoring the Future study show that among students surveyed as part of the last fifteen years, cocaine use has declined in all three grades; annual 12th grade use stands at a historical low of just 2.6% in 2014, with use by 8th and 10th graders still lower. [14]

Center for Behavioral Health Statistics and Quality. Behavioral Health Trends in the United States: Results from the 2014 National Survey on Drug Use and Health. SAMHSA. Available at September 2015; Accessed: December 10, 2015.

NIDA. Cocaine abuse and addiction. National Institute on Drug Abuse: Research Report Series. 1999.

SAMHSA. Overview of Findings from the 2004 National Survey on Drug Use and Health. 2005.

Flórez-Salamanca L, Secades-Villa R, Hasin DS, Cottler L, Wang S, Grant BF, et al. Probability and predictors of transition from abuse to dependence on alcohol, cannabis, and cocaine: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Am J Drug Alcohol Abuse. 2013 May. 39(3):168-79. [Medline]. [Full Text].

Delaney-Black V, Chiodo LM, Hannigan JH, Greenwald MK, Janisse J, Patterson G, et al. Prenatal and postnatal cocaine exposure predict teen cocaine use. Neurotoxicol Teratol. 2011 Jan-Feb. 33(1):110-9. [Medline].

Gerteis J, Chartrand M, Martin B, Cabral HJ, Rose-Jacobs R, Crooks D, et al. Are there effects of intrauterine cocaine exposure on delinquency during early adolescence? A preliminary report. J Dev Behav Pediatr. 2011 Jun. 32(5):393-401. [Medline]. [Full Text].

Buckingham-Howes S, Berger SS, Scaletti LA, Black MM. Systematic review of prenatal cocaine exposure and adolescent development. Pediatrics. 2013 Jun. 131(6):e1917-36. [Medline]. [Full Text].

Boghdadi MS, Henning RJ. Cocaine: pathophysiology and clinical toxicology. Heart Lung. 1997 Nov-Dec. 26(6):466-83; quiz 484-5. [Medline].

Chasnoff IJ, Lewis DE, Griffith DR. Cocaine and pregnancy: clinical and toxicological implications for the neonate. Clin Chem. 1989 Jul. 35(7):1276-8. [Medline].

Chasnoff IJ, Burns WJ, Schnoll SH. Cocaine use in pregnancy. N Engl J Med. 1985 Sep 12. 313(11):666-9. [Medline].

Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality. The DAWN Report: Highlights of the 2011 Drug Abuse Warning Network (DAWN) Findings on Drug-Related Emergency Department Visits. SAMHSA. Available at February 22, 2013; Accessed: December 10, 2015.

Kann L, Kinchen S, Shanklin SL, Flint KH, Kawkins J, Harris WA, et al. Youth risk behavior surveillance–United States, 2013. MMWR Surveill Summ. 2014 Jun 13. 63 Suppl 4:1-168. [Medline].

Wu LT, Woody GE, Yang C, Pan JJ, Blazer DG. Racial/Ethnic variations in substance-related disorders among adolescents in the United States. Arch Gen Psychiatry. 2011 Nov. 68(11):1176-85. [Medline].

Johnston, L. D., O’Malley, P. M., Miech, R. A., et al. Monitoring the Future national survey results on drug use: 1975-2014: Overview, key findings on adolescent drug use. Available at 2015; Accessed: December 10, 2015.

Wong SS, Zhou B, Goebert D, Hishinuma ES. The risk of adolescent suicide across patterns of drug use: a nationally representative study of high school students in the United States from 1999 to 2009. Soc Psychiatry Psychiatr Epidemiol. 2013 Oct. 48(10):1611-20. [Medline].

Aleksa K, Walasek P, Fulga N, Kappur B, Gareri J, Koren G. Simultaneous detection of seventeen drugs of abuse and metabolites in hair using solid phase micro extraction (SPME) with GC/MS. Forensic Sci Int. 2011 Oct 31. [Medline].

Warner TD, Behnke M, Eyler FD, Szabo NJ. Early adolescent cocaine use as determined by hair analysis in a prenatal cocaine exposure cohort. Neurotoxicol Teratol. 2011 Jan-Feb. 33(1):88-99. [Medline].

Weekes AJ, Quirke DP. Emergency echocardiography. Emerg Med Clin North Am. 2011 Nov. 29(4):759-87. [Medline].

Lundqvist T. Imaging cognitive deficits in drug abuse. Curr Top Behav Neurosci. 2010. 3:247-75. [Medline].

Cummings JR, Wen H, Druss BG. Racial/Ethnic differences in treatment for substance use disorders among u.s. Adolescents. J Am Acad Child Adolesc Psychiatry. 2011 Dec. 50(12):1265-74. [Medline].

Kann L, Kinchen SA, Williams BI. Youth risk behavior surveillance–United States, 1999. MMWR CDC Surveill Summ. Jun 2000. 49(5):1-32. [Medline]. [Full Text].

Bracken BK, Rodolico J, Hill KP. Sex, age, and progression of drug use in adolescents admitted for substance use disorder treatment in the northeastern United States: comparison with a national survey. Subst Abus. 2013. 34(3):263-72. [Medline]. [Full Text].

Bukstein O. Practice parameters for the assessment and treatment of children and adolescents with substance use disorders. American Academy of Child and Adolescent Psychiatry. J Am Acad Child Adolesc Psychiatry. 1997 Oct. 36(10 Suppl):140S-56S. [Medline].

Das G, Laddu A. Cocaine: friend or foe? (Part 2). Int J Clin Pharmacol Ther Toxicol. 1993 Oct. 31(10):489-96. [Medline].

Dressler FA, Malekzadeh S, Roberts WC. Quantitative analysis of amounts of coronary arterial narrowing in cocaine addicts. Am J Cardiol. 1990 Feb 1. 65(5):303-8. [Medline].

Green RM, Kelly KM, Gabrielsen T. Multiple intracerebral hemorrhages after smoking “crack” cocaine. Stroke. 1990 Jun. 21(6):957-62. [Medline].

Marzuk PM, Tardiff K, Leon AC. Fatal injuries after cocaine use as a leading cause of death among young adults in New York City. N Engl J Med. 1995 Jun 29. 332(26):1753-7. [Medline].

Miller NS, Brady KT. Addictive disorders. Psychiatr Clin North Am. 2004 Dec. 27(4):[Medline].

Ross SM, Chappel JN. Substance use disorders. Difficulties in diagnoses. Psychiatr Clin North Am. 1998 Dec. 21(4):803-28. [Medline].

Schuler ME, Nair P, Kettinger L. Drug-exposed infants and developmental outcome: effects of a home intervention and ongoing maternal drug use. Arch Pediatr Adolesc Med. 2003 Feb. 157(2):133-8. [Medline].

Anthony J Weekes, MD, RDMS, RDCS Ultrasound Fellowship Director, Associate Director of Emergency Ultrasound, Department of Emergency Medicine, Carolinas Medical Center

Anthony J Weekes, MD, RDMS, RDCS is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Douglas S Lee, MD Attending Physician, Department of Emergency Medicine, Naples Community Hospital

Douglas S Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Caroly Pataki, MD Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Chet Johnson, MD Professor of Pediatrics, Associate Director and Developmental-Behavioral Pediatrician, KU Center for Child Health and Development, Shiefelbusch Institute for Life Span Studies; Assistant Dean, Faculty Affairs and Development, University of Kansas School of Medicine

Chet Johnson, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Pediatric Cocaine Abuse

Research & References of Pediatric Cocaine Abuse|A&C Accounting And Tax Services