eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics

Substance Abuse: Cocaine

Anthony J Weekes, MD, RDMS, RDCS, Assistant Professor of Emergency Medicine, Albert Einstein College of Medicine; Director of Emergency Ultrasound, Department of Emergency Medicine, Montefiore Medical Center
Douglas S Lee, MD, Attending Physician, Department of Emergency Medicine, Naples Community Hospital

Updated: Mar 12, 2008

Introduction

Background

The 1998 National Household Survey on Drug Abuse revealed that 0.8% of US children aged 12-17 years had used cocaine in the previous month.¹ In June 2000, the Centers for Disease Control and Prevention (CDC) reported that 4% of 15,349 students in grades 9-12 reported cocaine use at least once in the prior month.² In 1991, 1.9% of students reported cocaine use at least once in the previous month.

Most recently, the 2004 National Survey on Drug Use and Health (NSDUH), formerly called the National Household Survey on Drug Abuse, focused on 3 major age groups, including the 12- to 17-year-old age group.³ The drug use information gathered was pertinent to civilians (nonmilitary) and residents of households and noninstitutional group housing facilities. Military personnel, residents of institutionalized group housing centers (eg, jails, hospitals), and homeless individuals not in shelters were not included. The 2004 NSDUH reported that 2.4% of the 12- to 17-year-old age group used cocaine at some point in their life, 1.6% used cocaine within the past year, and 0.5% used cocaine within the past month. Prevalence of cocaine use in this age group was similar to the use of ecstasy and inhalants but was notably less than cigarettes, alcohol, or marijuana.

The National Institute on Drug Abuse (NIDA) estimates that 10% of people who begin to use cocaine graduate to heavy use.⁴ 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. 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 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 strawlike 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 serum 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. Pregnancy significantly enhances metabolism. In addition, 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. Urinalysis can detect cocaine 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.

Pathophysiology

Cardiac

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).⁵ 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 quinidinelike effects. Resultant intraventricular conduction delays can lead to cardiac output corrected for heart rate (QTc) prolongation and electrocardiographic wave (QRS) complex widening. Large cocaine doses can induce a state of negative inotropy that may lead to bradycardia and even death.

Neurologic

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).

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.

Pulmonary

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.

GI

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.

Renal

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

Obstetrical

Cocaine use has well-known negative effects on pregnancy, including an increased risk of preterm labor, abruptio placentae, spontaneous abortions, and intrauterine growth retardation.^6,7 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
• Stillbirth
• Intrauterine fetal demise
• Breech presentation
• Low birth weight

Psychiatric

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.

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.

Frequency

United States

Approximately 50 million Americans have used cocaine at least once. According to preliminary results of the 1997 National Household Survey, approximately 1.5 million Americans currently use cocaine.¹ In 1985, approximately 3% of the population used cocaine (5.7 million people). In 1992, usage rates declined to 0.7% (1.4 million people) and remained essentially unchanged in 1997. Rates of frequent use, defined as cocaine use on 51 or more days in the past year, remained similar from 1985-1997; 600,000-700,000 Americans described themselves as frequent cocaine users. One quarter of the 12- to 17-year-old age group in the 2004 NSDUH reported that obtaining cocaine or crack was easy.³

International

Cocaine abuse has become an increasingly international public health concern.

Mortality/Morbidity

According to the National Household Survey, one third of deaths after cocaine use were due to drug intoxication; the remaining two thirds were associated with traumatic injuries (eg, homicides, suicides, falls, motor vehicle collisions).¹ For morbidity information, see Pathophysiology.

Race

The 2004 NSDUH reported current illicit drug in the 12- to 17-year-old age group of 26% among American Indians or Alaskan Natives, 12.2% of those reporting 2 or more races, 11.1% among whites, 10.2% among Hispanics, 9.3% among blacks, and 6% among Asians.¹

Sex

In 1997, men continued to have a higher rate of current cocaine use (0.9%) than women (0.5%). In the 2004 NSDUH report, the rate of substance abuse or dependence was similar among females and males in the 12- to 17-year-old age group.¹

Age

• A few other studies have examined cocaine use among teenagers. The NIDA, part of the National Institute of Health (NIH), funds the Monitoring the Future Survey, conducted by the University of Michigan's Institute for Social Research.⁴ Since 1975, this survey has tracked illicit drug use and related attitudes of 12th-grade students; in 1991, students in the eighth and 10th grades were added to the study. For the 1999 study, 49,866 students were surveyed from a representative sample of 422 public and private schools nationwide. This survey noted that lifetime prevalence of cocaine use was 4.7% for students in the eighth grade, 7.7% for students in 10th grade, and 9.8% for students in 12th grade.
• According to the NIH, the highest rate of current cocaine use in 1997 was among persons aged 18-25 years (1.2%).⁴ In other age groups, rates were 1% for persons aged 12-17 years, 0.9% for persons aged 26-34 years, and 0.5% for persons aged 35 years and older.
• Rates declined from 1996-1997 for adults aged 18-25 years and 26-34 years; rates remained stable for other age groups.

Clinical

History

Any patient who presents with symptoms of a cardiac, vascular, pulmonary, neurologic, or psychological problem should provide a drug history. Coordination, response, and judgment may have been influenced by psychoactive drugs in patients involved in vehicular accidents, falls, near-drowning experiences, domestic violence, rapes, and other violent acts or misfortunes. The history should attempt to elicit answers to the following questions:

• Identifying the drug or drugs
  • Which drug was used?
  • Was the drug used with any other drugs?
  • How much of the drug was used?
  • The use occurred over what period of time?
  • Was the drug obtained from a usual source?
• Prior cocaine use
  • Has the patient used cocaine before?
  • How often?
  • How much?
  • By what route?
  • How long?
  • Has tolerance developed?
  • What withdrawal signs have developed in the past?
• Alcohol and nicotine use
  • Does the patient use nicotine or alcohol?
  • What is the extent of either use or dependence?
  • Does the patient smoke or drink before or during cocaine use?
• Existing symptoms
  • What symptoms present?
  • Are pain (eg, headache, chest, extremity, abdominal), respiratory problems, anxiety, confusion, seizures, hallucinations, altered mental status, syncope, or dizziness present?
  • Did these symptoms occur with prior use of cocaine?
  • How long after cocaine use did symptoms begin?
  • Are these symptoms due to withdrawal from cocaine?
• Comorbid medical conditions
  • Does the patient have other medical conditions (eg, liver disease, pregnancy [lowered serum cholinesterases]) that may lead to greater toxicity from cocaine?
  • Comorbid disorders may include the following:
    • Suicidal ideation or behavior
    • Mood disorders
    • Attention deficit hyperactivity disorder
    • Anxiety disorder
    • Sleep disturbances
    • Oppositional defiant disorder/behavior
    • Schizophrenia or psychotic symptoms
    • Conduct disorder or antisocial behavior
    • Eating disorder
    • Aggressive behavior
    • Developmental problems
• Behaviors prompting this evaluation: What behaviors prompted this evaluation? Many psychiatrically disturbed adolescents and young adults brought into emergency departments (EDs) because of emotional outbursts or demonstrative, even dangerous, extremes of behavior may be intoxicated with psychoactive drugs, such as phencyclidine (PCP), cocaine, amphetamines, and lysergic acid diethylamide (LSD). Knowing the duration of action of the various illicit drugs (eg, cocaine's stimulatory effects typically last for 1 h, whereas amphetamines usually cause stimulation for several hours) can help the clinician to determine if behavior displayed is due to a drug or due to an underlying psychiatric illness.
• History of present illness from caregiving sources: Elicit reasons for the concern if it is a referral or complaint. What led to the referral and what outcome is expected by the referring person? Determine parents' knowledge of the child's cocaine use patterns and any response and attitude to prior substance abuse treatment.
• Interactions with peers and environment
  • Does the patient show any signs of disruptive behaviors or practices present?
  • Does the patient have prosocial hobbies, interests, or recreational activities?
• Family history
  • Do any family members have histories of substance use or abuse?
  • Are any family members currently involved in substance use or abuse?
  • What are family members' attitudes about substance abuse?
  • Do any family members have a history of psychiatric disorders?
  • What is the family's socioeconomic status?
  • What is the nature of family functioning (ie, support styles, interaction of family members, demonstrated behaviors and emotions, supervision, disciplinary methods, family stressors)?
  • What family stressors (eg, physical or sexual abuse, neglect, violence, other trauma) are present?
• Developmental history
  • Does the patient have developmental delays that may affect current functioning?
  • Does the patient have social skills or communication deficits?
  • What was the patient's highest level of functioning prior to substance use?
• Full medical history
• School performance and attitudes toward school
• Job history
• RAFFT questionnaire: The RAFFT questionnaire is a sensitive screening instrument for identifying substance abuse.
  • R (relax): Does the individual drink or take drugs to relax, improve self-image, or fit in?
  • A (alone): Does the individual ever drink or take drugs while alone?
  • F (friends): Do any close friends drink or use drugs?
  • F (family): Does a close family member have a problem with alcohol or drugs?
  • T (trouble): Has the individual ever gotten into trouble from drinking or taking drugs?

Physical

Because of the myriad of acute and chronic effects of cocaine use and abuse, the physical examination can be revealing, even in patients who are not acutely intoxicated.

• Vital signs: The patient may be hyperthermic, tachycardic, and hypertensive; however, a patient who abuses cocaine and is not currently intoxicated may have normal vital signs.
• Head, ears, eyes, nose, and throat (HEENT): Nasal septal ulcerations or perforations with atrophy of the mucosa suggest IN cocaine abuse. Patients intoxicated with cocaine may have a sympathomimetic syndrome with mydriasis. The patient may have "crack eye," with corneal abrasions and ulcerations from the heat and particulate smoke of crack. Singed nasal hairs and carbonaceous sputum may suggest thermal burns of the respiratory tract.
• Lungs: Pneumothorax and pneumomediastinum may result from crack use. Careful listening to the lungs and assessing for any subcutaneous air is important. Cocaine use may also lead to noncardiogenic pulmonary edema or to diffuse alveolar hemorrhage. Wheezing may occur from exacerbated asthma or hypersensitivity pneumonitis.
• Cardiac: Cocaine use is associated with MI, aortic dissection, endocarditis, cardiomyopathy, and bradycardia, as well as virtually all types of tachydysrhythmia. Careful auscultation of the heart, close monitoring, assessment of the pulses, and an ECG are important.
• GI: Inspect the abdomen for distension, ecchymosis, and bowel sounds. Pain out of proportion to tenderness may suggest bowel ischemia. A rectal examination to detect GI bleeding is indicated.
  • Body packers: Cocaine is carefully wrapped in small well-sealed packets. If body packing is suspected, carefully search the patient's body cavities.
  • Body stuffers: Cocaine is hastily ingested. Carefully search the patient's body cavities if stuffing is suspected.
• Skin: Inspect skin for needle punctures (ie, "track marks") or evidence of "skin-popping." Cellulitis, abscesses, and retained needles are complications. Acutely intoxicated patients may be warm and diaphoretic, in contrast to patients who have anticholinergic toxicity, who present with hot and dry skin.
• Neurologic: Conduct a thorough neurologic examination of any patient with possible cocaine abuse. Mental status, strength, reflexes, sensation, and gait help determine the possibility of cerebral ischemia, infarction, subarachnoid hemorrhage, movement disorders, or seizures.
• Obstetrical: Assess both fetal and maternal health. Fetal heart and motion monitoring is important. Withhold bimanual examination for third-trimester bleeding until ultrasonography can exclude a placenta previa or abruptio diagnosis.

Causes

The NIDA has identified the following risk factors for the development of drug use and abuse:⁴

• Unstable home environment due to parental substance abuse or mental illness
• Fractured relationship of parents and adolescent or child
• Poor level of supervision of the adolescent's activities
• Peer use of drugs
• Liberal parental attitude of their own drug use or adolescent's use of drugs
• Children with conduct disorder or difficult temperaments coupled with ineffective parenting
• Poor performance in school
• Apparent ambivalence or approval of drug-using behavior in the school, peer group, or the community
• Availability of drugs in the community, peer group, or home environment

Differential Diagnoses

Other Problems to Be Considered

Amphetamine abuse
Anticholinergic toxicity
Neuroleptic malignant syndrome
Serotonin syndrome
Withdrawal syndromes

Workup

Laboratory Studies

• CBC count can reveal suspected infection or anemia.
• Assess electrolytes and glucose levels.
• Creatine kinase with isoenzyme containing M and B subunits (MB) index may be diagnostic.
  • Rhabdomyolysis is a common complication of cocaine use, and muscle symptoms fail to predict its development.
  • Cocaine use can cause MI in patients with no other cardiac risk factors.
• Perform a urinalysis with drug screening.
  • Dipstick can detect myoglobin in the urine.
  • Initial urine screening is performed by an immunochemical assay and is not 100% specific.
• Gas chromatography-mass spectrometry detects cocaine and its metabolites as many as 14 days after significant cocaine use.

Imaging Studies

• Clinical findings dictate the need for imaging studies.
• Chest radiography can help reveal pulmonary edema, focal infiltrates, inhaled foreign bodies, pneumothorax, and pneumomediastinum. Also, chest radiographic findings can reveal cardiomyopathies and aortic dissection. Upright films are used to reveal free air in the abdomen.
• Abdominal radiography is used to identify body packers.
• Ultrasonography is useful in a trauma situation and can also be used to detect placental and fetal insult. Myocardial injury can be detected as hypokinesis or akinesis.
• Head CT scanning detects intracranial hemorrhage or cerebral infarction in patients complaining of cocaine-associated headaches, seizures, or neurologic deficits.
• Abdominal CT scanning can identify a segment of ischemic bowel.
• Brain CT scanning is highly recommended in patients with cocaine-induced seizures because of the risk of intracranial hemorrhages.

Other Tests

• Use 12-lead ECG and cardiac monitoring to evaluate for arrhythmias or ST- or T-wave abnormalities that suggest ischemia or infarction and conduction abnormalities.
• Consider human immunodeficiency virus (HIV) counseling and testing, especially if physical health is deteriorating or when risk factors for HIV infection are noted. Consent is necessary. Hepatitis viral serologies may be indicated. A history of IV use of cocaine with or without other drugs puts the young patient at an increased risk for acquiring new hepatitis C virus infections or developing chronic hepatic C infections.
• Consider sexually transmitted disease exposure and testing for infections in patients using cocaine or other illicit drugs.

Treatment

Medical Care

Unless a patient presents in an acutely intoxicated state or with cocaine-related complaints, the most important intervention is education and prevention. Most mild intoxications require only supportive care. Prevention of absorption is difficult because most cocaine exposures travel through IN, IV, or intrapulmonary routes.

Cocaine abuse and addiction is a complex mixture of neurobiologic, social, environmental, and familial problems. No pharmacologic agents have proven effective to treat or counteract cocaine addiction, although the NIDA is actively involved in research on this problem. Antidopaminergic agents, disulfiram, and antidepressants for the mood swings of early abstinence have been investigated. In 1999, selegiline entered phase III of a multicenter clinical trial and has shown some promise.

• The most effective therapies available focus on behavioral interventions. Intervention should involve several approaches and should address associated psychiatric disorders.
  • Discuss the medical, behavioral, psychological, and social effects of cocaine use with patients, patients' families, and others who provide support. Family therapy and self-help groups such as Cocaine Anonymous, which use 12-step programs, can have important support roles.
  • Behavioral interventions are effective for cocaine addiction. Contingency management is a popular and effective form of behavioral therapy. Patients are awarded points for drug-free urine samples. These points then can be traded for positive prosocial items (eg, passes to a gymnasium, tickets to a movie). Cognitive-behavioral therapy's aim is to maintain recovery states by helping patients "...recognize, avoid, and cope." Substance refusal, anger control, problem solving, and leisure-time management are crucial skills needed for successful recovery.
  • Relapse prevention is challenging. Therapy provided in an outpatient setting requires frequent follow-up appointments. Missed appointments commonly signal a relapse. Examples of relapse prevention include monitoring the temptations and urges to use cocaine or other drugs, rehearsing ways to avoid friends who encourage drug use, and living with relatives who are drug-free. Relapses can range in severity from slips involving several days of drug use to resumption of regular drug use and addiction.
  • Inpatient treatments (eg, residential communities) offer 6- to 12-month stays designed to provide comprehensive treatment. Programs may include treatment for coexisting mental problems, vocational rehabilitation, and other services to help the cocaine or polydrug-addicted patient return to constructive activity in society and avoid relapse.
  • Coexisting psychiatric disorders may require treatment. Early symptoms of abstinence may resemble symptoms of a psychiatric disorder. Depression during early abstinence may be sufficiently severe to cause suicidal ideation or attempts; therefore, carefully assess cocaine users in early abstinence for mood disorder and maintain concern for their safety. Medication for psychiatric syndromes may be indicated when symptoms persist beyond a few weeks into the abstinence period. Medication may be initiated more rapidly in cases involving a documented comorbid psychiatric disorder.
  • Encourage the patient toward a community environment or activities that limit temptations for relapse and that promote prosocial alternatives to deviant behavior and relationships. Some patients' interests may be served by relocating to another neighborhood.
• Agitation and hyperthermia are the major causes of death due to cocaine toxicity. Medical treatment for these conditions includes the following:
  • Establish airway control, if necessary, and IV access.
  • Obtain a core temperature.
  • Sedation is the mainstay of treatment. Benzodiazepines are very useful in the management of toxicity. Administer benzodiazepines titrated to sedation. (Avoid neuroleptic agents, if possible, because they may impair heat dissipation, lower the seizure threshold, and cause a dystonic reaction.)
  • Avoid restraints because they may exacerbate hyperthermia and acidosis and may cause death if used alone. If necessary, use restraints only until the person is calm.
  • Aggressive cooling with ice water baths, mist and fans, and ice packs is important until a core temperature of 101-102°F is reached within 30-45 minutes.
• To treat seizures, initial airway control and IV access are critical. Subsequent management steps include the following:
  • Evaluate for hypoxia, hypoglycemia, and electrolyte disturbances.
  • Treat seizures with benzodiazepines; however, refractory cases may require phenobarbital or neuromuscular blockade. Avoid succinylcholine because of the risk of exacerbating hyperkalemia in a patient with cocaine-induced rhabdomyolysis.
  • Brain CT scanning is highly recommended in patients with cocaine-induced seizures because of the risk of intracranial hemorrhages.
• Treat hypertension as follows:
  • Treatment for agitation and anxiety often reduces the elevated blood pressure (BP); therefore, sedation with benzodiazepines is a prudent initial therapy.
  • Some patients continue to have high BP despite sedation; these individuals require other pharmacologic agents as well as sedation and decreased environmental stimuli.
  • Nitroprusside, nitroglycerin, or phentolamine can be used to lower BP more aggressively.
  • Avoid beta-blocker use because of the unopposed alpha stimulation that results. Labetalol has both alpha and beta antagonism but in a 1:7 ratio. Theoretically, labetalol has insufficient alpha blockage. Esmolol has a safer profile because of its beta-1 selective antagonism, rapid onset, and short duration of activity.
• Cardiovascular treatment includes the following:
  • Use aspirin, nitrates, and benzodiazepines to treat patients with cocaine-related myocardial ischemia.
  • Although thrombolysis may be considered, the authors strongly recommend consultation with a cardiologist.
  • The efficacy of calcium channel blockers is controversial.
  • Treatment with nonselective beta-blockers is contraindicated because they may potentiate cocaine-induced coronary vasoconstriction.
  • Depleted norepinephrine stores may result in hypotension, which necessitates treatment with dopamine or norepinephrine.
  • Ventricular dysrhythmias can be treated with bretylium.
  • Lidocaine is usually the advanced cardiac life support (ACLS) drug of choice in ventricular tachydysrhythmia. However, lidocaine may lower the seizure threshold in a patient with cocaine intoxication patient.
• Treatment for patients with rhabdomyolysis requires aggressive hydration. Diuretics, such as mannitol or furosemide, can be used to ensure that urine output is at least 3 mL/kg/h. Dialysis may be needed to treat renal failure.

Surgical Care

• Neurosurgical care may be necessary for intracranial bleeding (eg, to monitor for intracranial pressure or to surgically decompress subdural or epidural hematomas).
• Other cocaine-related complications and pertinent surgical care include the following:
  • Pneumothorax - Chest tube placement
  • Abscess - Incision and drainage
  • Fractures or dislocations - Orthopedic reduction/immobilization or intraoperative repair

Consultations

Referral to a primary care physician to exclude medical causes is recommended. A more encompassing evaluation by a child and adolescent psychiatrist is then indicated. Input from behavioral and developmental pediatric specialists should be sought for truly specialized and long-term care especially with the large volume of patients that are in need. The following additional consultants may be needed:

• Cardiologist
• Toxicologist
• Drug counselor
• Neurologist
• Neurosurgeon
• Infectious diseases specialist

Medication

Sedative-hypnotics are used to treat seizures or anxiety in agitated patients. Antihypertensive agents may be required for hypertensive emergencies.

Cardiac resuscitation in cocaine-provoked ventricular fibrillation (VF) or unstable ventricular tachycardia (VT) may be required (see Ventricular Fibrillation). Use antiarrhythmic agents after preliminary defibrillation attempts fail. Follow current ACLS guidelines.

Sedative-hypnotics

Increase release of gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter of the CNS. This category, which includes benzodiazepines and barbiturates, is useful for an agitated patient (eg, seizure control, anxiolytic, sedating). Use of these drugs is an important part of attenuating cocaine-induced chest pain, especially in patients with tachycardia and agitation.

Diazepam (Valium, Diazemuls, Diastat rectal gel)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Dosing

Adult

5-10 mg IV over 2-3 min; repeat q5-10min prn, while monitoring for hypotension and respiratory depression

Pediatric

0.2-0.5 mg/kg IV q5min (administer PR if IV access cannot be established)

Interactions

CNS toxicity increases with coadministration of phenothiazines, barbiturates, alcohols, MAOIs; Inhibitors of CYP450 isoenzymes 1A2, 2C19, 3A4 may decrease elimination and increase toxicity of diazepam

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Hypotension or respiratory depression requiring intubation; caution with use of other CNS depressants and in patients with low albumin levels or hepatic disease (may increase toxicity)

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. May depress all levels of CNS, including limbic and reticular formation, by increasing action of GABA (a major inhibitory neurotransmitter in the brain).

Dosing

Adult

4-8 mg IV at a rate of <2 mg/min; can repeat in 10-15 min if seizures persist

Pediatric

0.05-0.1 mg/kg IV infused over 2-5 min; not to exceed 4 mg/dose; may repeat with 0.05 mg/kg in 15-20 min if seizures persist

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs; CYP450 3A4 inhibitors may decrease elimination and increase toxicity

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Hypotension or respiratory depression requiring intubation; caution in patients with renal or hepatic impairment, myasthenia gravis, and organic brain syndrome

Phenobarbital (Luminal)

IV dose may require about 15 min to attain peak levels in the brain. If injected continuously until convulsions stop, brain concentrations may continue to rise and can exceed amount required to control seizures. Important to use minimal amount required and to wait for anticonvulsant effect to develop before administering a second dose.

Dosing

Adult

300-800 mg IV followed by 120-240 mg/dose at 20-min intervals until seizures controlled or total dose of 1-2 g administered

Pediatric

15-20 mg/kg over 10-15 min IV in single or divided dose; some patients may require 5 mg/kg/dose q15-30 min until seizure is controlled or 40 mg/kg administered

Interactions

Coadministration with alcohol may produce additive CNS effects and death; chloramphenicol and MAOIs may increase effects; may decrease chloramphenicol effects; MAOIs may enhance sedative effects; rifampin may decrease effects; valproic acid appears to decrease barbiturate metabolism and increase toxicity; can decrease effects of anticoagulants, and patients stabilized on anticoagulants may require dosage adjustments if barbiturates added to or withdrawn from their regimen
May decrease serum carbamazepine levels; decreased effects of contraceptives may occur because of induction of microsomal enzymes; in women, menstrual irregularities and pregnancy may occur; may decrease corticosteroid effects by inducing hepatic microsomal enzymes; may increase digitoxin metabolism; may decrease antimicrobial effects of metronidazole; decrease theophylline levels, possibly resulting in decreased effects; may decrease bioavailability of verapamil

Contraindications

Documented hypersensitivity; patients with severe respiratory disease; marked impairment of liver function; nephritis

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Hypotension or respiratory depression requiring intubation; serum levels must be monitored; in prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; use with caution in patients with fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; use with caution in patients with myasthenia gravis and myxedema

Antihypertensive agents

These agents are used to treat hypertensive emergencies.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Dosing

Adult

0.3-0.5 mcg/kg/min IV initial and use increments of 0.5 mcg/kg/min; titrate to desired effect; average dose is 1-6 mcg/kg/min; infusion rates >10 mcg/kg/min may lead to cyanide toxicity

Pediatric

Administer as in adults

Interactions

Coadministration with other hypotensive agents may increase effect

Contraindications

Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, hypothyroidism; in patients with renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside can lower BP and, thus, should be used only in patients with mean arterial pressures >70 mm Hg

Nitroglycerin (Nitro-Bid IV, Tridil)

Treats hypertension. DOC in coronary artery disease and/or vasospasm-related chest discomfort. Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production.

Dosing

Adult

12.5-25 mcg IV initial bolus; then 10-20 mcg/min IV infusion, increase by 5-10 mcg/min q5-10min until desired response

Pediatric

0.5 mcg/kg/min IV infusion; increase by 0.5-1 mcg/kg/min q20-60min until desired response

Interactions

Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of CCBs (dose adjustment of either agent may be necessary)

Contraindications

Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Requires hemodynamic monitoring and a precise infusion system; use with caution in patients with coronary artery disease and low systolic BP

Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on alpha receptors.

Dosing

Adult

2.5-5 mg IV q5min; titrate to desired response

Pediatric

0.05-0.1 mg/kg IV q5min until hypertension is controlled

Interactions

Concurrent administration of epinephrine or ephedrine may decrease phentolamine effects; ethanol increases phentolamine toxicity

Contraindications

Documented hypersensitivity; coronary or cerebral arteriosclerosis; renal impairment

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution with tachycardia, peptic ulcer, or gastritis; cerebrovascular occlusions or myocardial infarctions can occur following administration

Follow-up

Further Inpatient Care

• Admit patients who have any of the major toxicologic complications of cocaine use or when inpatient drug counseling is deemed necessary.

Further Outpatient Care

• Close medical follow-up is important for any comorbid conditions (eg, sexually transmitted diseases and HIV counseling and testing).
• Refer to a behavioral and developmental pediatric specialist, if available.

Deterrence/Prevention

• Predicting whether a given adolescent will experiment with drugs is difficult, as is determining which individuals who experiment will proceed to abuse or dependence. Parents can lessen the chance of a child or adolescent developing a substance abuse problem by providing positive role modeling, open communication, and education on the nature and dangers of drug use. Children who abuse drugs have increased risk for involvement in crime, violence, and unprotected sex and its attendant consequences. Such involvement negatively impacts not only the individual but also family, friends and acquaintances, and society as a whole. Risk factors for developing a drug problem include the following:
  • Depression
  • Low self-esteem
  • Family history of substance abuse
• Early recognition of warning signs and intervention are crucial to avert a serious drug habit. Parents should be made aware that these findings might suggest other problems and indicate the need for referral to a primary care physician and a child and adolescent psychiatrist. Warning signs include the following:
  • School - Drop in performance and/or interest, increase in absences, problems with discipline
  • Social - Change in friendships, fewer prosocial activities, problems with police
  • Emotional - Withdrawal, mood swings, very argumentative behavior, depressed state, low self-esteem, irresponsibility, apathy, poor judgment
  • Physical - Weight loss, fatigue, frequent ailments, glazed/red eyes

Complications

• Parents should be made aware that early warning signs listed above might suggest other problems. Referral to a primary care physician to exclude medical causes is recommended. A more encompassing evaluation by a child and adolescent psychiatrist is then indicated.

Patient Education

• Provide patients with information about the serious dangers cocaine use poses to their health, and present a candid picture of cocaine's effects on their psychosocial functioning.
• Discuss the high risk of relapse and the efforts necessary to combat relapse.
• Adolescents are more receptive to nonjudgmental discussions. Address an adolescent's sense of immortality by emphasizing the powerful dangers of cocaine and addiction.
• Behavioral and developmental pediatric specialists serve an important role in dealing with the volatile and/or difficult to understand child or adolescent.
• For excellent patient education resources, visit eMedicine's Substance Abuse Center. Also, see eMedicine's patient education articles Cocaine Abuse, Drug Dependence and Abuse, and Substance Abuse.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider/treat hypoglycemia: Hypoglycemia can present with symptoms ranging from mild confusion to irrational and bizarre behavior and labile mood. A rapid bedside fingerstick glucose measurement to exclude this possibility can avert a potentially fatal, yet easily correctable, medical cause of altered mental status or psychosis. Administration of IV dextrose 50% in water (D50W) solution can restore normal behavior within minutes.
• Improper restraint use: Improper restraints can lead to further muscular exertion, exacerbation of hyperthermia, lactic acidosis, rhabdomyolysis, and death. Overly aggressive restraint techniques may cause injuries (eg, lacerations, abrasions, fractures, choking). Asphyxia is possible if the patient is restrained in a prone position or is not provided adequate ventilation. If restraints are needed, use the following criteria:
  • Use of restraints should be temporary.
  • Restraints should be used with sedation that allows heat dissipation (eg, benzodiazepines). Use of butyrophenones and phenothiazines is controversial.
  • Medical personnel must monitor restrained patients.
  • Restraints should be used in conjunction with IV hydration, cooling, and adequate ventilation.
• Failure to provide accurate chest pain management: Chest pain with acute cocaine use is common, and cocaine-associated chest pain evaluation is a medicolegal minefield.
  • Aspirin remains strongly indicated.
  • Beta-blocker use is relatively contraindicated and is replaced by benzodiazepine use to treat tachycardia and hypertension.
  • Chest pain evaluation should include recent use of cocaine or any alpha stimulants as recent use of either modifies the physician's approach.
  • Chest pain in the young with cocaine use should be considered vasospastic in etiology and not discounted.
  • Cocaine-induced myocardial ischemia and myocardial infarctions are as likely to be revealed on initial ECG as normal or nonspecifically abnormal as an MI unrelated to cocaine use.
  • Acute cocaine-related chest pain typically occurs approximately 30 minutes after IV cocaine use and 2.5 hours after IN ingestion. However, chest pain occurring several hours after cocaine use should not be discounted as unrelated. If alcohol was also used, chest pain may be due to prolonged effects of the unique metabolites. A person who uses cocaine over long periods may experience coronary spasm in the dopamine-depleted state.
• Failure to thoroughly assess headaches (especially with fever, altered behavior, or sudden severe onset) in a patient with cocaine use
  • CT scanning may reveal etiology.
  • With negative CT scan findings, consider lumbar puncture to rule out subarachnoid bleeds or meningeal infection.
  • Serotonin depletion can lead to headache in a patient who uses cocaine.
• Failure to evaluate for and treat rhabdomyolysis
• Failure to recognize the heightened risk of suicide in a patient who is abusing drugs, especially during early withdrawal: Acute cocaine toxicity may also be the red flag of a suicide gesture or a consequence of an underlying unstable psychiatric condition.
• Failure to evaluate for the medical or organic causes for psychoses or acute behavioral changes before psychiatric diagnosis and management
• Failure to recognize or explain abnormal vital signs
• Failure to consider concomitant physical or sexual abuse in pediatric patients diagnosed with substance abuse
• Failure to consider substance abuse because of age, background, or gender

Special Concerns

• Cocaine-induced dysrhythmias may require special considerations. Wide-complex tachycardias may have the following responses to sodium bicarbonate:
  • Increasing serum sodium concentration, competing with cocaine's effect on sodium channel blockage and its slowing of phase 0 of the cardiac action potential
  • Altering the serum pH and possibly the sodium channels' conformation
• Lidocaine has received a fair share of controversy. Bretylium has not been controversial.
• Caring for the neonate exposed to cocaine includes catering to higher caloric demands, providing a quiet area with low lighting, and handling the infant gently. A pacifier can be used for excessive sucking. Withhold breastfeeding if HIV or drug use is suspected or known.
• Maternal malnutrition is a more likely cause of infant growth restriction than the effects of maternal cocaine use. When growth restriction is due solely to maternal cocaine use, the child usually can achieve normal growth in 2 years.
• The large number of patients requiring detailed and sensitive care is very demanding on the primary care physician. Multidisciplinary input should also include behavioral and developmental pediatric consultation.
• Confidentiality concerns may differ from state to state and require individual assessment.

References

1. SAMHSA. Summary of Findings from the 1998 National Household Survey on Drug Abuse. Office of Applied Studies. Available at http://www.oas.samhsa.gov/nhsda/98SummHtml/TOC.htm. Accessed April 28, 2006.

2. 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].

3. SAMHSA. Overview of Findings from the 2004 National Survey on Drug Use and Health. Rockville, MD: Department of Health and Human Services; 2005. Office of Applied Studies, NSDUH Series H-27.

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

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

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

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

8. 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. Oct 1997;36(10 Suppl):140S-56S. [Medline].

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

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

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

12. 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. Jun 29 1995;332(26):1753-7. [Medline].

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

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

15. 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. Feb 2003;157(2):133-8. [Medline].

Keywords

substance abuse disorder, street drug, drug abuse, coke, Erythroxylon coca, freebase, crack, blow, snow, toot, nose candy, benzoylmethylecgonine, cocaine abuse, role impairment, mood disorder, anxiety disorder, attention deficit hyperactivity disorder, antisocial personality disorder, major depressive episode, depression, asthma, syphilis, tachycardia, hypertension, increased myocardial oxygen consumption, myocardial ischemia, myocardial infarction, atherosclerosis, pulmonary hemorrhage, pneumonitis, pneumomediastinum, pneumothorax, pulmonary edema, rhabdomyolysis, hyperthermia, seizures, abruptio placentae, spontaneous abortions, intrauterine growth retardation, placental insufficiency, stillbirth, low birth weight

Contributor Information and Disclosures

Author

Anthony J Weekes, MD, RDMS, RDCS, Assistant Professor of Emergency Medicine, Albert Einstein College of Medicine; Director of Emergency Ultrasound, Department of Emergency Medicine, Montefiore Medical Center
Anthony J Weekes, MD, RDMS, RDCS is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

Chet Johnson, MD, Medical Director, Child Development Unit, Department of Pediatrics, Professor, University of Kansas Medical Center
Chet Johnson, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

CME Editor

Carrie Sylvester, MD, MPH, Director of Education in Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Pediatrics, Northwestern University Medical School
Carrie Sylvester, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics, American Medical Women's Association, American Psychiatric Association, and American Society for Adolescent Psychiatry
Disclosure: Nothing to disclose.

Chief Editor

Caroly Pataki, MD, Professor of Clinical Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Division Chair of Child and Adolescent Psychiatry, Director of Training, Child and Adolescent Psychiatry Residency Program, University of Southern California Keck 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, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

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