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.
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). 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.
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.
Temperature
Cocaine toxicity and resultant hyperactivity may lead to hyperthermia.
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.[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
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.
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.
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]
International
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.
Mortality/Morbidity
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]
Race
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]
Sex
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]
Age
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]
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?
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.
Consider diagnostic imaging including CT scan if suspected packets are not detected by abdominal X-ray.
Consider administering golytely or whole bowel irrigation.
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.
Adulterants used in cocaine such as levamisole may confound and add to the complexity of the side-effect profile.
The NIDA has identified the following risk factors for the development of drug use and abuse[2] :
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
The consequences of cocaine use, abuse, and dependence include lowered educational achievements, increased trouble with law enforcement (including increased arrests, incarcerations, longer sentences), limited and more limited employment options with worse outcomes, and increased suicidal attempts and completed suicides.[15]
CBC count can reveal suspected infection or anemia. Cocaine tainted with levamisole can lead to neutropenia.
Assess electrolytes and glucose levels.
Troponin is especially helpful for detecting myocardial injury. Creatine kinase (CK) with isoenzyme containing M and B subunits (MB) index may be diagnostic. Myoglobin is the least helpful for cardiac ischemia.
Rhabdomyolysis is a common complication of cocaine use, and muscle symptoms fail to predict its development.
CK is more sensitive than myoglobin for the detection of skeletal muscle injury.
Dipstick can detect myoglobin in the urine (a good screen for rhabdomyolysis but not for myocardial ischemia) and shows up without red blood cells in the microscopic urinalysis.
Cocaine use can cause MI in patients with no other cardiac risk factors.
Perform a urinalysis with drug screening.
Initial urine screening is performed by an immunochemical assay and is not 100% specific.
In newborns, perform meconium testing.
Positive urine testing in children may suggest abuse or neglect.
Gas chromatography-mass spectrometry detects cocaine and its metabolites as many as 14 days after significant cocaine use.
Studies can now determine cocaine use by an analysis of hair, using solid phase microextraction.[16, 17]
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 but is unreliable in body stuffers.
Ultrasonography is useful in a trauma situation and can also be used to detect placental and fetal insult in the pregnant patient. Bedside echocardiography may be necessary if there are suspicions for myocardial dysfunction with signs such as hypotension, dyspnea, rales, or persistent chest pain. Myocardial injury can be detected as left ventricular hypokinesis or akinesis with cardiac ultrasound.
Chest pain with radiation to the back or associated with neurologic symptoms or hemodynamic deterioration may warrant urgent cardiac ultrasound and/or CT chest and abdomen contrast-enhanced imaging to evaluate for an intimal flap, dissection signs (including pericardial effusion), or signs of tamponade.
Cocaine-provoked cardiac dysfunction can be especially concerning and severe in patients with unsuspected or preexisting cardiomyopathies.[18]
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 and packets of cocaine.
Brain CT scanning is highly recommended in patients with cocaine-induced seizures because of the risk of intracranial hemorrhages.
In conjunction with other diagnostic tools, imaging techniques can help identify cognitive deficits in drug abuse.[19]
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.
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 physical restraints because they may exacerbate hyperthermia and acidosis and may cause death if used alone. If necessary, use restraints to allow administration of chemical sedation.
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 GABA-ergic drugs such as benzodiazepines; however, refractory cases may require propofol or phenobarbital. GABE-ergic drugs also decrease CNS catecholamine release. Avoid succinylcholine because of the risk of exacerbating hyperkalemia in a patient with cocaine-induced rhabdomyolysis. Avoid sodium channel blocking anticonvulsant drugs like phenytoin.
Temporary neuromuscular blockade may be necessary for rapid sequence intubation but the absence of motor activity due to paralysis does not stop brain injury or ongoing seizures.
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. These agents are short-acting, similar to cocaine, and can be rapidly titrated off as the patient improves, thus avoiding potential hypotension that might occur with use of longer-acting vasodilators.
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.
Calcium channel blockers are alpha antagonists and make more sense than beta-blockers.
Treatment with nonselective beta-blockers is relatively contraindicated because they may potentiate cocaine-induced coronary vasoconstriction.
Depleted norepinephrine stores may result in hypotension, which necessitates treatment with dopamine or norepinephrine.
Although advanced cardiovascular life support (ACLS) guidelines recommend treatment of ventricular dysrhythmias with lidocaine, the focus of ACLS is usually coronary artery disease-induced myocardial dysfunction. Sodium bicarbonate is a better, evidenced-based first choice for any wide-complex dysrhythmia due to sodium channel blockade, followed by lidocaine, then cardioversion. Lidocaine (also a sodium channel blocker) seems contradictory, but because it is a fast-on, fast-off sodium channel blocker, it competes with agents that bind the channel longer, thus freeing up channels to function normally.
Class 1A and 1C antiarrhythmic agents are contraindicated.
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.
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
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.
Specialized psychiatric/mental health care, also called substance use disorder (SUD) treatment, must be emphasized. SUD treatment helps identify risks factors for cocaine relapse and provides effective strategies to reduce the risk of cocaine relapse. According to the 2008 National Survey on Drug Use and Health, only 7% of adolescents who were candidates for SUD treatment actually received the treatment. An 8-year (2001-2008) cross-sectional survey of data from the National Survey of Drug Use and Health revealed that while substance use disorder referral and treatment is quite low amongst all adolescents, it is especially low in African American and Latino adolescents (8.4%) and up to 23.5% in Native Hawaiian/Pacific Islander adolescents.[20]
The following additional consultants may be needed:
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.
Clinical Context:
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).
Clinical Context:
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.
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.
Clinical Context:
Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.
Clinical Context:
Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on alpha receptors.
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
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.
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, see eMedicineHealth's patient education articles Cocaine Abuse, Drug Dependence and Abuse, and Substance Abuse.
Anthony J Weekes, MD, RDMS, RDCS, Ultrasound Fellowship Director, Associate Director of Emergency Ultrasound, Department of Emergency Medicine, Carolinas Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Douglas S Lee, MD, Attending Physician, Department of Emergency Medicine, Naples Community Hospital
Disclosure: Nothing to disclose.
Specialty Editors
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.
Chief Editor
Caroly Pataki, MD, Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
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
Disclosure: Nothing to disclose.
References
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 http://www.samhsa.gov/data/sites/default/files/NSDUH-FRR1-2014/NSDUH-FRR1-2014.pdf. 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.
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 http://www.samhsa.gov/data/sites/default/files/DAWN127/DAWN127/sr127-DAWN-highlights.htm. February 22, 2013; Accessed: December 10, 2015.
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. monitoringthefuture.org. Available at http://www.monitoringthefuture.org/pubs/monographs/mtf-overview2014.pdf.. 2015; Accessed: December 10, 2015.
