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Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations, medical consequences, and diagnosis
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Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations, medical consequences, and diagnosis
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2016. | This topic last updated: Aug 07, 2015.

INTRODUCTION — Cocaine is a tropane ester alkaloid found in leaves of the Erythroxylum coca plant, a bush that grows in the Andes Mountain region of South America [1]. Cocaine use can lead to addiction and adverse physical effects, such as stroke and cardiac arrest.

Cocaine is classified as a Schedule II medication under the Controlled Substances Act in the United States (US). Cocaine hydrochloride is still legally available in the US as a 4 or 10 percent solution for use as a local or topical anesthetic, although it has largely been replaced in clinical practice by synthetic local anesthetics [2].

The DSM-IV-TR psychiatric diagnoses cocaine abuse and cocaine dependence were replaced by one diagnosis, cocaine use disorder, in DSM-5 [3]. Although the crosswalk between DSM-IV and DSM-5 disorders is imprecise, cocaine dependence is approximately comparable to cocaine use disorder, moderate to severe subtype, while cocaine abuse is similar to the mild subtype [4].

This topic addresses the epidemiology, pharmacology, clinical effects, and diagnosis of cocaine use disorder in adults. Acute intoxication from cocaine use, specific cardiovascular and pulmonary complications related to cocaine, and treatment of stimulant use disorder are discussed separately. (See "Cocaine: Acute intoxication" and "Pulmonary complications of cocaine abuse" and "Evaluation and management of the cardiovascular complications of cocaine abuse" and "Pharmacotherapy for stimulant use disorders in adults" and "Psychosocial interventions for stimulant use disorder in adults".)

EPIDEMIOLOGY — Cocaine is used by an estimated 17 million people worldwide, about 0.4 percent of the global population age 15 to 64 years [5]. Use is most prevalent in North America (5.3 million people, 1.7 percent of population older than 14 years) and Central and South America (3.5 million people, 1.2 percent) and in Western and Central Europe (3.2 million people, 1.0 percent). Current use (3.4 percent in 2013) in the United Kingdom and Spain now exceeds population rates in the US [6], which have declined slightly over the past decade [5]. Common street names used in the US for cocaine are shown in a table (table 1).

There is less cocaine use in West and Central Africa, East and Southeast Asia, and Eastern and Southeastern Europe, with little use elsewhere in the world [5]. This pattern may be due to supply rather than demand factors, because of the difficulty in obtaining cocaine from its only source in South America and the ready availability of alternative synthetic stimulants such as amphetamines [7] or synthetic cathinones (“bath salts”).

Most cocaine use is by urban men age 15 to 35 years. About 3 percent of current users in the US are adolescents 12 to 17 years old [8]. Cocaine use has declined almost fourfold among this age group in the past decade, while declining about one-quarter in the overall population.

About one-fifth of the 4.2 million US residents estimated to use cocaine in a year meet DSM-IV diagnostic criteria for cocaine abuse or dependence (cocaine use disorder in DSM-5) [8]. Less than 600,000 cocaine users received specialty treatment for their cocaine use in 2013 [8].

Cocaine is the illegal drug most often associated with visits to US hospital emergency departments. In 2011, it was involved in an estimated 40.3 percent of illicit drug-related emergency department visits (about 505,000 visits), versus about 36 percent (456,000 visits) for marijuana and about 20.6 percent (258,000 visits) for heroin [9]. Nearly one-quarter of emergency room visits by patients seeking medical assistance for withdrawal (“detoxification”) involved cocaine use; 6.3 percent of emergency room visits for suicide attempts involved cocaine use.

Patterns of use — Cocaine is used in a variety of patterns [10,11]. The typical "binge" involves short periods of heavy use (eg, payday or weekends) separated by longer periods of little or no use. Others may use for an extended period until their finances are exhausted or access to cocaine is interrupted. A small number of users may be self-medicating an underlying neuropsychiatric disorder, such as attention deficit hyperactivity disorder (ADHD) [12], excessive daytime sleepiness [13], Parkinsonism [14], or cluster headaches [15]. Most cocaine users living in the community do not use very frequently. More than half (58 percent) of past-year users used less than 12 times in the year; only 22 percent used at least 50 times [8].

Risk factors — While cocaine use occurs in all sociodemographic groups, it is not equally distributed among the US population. The highest prevalence of use is among unemployed men in their 20s with no more than a high school education who live in urban areas.

Cocaine use is highly associated with use of other legal and illegal substances and with psychiatric disorders. Cigarette smokers and heavy alcohol drinkers are 10 and 20 times more likely, respectively, than non-users to also use cocaine [8]. Concurrent use of cocaine and alcohol produces a new compound, cocaethylene, which is pharmacologically active (see 'Metabolism' below).

Cocaine users are at high risk for developing a cocaine use disorder. Community-based interview surveys suggest that up to one in six persons who use cocaine will develop dependence by DSM-IV-TR criteria [16]. Heavier users and users who take the drug intravenously or by smoking are more likely to develop dependence than lighter users or intranasal and oral users [17-19]. The greater abuse potential of intravenous or smoked cocaine is attributed to the faster rate of drug delivery to the brain (within 10 seconds), and faster onset of psychological effects [20,21]. This faster onset is associated with a more intense pleasurable response (the so-called "rate hypothesis" of psychoactive drug action) [22]. Oral use of the coca leaf is not typically associated with significant adverse consequences [23]

The environment (including family, religious, and social factors) has the strongest influence on initial cocaine use [24]. Studies of drug use by pairs of fraternal (dizygotic) and identical (monozygotic) twins suggested a significant genetic influence on the risk of developing cocaine abuse or dependence after use has begun. Several promising candidate genes have been identified, including those for dopamine receptors and the dopamine transporter, but no specific gene has been clearly linked with cocaine addiction [25].

Co-occurring conditions — Many cocaine users use other substances either to enhance the "high" (eg, simultaneous use of opiates ["speedballing"]) or to ameliorate adverse effects of intoxication or withdrawal (eg, use of alcohol, cannabis, or benzodiazepines). Current cocaine users are twice as likely as non-users to have symptoms of depressive or anxiety disorders [26].

MECHANISM OF ACTION — Cocaine enhances monoamine neurotransmitter (dopamine, norepinephrine, and serotonin) activity in the central and peripheral nervous systems by blocking the presynaptic reuptake pumps (transporters) for these neurotransmitters [27,28]. Cocaine's positive psychological effects and abuse liability are considered to be due to its enhancement of brain dopamine activity, especially in the so-called corticomesolimbic dopamine reward circuit. Cocaine addiction has been conceptualized as a disease of the brain's dopamine reward system [29].

Cocaine is unique among stimulant drugs in having a second action of blocking voltage-gated membrane sodium ion channels. This action accounts for its local anesthetic effect, and may contribute to cardiac arrhythmias. (See "Evaluation and management of the cardiovascular complications of cocaine abuse".)

PHARMACOLOGY — Illegal cocaine comes in two forms: base (alkaloid, as in coca leaves) and salt [30,31]. Both forms consist of the same cocaine molecule and exert the same pharmacological actions once they reach the brain or other target organ. They differ in physical properties, which allow different routes of administration.

Cocaine base ("crack," "freebase") can be smoked because it has a relatively low melting point (98ºC) and vaporizes before substantial pyrolytic destruction has occurred. Cocaine base is difficult to dissolve for injection because it is relatively insoluble in water.

Cocaine salt, in contrast, cannot be efficiently smoked because it melts at 195ºC, with substantial breakdown of the cocaine molecule before vaporization. Cocaine salt is readily injected or insufflated ("snorted") through the nose; it is highly water soluble, making it easy to dissolve for injection purposes and facilitating absorption across mucus membranes.

The average purity of seized cocaine samples is 50 percent [32]. Common adulterants include both inert fillers that resemble cocaine in appearance (such as dextrose, lactose, mannitol, or starch) and active chemicals that may mimic the local anesthetic effect of cocaine (such as benzocaine, lidocaine, or procaine) or provide some psychoactive effect (such as ephedrine, amphetamine, caffeine, or PCP) [33,34]. Street cocaine also may contain contaminants from the preparation process (such as benzene, acetone, or sodium bicarbonate) [34]. An increasingly common cocaine adulterant is the veterinary anti-helminthic agent levamisole [35]. Cocaine adulterated with levamisole is associated with serious side effects, including leucopenia, agranulocytosis, and cutaneous vasculitis.

Absorption — Cocaine is readily absorbed through the mucous membranes of the nose and mouth, and from the genitourinary, gastrointestinal, and respiratory tracts. Passive absorption may occur through intact skin or by inhalation of second-hand cocaine smoke [36-38]. Such passive exposure can cause adverse effects in infants [39,40].

Distribution — Cocaine is rapidly taken up into most body organs, including the heart, kidney, adrenal glands, and liver [41]. Cocaine (and its hydrolytic metabolites) appears in blood, urine, hair [42], sweat [43], saliva [44], and breast milk [45,46]. It crosses the placenta to appear in meconium [47]. Analysis of these tissues and fluids is used for drug detection in workplace, legal, and treatment settings [48].

Onset of action — The onset of action for cocaine depends on the route of administration. Intravenous and inhaled (smoked) administration results in onset of action within seconds. Intranasal and gastrointestinal administration result in slower onsets of 20 to 30 minutes and up to 90 minutes, respectively.

Duration of action — The effects of intravenous or inhaled cocaine administration typically last 15 to 30 minutes; effects of intranasal and gastrointestinal administration are about one and three hours, respectively.

Metabolism — Cocaine is 95 percent metabolized by hydrolysis of its ester bonds to benzoylecgonine (by carboxyesterases in the liver) and to ecgonine methylester (by butyrylcholinesterase in the liver, plasma, brain, lung, and other tissues) [49-51]. The remaining 5 percent is N-demethylated to norcocaine by the liver cytochrome P450 microsomal enzyme system. The hydrolytic metabolites appear to be largely inactive. Norcocaine has some pharmacological actions similar to those of cocaine, and is hepatotoxic [52].

Smoked cocaine produces an additional series of pyrolysis products, the chief of which are anhydroecgonine methylester and noranhydroecgonine methylester [50,53].

Cocaine used together with alcohol leads to formation of a new compound, cocaethylene, by transesterification [50]. Cocaethylene has pharmacological actions similar to, but less potent than, those of cocaine, and has a longer half-life [54,55]. Formation of cocaethylene may contribute to more severe or longer lasting toxic effects of cocaine when it is used along with alcohol.

Elimination — Cocaine is largely eliminated in the urine [50]. Benzoylecgonine is the metabolite found in highest concentration in urine. It is this metabolite, rather than the parent drug cocaine, that is measured in urine drug tests for cocaine (see 'Screening' below).


Acute intoxication — Typical cocaine doses are 12 to 15 g orally (coca leaf), 20 to 100 mg intranasally, 10 to 50 mg intravenously, and 50 to 200 mg smoked. The intended effects include increased energy, alertness, and sociability; elation or euphoria; and decreased fatigue, need for sleep, and appetite [56-58]. The intense pleasurable feeling has been described as a "total body orgasm" [56].

There is wide variability in the acute response to cocaine and poor correlation between cocaine plasma concentrations and toxic effects [56,59]. Fatal cases of cocaine intoxication may present with 100-fold differences in plasma cocaine concentration [31].

Unintended adverse effects occur with increasing dose, duration of use, or a more efficient route of administration (eg, intravenous or smoked versus intranasal). These effects include dysphoric mood (anxiety, irritability), panic attacks, suspiciousness, paranoia, grandiosity, impaired judgment, and psychotic symptoms such as delusions and hallucinations. Up to one-quarter of non-treatment-seeking cocaine users may experience anxiety, depression, sleep disturbance, or weight loss (due to appetite suppression and changes in fat regulation) [60,61]. Concurrent behavioral effects include restlessness, agitation, tremor, dyskinesia, and repetitive or stereotyped behaviors such as picking at the skin or foraging for drugs ("punding," "hung-up activity") [62]. Associated physiological effects include tachycardia, pupil dilation, diaphoresis, and nausea, reflecting stimulation of the sympathetic nervous system.

Cocaine-associated psychotic symptoms (paranoia, delusions, hallucinations) are reported by up to 80 percent of individuals with a cocaine use disorder [63,64]. These symptoms may somewhat resemble those due to acute schizophrenia [65]. Cocaine-associated psychosis may differ from acute schizophrenic psychosis in being marked by less thought disorder and bizarre delusions and fewer negative symptoms such as alogia and inattention [64]. Hallucinations may be auditory, visual, or tactile, but the last two are much more common with cocaine use than with schizophrenia [63,66]. Tactile hallucinations are especially typical of stimulant-associated psychosis and include the sensation of something (eg, insects) crawling under the skin (“formication,” “cocaine bugs”).

The presentation and treatment of cocaine intoxication is discussed in greater detail separately (see "Cocaine: Acute intoxication").

Chronic use — Chronic cocaine use can result in either of two distinct pharmacological adaptations: sensitization (increased drug response) or tolerance (decreased drug response) [67,68]. In animal studies, sensitization results from low-dose, intermittent exposure, while tolerance results from frequent, high-dose, or long-term exposure.

The factors that determine sensitization and tolerance in humans, however, are not well understood. Sensitization to the cardiovascular effects of oral cocaine, but not to its psychological effects, has been demonstrated in laboratory studies [69]. Tolerance to the psychological, cardiovascular, and neuroendocrine effects of cocaine develops after several doses [70,71]. Tolerance to cardiovascular effects may develop more quickly and completely than does tolerance to psychological effects [71,72]. This rapid tolerance presumably allows binge users to take large cumulative doses of cocaine.

Chronic cocaine use is associated with cognitive impairment affecting visuo-motor performance, attention, verbal memory, and risk-reward decision-making [73]. These impairments persist for at least several weeks of abstinence.

Cocaine use is associated with suicidal ideation and suicide attempts [74,75]. The extent to which suicide is a direct consequence of use, rather than an associated sociodemographic or psychological factor, remains unclear [76,77]. Factors associated with increased risk of suicidality among cocaine users include depression, severe cocaine withdrawal, comorbid alcohol or opioid dependence, history of childhood trauma, and family history of suicidality [78,79].

Chronic cocaine use by any route of administration is associated with increased risk of infection, especially viral hepatitis [80] and HIV [81], and of risky sexual behavior (such as unprotected sex) [82].

Chronic cocaine use does not appear to increase the risk of general anesthesia, as long as the patient has normal cardiovascular parameters at the time of surgery [83].

Withdrawal symptoms — Cessation of heavy chronic cocaine use results in a withdrawal syndrome that has prominent psychological features, but is rarely medically serious [84-86]. Symptoms include depression, anxiety, fatigue, difficulty concentrating, decreased ability to experience pleasure (anhedonia), increased cocaine craving, increased appetite, increased sleep, and increased dreaming (due to increased REM sleep). An initial period of intense symptoms (commonly termed the "crash") may occur, including psychomotor retardation and severe depression with suicidal ideation. However, most users experience milder symptoms that resolve within one to two weeks without treatment.

Physical signs of cocaine withdrawal are usually minor and rarely require treatment. These include nonspecific musculoskeletal pain, tremors, chills, and involuntary motor movement [87]. The first week of stimulant withdrawal has been associated with myocardial ischemia [88], possibly due to coronary vasospasm.


Central nervous system — Cocaine euphoria is associated with transient increases in EEG activity followed by longer-lasting increases in activity [89]. Seizures may occur in persons without a seizure history, even with first time use of cocaine [90-92]. These are usually single, generalized tonic-clonic seizures occurring within 90 minutes of cocaine use.

Cerebral vasoconstriction, cerebrovascular disease, and hemorrhagic and ischemic stroke are increased in cocaine users, even in patients with no other risk factors [90-94]. Etiologic mechanisms include tachycardia and increased blood pressure from sympathetic activation, vasoconstriction, vasospasm, and intravascular thrombosis due to increased platelet aggregation [95].

MRI, SPECT, and PET imaging in chronic cocaine users demonstrate structural and functional brain abnormalities: cerebral gray matter atrophy and decreased glucose metabolism in the frontal and temporal lobes, small cerebral perfusion defects, increased creatine concentration in parietal white matter (suggesting abnormal energy metabolism), and decreased D2 dopamine receptors in the striatum [95-97]. Impairment of behavioral inhibition in cocaine users has been associated with reduced activity in the anterior cingulate and prefrontal cortices [97].

A pathologic study using melanin immunoreactivity found cocaine users to have 16 percent fewer midbrain dopamine neurons than non-using subjects. This and related findings above suggest that cocaine may have a neurotoxic effect on dopamine neurons, contributing to development of cocaine dependence in some users [98]. Parkinson's disease has not been associated with cocaine use.

Cocaine use is associated with a variety of movement disorders, including stereotyped behaviors, acute dystonic reactions, choreoathetosis and akathisia (so-called "crack dancers"), buccolingual dyskinesias ("twisted mouth" or "boca torcida"), and exacerbation of Tourette's syndrome and tardive dyskinesia [56,90,99]. Cocaine users are at increased risk of acute dystonic reactions from neuroleptic (antipsychotic) medications [100].

Cardiovascular system — Cardiopulmonary symptoms are the most frequent complaints in cocaine users who seek medical help, with chest pain being the most frequent symptom [101]. Cocaine acutely increases heart rate, blood pressure, and systemic vascular resistance by increasing adrenergic activity in the heart, and indirectly via the CNS [101,102]. The increased myocardial oxygen demand, coupled with decreased coronary blood flow from vasospasm and vasoconstriction, can cause acute myocardial infarction, even in young persons without atherosclerosis. Cocaine use is a factor in about one-quarter of nonfatal heart attacks in persons younger than 45 years [103].

Cocaine use is not usually associated with chronic hypertension [104], but appears to enhance the progression of renal disease in patients with hypertension (see 'Kidneys' below) [105,106].

Cocaine use increases risk for cardiac arrhythmias and sudden death [107,108]. Chronic use is associated with left ventricular hypertrophy, cardiomyopathy, myocardial fibrosis, and myocarditis. (See "Evaluation and management of the cardiovascular complications of cocaine abuse".)

Respiratory system — The effects of cocaine on the respiratory system depend on the route of administration. Intranasal cocaine use ("snorting") may cause chronic rhinitis, perforation of the nasal septum, oropharyngeal ulcers, and osteolytic sinusitis, due to vasoconstriction and resulting ischemic necrosis [90,99]. Anosmia is rare.

Smoked (“crack”) cocaine produces acute respiratory symptoms in up to half of users, including productive cough, shortness of breath, wheezing, chest pain, and hemoptysis [109], and is a factor in up to one-third of young adult cases of acute asthma exacerbation seen in hospital emergency departments [110]. Rarer pulmonary complications of smoked cocaine use include pulmonary edema, pulmonary hemorrhage, pneumothorax, pneumomediastinum, and thermal airway injury [109,111]. These effects are due to a combination of direct damage to the alveolar-capillary membrane by cocaine or inhaled microparticles, damage to the pulmonary vascular bed from vasoconstriction, interstitial disease, and/or toxicity from adulterants such as levamisole [112]. Chronic cocaine smokers generally have normal spirometry tests, but may have increased alveolar epithelial permeability and moderately decreased pulmonary diffusion capacity, even when asymptomatic. “Crack lung” refers to an acute pulmonary syndrome, associated with smoked cocaine use, whose pathophysiology and optimum treatment remain unclear [109,111]. It is associated with fever, hypoxemia, hemoptysis, respiratory failure, and diffuse alveolar infiltrates (usually eosinophil-rich). (See "Pulmonary complications of cocaine abuse".)

Gastrointestinal system — Cocaine use by any route of administration reduces salivary secretions (xerostomia) and causes bruxism [113]. Cocaine reduces gastric motility and delays gastric emptying [90]. Cocaine-induced vasoconstriction and ischemia may result in gastrointestinal ulceration, infarction, perforation, and ischemic colitis [90,99]. Cocaine-associated ulcers are distributed primarily in the greater curvature and prepyloric region of the stomach, pyloric canal, but, similar to peptic ulcers, also occur in the first portion of the duodenum.

Liver — Cocaine users may have mild, transient elevation in transaminases [114], but there is no direct evidence that cocaine is hepatotoxic in humans. Cocaine does cause liver damage in rodents; however, the responsible hepatotoxins are oxidative metabolites such as norcocaine, which are very minor metabolites in humans (see 'Metabolism' above). Liver abnormalities in cocaine users can almost always be accounted for by viral hepatitis from injection drug use, alcoholic liver disease, concurrent rhabdomyolysis [114], use of other hepatotoxic drugs (such as MDMA [“ecstasy”]), or other consequences of a drug-using lifestyle. Concurrent alcohol intake may sensitize hepatocytes to damage by cocaine, as well as generating the hepatotoxic metabolite cocaethylene [115].

Kidneys — Cocaine use can impair kidney function by a variety of mechanisms [116,117]. Cocaine-induced rhabdomyolysis is a significant cause of acute renal failure [118] (see "Drug-induced myopathies" and "Clinical features and diagnosis of heme pigment-induced acute kidney injury (acute renal failure)"). Cocaine use by hypertensive patients enhances their decline in kidney function [105] and the progression from hypertensive nephrosclerosis to end-stage renal disease [106]. While cocaine promotes atherosclerosis in renal vessels, cocaine-induced renal infarction is relatively rare [119].

Endocrine — Acute cocaine use activates the hypothalamic-pituitary-adrenal (HPA) axis, increasing levels of epinephrine, corticotropin-releasing hormone (CRH), ACTH, cortisol, and luteinizing hormone, and decreasing plasma prolactin levels [99,120,121]. Chronic cocaine users, however, usually have normal plasma levels of prolactin, testosterone, cortisol, luteinizing hormone, and thyroid hormones.

Skin — Cocaine use is associated with a variety of pseudovasculitic lesions that may mimic rheumatologic syndromes such as Wegener's granulomatosis, necrotizing vasculitis, and Henoch-Schönlein purpura (IgA vasculitis) [122]. Use of cocaine contaminated with levamisole (an anti-helminthic now approved in the US only for veterinary use) has been associated with cutaneous vasculitis or vasculopathy (picture 1) [123,124]. (See "Evaluation of adults with cutaneous lesions of vasculitis", section on 'Etiology' and "Evaluation of adults with cutaneous lesions of vasculitis", section on 'Evaluation for vasculitis due to levamisole-contaminated cocaine'.)

Sexual dysfunction — Although cocaine is often considered an aphrodisiac, it actually may impair sexual function, especially with chronic use, and may cause delayed or inhibited ejaculation in men [125-127].

Reproductive, fetal, and neonatal health — Cocaine may cause irregular menses in women [126,127].

Topical cocaine is classified as pregnancy category C (risk cannot be ruled out because human studies are lacking) by the US Food and Drug Administration (FDA). Maternal cocaine use has been associated with vaginal bleeding, abruptio placenta, placenta previa, premature rupture of membranes, premature birth, decreased head circumference, low birth weight, and autonomic instability [128,129]. However, it is unclear to what extent these adverse effects are due to prenatal (in utero) cocaine exposure, rather than to other factors in the cocaine-using lifestyle, such as concomitant drug use (including alcohol, nicotine, and opiates), poor nutrition, and lack of prenatal care. Rodent and monkey studies, in which these confounding factors are excluded, show few direct adverse effects of prenatal exposure to cocaine [130].

The long-term effects of prenatal exposure to cocaine are also unclear [131]. Well-controlled, prospective studies of children born to cocaine-using mothers have not confirmed most earlier concerns regarding long-term cognitive impairment and behavioral problems.

Cocaine appears in breast milk and may cause irritability, sleep disturbance, and tremors in the nursing infant [45,46].

ASSESSMENT — Initial assessment of the cocaine-abusing patient addresses the following areas [132].

Patient history

Use of all psychoactive substances (not just cocaine), including illegal, prescription, and over-the-counter as well as duration, quantity, frequency, route of administration, and effects for each substance used

Prior treatment, if any

Psychiatry history, including relationship of any psychiatric symptoms to substance use or withdrawal

Medical history

Social and developmental history, especially current social network

Family history

Substance use

Psychiatric history

Mental status

Insight into condition

Motivation and preferences for treatment

Cognitive function


Attention span

Memory, short- and long-term

Decision-making capacity

Presence of thought disorder, eg, delusions, hallucinations

Mood and affect

Physical examination

Vital signs

Heart, lungs, abdomen, extremities, skin

Neurological examination

Stigmata of cocaine use, eg, skins lesions from injection, perforated nasal septum from insufflation (“snorting”)

Laboratory tests

Blood or urine drug testing


Complete blood count (CBC)

Blood chemistries, including liver tests

Blood-borne and sexually transmitted diseases, eg, HIV, syphilis, hepatitis B and C

Goals of the initial psychiatric assessment are to:

Determine the severity of the addiction problem

Identify concurrent substance use (alcohol, opiates, or cannabis)

Diagnose co-occurring psychiatric or medical disorders

Identify strengths (eg, employment, supportive social network)

Identify weaknesses (criminal behavior, poor social skills)

Evaluate motivation for treatment

Discuss treatment preferences

Screening — The two question Two-item Conjoint Screen (TICS) and the four-question CAGE screen for a DSM-IV diagnosis of cocaine dependence (table 2 and table 3) [133,134]. Both tests have sensitivities and specificities of 80 percent or greater in primary care settings for populations including women [135], pregnant women [134], the elderly [136], and patients with HIV infection [137].

Drug testing — Drug testing detects cocaine use, but is not diagnostic of a cocaine use disorder, which implies adverse consequences from use. Conversely, a negative drug screen may only indicate lack of recent use. Cocaine and its metabolites can be measured in urine, blood, oral fluid, sweat, and hair [48,138]. The window of detection is shorter for cocaine than for its major metabolite, benzoylecgonine, and varies with the sensitivity of the assay method.

Urine testing (which measures benzoylecgonine, not cocaine), including rapid point-of-care methods, is common in clinical settings because the sample can be collected non-invasively. It has a detection window of about two to three days after cocaine use, but may be positive up to two weeks after chronic heavy use [139,140].

Blood testing has a detection window of 12 hours for cocaine and 48 hours for benzoylecgonine. It is rarely used outside the setting of acute intoxication. Actual blood cocaine concentrations have little correlation with acute symptoms of cocaine intoxication in the emergency department setting [59].

Oral fluid testing has a detection window similar to that of blood, with the advantage of non-invasive collection and better patient acceptability [44]. Sweat testing (via patches worn on the skin) has a detection window of several weeks, but is useful only for prospective evaluation (ie, monitoring future drug intake). Results may be influenced by location of the skin patch and environmental exposure to cocaine [141].

Hair testing has the longest detection window (potentially years), but valid results require careful technique, and some questions remain unresolved. Results may be influenced by hair location, racial/ethnic differences in hair composition, prior hair treatments, and environmental exposure to cocaine [142]. Cocaine continues to be incorporated into hair for a few months after last use [143].

A variety of relatively inexpensive commercial assays are available for testing of urine and oral fluid, including disposable kits that allow on-site testing with results available within minutes. Results from such screening tests should be confirmed by a standard laboratory assay, especially in legal or workplace settings.

DIAGNOSIS — The diagnosis of cocaine use disorder is made on the basis of history, obtained primarily from the patient and from collateral sources (eg, family, friends, and medical records) when available.

Diagnoses of cocaine abuse and cocaine dependence in DSM-IV-TR were replaced by the single diagnosis, cocaine use disorder, in DSM-5 [3]. DSM-5 diagnostic criteria for cocaine use disorder are described below.

DSM-5 criteria — A problematic pattern of cocaine use leading to clinically significant impairment or distress, as manifested by two or more of the following within a 12-month period:

Cocaine is often taken in larger amounts or over a longer period than was intended

There is a persistent desire or unsuccessful efforts to cut down or control cocaine use

A great deal of time is spent in activities necessary to obtain cocaine, use cocaine, or recover from its effects

Craving, or a strong desire or urge to use cocaine

Recurrent cocaine use resulting in a failure to fulfill major role obligations at work, school, or home

Continued cocaine use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of cocaine

Important social, occupational, or recreational activities are given up or reduced because of cocaine use

Recurrent cocaine use in situations in which it is physically hazardous

Continued cocaine use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by cocaine



Specifiers for the diagnosis include:

In early remission – After full criteria for cocaine use disorder were previously met, none of the criteria for cocaine use disorder have been met (with the exception of craving) for at least three months but less than 12 months

In sustained remission – After full criteria for cocaine use disorder were previously met, none of the criteria for cocaine use disorder have been met (with the exception of craving) during a period of 12 months or longer

In a controlled environment – If the individual is in an environment where access to cocaine is restricted

The severity of cocaine use disorder at the time of diagnosis can be specified as a subtype based on the number of symptoms present:

Mild: Two to three symptoms

Moderate: Four to five symptoms

Severe: Six or more symptoms

Most clinical trials of treatments for cocaine use were conducted in samples limited to patients with cocaine dependence (DSM-IV-TR or earlier criteria). Applying trial results to patients diagnosed with DSM-5 cocaine use disorder is imprecise; the most closely comparable patients are those with cocaine use disorder, moderate to severe subtype [4]. Cocaine abuse is similar to the mild subtype of cocaine use disorder. (See "Pharmacotherapy for stimulant use disorders in adults" and "Psychosocial interventions for stimulant use disorder in adults".)

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Basics topic (see "Patient education: Cocaine use disorder (The Basics)")


Cocaine use is most prevalent in North and South America, and increasingly in Western Europe, especially among urban men aged 15 to 35 years. It is the illegal drug most often associated with emergency department visits in the US. (See 'Introduction' above.)

Up to one in six persons who use cocaine will develop dependence (DSM-IV-TR criteria) or moderate to severe cocaine use disorder (DSM-5 criteria); abuse liability is greater with intravenous and smoked cocaine, compared to intranasal and oral use. Cocaine base has a low melting point and can be smoked; cocaine salt is water soluble and can be injected or absorbed across mucous membranes. (See 'Risk factors' above and 'Pharmacology' above.)

Cocaine is largely metabolized to inactive hydrolytic products in the liver and plasma. Use of alcohol with cocaine produces a new metabolite, cocaethylene, which has actions similar to cocaine but a longer half-life. Concurrent alcohol use with cocaine may cause more severe and longer lasting toxic effects. (See 'Metabolism' above.)

Drug testing detects the metabolite benzoylecgonine, which is usually detectable two to four days after the last cocaine use, although this can be up to 14 days after heavy, prolonged use. (See 'Elimination' above.)

Cocaine use increases energy and alertness, can produce euphoria, and decreases appetite and need for sleep. Adverse effects may include anxiety, irritability, paranoia, delusions, and hallucinations. These may be accompanied by tachycardia, diaphoresis, nausea, and pupil dilatation. There is poor correlation between cocaine plasma concentrations and toxicity. (See 'Acute intoxication' above.)

Withdrawal symptoms from chronic cocaine use are predominantly psychological: depression, anxiety, anhedonia, cocaine craving, and increased sleep. Most symptoms are self limited and resolve within one to two weeks. (See 'Withdrawal symptoms' above.)

Effects of cocaine on specific organ systems are (see 'Effects on specific organ systems' above):

CNS: seizures, stroke, movement disorders

Cardiovascular: myocardial infarction, arrhythmia, cardiomyopathy, myocarditis

Respiratory: rhinitis and septal perforation (with intranasal use) cough, wheeze, chest pain (with smoked use)

GI: xerostomia, gastric ulcers, ischemic colitis

Diagnoses of cocaine abuse and cocaine dependence in DSM-IV-TR were replaced by the single diagnosis, cocaine use disorder, in DSM-5. (See 'Diagnosis' above.)

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