Cocaine Addiction: Symptoms and Treatment

Cocaine is a powerful central nervous system stimulant that increases dopamine and norepinephrine levels, causing a brief surge of energy and mood, followed by a sudden drop in energy, anxiety, dysphoria, and cravings for more use. In Europe, cocaine consistently ranks second in prevalence after cannabis, and its availability remains high, reflected in record seizures and a rise in related medical treatment requests. [1]

Despite improvements in overdose mortality in a number of countries, cocaine continues to contribute significantly to the overall burden, particularly when used in combination with synthetic opioids. This requires healthcare systems to be prepared to simultaneously treat acute conditions and provide long-term addiction care. [2]

The current approach combines emergency toxicology support, proven behavioral therapy, and, when necessary, the use of individual off-label medications in carefully selected patients. Particular attention is paid to harm reduction, as fentanyl adulterants are commonly found in illicit circulation, increasing the risk of death. [3]

ICD-10 and ICD-11 codes

The International Classification of Diseases (ICD) identifies a wide range of cocaine-related disorders, including harmful use, dependence syndrome, intoxication, withdrawal symptoms, and induced mental disorders. Proper coding is essential for statistics, patient routing, and reimbursement. [4]

In the ICD-11 version, the "Cocaine Use Disorders" block includes harmful episode, harmful pattern, dependence, intoxication, withdrawal, and induced states, with clarifications on severity and context. This facilitates clinicians' documentation and selection of monitoring tactics. [5]

Table 1. ICD-10 and ICD-11 codes for cocaine-related disorders

Classification	Main code	Examples of clarifications
ICD-10	F14.1	Harmful use, including intoxication or psychotic symptoms
ICD-10	F14.2	Cocaine addiction, course variants
ICD-10	F14.3-F14.5	Withdrawal symptoms, delirium, psychotic disorders
ICD-11	6C45.0-6C45.2	Harmful episode, harmful pattern, addiction
ICD-11	6C45.3-6C45.7	Intoxication, withdrawal, delirium, psychosis, other induced disorders
Source: official reference books ICD-10 and ICD-11. [6]

Epidemiology

In Europe, cocaine remains the second most widely used illicit substance. A long-standing trend of increasing seizures and high purity of the product has been documented, which correlates with its availability and medical consequences, including cardiovascular complications and hospitalizations. [7]

At the same time, the incidence of polysubstance use, in which cocaine is combined with alcohol and opioids, is growing. This increases toxicity, increases the risk of overdose, and worsens outcomes, including due to the formation of cocaethylene when taken with ethanol. [8]

Outside Europe, a significant decline in overall overdose mortality was observed in 2024, but the burden remains high, and stimulants continue to contribute to mortality, particularly with fentanyl. This context is important for risk prediction and harm reduction program planning. [9]

Localized spikes in cocaine-related cases are being recorded in urban and port areas, reflecting supply chain issues and episodes of high-purity drug influxes. Monitoring wastewater and clinical encounters helps quickly assess the situation. [10]

Reasons

The biological basis of cocaine addiction is linked to repeated enhancement of dopaminergic transmission due to blockade of the dopamine transporter protein, which perpetuates the "seeking-use-reinforcement" pattern. Combined with individual vulnerabilities, this leads to the development of persistent cravings. [11]

Social and psychological factors play a significant role: stress, depression, anxiety, traumatic experiences, and the availability of the substance in the environment. These factors increase the likelihood of transitioning from occasional to regular use. [12]

Genetic and neurobiological characteristics determine sensitivity to the effects of cocaine, differences in the intensity of euphoria and the severity of dysphoric “rebounds”, which affects the rate of addiction development. [13]

Combination with alcohol increases the likelihood of severe toxic effects due to the formation of cocaethylene, which has a long period of action and increased cardiotoxicity. [14]

Risk factors

The risk increases with early initiation of use, high doses, short intervals between "lines" or "sessions," and with inhalation and intravenous administration, which provide a sharp rise in brain concentrations. Polysubstance use significantly worsens the safety profile. [15]

Comorbid mental disorders, attention-deficit hyperactivity disorder, depression, anxiety, post-traumatic stress disorder, and social determinants of health increase the likelihood of transition to an addictive pattern. Concurrent treatment of comorbidity is required. [16]

Regular, concomitant use of alcohol forms cocaethylene and increases the risk of arrhythmias, myocardial infarction, stroke, and sudden death. This risk exceeds the combined toxicity of each substance individually. [17]

Contamination of illicit stimulants with synthetic opioids increases the risk of fatal overdose even in people who do not intend to use opioids, so carrying naloxone and using fentanyl test strips is recommended.[18]

Pathogenesis

Cocaine blocks the reuptake of dopamine, norepinephrine, and serotonin, causing hyperactivation of mesolimbic neural networks and increasing the motivation for repeated use. This is accompanied by vasoconstriction, tachycardia, increased blood pressure, and hyperthermia. [19]

Cardiovascular effects include coronary vasospasm, increased myocardial oxygen demand, and a tendency toward arrhythmias. These mechanisms underlie cocaine-associated acute coronary syndromes and sudden cardiac death.[20]

When combined with alcohol, cocaethylene is formed with a longer half-life and increased cardiotoxicity, which enhances ischemic and arrhythmogenic effects. [21]

Chronic intranasal exposure results in ischemic mucosal damage, perforation of the nasal septum and destruction of midfacial structures up to severe defects of the palate and nose, reflecting local vasospasm and tissue ischemia. [22]

Symptoms

Acute intoxication: euphoria, hyperactivation, insomnia, anxiety, mydriasis, sweating, tachycardia, increased blood pressure, tremor. Hyperthermia, arrhythmia, myocardial ischemia, stroke, seizures, rhabdomyolysis are possible. [23]

Post-intoxication state: dysphoria, irritability, fatigue, hypersomnia, increased cravings. Against this background, the risk of repeated use and polysubstance "smoothing" with alcohol or sedatives increases. [24]

Withdrawal symptoms: cravings, anxiety, depressed mood, sleep disturbances, anergia, anedonia. Some patients develop transient suicidality and psychotic symptoms requiring urgent evaluation. [25]

Local complications depend on the route of administration: with intranasal administration - chronic rhinitis and perforation of the septum, with crack smoking - bronchospasm and pneumonitis, with injections - local infections, thrombosis, risk of viral hepatitis and HIV. [26]

Table 2. Clinical manifestations by phase

Phase	Neuropsychiatric	Somatic	Special risks
Intoxication	Euphoria, anxiety, paranoia	Tachycardia, hyperthermia	Heart attack, stroke
Post-intoxication	Dysphoria, irritability	Exhaustion, hypersomnia	Breakdown, polysubstances
Abstinence	Cravings, depression	Asthenia	Suicidality, psychosis
Rationale: Summary of toxicological profile and observations in clinical guidelines. [27]

Classification, forms and stages

Harmful use, dependence, episodic and continuous patterns of use, as well as intoxication and withdrawal as acute conditions are distinguished. ICD-11 allows for clarification of severity and context, which is important for care planning. [28]

Administration routes include intranasal inhalation of powder, smoking crack, intravenous, and intraoral. The route of administration determines the speed of onset of effect, the intensity of euphoria, the risk profile, and the likelihood of severe complications. [29]

Staging according to the clinical course includes an early episodic phase, pattern formation, dependence with loss of control, and a chronic course with alternating remissions and relapses. [30]

Table 3. Routes of use and typical risks

Path	The beginning of the effect	Peak and duration	Specific risks
Intranasal	Minutes	Short	Septal perforation, sinusitis
Smoking	Seconds	Very short	Bronchospasm, pneumonitis
Intravenous	Almost instantly	Short	Infections, thrombosis, HIV, viral hepatitis
Source: epidemiological and clinical reports. [31]

Complications and consequences

Cardiological: acute coronary syndrome, life-threatening arrhythmias, cardiomyopathy, coronary artery dissection, sudden death. The risk increases with concomitant alcohol consumption due to cocaethylene. [32]

Neurological: ischemic and hemorrhagic stroke, seizures, cerebral vasoconstriction. Cognitive impairment is possible with long-term use. [33]

Otolaryngological and maxillofacial: perforation of the nasal septum, destruction of the hard palate and medial structures, facial deformities. Reconstructive surgery is often required. [34]

Pregnancy: Increased maternal and fetal risks, including growth retardation and adverse neurodevelopmental outcomes in the child, requiring multidisciplinary monitoring and substance abstinence support. [35]

Table 4. Complications by organ system

System	Examples of complications
Cardiovascular	Vasospasm, infarction, arrhythmias
Nervous	Stroke, seizures
Respiratory	Bronchospasm, pneumonitis
ENT and maxillofacial surgery	Perforations, necrosis, deformations
Kidneys and muscles	Rhabdomyolysis, acute renal failure
Based on clinical reviews of cardiovascular toxicity and toxicology.[36]

When to see a doctor

Immediately if you experience chest pain, shortness of breath, severe weakness, slurred speech, facial asymmetry, seizures, fever above 39°C (102.5°F), persistent vomiting, confusion, or severe psychosis. These are potential signs of a heart attack, stroke, hyperthermia, or intoxication. [37]

Immediately respond to any loss of consciousness, suspected overdose, or combination of cocaine with alcohol or unknown substances, given the risk of fentanyl contamination. Naloxone can be lifesaving. [38]

On a planned basis - in the presence of signs of addiction, decreased control, problems at work and relationships, in the presence of mental symptoms or somatic complications requiring examination and initiation of therapy. [39]

A special risk group includes pregnant women, adolescents, and patients with cardiovascular diseases. For them, even small doses can be dangerous. [40]

Diagnostics

Diagnosis is based on clinical presentation, medical history, and toxicology screening data. Benzoylecgonine, the primary metabolite of cocaine, is typically detected in urine. If necessary, confirmatory testing using high-throughput methods is performed. [41]

Approximate detection windows in urine: up to 2-3 days for occasional users; longer for regular users, sometimes up to 7-12 days, depending on the sensitivity of the method and individual factors. In saliva, the window is shorter, usually up to 1-2 days. [42]

In acute conditions, ECG, cardiac troponins, temperature monitoring, electrolytes, and renal function are indicated; in case of neurological symptoms, brain imaging is indicated. The examination tactics depend on clinical signs and risks. [43]

Table 5. Cocaine tests and approximate detection windows

Material	What is determined	Detection window
Urine	Benzoylecgonine	Usually 1-3 days, longer for regular people
Saliva	Cocaine and metabolites	Usually up to 1-2 days
Confirmation	Gas or liquid chromatography with mass spectrometry	According to the readings
Based on laboratory manuals and reviews.[44]

Differential diagnosis

Acute intoxication can mimic thyrotoxicosis, pheochromocytoma, anxiety disorder, panic attack, delirium, sepsis, and heatstroke. Hypoglycemia, epilepsy, and intoxication with other stimulants are also considered. [45]

Cocaine-associated chest pain is differentiated from acute coronary syndrome of other etiologies, myocarditis, aortic dissection, pneumothorax, and pulmonary embolism. A risk assessment algorithm and instrumental diagnostics are needed. [46]

Psychotic symptoms require the exclusion of primary psychoses induced by other substances, as well as organic causes. It is important to determine the time of last use and the dynamics of symptoms. [47]

Treatment

The behavioral methods with the best evidence base are contingent management, which provides non-material or small material reinforcements for confirmed sobriety, combined with cognitive behavioral therapy and a community-based approach. These programs demonstrate the greatest effectiveness and are the standard. [48]

Medication for acute intoxication: benzodiazepines are the primary treatment for agitation, tachycardia, and hypertension. Vasodilators and nitroglycerin may be used for persistent pain and vasospasm, and active external cooling may be used for hyperthermia. The choice of medication and the sequence of treatment depend on the clinical situation. [49]

Historically, pure beta-blockers were avoided due to the risk of "unopposed" alpha stimulation. Recent reviews suggest that combined alpha-beta blockers may be safe in selected cases, but routine use for acute cocaine-associated chest pain remains avoided. Sedative therapy and vasodilators are the mainstays of treatment. [50]

Long-term pharmacotherapy for cocaine addiction has no registered medications, but certain regimens are considered off-label in carefully selected patients. Professional association guidelines permit the use of topiramate, long-acting amphetamine forms, and their combinations to reduce use and cravings, subject to strict monitoring and physician expertise in addiction medicine. [51]

Comorbid conditions require simultaneous treatment: depression, anxiety disorders, attention-deficit hyperactivity disorder, and sleep disorders. Adequate treatment of comorbid conditions improves program retention and reduces the risk of relapse. [52]

Harm reduction measures include risk education, advice against using alone, access to fentanyl test strips, training in recognizing the signs of opioid overdose, and availability of naloxone. This is especially important when the purity of the substance is unknown. [53]

The maintenance phase includes developing a relapse prevention plan, support groups, digital monitoring, family involvement, working with triggers and stress, and sleep and exercise modification. Regular visits and program flexibility increase the chances of remission. [54]

Table 6. Treatment of acute conditions: clinical emphases

Situation	First steps	Additional measures
Agitation, hypertension	Benzodiazepines titrated	Nitroglycerin, vasodilators for spasms
Hyperthermia	Active external cooling	Correction of electrolytes, monitoring of renal function
Chest pain	Nitrates, benzodiazepines	Avoid pure beta blockers, consider alpha-beta in selection
Arrhythmia, wide QRS	Algorithm support, sodium bicarbonate when indicated	Council, monitoring
Rationale: Toxicological and cardiological guidelines. [55]

Table 7. Long-term help for cocaine addiction

Component	Evidence base	Notes
Contingent management	High	Basic element of programs
Cognitive behavioral therapy	Average	In combination with reinforcement
Topiramate	Low-moderate	Off-label patient selection
Long-acting amphetamine forms	Low-moderate	Off-label, specialist observation
Combination of topiramate plus prolonged-release amphetamines	Moderate	To reduce consumption and cravings
Source: Clinical practice guideline for stimulants. [56]

Prevention

The key is community-level supply and demand reduction, early identification of risky use, information about multi-substance risks, and access to evidence-based support programs. Overdose recognition skills and the availability of naloxone are important for the community. [57]

Health services should provide screening in primary care, rapid referral to behavioral programs with contingent management, and consideration of age, gender, pregnancy, and comorbidity when choosing tactics. [58]

Harm reduction policies include substance testing when available, information about impurities, and linkage to infection control services for people using invasive routes of administration.[59]

Forecast

The prognosis depends on the duration and intensity of use, comorbid disorders, social support, and access to reinforcement programs. Participation in structured behavioral programs increases the chance of long-term remission. [60]

Polysubstance use, especially in combination with alcohol and opioids, worsens the prognosis and increases the risk of cardiac and neurological catastrophic events. Targeted harm reduction can reduce mortality even while use persists. [61]

FAQ

Is it "safe" to use cocaine only on weekends
? No. Occasional use is also associated with the risk of heart attack, stroke, and psychotic reactions, especially when combined with alcohol and unknown additives. [62]

Are there "pills for cocaine addiction?"
There are no registered medications. The best evidence supports contingent management and cognitive behavioral therapy. Specialists are considering off-label regimens with topiramate and long-acting stimulants in carefully selected patients. [63]

How to tell if it's cocaine in a urine test:
Routine urine screening detects the metabolite benzoylecgonine. In case of doubt, a confirmatory test is performed at a reference laboratory. The detection window for most users is up to 2-3 days. [64]

What to do if chest pain occurs due to cocaine use:
Call emergency medical services immediately. Until contraindications are assessed, benzodiazepines and nitrates are standard treatment, along with cooling for hyperthermia. Prescribing pure beta-blockers in the acute phase is not routine practice. [65]

Is naloxone necessary if "stimulants only" are used
? Yes, due to the risk of fentanyl contamination. It is recommended that loved ones have naloxone available and be trained in its use. [66]

Additional Table: Red Flags and Actions

Sign	Possible condition	Action
Chest pain, sweating, nausea	Acute coronary syndrome	Urgent Care
Facial asymmetry, limb weakness, speech impairment	Stroke	Urgent hospitalization
Temperature ≥ 39, convulsions	Hyperthermia, toxic syndrome	Cooling, first aid
Psychosis, suicidal thoughts	Acute mental state	Safety, emergency assistance
Based on cardiology and toxicology guidelines.[67]