Drug use disorder is a recurring pattern of harmful use of a substance despite adverse consequences to work, school, relationships, the legal system, or physical health. This may occur concurrently with or independently from substance dependence, in which the impairment or distress is more pervasive and often (though not necessarily) includes physical dependence and withdrawal symptoms

Substance use disorder

Substance abuse

Substance dependence

Addiction

• Polysubstance use and comorbidity with psychiatric disorders are common.
• History often reveals recurring behavioral and psychosocial problems, such as relationship, work, financial, housing, or legal problems; violence and traumatic injuries; and anxiety, depression, insomnia, and cognitive and memory dysfunction.
• Repeated requests for early refills of controlled substances and obtaining prescriptions from multiple providers should raise concern for prescription drug use disorder.
• Physical findings may include injection marks, nasal lesions or recurrent epistaxis, poor dentition, scars or bruises from falls or trauma, sudden weight change, and poor nutritional status. Signs/symptoms of intoxication (e.g., dilated or constricted pupils, involuntary head nodding) or withdrawal are highly suggestive of substance use disorder.

Several models of addiction have been proposed, with consensus that addiction likely results from a combination of both biologic/genetic and social/environmental factors.

• Disease model: Addiction is a chronic brain disease, which occurs as a result of the impairment of healthy neurochemical or behavioral processes.
• Genetic model: Genetic predisposition is often a factor in dependency and certain addictive behaviors.
• Social model: Person-environment interactions (i.e., socialization, imitation of observable behavior and the influence of modeling) shape addictive behavior.

• Psychiatric disorders and symptoms such as depression, mania, psychosis, insomnia, posttraumatic stress disorder, and anxiety disorders may coexist or occur as a consequence of substance use.
• Rule out seizure disorder and underlying medical illness.

• A thorough history is crucial for diagnosis.
• The physician’s history-taking style and techniques strongly affect patient’s willingness to report use and to participate in future treatment activities.
• A structured, nonjudgmental approach is generally preferable:
  1. Ask about quantity and frequency of alcohol or drug use, as well as method of administration (e.g., IV, smoke). The National Institute on Alcohol Abuse and Alcoholism (NIAAA) declares that problem drinking is defined as more than two drinks per day for men and more than one drink per day for women or anyone older than age 65.
  2. Use a short screening instrument such as the CAGE questionnaire (“1. Have you ever felt you need to Cut down on your alcohol or drug use? 2. Have people Annoyed you by criticizing your alcohol or drug use? 3. Have you ever felt Guilty about alcohol or drug use? 4. Have you ever felt you need to drink first thing in the morning [Eye opener] to stop shakiness?”).
• Problematic behavior during intoxication or withdrawal is diagnostic.
• Because self-report of substance use and its consequences can be unreliable, laboratory tests and obtaining corroborating information, such as from family members, past detoxifications, or drug rehabilitations, is often helpful.

• Blood alcohol content (BAC) measured on the breath is practical to define intoxication and provides a rough measure of impairment. In general, two standard drinks may cause BAC 0.08% or higher, which is considered legally impaired.
• Obtain toxicology screen in urine, oral swab, or blood samples. Oral swabs are more resistant to tampering than are urine screens.
• Biologic markers such as elevated mean corpuscular volume (MCV), γ-glutamyltransferase (GGT), liver function tests (AST and ALT; AST/ALT ratio of 2:1 or greater is suggestive of alcoholic liver disease), and carbohydrate-deficient transferrin (CDT) may also be used to diagnose and monitor.

Not helpful in routine diagnosis and management of substance misuse but possibly useful in the management of sequelae of substance misuse (e.g., brain imaging to evaluate the alcohol abuse-associated increased risk of subdural hematomas or increased evidence of cerebral atrophy). Imaging studies have also revealed adaptations within the brain’s reward circuit following repeated alcohol and drug use; these adaptations reduce the impact of dopamine, often resulting in depressed mood and anhedonia among persons who misuse substances.

• Motivational interviewing (MI) is an evidence-based approach that preserves patient autonomy in defining treatment goals and working toward change. For patients who express lack of readiness/commitment to change, it can be helpful to discuss the functions of their use and advantages/disadvantages the patient has personally experienced. Use an Elicit-Provide-Elicit format to counsel about risks of use and benefits of abstinence; in other words, elicit a patient’s consent and feedback before and after providing information.
• Nonpharmacologic strategies have the greatest documented efficacy: Education, feedback, goal setting, problem solving, and additional contacts for further assistance.
• Opiate contracts, prohibiting a patient from getting early refills, or obtaining opiates from multiple prescribers should be considered for all patients with chronic pain receiving opioid painkillers, especially for patients with a history of substance misuse or misuse of prescribed medication.
• Behavioral relapse prevention approaches teach patients how to avoid trigger stimuli or uncouple trigger stimuli from substance ingestion.
• Self-help and 12-step support groups such as Alcoholics Anonymous and Narcotics Anonymous are helpful in achieving and maintaining sobriety. Alternative self-help and peer groups include SMART Recovery, Dharma Recovery, Refuge Recovery, and Recovery Coach services.
• Consider psychotherapy/psychiatry referrals to address co-occurring psychiatric conditions, as well as case management referrals to address common barriers to recovery (e.g., safe housing).
• Residential or inpatient treatment programs should be a consideration for any individual with continued or escalating use despite outpatient treatment.

• Detoxification is an important first step. Seizure risk is greatest within the first 48 hours of alcohol abstinence. Detoxification goals are to facilitate withdrawal and initiate abstinence safely, prevent withdrawal seizures and reduce symptoms, and refer the patient to ongoing treatment.
• Benzodiazepines are effective in acute alcohol withdrawal for the management of symptoms as well as the prevention of seizures. One strategy is to give the patient a loading dose of a long-acting benzodiazepine (e.g., 20 mg of diazepam) and then continue the benzodiazepine as scheduled while tapering the dose gradually. An example would be chlordiazepoxide 25 to 50 mg q6h on day 1, 25 to 50 mg q8h on day 2, 25 to 50 mg q12hr on day 3, and 25 to 50 mg at hour of sleep on day 4 and day 5 and then discontinue. An alternative “symptom-driven” strategy is to follow the patient closely with serial assessments, such as the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) scale, and to dose with 1 to 2 mg of lorazepam as needed to treat specified withdrawal symptoms.
• The prophylactic administration of thiamine and folic acid (first intravenously or intramuscularly followed by supplemental oral doses) in alcohol withdrawal is recommended before starting any carbohydrate-containing fluids or food to prevent Wernicke-Korsakoff syndrome (alcoholic encephalopathy and psychosis). Magnesium appears to be effective in the treatment of alcohol withdrawal-related cardiac arrhythmias, but not other symptoms of alcohol withdrawal.
• Beta-blockers and clonidine generally should be avoided in alcohol withdrawal; they may mask markers of the severity of the withdrawal (blood pressure and pulse rate).
• Unlike withdrawal from alcohol or benzodiazepines, opioid withdrawal is not life threatening.
• Clonidine alleviates the discomfort of opiate withdrawal. Clonidine tablets, 0.1 mg q4 to 6h as needed, can be used while monitoring patient’s blood pressure. Clonidine transdermal patch, 0.1 mg/24 hr, can be used to treat autonomic hyperactivity symptoms; however, it has a very slow onset and may take 2 to 3 days to achieve therapeutic levels. Antidiarrheals, ibuprofen, and dicyclomine can be used as adjuncts to treat opiate withdrawal symptoms.
• Methadone taper is an effective approach for detoxification in opioid dependence.
• Buprenorphine is a partial μ-opioid receptor agonist that may be used for detoxification and maintenance in treatment of opioid dependence (see dosing in next section).

• Naltrexone helps reduce craving for alcohol. Naltrexone 50 mg once daily for 12 wk can be a useful adjunct to substance abuse counseling or rehabilitation programs. Randomized treatment studies are equivocal for long-term outcomes. Naltrexone reduces relapse and the intensity or frequency of any drinking that does occur. It can be hepatotoxic and is contraindicated in opiate users. IM naltrexone (380 mg/mo) may be considered if adherence is an issue.
• Acamprosate also helps reduce craving for alcohol. Acamprosate 666 mg tid may be an effective adjunct to counseling. A recent meta-analysis showed overall benefit with increase in the number of abstinent days.
• Disulfiram provokes acetaldehyde accumulation after alcohol ingestion, producing a toxic state manifested by nausea, headache, flushing, and respiratory distress. Studies have shown limited efficacy mostly due to noncompliance.
• Topiramate may be an alternative treatment for alcoholism. In a 12-wk randomized trial, topiramate up to 300 mg/day significantly reduced the number of heavy drinking days.
• Methadone maintenance for opiate addiction is effective and involves once-daily dosing of methadone in a controlled setting by methadone clinics.
• Buprenorphine is as effective as low-dose methadone and may be prescribed by physicians who have completed approved training. For induction, initiate 12 to 24 hr after short-acting opioid use and 24 to 48 hr after long-acting opioid use. Use buprenorphine/naloxone (Suboxone) tablets in most patients, since buprenorphine-only tablets have risk of abuse. Maximum first-day dosage is 4 to 8 mg of buprenorphine. Titrate buprenorphine dose up to 12 mg on day 2 for signs of withdrawal. Then adjust dosage in frequent outpatient visits (weekly) to minimum needed for maintenance (up to 32 mg/day).
• Naltrexone (oral or injectable) may also be used for maintenance in opioid dependence treatment, though evidence of effectiveness is limited.
• Always combine pharmacotherapy with counseling. There is good evidence that this combination improves outcome.
• Treatment of comorbid psychiatric disorders improves outcomes.

• Drug use disorders are chronic relapsing illnesses, so relapses are best approached as part of the course of the illness, as opposed to treatment failure.
• The goal of treatment is often abstinence, but success of treatment is measured by return of function, increasing duration between relapses, and prevention of sequelae of use.

Physicians should refer patients who do not make progress on changing substance use patterns to addiction specialists and/or specialized substance use disorder or dual-diagnosis (mental health and addiction) programs. Patients with comorbid psychiatric illness should be referred for mental health care.