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Harrison's Manual of Medicine, 19e

Chapter 199: Alcohol Use Disorder

INTRODUCTION

Alcohol use disorder is defined as repeated alcohol-related difficulties in at least 2 of 11 life areas that cluster together in the same 12-month period (Table 199-1). Severity is based on the number of items endorsed: mild is two or three items, moderate is four or five, and severe is six or more.

TABLE 199-1DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS, FIFTH EDITION, CLASSIFICATION OF ALCOHOL USE DISORDER (AUD)

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TABLE 199-1DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS, FIFTH EDITION, CLASSIFICATION OF ALCOHOL USE DISORDER (AUD)

Criteria

Two or more of the following items occurring in the same 12-month period must be endorsed for the diagnosis of an AUD^a:

Drinking resulting in recurrent failure to fulfill role obligations

Recurrent drinking in hazardous situations

Continued drinking despite alcohol-related social or interpersonal problems

Tolerance

Withdrawal, or substance use for relief/avoidance of withdrawal

Drinking in larger amounts or for longer than intended

Persistent desire/unsuccessful attempts to stop or reduce drinking

Great deal of time spent obtaining, using, or recovering from alcohol

Important activities given up/reduced because of drinking

Continued drinking despite knowledge of physical or psychological problems caused by alcohol

Alcohol craving

^aMild AUD: 2–3 criteria required; moderate AUD: 4–5 items endorsed; severe AUD: 6 or more items endorsed.

CLINICAL FEATURES

Lifetime risk for alcohol use disorder is 10–15% for men and 5–8% for women. Typically, the first major life problem from excessive alcohol use appears in early adulthood, followed by periods of exacerbation and remission. The course is not hopeless; following treatment, between half and two-thirds of pts maintain abstinence for years and often permanently. If the alcoholic continues to drink, life span is shortened by an average of 10 years due to increased risk of death from heart disease, cancer, accidents, or suicide.

Screening for alcoholism is important given its high prevalence. Standardized questionnaires can be helpful in busy clinical practices including the 10-item Alcohol Use Disorders Identification Test (AUDIT) (Table 199-2).

TABLE 199-2THE ALCOHOL USE DISORDERS IDENTIFICATION TEST (AUDIT)^a

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TABLE 199-2THE ALCOHOL USE DISORDERS IDENTIFICATION TEST (AUDIT)^a

Item

5-Point Scale (Least to Most)

1. How often do you have a drink containing alcohol?

Never (0) to 4+ per week (4)

2. How many drinks containing alcohol do you have on a typical day?

1 or 2 (0) to 10+ (4)

3. How often do you have six or more drinks on one occasion?

Never (0) to daily or almost daily (4)

4. How often during the last year have you found that you were not able to stop drinking once you had started?

Never (0) to daily or almost daily (4)

5. How often during the last year have you failed to do what was normally expected from you because of drinking?

Never (0) to daily or almost daily (4)

6. How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session?

Never (0) to daily or almost daily (4)

7. How often during the last year have you had a feeling of guilt or remorse after drinking?

Never (0) to daily or almost daily (4)

8. How often during the last year have you been unable to remember what happened the night before because you had been drinking?

Never (0) to daily or almost daily (4)

9. Have you or someone else been injured as a result of your drinking?

No (0) to yes, during the last year (4)

10. Has a relative, friend, doctor, or other health worker been concerned about your drinking or suggested that you should cut down?

No (0) to yes, during the last year (4)

^aThe AUDIT is scored by simply summing the values associated with the endorsed response. A score ≥8 may indicate harmful alcohol use.

Routine medical care requires attention to potential alcohol-related illness and to alcoholism itself:

Neurologic: blackouts, seizures, delirium tremens (DTs), cerebellar degeneration, neuropathy, myopathy
GI: esophagitis, gastritis, pancreatitis, hepatitis, cirrhosis, GI hemorrhage
Cardiovascular: hypertension, cardiomyopathy
Hematologic: macrocytosis, folate deficiency, thrombocytopenia, leukopenia
Endocrine: gynecomastia, testicular atrophy, amenorrhea, infertility
Skeletal: fractures, osteonecrosis
Cancer: breast cancer, oral and esophageal cancers, rectal cancers

Alcohol Intoxication

Alcohol is a CNS depressant that acts on receptors for γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the nervous system. Behavioral, cognitive, and psychomotor changes can occur at blood alcohol levels as low as 0.02–0.03 g/dL, a level achieved after the ingestion of one or two typical drinks. “Legal intoxication” in most states requires a blood alcohol concentration of 0.08 g/dL; levels twice this can lead to deep but disturbed sleep. Incoordination, tremor, ataxia, confusion, stupor, coma, and even death occur at progressively higher blood alcohol levels.

Alcohol Withdrawal

Chronic alcohol use produces CNS dependence, and the earliest sign of alcohol withdrawal is tremulousness (“shakes” or “jitters”), occurring 5–10 h after decreasing ethanol intake. This may be followed by generalized seizures in the first 24–48 h; these do not require initiation of antiseizure medications. With severe withdrawal, autonomic hyperactivity ensues (sweating, hypertension, tachycardia, tachypnea, fever), accompanied by insomnia, nightmares, anxiety, and GI symptoms.

Delirium Tremens (DTs)

A very severe withdrawal syndrome characterized by profound autonomic hyperactivity, extreme confusion, agitation, vivid delusions, and hallucinations (often visual and tactile) that begins 3–5 days after the last drink. Mortality is 5–15%.

Wernicke’s Encephalopathy

An alcohol-related syndrome characterized by ataxia, ophthalmoplegia, and confusion, often with associated nystagmus, peripheral neuropathy, cerebellar signs, and hypotension; there is impaired short-term memory, inattention, and emotional lability. Wernicke-Korsakoff’s syndrome follows, characterized by anterograde and retrograde amnesia and confabulation. Wernicke-Korsakoff’s syndrome is caused by chronic thiamine deficiency, resulting in damage to thalamic nuclei, mammillary bodies, and brainstem and cerebellar structures.

LABORATORY FINDINGS

Include mild anemia with macrocytosis, folate deficiency, thrombocytopenia, granulocytopenia, abnormal liver function tests, hyperuricemia, and elevated triglycerides. Two blood tests with ≥60% sensitivity and specificity are γ-glutamyl transferase (GGT) (>35 U) and carbohydrate-deficient transferrin (CDT) (>20 U/L or >2.6%); the combination of the two is likely to be more accurate than either alone. A variety of diagnostic studies may show evidence of alcohol-related organ dysfunction.

TREATMENT: ALCOHOLISM ACUTE WITHDRAWAL

Acute alcohol withdrawal is treated with multiple B vitamins including thiamine (50–100 mg IV or PO daily for ≥1 week) to replenish depleted stores; use the IV route if Wernicke-Korsakoff’s syndrome is suspected since intestinal absorption is unreliable in alcoholics.
CNS depressant drugs are used when seizures or autonomic hyperactivity is present to halt the rapid state of withdrawal in the CNS and allow for a slower, more controlled reduction of the substance. Low-potency benzodiazepines with long half-lives are preferred (e.g., diazepam 10 mg PO q4–6h, chlordiazepoxide 25–50 mg PO q4–6h) because they produce fairly steady blood levels of drug within a wide dose range. Risks include overmedication and oversedation, which occur less commonly with shorter-acting agents (e.g., oxazepam, lorazepam).
In severe withdrawal or DTs, high doses of benzodiazepines are usually required. Fluid and electrolyte status and blood glucose levels should be closely followed. Cardiovascular and hemodynamic monitoring is crucial, as hemodynamic collapse and cardiac arrhythmia are not uncommon.
Generalized withdrawal seizures rarely require aggressive pharmacologic intervention beyond that given to the usual pt undergoing withdrawal, i.e., adequate doses of benzodiazepines.

RECOVERY AND SOBRIETY Counseling, Education, and Cognitive Approaches

First, attempts should be made to help the alcoholic achieve and maintain a high level of motivation toward abstinence. These include education about alcoholism and instructing family and/or friends to stop protecting the person from the problems caused by alcohol.
A second goal is to help the pt to readjust to life without alcohol and to reestablish a functional lifestyle through counseling, vocational rehabilitation, and self-help groups such as alcoholics anonymous (AA).
A third component, called relapse prevention, helps the pt to identify situations in which a return to drinking is likely, formulate ways of managing these risks, and develop coping strategies that increase the chances of a return to abstinence if a slip occurs.
There is no convincing evidence that inpatient rehabilitation is more effective than outpatient care.

Drug Therapy

Several medications may be useful in alcoholic rehabilitation; usually medications are continued for 6 months if a positive response is seen.

The opioid-antagonist drug naltrexone (50–150 mg/d PO or monthly 380-mg injection) decreases the probability of a return to drinking and shortens periods of relapse.
A second medication, acamprosate (2 g/d divided into three oral doses), an N-methyl-D-aspartate receptor inhibitor, may be used; efficacy appears similar to naltrexone.
A combination of naltrexone and acamprosate may be superior to either drug alone, although not all studies agree.
Disulfiram (250 mg/d), an aldehyde dehydrogenase inhibitor, produces an unpleasant and potentially dangerous reaction in the presence of alcohol.

For a more detailed discussion, see Schuckit MA: Alcohol and Alcoholism, Chap. 467, p. 2723, in HPIM-19.

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