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Information ⬇

[Section Outline]

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 with leading causes of increased death stemming from enhanced rates of 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 202-2 The Alcohol Use Disorders Identification Test (AUDIT)a ).

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

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

Alcohol Intoxication !!navigator!!

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 0.02-0.04 g/dL, a level achieved after the ingestion of one or two typical drinks. “Legal intoxication” in most states is based on 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 !!navigator!!

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) !!navigator!!

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 as high as 5%.

Wernicke's Encephalopathy !!navigator!!

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 !!navigator!!

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 for heavy alcohol consumption 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 on the first day and then decreased over the next 5 days) 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 education, helps the pt to identify situations in which a return to drinking is likely, formulate ways of managing these risks or avoid the risky situation, and develop coping strategies that increase the chances of a return to abstinence quickly after an episode of drinking.
  • 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 6-12 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.
  • Additional drugs under investigation include another opioid antagonist nalmefene, the nicotinic receptor agonist varenicline, the serotonin antagonist ondansetron, the α-adrenergic agonist prazosin, the GABAB receptor agonist baclofen, the anticonvulsant topiramate, and cannabinol receptor antagonists; few data yet offer solid support for their routine use in clinical settings.

Outline ⬆

Section 15. Psychiatry and Substance Abuse