Harrison’s Manual of Medicine
Alcoholism and alcohol abuse are defined by the regular and excessive use of alcohol with concomitant social, occupational, and/or physical problems; alcohol is associated with half of all traffic fatalities and half of all homicides. In alcohol dependence, the regular use of alcohol has resulted in a state of physiologic tolerance and dependence. A pt may never suffer from withdrawal symptoms and still meet criteria for alcohol abuse.
Alcoholism is a multifactorial disorder in which genetic, biologic, and sociocultural factors interact. Typically, the first major life problem from excessive alcohol use appears in early adulthood, followed by periods of exacerbation and remission; the lifespan of the alcoholic is shortened by an average of 15 years due to increased risk of death from heart disease, cancer, accidents, or suicide.
One out of five of the average physician’s pts will suffer from alcoholism. Routine medical care requires attention to potential alcohol-related illness and to alcoholism itself:
Neurologic—blackouts, seizures, delirium tremens, cerebellar degeneration, neuropathy, myopathy
Gastrointestinal—esophagitis, gastritis, pancreatitis, hepatitis, cirrhosis, GI hemorrhage
Hematologic—macrocytosis, folate deficiency, thrombocytopenia, leukopenia
Endocrine—gynecomastia, testicular atrophy, amenorrhea, infertility
Cancer—breast cancer, oral and esophageal cancers, rectal cancers.
Most alcoholic pts do not have dramatic physical symptoms but instead present with psychosocial difficulties. Most common are marital difficulties, job problems (tardiness, absenteeism), and legal problems resulting from driving while intoxicated. A positive answer to any of the “CAGE questions” indicates a high probability of alcoholism: Are you . . . Cutting down, or feel the need to? Annoyed when people criticize your drinking? Guilty about your drinking? Eye-opening with a drink in the morning? Typically, pts will describe a host of difficulties but will then deny that they have a problem with alcohol abuse. Denial is a characteristic, if not the core, symptom of alcoholism.
Alcohol is a CNS depressant that acts on receptors for g-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 4–7 mmol/L (20–30 mg/dL), a level achieved after the ingestion of one or two typical drinks. Mild to moderate intoxication occurs at 17–43 mmol/L (80–200 mg/dL). Incoordination, tremor, ataxia, confusion, stupor, coma, and even death occur at progressively higher blood alcohol levels.
Chronic alcohol use produces CNS dependence. In such individuals, the earliest sign of alcohol withdrawal is tremulousness (“shakes” or “jitters”), which usually occurs 8–24 h after the last drink. This may be followed by generalized seizures (“rum fits”) in the first 24–48 h; these do not require initiation of anti-seizure medications. With severe withdrawal, autonomic hyperactivity ensues (sweating, hypertension, tachycardia, tachypnea, fever), accompanied by insomnia, nightmares, anxiety, and GI symptoms.
Delirium tremens (DTs), which may begin 3–5 days after the last drink, is a very severe withdrawal syndrome characterized by profound autonomic hyperactivity, extreme confusion, agitation, vivid delusions, and hallucinations (often visual and tactile); mortality is 5–15%. Wernicke’s encephalopathy is 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. Korsakoff’s syndrome follows as the encephalopathy and ocular findings resolve; it is characterized by anterograde and retrograde amnesia and confabulation. Wernicke-Korsakoff’s syndrome is caused by chronic thiamine deficiency, resulting in damage to thalamic nuclei, mamillary bodies, and brainstem and cerebellar structures.
Clues to alcoholism include mild anemia with macrocytosis, folate deficiency, thrombocytopenia, granulocytopenia, abnormal LFTs, hyperuricemia, and elevated triglycerides. Decreases in serum K, Mg, Zn, and PO4 levels are common. Diagnostic studies such as GI radiology or endoscopy, abdominal ultrasound or CT, liver-spleen scan, liver biopsy, ECG, echocardiogram, brain CT or MRI, EEG, and nerve conduction studies may show evidence of alcohol-related organ dysfunction.
Acute Withdrawal Acute alcohol withdrawal is treated with thiamine (50–100 mg IV or 100 mg PO daily for 5 d) to replenish depleted stores; if Wernicke-Korsakoff’s syndrome is suspected, the IV route must be used, since intestinal absorption is unreliable in alcoholics. CNS depressant drugs that enhance GABA-mediated inhibition are used when seizures or autonomic hyperactivity are present. These drugs 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 the medication of choice (e.g., diazepam, chlordiazepoxide), because they produce fairly steady blood levels of drug and there is a wide dose range within which to work. These benefits must be weighed against the risk of overmedication and oversedation, which occur less commonly with shorter-acting agents (e.g. oxazepam, lorazepam). Typical doses are diazepam 5–10 mg or chlordiazepoxide 25–50 mg PO every 1–4 h prn objective signs of alcohol withdrawal (such as pulse < 90). Extremely high doses are sometimes required for the chronic alcoholic.
In severe withdrawal or DTs, the physician must also look for evidence of trauma or infection that may be masked by prominent withdrawal symptoms or that contribute to the pt’s debilitated state. Fluid and electrolyte status and blood glucose levels should be closely followed as well. Cardiovascular and hemodynamic monitoring are crucial, as hemodynamic collapse and cardiac arrhythmia are not uncommon.
Recovery and Sobriety The definitive treatment of alcoholism requires a successful confrontation of the pt’s denial, followed by the pt’s motivation to change. It may take multiple encounters between physician and pt over a period of years for a pt to achieve this level of motivation. Once pts commit to treatment, an initial stage of recovery (early abstinence) is followed by ongoing sobriety. The physician should counsel the pt about the need for continued abstinence as a primary treatment goal and about the usefulness of regular participation in self-help resources such as AA (and Alanon for family members).
Once sobriety has been achieved, pts should be evaluated for the presence of any other underlying psychiatric disorder (such as major depression) and vigorously treated. The physician should also recognize the relapsing/remitting nature of alcoholism, and be prepared to help pts reenter treatment periodically.
Disulfiram (Antabuse), a drug that inhibits aldehyde dehydrogenase and results in toxic symptoms (nausea, vomiting, diarrhea, tremor) if the pt consumes alcohol, is used in some centers but is not an effective therapy in the absence of psychosocial intervention. Preliminary studies show that naltrexone and acamprosate may reduce recidivism in abstinent alcoholics.
For a more detailed discussion, see Schuckit MA: Alcohol and Alcoholism, Chap. 387, p. 2561, in HPIM-15.