Psychiatry of Alcohol
Alcohol is the major substance of abuse. About 55% of Americans drink; 7% are heavy drinkers (men, 3:1); 20%+ have alcohol-abuse problems at some time (peak at age 21); the lifetime risk for alcoholism is 10% to 14%; and 40% of homicides and automobile deaths are alcohol related (1). Certain populations are at risk (e.g., elderly urban blacks, urban Indians, bartenders, musicians). Finally, mixed abuse of alcohol and other drugs is extremely common.
CLASSIFICATION
Normal (recreational) drinking grades into pathologic use. ALCOHOL ABUSE (DSM p. 214, 305.00) exists if clearly recurrent (not continuous) impaired social and occupational functioning due to alcohol use is present over a 1-year period. Individual patterns can vary from steady sporadic consumption to periodic binges. All demonstrate the inability to abstain from drinking or to stop drinking once started, despite an obvious downward spiral. Such drinking may result in depression and anxiety. Beginning often as evening and weekend drinking, the pattern usually becomes established by the late 20s in men (later in women) with gradual deterioration in some during their 30s and 40s. Spontaneous remissions can occur: they are the norm, but they are temporary. Blackouts (anterograde amnesia for events that occurred during acute intoxication but while the patient was conscious, functional, and appearing normal to those around him or her) often develop as abusive drinking becomes more serious.
If the patient also demonstrates tolerance (increased amounts needed to achieve effect), withdrawal, compulsive and continuous use, or a combination of these, he has ALCOHOL DEPENDENCE (ALCOHOLISM) (DSM p. 213, 303.90). Cultural groups are differently affected [e.g., low among Jews and Asians: 50%+ of Asians have genetic polymorphisms that metabolize alcohol (ethanol) rapidly and its metabolite, acetaldehyde, slowly, producing unpleasant acetaldehyde side effects such as “flushing”]. All social strata are
affected—fewer than 5% are “skid row” types. No “typical alcoholic personality” exists. Alcoholism is comorbid with chronic anxiety disorders, mood disorders (particularly in women), schizophrenia, dementia, and antisocial personality disorder; the presence of these conditions is often both (and/or) an effort to “self-medicate” with alcohol and the aftereffect of primary alcoholism. Nevertheless, always rule out (or treat) these psychiatric disorders.
affected—fewer than 5% are “skid row” types. No “typical alcoholic personality” exists. Alcoholism is comorbid with chronic anxiety disorders, mood disorders (particularly in women), schizophrenia, dementia, and antisocial personality disorder; the presence of these conditions is often both (and/or) an effort to “self-medicate” with alcohol and the aftereffect of primary alcoholism. Nevertheless, always rule out (or treat) these psychiatric disorders.
The etiology of alcoholism is unknown. Evidence for genetic biologic characteristics grows but is not without controversy (risk of developing alcoholism: one alcoholic parent, 4 times normal risk; both parents alcoholic, 60% risk). Adoption studies indicate a genetic factor in some families: increased frequency of alcohol abuse and sociopathy among male relatives and possibly increased somatization among female relatives of alcoholics. Recent research identifies two groups of alcoholics (2):
Type 1: adult onset; steady, gradually escalating consumption; guilty, worried, rigid, perfectionistic, dependent, introverted; modest family history; both men and women; some recover completely; 75% of alcoholics.
Type 2: alcohol seeking from adolescence and early adulthood; impulsive; distractible; risk taking; antisocial characteristics with recklessness and aggression; strong family history; primarily men; very treatment resistant; 25% of all alcoholics.
Moreover, certain predictive biologic features of future alcoholism may be inherited by some first-degree relatives (particularly men) of alcoholics [e.g., a resistance to intoxication (the person who can “really hold his liquor” from an early age is at a very high risk to develop alcoholism), a subnormal cortisol increase after drinking, and a subnormal epinephrine release after stress]. Alcohol stimulates the release of dopamine from the nucleus accumbens, producing euphoria. Over time, the dopaminergic neurons atrophy and natural level of dopamine decreases, producing malaise unless the level is stimulated by alcohol (i.e., very reinforcing). With abstinence, the alcoholic’s dopamine level may take months or years to recover.
RECOGNIZING THE ALCOHOLIC
Clinical Markers
The majority of alcoholics function fairly well most of the time and go unrecognized by physicians until their social and occupational
lives and their physical health have been significantly harmed. Early recognition is important. These patients frequently conceal alcohol use; keep a high index of suspicion if the predominant complaints include chronic anxiety and tension, insomnia, chronic depression, headaches, blackouts, nausea and vomiting, vague gastrointestinal problems, tachycardia, palpitations, and frequent falls or minor injuries. Ask about absenteeism, job loss, financial difficulties, and family trouble. Ask “Do you drink?” Be encouraging and nonjudgmental. Get drinking specifics (number of beers per day, oz/glass, drink alone?, etc). Interview relatives and friends, if possible.
lives and their physical health have been significantly harmed. Early recognition is important. These patients frequently conceal alcohol use; keep a high index of suspicion if the predominant complaints include chronic anxiety and tension, insomnia, chronic depression, headaches, blackouts, nausea and vomiting, vague gastrointestinal problems, tachycardia, palpitations, and frequent falls or minor injuries. Ask about absenteeism, job loss, financial difficulties, and family trouble. Ask “Do you drink?” Be encouraging and nonjudgmental. Get drinking specifics (number of beers per day, oz/glass, drink alone?, etc). Interview relatives and friends, if possible.
Screening Tests
Use a brief screening questionnaire (but remember, patients often “fake good”). Two that are quick and reliable are the SAAST (Self-Administered Alcoholic Screening Test; can be computer scored; takes 10 minutes; accurate when completed by a relative) and the CAGE (consists of four “mnemonic” questions; two or more positive answers are suggestive of alcoholism) (3):
“Have you ever felt you should Cut down on your drinking?”
“Have people Annoyed you by criticizing your drinking?”
“Have you ever felt bad or Guilty about your drinking?”
“Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (Eye opener)?”
A subscale of the MMPI, the MacAndrew Scale (Mac), consists of 49 MMPI items and provides a degree of reliability when coupled with the MMPI validity scales.
Biologic Markers
Chronic drinking frequently elevates serum γ-glutamyltransferase (GGT) and RBC MCV (together they identify 90% of alcoholics). These measures, coupled with evidence of more acute alcoholic insult (protein, Alk Phos, LDH, SGOT, SGPT, etc.), constitute a fairly reliable laboratory screen for alcoholism. A new blood test, carbohydrate-deficient transferrin (CDT), has demonstrated a sensitivity of 82% and specificity of 97%. It could be very useful but primarily when used with other tests because its sensitivity is very high, and it is likely to pick up “normal heavy drinkers” (like college students).
CLINICAL PRESENTATIONS OF ALCOHOL SYNDROMES
When suspecting alcohol problems, always determine whether (a) the patient is currently intoxicated, and (b) the time since the patient’s last drink.
Intoxication Syndromes
▪ Alcohol Intoxication (DSM p. 214, 303.00)
Alcohol is a CNS depressant that initially disinhibits and then depresses. Early intoxication includes liveliness, a sense of well-being, and a smell of alcohol on the breath [blood alcohol levels (BALs) up to 100 mg/dl, 100 mg%, or 0.1%]; grading into irritability, emotional lability, and incoordination (0.1% to 0.15%); which grades into apathy, slurred speech, and ataxia (0.15% to 0.25%); which can become alcoholic coma (above 0.25% to 0.4%, an emergency—get blood alcohol level and check for presence of other drugs; treat with intubation, CPR, etc., if necessary). Blood alcohol levels vary with drinking history and thus are only approximate; behavior may vary from depressed and maudlin to agitated and aggressive. As intoxication wanes over a period of 6 to 12+ hours, a “hangover” usually supervenes (headache, malaise, dysphoria, nausea, shakes, diaphoresis), which can last the better part of a day.
Acute intoxication can mimic schizophrenia, mania, depression, hysteria, etc., so delay detailed interview and final diagnosis until the patient is sober. Evaluate carefully for medical problems (see later)—differential includes hypoglycemia, CNS infection, and toxic psychosis of other etiology. Intoxicated patients may be uncooperative, assaultive, and dangerous—be civil, nonthreatening, accepting, respectful, patient, but prepared with force. Attempt nonpharmacologic management (quiet room, support, coffee), but sedation may be necessary (e.g., diazepam, 5 to 20 mg i.m., erratically absorbed), but be cautious of oversedation. Decide if the patient just needs to “sleep it off” (most common), is at risk for withdrawal, or is becoming comatose. Should the patient go home with family, be observed overnight, be hospitalized, or go to jail? Be familiar with community resources.
Alcohol idiosyncratic intoxication or pathologic intoxication is an unusual and controversial condition (not currently in DSM-IV) of marked aggressiveness and emotional lability, occasionally of psychotic proportions, that follows ingestion of small quantities of alcohol in an otherwise normal person. Etiology is unknown.
Some patients retain this pattern for life. Episodes appear suddenly and may last for hours or a day or more, often with amnesia for the episode afterward. Sedate [benzodiazepines, haloperidol (Haldol)], and control until sober. Rule out temporal lobe epilepsy. Alcoholic paranoia (DSM p. 338, 291.5) has a similar presentation but with strong paranoid delusions, typically of jealousy: it usually occurs in chronic alcoholics who are actively drinking and who can become violent.
Some patients retain this pattern for life. Episodes appear suddenly and may last for hours or a day or more, often with amnesia for the episode afterward. Sedate [benzodiazepines, haloperidol (Haldol)], and control until sober. Rule out temporal lobe epilepsy. Alcoholic paranoia (DSM p. 338, 291.5) has a similar presentation but with strong paranoid delusions, typically of jealousy: it usually occurs in chronic alcoholics who are actively drinking and who can become violent.
Alcohol-withdrawal Syndromes
These may occur in heavy drinkers or alcoholics who stop drinking or who just reduce their consumption. Do not overlook them in the “closet” alcoholic (e.g., the businessman or housewife who temporarily abstains while in the hospital for other reasons). If the patient is withdrawing, delay final diagnostic conclusions.
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