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20.

ALCOHOL USE DISORDERS


lane A. Kemedy, D.O.
1. Who drinks alcohol? About 75% of the population in the United States drinks, and about 23% reported alcohol abuse or dependence in the National Comorbidity Survey reported in 1994. Men are 2-3 times more likely than women to be problem drinkers, although women may hide their drinking more frequently.

2. Does alcoholism run in families?


Good evidence suggests a genetic link, and the strongest vulnerability appears to be for sons of alcoholic fathers. Several studies, including twin and adoption studies, show that children of alcoholics are about 4 times more likely to develop alcohol problems. Specific biologic abnormalities have been noted, such as decreased brain-wave reactivity (P300, a measure of visual evoked response) in children of alcoholics and decreased intensity of reaction to alcohol in sons of alcoholics.

3. What are the signs and symptoms of alcohol intoxication? A person intoxicated by alcohol may have ataxia, slurred speech, mood lability, decreased concentration and memory, poor judgment, facial flushing, enlarged pupils, and nystagmus. Although alcohol initially has a stimulant effect, increasing levels result in depression of respiration, reflexes, blood pressure, and body temperature, potentially followed by stupor, coma, and death. Blood alcohol levels are measured in grams percent (8%) or milligrams per 100 milliliters (mg/dl); in most states drivers are said to be impaired at levels of 0.05 g% (50 mg/dl) and under the influence at levels of 0.1 g% (100 mg/dl). Lack of intoxication at a level of 100 mg/dl is evidence of tolerance, and alcohol dependence disorder should be suspected.
4. What are the usual symptoms and time course of alcohol withdrawal? In someone dependent on alcohol, stopping or suddenly decreasing the amount of alcohol intake may result in withdrawal symptoms, which reflect central nervous system and autonomic hyperactivity. Symptoms begin to appear in 4-24 hours, usually peak at 36-48 hours, and subside in about 5 days. Symptoms typically are in proportion to duration of drinking, but the presence of medical illness may increase the severity. Mild withdrawal may manifest as insomnia, irritability, anxiety, and mild gastrointestinal problems that start a few hours after stopping alcohol and last up to 48 hours. Symptoms may progress first to tremor, sweating, tachycardia, elevated blood pressure, nausea, vomiting, and diarrhea and then to fever, hallucinations, delusions, confusion, agitation, and grand ma1 seizures. Hallucinations may appear within 24-96 hours and may be auditory, tactile, or visual (most common). Delirium tremens usually appears between 24 and 72 hours and may have a mortality rate of 5 1 5 % ; this syndrome, which is characterized by extreme agitation, delirium, psychosis (delusions and hallucinations), and fever, may last up to 5 days. 5. What about alcohol withdrawal seizures? Alcohol withdrawal seizures (rum fits) most often occur M 8 hours after stopping or reducing alcohol and may occur in 5-10% of patients in alcohol withdrawal. The seizures generally stop within 6-12 hours; they may be multiple and are usually grand mal. If a patient has a past history of alcohol withdrawal seizures, the risk of recurrence is increased 10-fold. Because < 5% of alcohol withdrawal seizures are focal, other causes, such as subdural hematoma, should be evaluated. Seizures that occur beyond 48 hours may be due to causes such as withdrawal from sedatives. Many alcoholics have chronic obstructive pulmonary disease, and
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seizures may be related to theophylline toxicity. Seizures also may be caused by metabolic disorders such as hypoglycemia or hypomagnesemia, which are not uncommon in alcoholics.

6. What is the treatment of alcohol withdrawal? Removal of alcohol leads to a state of hyperexcitability. Most patients are able to withdraw without medication, but patients with moderate-to-severe symptoms are best treated with a sedative. Overall, the benzodiazepines have been found to be the most useful and the most practical. The long-acting benzodiazepines, such as chlordiazepoxide, diazepam, and chlorazepate, are used in decreasing doses to prevent seizure and to decrease the other symptoms of hyperexcitability. For patients with severe liver disease, who may encounter problems with accumulation of long-acting benzodiazepines and their metabolites, oxazepam is recommended because of its lack of active metabolites and its independence of liver metabolism. Oxazepam and lorazepam may be given intramuscularly, whereas other benzodiazepines are poorly absorbed with intramuscular administration. Other agents have been examined for treatment of alcohol withdrawal, with various success: Alpha2 adrenergic agonists: clonidine and lofexidine reduce noradrenergic symptoms, but have no anticonvulsant effects and may cause hypotension. Antipsychotics: haloperidol in low doses may be useful in patients with hallucinations and agitation that do not respond to benzodiazepines, but they should not be used alone. Antipsychotics do not prevent seizures and may lower seizure threshold. Thorazine, which may cause severe hypotension and lower seizure threshold, should not be used. Barbiturates: effective anticonvulsants but narrow therapeutic index and greater tendency to induce respiratory depression. Anticonvulsants: both carbamazepine and divalproex have been used effectively in small studies. In particular, divalproex seems to have considerably less effect on cognition and psychomotor performance. Ethanol: contraindicated because of toxicity and potential to cause high fluid load. Propranolol: contraindicated because it does not prevent seizures, may obscure withdrawal signs, and is contraindicated in various conditions seen in chronic alcoholics, such as lung diseases with bronchospasm, congestive heart failure, hypotension, and insulin-dependent diabetes.
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7. What is the treatment of alcohol withdrawal seizures? Benzodiazepines should be used for the treatment of withdrawal seizures-most commonly, the long-acting drugs such as chlordiazepoxide, diazepam, or chlorazepate. Some clinicians avoid the use of diazepam, because it may cause euphoria. For elderly patients or patients with compromised liver function, short-acting benzodiazepines, such as oxazepam or lorazepam, avoid accumulation of metabolites and may be administered parenterally.
8. Do patients need phenytoin for prophylaxis of alcohol withdrawal seizures? Little evidence supports the use of phenytoin for the treatment or prophylaxis of alcohol withdrawal seizures unless the patient has a preexisting seizure disorder.

9. What is Wernicke-Korsakoffsyndrome?
Wemickes disease, or Wernickes encephalopathy, is characterized by confusion and drowsiness, ataxia, and ocular disturbances (usually due to weakness or paralysis of the sixth cranial nerve), including nystagmus. Wernickes syndrome may have acute onset or develop slowly over 1 week or so. Korsakoffs psychosis is a state of amnesia that usually follows Wernickes syndrome; patients have anterograde amnesia (inability to retain new memories, even their physicians name) and possibly retrograde amnesia (inability to recall the past). Otherwise they appear alert, responsive, and normal and may try to cover their memory problem by fabricating answers or confabulating. In the string test, which has been used in diagnosis of Korsakoffs psychosis, the physician asks the patient to take an imaginary string in his or her hands, and the patient complies, as though the string were real. Treatment with thiamine may reverse the ocular abnormalities and ataxia almost completely, but the confusion and amnestic problems may not respond as well. Rapid treatment of Wernickes syndrome

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may prevent the onset of Korsakoffs psychosis; if treatment is delayed, the patient may become demented and unable to care for him- or herself. Thus, Wemickesencephalopathy is a medical emergency.

10. When is thiamine needed?


Chronic alcoholics often are malnourished. Thiamine deficiency is common and may cause Wernicke-Korsakoff syndrome. The treatment is immediate administration of thiamine, 100 mg intramuscularly, followed by 100 mg intramuscularly or orally for the next 2 days. Because administration of glucose may deplete already deficient B-vitamins, thiamine should be given before glucose is administered.

11. What are the medical complicationsof chronic alcohol use? Gastrointestinal complications. Gastrointestinal problems include gastritis, peptic and gastric ulcer, esophagitis, esophageal varices, alcoholic hepatitis, cirrhosis, and pancreatitis. Except for cirrhosis, these conditions are often reversible with abstinence from alcohol. Although a minority of alcoholics (15-20%) develop cirrhosis, the majority of patients with cirrhosis are alcoholics (50-80%). Therapeutic doses of acetaminophen are associated with hepatoxicity in alcoholics. Neurologic complications. Wernicke-Korsakoff syndrome is a medical emergency (see Question 9). Hepatic encephalopathy may occur because the liver is no longer able to metabolize and detoxify substances. Asterixis, or liver flap, appears late; early symptoms include confusion, agitation, and personality changes. Peripheral neuropathy is usually symmetrical and in the lower extremities. With prolonged drinking, alcohol dementia may occur with memory defects and difficulty with abstract thinking and new learning. Cerebellar degeneration, which causes a wide-spread gait, may be associated with Wernicke-Korsakoff syndrome. Stopping alcohol intake and vitamin treatment can improve these conditions. Cardiovascular complications. Hypertension is associated with excessive alcohol intake, and patients who continue to drink heavily may not respond as well to antihypertensive medication. With abstinence, many patients become normotensive. Alcoholic cardiomyopathy has a fairly nonspecific presentation, and the diagnosis is usually based on the alcohol history; it should be suspected in patients under age 50 who present with heart failure. Alcohol ingestion and alcohol withdrawal cause sinus tachycardia. Pulmonary complications. Alcoholics show increased incidence of tuberculosis and bacterial pneumonias; in addition, aspiration pneumonia may occur with vomiting and altered levels of consciousness. Because at least 80% of alcoholics are smokers, the incidence of bronchitis, emphysema, and chronic obstructive pulmonary disease is increased. Hematologic complications. Macrocytosis (enlarged red blood cells) is an early laboratory manifestation of chronic alcoholism. It may be caused by folate deficiency or the direct toxicity of alcohol (unrelated to vitamin depletion). Iron deficiency anemia may occur in alcoholics because of chronic gastrointestinal bleeding, but the associated low mean corpuscular volume may be hidden by concurrent macrocytosis. Alcohol impairs the production and function of white blood cells, both neutrophils and lymphocytes, and increases the risk of infection. Blood platelet production also may be suppressed, and platelet function may be impaired. In addition, splenic enlargement secondary to liver disease may cause thrombocytopenia through increased sequestration of platelets. Endocrine complications.Alcohol suppresses testosterone levels in men by effects on the pituitary gland and the testicle, and impaired metabolism of estrogen by the liver increases estrogen levels. Both events may result in signs of feminization, such as gynecomastia and feminine fat distribution; decreased libido; testicular atrophy; and impotence. Women experience menstrual irregularities, ranging from cessation of menses to excessive bleeding. 12. Is smoking associated with drinking? At the minimum, 80-90% of alcoholics are regular and often heavy smokers. Some of the medical complications of alcoholism may be caused by cigarette smoking, and increased mortality also may be due to complications from smoking. A higher rate of alcoholism should be expected in smoking populations, such as patients with chronic obstructive pulmonary disease.

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Alcohol Use Disorders

13. How can the physician detect alcohol problems in patients? The history and physical exam of a patient reveal a great deal. Certainly the diagnosis of alcohol abuse or dependence must be pursued in a patient who shows withdrawal symptoms such as tremors and diaphoresis or who is intoxicated and smells of alcohol. Symptoms of medical conditions associated with excessive alcohol use, such as diarrhea, anemia, or impotence, also should suggest the diagnosis. Patients have been known to receive an extensive work-up for diarrhea caused by alcohol withdrawal, because the physician did not ask about drinking. The physician should ask about alcohol intake without being accusatory; problem drinkers may be honest if they do not feel threatened.

14. What physical findings are common in chronic heavy drinkers?


Flushed facies Parotid gland enlargement Gynecomastia in men Spider angiomata Abdominal distension from ascites Abnormal gait due to cerebellar degeneration Dilated superficial veins on the abdomen Right upper quadrant tenderness Hepatomegaly Muscle wasting or tenderness Paresthesias in feet and calves

15. Can laboratory tests diagnose alcohol abuse and dependence?


Verbal questioning is more sensitive than laboratory tests for detecting alcohol problems; no one test can prove their presence. Several tests evaluated together, however, are sometimes useful, although often in the later stages of disease. The gamma-glutamyltransferase (GGT) test has been used most commonly; although not specific (many other factors may cause increased GGT), abnormally high values are seen in most chronic alcoholics. An elevated mean corpuscular volume (MCV) may be a sign of chronic heavy alcohol consumption and is thought to be a direct effect of alcohol on bone marrow or folate metabolism; again, an elevated MCV may have many other causes. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are nonspecific indicators of hepatic damage but are frequently elevated in alcoholic liver disease; an ALT/AST ratio of > 2 is especially suspicious. Other blood tests found to be elevated with chronic alcohol intake are alkaline phosphatase, high-density lipoprotein cholesterol, and uric acid. It is best to look at laboratory markers in combination; the more tests that are elevated, the more likely the patient will be a heavy drinker. The carbohydrate-deficient transfemn test, which is being evaluated as a state marker for alcoholism, appears promising.

16. What is fetal alcohol syndrome? The fetus is affected by maternal alcohol intake, probably in a dose-dependent manner. The minimal safe amount o f alcohol that will not cause fetal problems is unknown, but certainly the likelihood of fetal alcohol syndrome (FAS) increases with increasing amounts of alcohol intake. The early weeks of the first trimester are thought to be the time of greatest vulnerability. Infants with FAS are smaller, may have mental retardation, and have characteristic facial features, such as no philtrum (ridge between nose and upper lip), thin upper lip, low-set ears, and short palpebral fissures. Cigarette smoking, malnutrition, and drug use may be complicating factors in the spectrum of clinical problems seen in these infants.
17. Are there any useful pharmacologic approaches in the treatment of alcohol abuse and dependence afer withdrawal? Disulfiram (Antabuse) has been used as a deterrent to drinking; it inhibits aldehyde dehydrogenase, which breaks down acetaldehyde, a metabolite of alcohol. If a patient drinks while taking disulfiram, the increased level of acetaldehyde causes flushing, throbbing headache, nausea, vomiting, tachycardia, hypotension, and hyperventilation; rarely, cardiovascular collapse and death may occur. A large study showed marginal efficacy of disulfiram, but patients were not monitored. Results are improved if the patient is required to take the disulfiram under observation. Naltrexone, an opioid blocker, has been approved for use in the treatment of alcohol problems; it decreases craving, and reduces likelihood of continued drinking if the patient relapses. Because

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the reinforcing property of alcohol seems to be attenuated for some drinkers, naltrexone is helpful as an adjunct to treatment of alcohol dependence. No studies have reported the use of naltrexone beyond 12 weeks. Nalmefene, an experimental oral opioid antagonist, appears as effective as naltrexone and possibly has less risk of liver toxicity. Acamprosate, an analog of homocysteic acid, has produced higher continuous abstinence rates and fewer drinking days. It seems to affect excitatory amino acid neurotransmitters and possibly the GABA system. It is not yet available in the U S . Gamma hydroxybutyrate has been used to treat alcohol and opiate withdrawal outside the U.S., but it is an abusable drug.

BIBLIOGRAPHY
I . Brewer C: Combining pharmacological antagonists and behavioral psychotherapy in treating addictions. Br J Psychiatry 157:3440, 1990. 2. Fuller RF, Branchey L, Brightwell DR, et al: Disulfiram treatment of alcoholism: A Veterans Administration cooperative study. JAMA 256:1449-1455, 1986. 3. Garbutt JC, West SL, Carey TS, et al: Pharmacological treatment of alcohol dependence: A review of the evidence. JAMA 281:1318-1325, 1999. 4. Johnston SC, Pelletier LL Jr: Enhanced hepatoxicity of acetorninophen in the alcoholic patient. Medicine (Baltimore) 76:185-191, 1997. 5. OConnor PG, Schottenfeld R: Patients with alcohol problems. New Engl J Med 338:592400, 1998. 6. OMalley SS: Opioid antagonists in the treatment of alcohol dependence: Clinical efficacy and prevention of relapse. Alcohol Alcohol 31(Suppl 1):77-81, 1996. 7. Sass H, Soyka M, Mann K, Zieglgansberger W: Relapse prevention by acamprosate. Arch Gen Psychiat 53~673-680, 1996. 8. Stibler H: Carbohydrate-deficient transferrin in serum: A new marker of potentially harmful alcohol consumption reviewed. Clin Chem 37:2029-2037, 1991.

2 1. OPIOID USE DISORDERS


Jane A. Kennedy, D.O.
1. What are opioids?
Opioids include naturally occurring substances such as opium and morphine, semisynthetic drugs such as heroin and hydromorphone, and totally synthetic drugs such as methodone or meperidine. These substances act at specific opioid receptors in the brain and the body, as do the endogenous opioids (endorphins, enkephalins, and dynorphins).

2. Who abuses opioids? Opioid abusers sometimes are divided into heroin addicts and prescription opioid abusers (medical addicts). In the United States, approximately one-half million people are dependent on heroin, but only about 140,000 are in methadone maintenance treatment. In 1995, there were 141,000 new users, and most were under age 26; in 1997,2.1% of high school seniors reported using heroin at least once. Although most users are still injecting heroin, there is an increase in intranasal use and smoking, due to increased purity and fear of HIV transmission with needles. Prescription drug abusers frequently are patients with real or fabricated pain, or health professionals with access to medications by prescription or diversion.

3. Describe the signs and symptoms of opioid intoxication.


Soon after injecting heroin, the person may vomit because of activation of the chemoreceptor trigger zone in the medulla; for the heroin user, this reaction often indicates good heroin. Feeling sedation, warmth, and euphoria (flush and rush), the user nods, with the head dropping toward

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