With respect to the use of medications to treat the withdrawal syndromes, it is important to distinguish between mild symptoms, which are essentially benign and responsive to practically any sedative drug, and full-blown delirium tremens. There is no certain way to predict whether a patient with the early signs of withdrawal will progress to delirium tremens. In the latter state, the object of therapy is to blunt the psychomotor and autonomic overactivity, prevent exhaustion, and facilitate the administration of parenteral fluid and nursing care; one should not attempt to suppress agitation “at all costs,” as doing so requires an amount of drug that might depress respiratory drive.
A wide variety of drugs are effective in controlling withdrawal symptoms. The more popular ones have been chlordiazepoxide (Librium), diazepam (Valium), and the ancillary medications, clonidine and beta-adrenergic blockers, and a number of both older and newer anticonvulsant drugs such as gabapentin, which may reduce the requirement for sedative drugs. There is little to choose among the primary sedative drugs in respect to their therapeutic efficacy. More importantly, there are few data to indicate that any one of them can prevent hallucinosis or delirium tremens, or shorten the duration, or alter the mortality rate of the latter disorder (Kaim et al). A contemporary summary of the medication management of withdrawal has been given by Kosten and O’Connor. In general, phenothiazine drugs should be avoided because they may reduce the threshold to seizures. Probably, the use of any of the diazepine medications is as effective as a single dose of lorazepam in prophylactically suppressing seizures (see earlier discussion).
If parenteral medication is necessary, we still prefer 10 mg of diazepam or chlordiazepoxide given intravenously and repeated once or twice at 20to 30-min intervals until the patient is calm but awake; we also favor midazolam in closely controlled circumstances when hyperactivity and hallucinosis are extreme. Beta-adrenergic-blocking agents, such as propranolol, labetalol, and atenolol, are helpful in reducing heart rate, blood pressure, and the tremor to some extent. Lofexidine, an alpha2-agonist that blocks autonomic outflow centrally, and clonidine may be similarly effective in reducing the severity of withdrawal symptoms, but clinical trials have given conflicting results for lofexidine and they are not recommended as the sole treatments. Corticosteroids have no place in the treatment of the withdrawal syndrome and more potent agents such as propofol are usually not necessary.
Wernicke-Korsakoff Syndrome and Alcoholic–Nutritional Diseases (See Chap. 40)
Alcoholism provides the ideal setting for the development of nutritional diseases of the nervous system. Although only a small proportion of alcoholics develop nutritional diseases, the overall number of these diseases is substantial because of the frequency of alcoholism. The importance of the alcohol-induced deficiency diseases relates to the fact that they are preventable and, if neglected, may lead to permanent disability. These illnesses, particularly the Wernicke-Korsakoff syndrome, are discussed fully in Chap. 40. Contrary to popular opinion with regard to the prevention of Wernicke disease, the content of B vitamins in American beer and other liquors is so low as to have little nutritional value (Davidson).
Disorders of Uncertain Pathogenesis Associated With Alcoholism