Patients With Alcohol Use Disorder

Overview

Alcohol remains one of the most prevalent and clinically relevant drugs of abuse, with an estimated 75 million people worldwide meeting criteria for an alcohol use disorder (AUD) in 2004. In the United States, two-thirds of all adults consume alcoholic beverages; an estimated 8 million Americans meet criteria for a severe AUD. Furthermore, approximately 500,000 individuals each year experience acute alcohol withdrawal severe enough to require pharmacologic management. The annual healthcare cost related to alcohol use exceeds US$250 billion, and an estimated 85,000 deaths a year in the United States alone can be attributed to alcohol use. Alcohol accounts for roughly one-tenth of all deaths among working-age US adults. Thus, it is no surprise that alcohol is responsible for more psychiatric and neuropsychiatric problems in general hospitals than from all other substances combined. Studies estimate that 25% to 50% of all patients hospitalized for injuries are intoxicated at the time of their trauma and that the prevalence of alcohol-related problems in medical inpatients ranges from 12.5% to 30%.

Given the prevalence of alcohol use in our society and the potential for significant medical, psychiatric, and psychosocial complications associated with chronic use and alcohol withdrawal, all psychiatrists who work in general hospitals should be skilled in the recognition and treatment of AUD. In fact, failure to diagnose and effectively treat alcohol use in hospitalized patients is exceedingly costly (in terms of morbidity and expense); a retrospective study at a major teaching hospital estimated that $4.3 million of charges were sustained by 160 patients with a substance use disorder (SUD) over a 23-day period and these could be attributed directly to the patients' SUD. Prompt identification of patients with AUD in particular, and initiation of acute inpatient treatment (including acute withdrawal management, engagement with an addiction consultation service and identification of suitable aftercare resources), has been associated with improved outcomes (e.g., abstinence, longer time since the last drink, job performance, and personal happiness).

Screening for Alcohol Use Disorder

Alcohol use is widespread; roughly 50% of the adult US population reports using alcohol within the past 30 days, although there is considerable variation in the pattern and severity of use. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines two categories of problematic drinking:

• Use of more than 14 drinks per week or more than 4 drinks on any day, for men under the age of 65 years

• Use of more than 7 drinks per week or more than 3 drinks on any day for women and/or any adult 65 years and older.

Nearly 30% of all US adults who use alcohol do so in a potentially unhealthy manner, including 15% who exceed the recommended daily limit, 10% who exceed both daily and weekly limits, and 2% who exceed the weekly limit alone. The highest rates of risky alcohol use occur in younger adults (18–29 years old), males, and Native Americans.

Many tools are available to providers to help identify risky alcohol use. These include a variety of questionnaires that can be administered to inpatients or outpatients. Laboratory testing can be useful (especially if there is a concern for minimization of reported use), although such tests are not routinely recommended for screening purposes. The most commonly encountered screening tools are outlined in Tables 14-1 and 14-2 , and include the AUDIT-C screening test ( Table 14-1 ) and the CAGE questionnaire ( Table 14-2 ). The AUDIT-C asks three questions and is considered positive when scores are >4 in men or are >3 in women, with a 90% sensitivity, and an 80% specificity rate. The CAGE asks four questions; >2 positive responses carries 77% sensitivity and 79% specificity for the detection of an AUD. If the CAGE is used for screening, even a single response should be considered as screening positive.

Acute Intoxication and the Psychiatric Sequelae of Alcohol Use

Ethanol, the primary active component of alcoholic beverages, is a water-soluble alcohol compound primarily absorbed via the gastrointestinal (GI) mucosa of the duodenum and small intestine (80%) and the stomach (20%). The compound undergoes hepatic metabolism via alcohol dehydrogenase; in fact, a smaller distribution volume and reduced expression of this enzyme in women is believed to account for their increased susceptibility to alcohol intoxication. In most individuals, peak serum alcohol levels are reached 30–90 minutes following ingestion. Resolution of the acute toxidrome follows steady-state kinetics, so that a 70-kg male is expected to metabolize approximately 10 mL of absolute ethanol or 1.5 to 2 drink equivalents (1.5 oz whiskey = 5 oz wine = 12 oz beer) per hour.

The effect of alcohol on the central nervous system (CNS) is surprisingly complex, and involves changes across multiple neurotransmitter systems. The primary mechanism of action is achieved through gamma amino butyric acid (GABA) agonism, which accounts for the CNS depressant effects of alcohol as well as for the behavioral disinhibition seen with use of the compound. With chronic exposure, further CNS changes occur, primarily in response to exogenously increased GABA tone, including a decrease in GABA receptors, decreased GABA production and decreased binding affinity to the receptor complex. More importantly, these changes also lead to an increase in endogenous glutaminergic tone (an attempt to maintain homeostasis) and the development of complicated alcohol withdrawal symptoms.

Signs and symptoms associated with acute alcohol intoxication are undoubtedly familiar to virtually all clinicians. Mild intoxication can present as impulsivity, elation, slight slurring of speech, and gait impairment. As the blood alcohol content increases, these findings become more pronounced, and include marked disinhibition, irritation, or even frankly aggressive behavior. The neurologic examination is notable for nystagmus, impaired coordination (ataxia), and unsteady gait. Attention and memory consolidation are commonly impaired, resulting in reduced recall of the intoxication, or even full “blackouts” in more severe cases. With severe alcohol poisoning, CNS depression becomes prominent, leading to stupor and coma.

The clinical effect is dose-dependent, although much variability (based on the patient's gender, genetics, amount/rate of intake, co-ingestion of other drugs, and overall duration of alcohol use) exists. While the blood alcohol level (BAL) can reliably predict clinical effects in patients who only use alcohol socially, habituation and tolerance are common with chronic use, and in these individuals, little clinical evidence of intoxication may be seen despite an extremely elevated BAL. In patients who use alcohol intermittently, a BAL <100 mg/dL, will produce euphoria, problems with coordination, and impaired attention. Higher levels (e.g., BAL 100–200 mg/dL) are associated with a worsening of motor deficits, impaired judgment, and an increased chance of assaultive/aggressive behavior. As BAL exceeds 300 mg/dL encephalopathy and CNS depression become prominent, and coma (and even death) can occur at BAL 400–500 mg/dL.

Initial work-up of acute alcohol intoxication should involve checking basic chemistry studies (as electrolyte imbalance is common with acute intoxication), a serum glucose, hepatic function, and a BAL. If co-ingestion is suspected, screening for other drugs of abuse is recommended, though it may not always be necessary with isolated alcohol intoxication. Treatment depends largely on the degree of intoxication observed:

• Mild to moderate intoxication can be managed supportively and patients may require little more than observation and serial assessments. IV fluids may be warranted if there is evidence (e.g., persistent tachycardia) of volume depletion. Agitation, if present, may respond to reduced stimulation/isolation, and in more severe cases, use of dopamine antagonists such as intravenous (IV) haloperidol (e.g., 2–5 mg), as it does not exacerbate sedation, and can be administered easily. In patients with a preference for the parenteral route, various atypical agents (e.g., olanzapine, quetiapine) should be considered. Benzodiazepines are also commonly used in this setting, although using them as sole agents for management of agitation may exacerbate acute intoxication and worsen agitation, over-sedation, and respiratory depression. Once an individual is no longer intoxicated, he or she can usually be discharged home, after screening for the severity/extent of use and discussing aftercare resources.

• Severe intoxication may require intensive supportive measures, including frequent assessment of physiologic parameters. With severe obtundation, patients may not be able to protect their airway and may require intubation. Hemodynamic changes may be seen, including tachycardia and hypotension, and patients may require IV hydration.

Alcohol Withdrawal Syndrome: Identification and Management

Alcohol withdrawal can range from a state of mild discomfort that requires no medication to multi-organ failure that requires intensive care. In large part, this variability is a reflection of a series of changes in CNS receptor expression and function associated with chronic alcohol use ( Figure 14-1 ). As previously discussed, alcohol enhances GABA activity and inhibits glutamate activity; this leads to a CNS depressant effect. In the setting of chronic alcohol use, the GABA system habituates, leading to a decrease in the number of GABA receptors, to changes in configuration of the receptor subunits, and to reduced rates of GABA synthesis. The result is one of decreased endogenous GABA tone. Similarly, chronic exposure to alcohol leads to changes in the glutamate neurotransmitter system, namely with an increase in the number of glutamate receptors. The overall effect is that of increased endogenous excitatory tone, representing an attempt to restore homeostasis and balance the increase in exogenous GABA tone caused by the use of alcohol. With abrupt cessation of alcohol use, this tenuous balance becomes disturbed quickly and a state marked by over-expression of excitatory neurotransmitters (glutamate, norepinephrine, dopamine) and reduced GABA tone develops. The specific types of neurotransmitters affected and the severity of aberration seen determine the clinical symptoms and the severity of the alcohol withdrawal syndrome observed.

Table 14-3 summarizes three key clusters of symptoms observed in alcohol withdrawal. Type A symptoms are associated with minor (uncomplicated) withdrawal and reflect an overall decrease in GABA activity. The most common clinical findings with this type are anxiety, restlessness/irritability, insomnia, general malaise, and a fine tremor. Symptoms of types B and C are more prevalent in cases of severe (complicated) withdrawal and reflect an increase in noradrenergic and dopaminergic tone, respectively. Type B withdrawal symptoms include the hallmark increased sympathetic tone, with resultant coarse bilateral tremor, hypertension, tachycardia, fever, and diaphoresis. Since some patients attempt to fabricate type B findings (e.g., tremor), clinicians should examine patients for tongue fasciculations and monitor for the absence of tremor with distraction (e.g., observation from outside the room or providing a glass of water to consume while conducting the examination and observing for the presence of end-point tremor). Type C symptoms are marked by impairments of attention and by confusion, as well as by the symptoms of acute psychosis, including hallucinations (visual more often than auditory), paranoid ideation, and delusional thinking.

Given the range of neurotransmitters involved, treatment of alcohol withdrawal should be tailored to the specific symptom cluster observed, including use of benzodiazepines for type A symptoms, use of beta-blockers and alpha-adrenergic agents to treat refractory tachycardia/hypertension (type B symptoms), and use of dopamine antagonists for management of hallucinations, agitation, and paranoid delusions (type C symptoms). The clinician, however, should always ensure that one prioritizes type A > type B > type C unless there are type B or type C emergencies that need to be managed and treated acutely (e.g., concern for demand ischemia or hypertensive emergency).