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Alcohol-Related Disorders


Key Points

Incidence

  • Alcohol misuse is one of the leading causes of morbidity and mortality in the US.

Epidemiology

  • The highest rates of alcohol use, heavy binge use, and alcohol use disorders occur between the ages of 18 and 29 years.

Pathophysiology

  • Alcohol causes harm through three distinct, but related pathways: intoxication, toxicity, and alcohol use disorder.

Clinical Findings

  • Alcohol use disorders are heterogeneous disorders that require assessment and an individualized clinical approach.

  • It is possible to screen effectively and efficiently for the presence of an alcohol use disorder using brief, validated measures.

Differential Diagnoses

  • Presentation of an alcohol use disorder is often complicated by the presence of co-morbid psychiatric symptoms and disorders that require assessment and monitoring, as well as an integrated treatment approach.

Treatment Options

  • A number of effective pharmacological and psychosocial treatment approaches exist for alcohol use disorders that produce outcomes similar to, or better than, outcomes for other chronic illnesses.

Complications

  • Heavy drinking can lead to accidents, violence, unwanted pregnancies, and overdoses.

Overview

Alcohol is an ambiguous molecule often referred to as “man's oldest friend and oldest enemy”. Compared to more structurally complicated substances, such as cannabis (C 21 H 30 O 2 ), cocaine (C 17 H 21 NO 4 ), or heroin (C 21 H 23 NO 5 ), beverage alcohol (ethanol) possesses a simple chemical structure (C 2 H 5 OH) that belies the complexities of its medical, psychological, and social impact ( Figure 15-1 ).

Figure 15-1, Molecular structure of beverage ethyl alcohol.

When the alcohol molecule reaches the human brain it is generally perceived as good news; pleasant subjective experiences of euphoria, disinhibition, anxiety reduction, and sedation, are the most likely outcomes. These are often encouraged and enhanced by social contexts and by culture-bound customs. If too high a dose is imbibed too rapidly, however, acute intoxication occurs, leading to a predictable sequence of behavioral disinhibition and cognitive and motor impairments. If a large quantity of alcohol is consumed, especially if it is done rapidly, alcohol-induced amnesia (“blackouts”), coma, and death, can occur.

Like several other drugs, alcohol causes harm in three distinct, but related, ways: through intoxication, toxicity, and alcohol use disorder. As depicted in Figure 15-2 , the acute intoxicating effects of alcohol produce physical and psychological impairments (e.g., ataxia, poor judgment, visuo-spatial deficits, sensory distortions) and disinhibition can lead to aggression, that can result in accidents and injuries (e.g., from car crashes, falls, fights). The toxic effects of alcohol, on the other hand, produce harm through the chronic deleterious action of alcohol on the human body that can result in liver damage, including cirrhosis, as well as damage to the brain, heart, and kidneys. Because of the toxicity pathway to harm, it is possible for individuals who infrequently become intoxicated to, nevertheless, develop a variety of diseases associated with alcohol's toxic effects, such as cirrhosis of the liver or a variety of cancers (e.g., of the colon, rectum, breast, larynx, liver, esophagus, oral cavity, pharynx ; Figure 15-2 ). Somewhat paradoxically, cirrhosis is more common among individuals without alcohol addiction, since more florid manifestations of dependence are likely to result in more rapid remission, incarceration, or death, preventing the chronic damaging toxic effects associated with prolonged use of alcohol. Alcohol use disorder (AUD) is the third pathway through which alcohol use causes harm. AUD contributes to a range of changes in the brain that often result in alcohol addiction. This can take a heavy toll on individuals' lives (with serious domestic and social problems, family disintegration, loss of employment and increased risk of mortality). Related to these pathways is the volume and frequency at which alcohol is consumed. Low-risk consumption is, for men, no more than 14 drinks per week and, for women, no more than 7 drinks in any given week. The pattern of consumption is also critical, however, for obvious reasons; 14 drinks in one sitting for some could constitute a lethal dose. Thus, to minimize harm from intoxication, and to reduce the risk from AUDs, no more than 2 drinks on any given day for men and no more than 1 for women is recommended ( Figure 15-3 ). It should be emphasized, however, that this pattern of consumption is “ low risk” and not “ no risk”; meta-analyses reveal even less than 1 drink a day is associated with an increased risk for a number of cancers (including breast cancer in women). It is estimated that alcohol is responsible for about 20%–30% of esophageal cancers, liver cancer, cirrhosis of the liver, homicide, epileptic seizures, and motor vehicle accidents worldwide. Excessive or risky alcohol consumption is the third leading cause of death in the US, accounting for approximately 100,000 deaths annually. In terms of disability-adjusted life years (DALYs) lost, alcohol accounts for more disease, disability, and mortality combined in the United States than tobacco use, even though tobacco use accounts for a higher death rate. This is because alcohol causes more illness, impairment during the prime of individuals' lives, and death (e.g., alcohol is the leading risk factor for death among men 15–59 worldwide). The economic burden attributed to alcohol-related problems in the US approaches $224 billion annually.

Figure 15-2, Alcohol-related disorders associated with high-risk drinking.

Figure 15-3, Patterns of drinking and pathways to harm.

Alcohol-related disorders are common in the general population, are prevalent among general medical patients, and are endemic among psychiatric patients. An awareness of the substantial roles that alcohol use, misuse, and associated disorders play in medicine and psychiatry will enhance the detection of these problems and lead to more efficient and effective targeting of clinical resources.

In this chapter we review pertinent clinical manifestations of heavy alcohol use and outline strategies for effective management of alcohol-related problems. The nature, etiology, epidemiology, and typologies of alcohol-related disorders are described, and optimal screening and assessment methods (to facilitate detection and appropriate intervention) are outlined. In the final sections, details of current knowledge regarding the mechanisms of action of heavy alcohol use are provided and effective psychosocial and pharmacological treatment approaches are reviewed.

Description and Definition

Alcohol-related disorders can be divided into two main groups: alcohol-induced disorders (such as alcohol intoxication, delirium, alcohol withdrawal, persisting alcohol-induced amnestic disorders, and fetal alcohol spectrum disorders), and alcohol use disorder (DSM-5 , Box 15-1 ).

Box 15-1
Reprinted with permission from the Diagnostic and statistical manual of mental disorders , ed 5, (Copyright 2013). American Psychiatric Association.
The DSM-5 Diagnostic Criteria
Alcohol Use Disorder

  • A.

    A problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

    • 1.

      Alcohol is often taken in larger amounts or over a longer period than was intended.

    • 2.

      There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.

    • 3.

      A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recovery from its effects.

    • 4.

      Craving, or a strong desire or urge to use alcohol.

    • 5.

      Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home.

    • 6.

      Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol

    • 7.

      Important social, occupational, or recreational activities are given up or reduced because of alcohol use.

    • 8.

      Recurrent alcohol use in situations in which it is physically hazardous.

    • 9.

      Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.

    • 10.

      Tolerance, as defined by either of the following:

      • a.

        A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.

      • b.

        A markedly diminished effect with continued use of the same amount of alcohol.

    • 11.

      Withdrawal, as manifested by either of the following:

      • a.

        The characteristic withdrawal syndrome for alcohol

      • b.

        Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

Specify if:

  • In early remission : After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met).

  • In sustained remission : After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use alcohol,” may be met).

Specify if:

  • In a controlled environment : This additional specifier is used if the individual is in an environment where access to alcohol is restricted.

    • Coding note based on current severity, for ICD-10-CM codes: If an alcohol intoxication, alcohol withdrawal, or another alcohol-induced mental disorder is also present, do not use the codes below for alcohol use disorder. Instead, the comorbid alcohol use disorder is indicated in the 4th character of the alcohol-induced disorder code (see the coding note for alcohol intoxication, alcohol withdrawal, or a specific alcohol-induced mental disorder). For example, if there is comorbid alcohol intoxication and alcohol use disorder, only the alcohol intoxication code is given, with the 4th character indicating whether the comorbid alcohol use disorder is mild, moderate, or severe: F10.129 for mild alcohol use disorder with alcohol intoxication or F10.229 for a moderate or severe alcohol use disorder with alcohol intoxication.

Specify current severity:

  • 305.00 (F10.10) Mild : Presence of 2–3 symptoms.

  • 303.90 (F10.20) Moderate : Presence of 4–5 symptoms.

  • 303.90 (F10.20) Severe : Presence of 6 or more symptoms.

Heavy, chronic, alcohol use may also induce psychiatric symptoms and syndromes that mimic psychotic disorder, mood disorders, and anxiety disorders. Such syndromes most often remit with abstinence, but the diagnosis of an independent co-occurring psychiatric disorder is difficult to discern in an individual who is actively drinking. At least 4 weeks of sobriety is recommended to establish the diagnosis of an independent psychiatric disorder. The next sections describe alcohol-induced disorders and AUDs.

Alcohol-Induced Disorders

Alcohol Intoxication

The action of alcohol on the brain is complex. Low blood alcohol concentrations (BACs) produce activation and disinhibition, whereas higher BACs produce sedation. Behavioral disinhibition is mediated by alcohol's action as a γ-aminobutyric acid (GABA) agonist, and its interactions with the serotonin system may account for its association with violent behavior. The GABA, N- methyl- d -aspartate (NMDA), and serotonin systems have all been implicated in the escalation to violence. Blood alcohol concentrations (BACs, measured as the percentage of alcohol in the blood) from 0.19% to 29% may impair memory or lead to an alcoholic blackout, with argumentativeness or assaultiveness developing at levels of 0.10%–0.19% and coma or death occurring at 0.40%–0.50%. Yet, chronic alcoholics may be fully alert with a BAC of more than 0.40%, owing to tolerance. Resolution of intoxication follows steady-state kinetics, so that a 70-kg man metabolizes approximately 10 ml of absolute ethanol (or 1.5 to 2 drink equivalents; 1 standard drink = 0.5 oz of whiskey, 4 oz of wine, or 12 oz of beer) per hour ( Figure 15-4 ).

Figure 15-4, Impairment as a result of increased blood alcohol content (BAC).

Treatment

If it becomes necessary to sedate an intoxicated individual, one should begin with a smaller-than-usual dose of a benzodiazepine to avoid cumulative effects of alcohol and other sedative-hypnotics. Once the individual's tolerance has been established, a specific dose can be safely determined. Lorazepam (Ativan) (1 to 2 mg) is effectively absorbed via oral (PO), intramuscular (IM), or intravenous (IV) administration. Diazepam (Valium) and chlordiazepoxide (Librium) are erratically and slowly absorbed after IM administration unless they are given in large, well-perfused sites. When incoordination suggests that the additive effect of a benzodiazepine has produced excessive sedation, it may be advantageous to use haloperidol 5 to 10 mg PO or IM. The initial dose should be followed by a delay of 0.5 to 1 hour before the next dose. If there is no risk of withdrawal, the patient can safely be referred to an outpatient program. Inpatient detoxification is preferable to outpatient care if the patient is psychosocially unstable; has serious medical, neurological, or psychiatric co-morbidity; has previously suffered from complications of withdrawal (such as seizures or delirium tremens [DTs]); or is undergoing his or her first episode of treatment. Repeatedly undertreated withdrawal may place the patient at subsequent risk for withdrawal seizures and for other neurological sequelae through “kindling,” an electrophysiological effect that may be mediated, similar to other neurodegenerative effects of ethanol, via the glutamate excitatory neurotransmitter system.

Alcohol-induced Coma

Alcohol-induced coma, although rare, is a medical emergency. It occurs when extraordinary amounts of alcohol are consumed, and it can occur in conjunction with use of other drugs. Young adults/college-age youth may be particularly susceptible when goaded into drinking contests. This age group is also at significantly higher risk for alcohol-related injuries. A 2002 study by the federally supported Task Force on College Drinking estimated that 1,400 college students in the US are killed each year in alcohol-related accidents.

Alcohol Withdrawal Syndrome

The syndrome of alcohol withdrawal can range from mild discomfort (that requires no medication) to multi-organ failure (that requires intensive care). Uncomplicated withdrawal is surprisingly common and is frequently missed. Although more than 90% of alcoholics in withdrawal need nothing more than supportive treatment, those hospitalized with co-morbid medical conditions have a higher rate of complications. The most common features of uncomplicated alcohol withdrawal emerge within hours and resolve after 3 to 5 days. Early features (loss of appetite, irritability, and tremor) of uncomplicated withdrawal symptoms are predictable. A hallmark of alcohol withdrawal is generalized tremor (fast in frequency and more pronounced when the patient is under stress). This tremor may involve the tongue to such an extent that the patient cannot talk. The lower extremities may tremble so much that the patient cannot walk. The hands and arms may shake so violently that a drinking glass cannot be held without spilling the contents. Typically, the patient is hypervigilant, has a pronounced startle response, and complains of insomnia.

Less commonly, patients experience hallucinations (without delirium) or seizures associated with alcohol withdrawal. Illusions and hallucinations may appear and produce vague uneasiness. These symptoms may persist for as long as 2 weeks and then clear without the development of delirium. Grand mal seizures (“rum fits”) may occur, usually within the first 2 days. More than one out of every three patients who suffer seizures develops subsequent DTs ( Figure 15-5 ).

Figure 15-5, Progress of alcohol withdrawal syndrome.

Treatment

Rigid adherence to a single protocol for all cases of alcohol withdrawal is unrealistic. Symptom-triggered dosing, in which dosages are individualized and only administered on the appearance of early symptoms, is often recommended. Assessment of the severity of alcohol withdrawal's signs and symptoms is best accomplished with the use of standardized alcohol withdrawal scales, such as the CIWA-Ar. This reduces use of medication doses by a factor of four, substantially shortens the length of treatment, and shortens symptom duration by a factor of six, although the benefits may be less dramatic in medically ill inpatients. Chlordiazepoxide (50 to 100 mg PO) can be given initially, and be followed by 50 to 100 mg every 1 to 2 hours until the patient is sedated and the vital signs are within normal limits. Alternatively, diazepam (10 to 20 mg) may be given initially, and then repeated every 1 to 2 hours until sedation is achieved. Often a first day's dose of a long-acting benzodiazepine is sufficient for the entire detoxification process because of the self-tapering effect and slow elimination. Patients with impaired liver function, the elderly, or individuals with co-occurring medical or psychiatric conditions are often better managed with a shorter-acting agent, such as lorazepam 1 to 4 mg PO or IM, or 0.5 mg/min slow IV infusion in severe withdrawal, repeated after 1 to 2 hours, with dose tapering by 25% per day over the subsequent 3 to 6 days.

The α2-agonist dexmedetomidine is sometimes used in cases of alcohol withdrawal, especially when patients require escalating doses of benzodiazepines and additional intubation and mechanical ventilation to protect airways, which can lead to complications and prolonged hospital stays. Similarly, phenobarbital is used to augment benzodiazepine-assisted alcohol withdrawal to prevent the need for intubation and ICU admission. A prospective, randomized, double-blind, placebo-controlled study with 102 patients, half of whom received either a single dose of IV phenobarbital (10 mg/kg in 100 ml of normal saline) or placebo (100 ml of normal saline) in addition to a symptom-guided lorazepam-based alcohol withdrawal protocol, found that patients who received phenobarbital had fewer ICU admissions (8% vs. 25%), and there were no differences in adverse events.

Alcohol Withdrawal Seizures

Withdrawal seizures occur in roughly 1% of unmedicated alcoholics undergoing withdrawal, although the prevalence is increased in individuals with inadequately treated prior episodes of alcohol withdrawal, prior alcohol withdrawal seizures, seizure disorders, and previous brain injuries. Although brain imaging may not be necessary in patients with their first episode, seizures during alcohol withdrawal require careful evaluation for other causes. Indications for imaging include neurological and other physical findings suggestive of focal lesions, meningitis, or subarachnoid hemorrhage—all of which may occur in a patient with a history of alcohol withdrawal seizures. Multiple prior detoxifications predispose patients to withdrawal seizures more than the quantity or duration of a drinking history, implying a kindling cause. Seizures may occur following a rapid drop in the BAC or during the 6 to 24 hours after drinking cessation. Generalized seizures typically occur (i.e., in 75% of cases) in the absence of focal findings, and in individuals with otherwise unremarkable electroencephalogram (EEG) findings. Repeated seizures may occur over a 24-hour period; however, status epilepticus occurs in less than 10% of those who seize.

Treatment

In patients without a prior seizure disorder, diphenylhydantoin offers no benefit over placebo, and given the potential for side effects, diphenylhydantoin is therefore not recommended. Also, given that loading with carbamazepine or valproate may not address the rapid time course of withdrawal seizures, the most parsimonious approach remains effective treatment with benzodiazepines. Prompt treatment of early withdrawal symptoms, as described below, is the most effective measure to prevent the development of seizures. In cases where there is a known seizure disorder, however, conventional management with an anticonvulsant is in order.

Alcohol Withdrawal Delirium

Delirium tremens, or “DTs,” the major acute complication of alcohol withdrawal, was renamed “alcohol withdrawal delirium” in the Diagnostic and Statistical Manual of Mental Disorders, ed 4 (DSM-IV). Until open-heart procedures spawned new postoperative deliria, DTs were by far the most frequently encountered delirium in general hospitals, reportedly occurring in 5% of hospitalized alcoholics. Although it was first described in the medical literature more than 150 years ago and it has been frequently observed ever since, DTs still go undiagnosed in a large number of cases. It is missed because physicians tend to forget that alcoholism is rampant among people of all backgrounds and appearances. Because deaths have occurred in 10% of patients with untreated alcohol withdrawal delirium and in 25% of those patients with medical or concomitant surgical complications, it is imperative to be on the alert for this life-threatening condition.

It is difficult to predict who will develop DTs. Until a decade ago, DTs rarely developed in patients younger than 30 years of age. This is no longer true. Today the condition is frequently observed in young patients who may have had a decade or more of chronic heavy alcohol consumption. The mechanisms may involve NMDA-glutamate receptor supersensitivity. Although delirium is regarded as a withdrawal syndrome, some heavy drinkers fail to develop delirium after sudden withdrawal of ethanol. Infection, head trauma, and poor nutrition are potentially contributing factors to delirium. A history of DTs is the most obvious predictor of future DTs.

The incidence of DTs is approximately 5% among hospitalized alcoholics and about 33% in patients with alcohol withdrawal seizures. If DTs do occur, they generally do so between 24 and 72 hours after abstinence begins. There have been reports, however, of cases in which the clinical picture of DTs did not emerge until 7 days after the last drink. The principal features are disorientation (to time, place, or person), tremor, hyperactivity, marked wakefulness, fever, increased autonomic tone, and hallucinations. Hallucinations are generally visual, but they may be tactile (in which case they are probably associated with a peripheral neuritis), olfactory, or auditory. Vestibular disturbances are common and often hallucinatory. The patient may complain of the floor moving or of being on an elevator. The hallucinatory experience is almost always frightening, such as seeing spiders and snakes that may have additional characteristics (e.g., more vivid colors and mice or insects sensed on the skin). Once the condition manifests itself, DTs usually last 2 to 3 days, often resolving suddenly after a night of sound sleep. Should it persist, an infection or subdural hematoma may be the cause. There are, however, a small number of individuals whose course is characterized by relapses with intervals of complete lucidity. These patients offer the clinician the most challenging diagnostic opportunities. As a rule of thumb, it is always wise to include DTs in the list of diagnoses considered whenever delirium appears. Even skilled clinicians are apt to miss the diagnosis of DTs when the patient's manner, social position, or reputation belies a preconceived and distorted stereotype of an “alcoholic.” The clinician is also frequently misled when the delirium is intermittent and the patient is examined during a lucid stage. Although a course of intermittent episodes is highly atypical for DTs, it can occur.

The prognosis for DTs is reasonably good if the patient is aggressively medicated, but death can occur as the syndrome progresses through convulsions to coma and death. Death can also result from heart failure, an infection (chiefly pneumonia), or injuries sustained during the restless period. In a small proportion of patients the delirium may merge into Wernicke–Korsakoff syndrome, in which case the patient may not regain full mentation. This is more apt to happen in those with closely spaced episodes of DTs and in the elderly, but it should be assessed and continually monitored.

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