Foundations
Excess alcohol consumption places a significant burden on individuals and society. Globally, alcohol consumption is the seventh leading risk factor for both death and the burden of disease and injury. 2016 data from the World Health Organization (WHO) state that 5.3% of all deaths globally were attributable to alcohol consumption. The overall costs associated with alcohol use represent more than 1% of the gross national product in high- and middle-income countries, with the costs of social harm (e.g., violence and road accidents) being far greater than health costs alone. In short, except for tobacco, alcohol accounts for a higher burden of disease than any other drug.
From 2002 to 2010, the rate of emergency department (ED) visits for alcohol-related diagnoses increased by 38%. In addition to the number of visits, current National Hospital Ambulatory Care survey data indicates that the total time and the length of stay (LOS) for ethanol-related visits are increasing as well.
Twenty-seven percent of the US population admits to alcohol misuse. Alcohol misuse accounts for more than 100,000 deaths in the United States every year, making it the fourth leading preventable cause of death in the United States and the 12th leading cause of death overall and is associated with over 200 diseases. , Alcoholism permeates all levels of society. Studies reveal a complex association between alcohol consumption and socioeconomic status (SES), where people of lower SES show greater susceptibility to the damaging effects of alcohol.
Alcohol use and misuse also have social and financial costs, with estimates of over $220 billion in societal costs in the United States annually. The literature refers to harmful, hazardous, and risky drinking interchangeably as a pattern of drinking that increases the risk of harm for the person consuming alcohol or others. The International Classification of Disease 10th Revision (ICD-10), draft ICD-11, and the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-4) use the term “alcohol dependence.” Alcohol dependence is a result of repeated use leading to a person having impaired control over the use of alcohol despite physical, psychological, and social harms. The fifth edition of the Diagnostic and Statistical Manual (DSM-5) combines diagnostic criteria for alcohol abuse and dependence under the term “alcohol use disorder,” with severity modifiers of “mild,” “moderate,” or “severe,” based on the number of criteria met. DSM-5 AUD of moderate or greater severity is essentially equivalent to DSM-4 and ICD-10 criteria for alcohol dependence. DSM–5 integrates alcohol abuse and alcohol dependence into a single disorder called alcohol use disorder (AUD), with mild, moderate, and severe sub-classifications.
At least 24% to 31% of ED patients meet National Institute Alcohol Abuse and Alcoholism (NIAAA) criteria for “at-risk” or heavy drinking. At-risk drinking is defined as an average of 14 or more standard drinks/week or 5 or more per occasion for men and 7 or more drinks weekly or 3 or more per occasion for women and people older than 65 years. ( Table 137.1 : Terms and Definitions of Unhealthy Alcohol Use. )
TABLE 137.1
Terms and Definitions of Unhealthy Alcohol Use
Data from US Preventive Services Task Force, Curry SJ, Krist AH, et al. Screening and Behavioral Counseling Interventions to Reduce Unhealthy Alcohol Use in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement. JAMA . 2018;320(18):1899–1909.
| Term | Source | Definition |
|---|---|---|
| Low-risk use/lower-risk use | ASAM | Consumption of alcohol below the amount identified as hazardous and in situations not defined as hazardous |
| Risky/at-risk use | NIAAA | Consumption of alcohol above the recommended daily, weekly, or per-occasion amounts but not meeting criteria for alcohol use disorder |
| For all women and men 65 years or older: No more than 3 drinks/day and no more than 7 drinks/week for men (21 to 64 years): No more than 4 drinks/day and no more than 14 drinks/week | ||
| Should avoid alcohol completely: Adolescents, women who are pregnant or trying to get pregnant, and adults who plan to drive a vehicle or operate machinery, are taking medication that interacts with alcohol, or have a medical condition that can be aggravated by alcohol | ||
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For adolescents: NIAAA defines moderate- and high-risk use based on days of alcohol use in the past year, by age group:
Moderate risk: |
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| Ages 12–15 years: 1 day/year | ||
| Ages 16–17 years: 6 days/year | ||
| Age 18 years: 12 days/year | ||
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Highest risk:
Age 11 years: 1 day |
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| Ages 12–15 years: 6 days | ||
| Age 16 years: 12 days | ||
| Age 17 years: 24 days | ||
| Age 18 years: 52 days | ||
| Unhealthy use | ASAM | Any alcohol use that increases the risk or likelihood of health consequences (hazardous use [see below]) or has already led to health consequences (harmful use [see below]) |
| Hazardous use | WHO | A pattern of substance use that increases the risk of harmful consequences; in contrast to harmful use, hazardous use refers to patterns of use that are of public health significance, despite the absence of a current alcohol use disorder ¡ท the individual user |
| ASAM | Alcohol use that increases the risk or likelihood of health consequences; does not include alcohol use that has already led to health consequences | |
| Harmful use | WHO | A pattern of drinking that is already causing damage to health; the damage may be either physical (e.g., liver damage from chronic drinking) or mental (e.g., depressive episodes secondary to drinking) |
| The description for ICD-10 code F10.l, also labeled “Alcohol Abuse” in the 2018 ICD-10-CM codebook | ||
| ASAM | Consumption of alcohol that results in health consequences in the absence of addiction | |
| Alcohol use disorder | DSM-5 | A maladaptive pattern of alcohol use leading to clinically significant impairment or distress, as manifested by 2 (or more) of the following, occurring within a 12-month period: |
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Severity is determined based on the number of symptoms present:
Mild: 2–3 symptoms |
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| Moderate: 4–5 symptoms | ||
| Severe: ≥6 symptoms | ||
| Binge drinking/heavy drinking | NIAAA | A pattern of drinking that brings blood alcohol concentration levels to 0.08 g/dL, which typically occurs after 4 drinks for women and 5 drinks for men-in about 2 h |
| Episodes | SAMHSA | Drinking ≥5 alcoholic drinks on the same occasion on at least 1 day in the past 30 days |
| Heavy drinking | SAMHSA | Drinking ≥5 drinks on the same occasion on each of ≥5 days in the past 30 days |
| Alcohol dependence | WHO/ICD -10-CM | ≥3 of the following at some time during the previous year: |
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| Abbreviations: ASAM. American Society of Addiction Medicine; DSM-5. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; ICD-10-CM. International Classification of Diseases. Tenth Revision Clinical Modification NIAAA. National Institute on Alcohol Abuse and | Alcoholism; SAMHSA. Substance Abuse and Mental Health Services Administration; WHO. World Health Organization. | |
a According to the American Society of Addiction Medicine, the preferred term; is “heavy drinking episode.”
Patients, their families, and society, in general, should be aware that AUDs are not a result of any individual weakness or moral failing but arise from a complex interaction of individual, social, cultural, and biological factors. Most people with AUD are difficult to identify because they are likely to have jobs and families and to present with general complaints, such as malaise, insomnia, anxiety, sadness, or a range of medical problems.
In 2013, the US Preventive Services Task Force (USPSTF) recommended that clinicians screen adults 18 years or older for alcohol misuse and provide brief behavioral counseling interventions to those engaged in risky or hazardous drinking behaviors. Of the available screening tools, the USPSTF determined that 1-item to 3-item screening instruments have the best accuracy for assessing unhealthy alcohol use in adults 18 years or older. These instruments include the abbreviated Alcohol Use Disorders Identification Test–Consumption (AUDIT-C) and the NIAAA-recommended Single Alcohol Screening Questionnaire (SASQ). This high burden of alcohol-related injury and disease indicates a need to increase awareness of AUD and its effective treatment options (see Box 137.3 ).
BOX 137.3
AUDIT-C Questions
Adapted from Miller LB, Brennan-Cook J, Turner B, et al. Utilizing an Evidence-Based Alcohol Screening Tool for Identification of Alcohol Misuse. J Addict Nurs . 2018;29(2):90–95.
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1.
How often did you have a drink containing alcohol in the past year?
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a.
Never (0 points)
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b.
Monthly or less (1 point)
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c.
Two to four times a month (2 points)
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d.
Two to three times per week (3 points)
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e.
Four or more times a week (4 points)
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a.
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2.
How many drinks containing alcohol did you have on a typical day when you were drinking in the past year?
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a.
0–2 (0 points)
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b.
3–4(1 point)
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c.
5–6 (2 points)
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d.
7–9 (3 points)
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e.
10 or more (4 points)
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a.
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3.
How often did you have six or more drinks on one occasion in the past year?
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a.
Never (0 points)
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b.
Less than monthly (1 point)
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c.
Monthly (2 points)
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d.
Weekly (3 points)
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e.
Daily or almost daily (4 points)
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a.
Metabolism of Alcohol
While some alcohol is absorbed in the stomach, the vast majority is absorbed in the small intestine. It is distributed uniformly to all organ systems, including the placenta. Although 2% to 10% of alcohol is excreted through the lungs, urine, and sweat, most is metabolized to acetaldehyde, primarily by alcohol dehydrogenase (ADH). The oxidation of alcohol is a complex process involving three enzyme systems, all contained in the hepatocyte. Acetaldehyde is then quickly converted to carbon dioxide and water, primarily through aldehyde dehydrogenase (ALDH). The common forms of ADH decrease the alcohol concentration in blood by about 4.5 mmol/L ethanol/h (the equivalent of about one drink/h):
where NAD is nicotinamide adenine dinucleotide and NADH is reduced nicotinamide adenine dinucleotide.
At least two variations of ADH genes ( ADH1B∗2 and ADH1C∗1 ) produce a slightly more rapid breakdown of alcohol and therefore potentially faster production of acetaldehyde, which is rapidly metabolized by ALDH2 . However, about 40% of Asian people (Japanese, Chinese, and Koreans) have an inactive ALDH2 mutation that results in much higher acetaldehyde levels after drinking than normal. About 10% of people who are homozygous for this gene form cannot drink alcohol without becoming sick and have almost no risk of AUD, whereas those who are heterozygous have a relatively low rate of AUD.
An alternative pathway, the microsomal ethanol-oxidizing system (MEOS), is induced by chronic alcohol exposure. The primary component of the MEOS is the molecule cytochrome P 450 , which exists in several variants. The variant most important for alcohol metabolism is cytochrome P 450 2E1 (CYP2E1). Many effects of alcoholism are produced by the toxic byproducts (hydrogen, acetaldehyde), acceleration of the metabolism of other drugs, and activation of hepatotoxic compounds by these metabolic pathways.
Although the liver is the major site of ethanol metabolism, other tissues contribute to its metabolism. ADH is found in the gastric mucosa, but the gastric metabolism of alcohol is decreased in women and those of Asian descent. This increased bioavailability of ethanol or decreased first-pass metabolism may explain the greater vulnerability of women to acute and chronic complications of alcohol.
Alcohol metabolism has two elimination rates. The alcohol elimination rate approximates zero-order kinetics (constant rate) for lower ethanol levels and first-order kinetics (amount of drug removed over time is proportional to the concentration of the drug) for higher levels, especially in chronic alcoholics; most likely, through induction of the MEOS pathway, the elimination rate is increased at higher blood levels.
The absorption and elimination rates of alcohol vary by individual and depend on many factors. There is enormous variation among patients in the rate of elimination of ethanol from the blood, ranging from 9 to 36 mg/dL/h in published data. Although the clearance rate may be as high as 36 mg/dL/h in some chronic drinkers, 20 mg/dL/h is a reasonable rate to assume in a typical intoxicated ED patient.
Physiologic effects vary directly with the blood alcohol level ( Table 137.2 ). Diminished fine motor control and impaired judgment appear with alcohol concentrations as low as 20 mg/dL (0.02 mg%), but wide individual variability exists. Chronic alcoholics can exhibit impressive tolerance. The blood alcohol concentration of a person cannot be accurately determined without quantitative testing. More than 50% of the adult population is obviously intoxicated with a level of 150 mg/dL (0.15 mg%). As the ethanol level rises, the patient’s level of consciousness declines, eventually ending in a coma. Death is caused by aspiration or respiratory depression.
TABLE 137.2
Physiologic Effects and Blood Ethanol Levels
| Blood Ethanol Concentration (mg/dL) | Effects a |
|---|---|
| 20–50 | Diminished fine motor control |
| 50–100 | Impaired judgment, impaired coordination |
| 100–150 | Difficulty with gait and balance |
| 150–250 | Lethargy, difficulty sitting upright without assistance |
| 300 | Coma in the novice drinker |
| 400 | Respiratory depression |
Clinical Features
Alcohol Withdrawal Syndrome
Alcohol is a central nervous system (CNS) depressant. Chronic alcohol use results in a down-regulation of γ-aminobutyric acid (GABA) receptor activity and disinhibition of the dopaminergic reward pathway. This down-regulation of GABA receptors is thought to lead to an increase in the desirable effects of alcohol and vulnerability for dependence due to the presence of increased synaptic GABA. The hallmark of alcohol withdrawal is CNS excitation, with increased cerebrospinal fluid, plasma, and urinary catecholamine levels. Alcohol withdrawal syndrome (AWS) is a continuum of syndromes that begins after a decrease in the amount of intake of ethanol. Therefore, only a reduction, not the abrupt cessation, of ethanol intake may result in withdrawal.
AWS is often divided into three sets of symptoms. The first set consists of autonomic hyperactivity, which appears within hours of the last drink and usually peaks within 24 hours.
Symptoms may occur as early as 6 hours after cessation of or a significant decrease in alcohol intake and usually peaks at 24 to 36 hours. It is characterized by mild autonomic hyperactivity—anorexia, nausea, vomiting, anxiety, coarse tremor, tachycardia, hypertension, hyperreflexia, and sleep disturbances such as insomnia and vivid dreams.
The second symptom set includes additional neuronal excitation, with epileptiform seizures and global confusion, usually occurring within 24 to 48 hours of abstinence and usually peaks at 50 hours after cessation of or a significant decrease in alcohol intake but occasionally takes up to 5 days. The syndrome is characterized by pronounced anxiety, insomnia, irritability, tremor, anorexia, tachycardia, hyperreflexia, hypertension, fever, decreased seizure threshold, visual and auditory hallucinations, and finally delirium.
The third set of symptoms features delirium tremens or alcohol withdrawal delirium (AWD). While only 5% of patients hospitalized for alcohol withdrawal have delirium tremens, this syndrome is a life-threatening manifestation of alcohol withdrawal and consists of gross tremor, frightening visual hallucinations, profound confusion, agitation, and a hyperadrenergic state characterized by a temperature above 101°F (≈38.5°C), blood pressure higher than 140/90 mm Hg, and tachycardia. It seldom appears before the third post abstinence day.
The criteria for withdrawal delirium, as described in Box 137.1 , are delirium and alcohol withdrawal. Alcohol withdrawal is the most common alcohol-related illness that may require inpatient admission and is associated with adverse events such as uncontrolled agitation with the potential for over-sedation, generalized seizures, and prolonged hospital stay. Emergency clinicians should be familiar with the commonly used withdrawal rating instrument known as the Clinical Institute Withdrawal Assessment of Alcohol Scale, revised (CIWA-Ar). See Table 137.3 .
BOX 137.1
DSM-5 Criteria for Withdrawal Delirium (Delirium Tremens)
From the American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders . 5th ed. Washington DC: American Psychiatric Publishing; 2013.
Criteria for Alcohol Withdrawal
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Cessation of or reduction in heavy and prolonged use of alcohol
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At least two of eight possible symptoms after reduced use of alcohol:
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Autonomic hyperactivity
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Hand tremor
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•
Insomnia
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•
Nausea or vomiting
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•
Transient hallucinations or illusions
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•
Psychomotor agitation
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•
Anxiety
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•
Generalized tonic-clonic seizures
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•
Criteria for Delirium
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Decreased attention and awareness
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Disturbance in attention, awareness, memory, orientation, language, visuospatial ability, perception, or all these abilities change from the normal level and fluctuate in severity during the day
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No evidence of coma or other evolving neurocognitive disorders
TABLE 137.3
Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA-Ar)
Adapted from Sullivan JT, Sykora K, Schneiderman, J, et al. Assessment of alcohol withdrawal: The revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar). Br J Addict . 1989;84:1353–1357.
| Components of Scale | Most Severe Manifestations |
|---|---|
| Nine items a | |
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Constant nausea with vomiting |
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Severe tremor, even with arms extended |
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Drenching sweats |
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Acute panic |
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Continuous hallucinations |
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Continuous hallucinations |
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Continuous hallucinations |
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Extremely severe headache |
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Pacing during most of an interview with clinician or thrashing about |
| One item—orientation and clouding of sensorium b | |
Alcohol-Related Seizures
Patients presenting to the ED with seizures should be questioned about alcohol intake ( Box 137.2 ). Of seizure patients presenting to an ED, 20% to 40% will have their seizures related to alcohol use or abuse. The primary consideration in the initial care of seizure patients who regularly consume alcohol is the recognition of treatable, life-threatening causes. Alcohol may act in one of several ways to produce seizures in patients by its partial or absolute withdrawal after a period of chronic intake by, an acute alcohol-related metabolic disorder (e.g., hypoglycemia, hyponatremia), an acute event leading to cerebral trauma, precipitation of seizures in patients with idiopathic or posttraumatic epilepsy, or lowering of the seizure threshold in patients with prior existing intracerebral disease states.
BOX 137.2
Differential Diagnosis of Alcohol-Related Seizures
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Withdrawal (alcohol or drugs)
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Exacerbation of idiopathic or posttraumatic seizures
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Acute intoxication (e.g., amphetamines, anticholinergics, cocaine, isoniazid, organophosphates, phenothiazines, tricyclic antidepressants, salicylates, lithium)
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Metabolic (e.g., hypoglycemia, hyponatremia, hypernatremia, hypocalcemia, hepatic failure)
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Infectious (e.g., meningitis, encephalitis, brain abscess)
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Trauma (e.g., intracranial hemorrhage)
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Cerebrovascular accident
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Sleep deprivation
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Noncompliance with anticonvulsants
Alcohol Withdrawal Seizures
Withdrawal seizures may occur 6 to 48 hours after the cessation of drinking. Of patients with seizures, 90% have one to six generalized tonic-clonic seizures, and 60% experience multiple seizures within a 6-hour period. The incidence of partial seizures, common with posttraumatic epilepsy, is increased during alcohol withdrawal. The term alcohol withdrawal seizure is reserved for seizures with these characteristics. The term alcohol-related seizure is used to refer to all seizures in the aggregate associated with alcohol use, including this subset of alcohol withdrawal seizures.
Alcoholic Hallucinosis
Alcoholic hallucinosis is clinically distinct from delirium tremens and is characterized by hallucinations presenting within 12 to 24 hours of abstinence and resolve within 24 to 48 hours, in contrast to delirium tremens that presents at least 48 to 72 hours after abstinence. Hallucinations are typically visual, although tactile hallucinations have been described. Alcoholic hallucinosis is also generally not associated with autonomic instability such as tachycardia, hypertension, or hyperthermia.
Cardiovascular Effects
Acute and chronic ethanol consumption can affect the mechanical function of the heart, produce dysrhythmias, and exacerbate coronary artery disease (CAD). It may alter myocardial function by direct toxic effects, by associated hypertension, or indirectly by altering specific electrolytes. Acute intoxication can decrease cardiac output in alcoholic and nonalcoholic patients with preexisting cardiac disease (see Table 137.4 ).
Table 137.4
Cardiovascular Effects of Alcohol
Data from Klatsky AL. Alcohol and cardiovascular diseases: where do we stand today? J Intern Med . 2015;278(3):238-–250.
| Condition | Probable Relationship With Alcohol | Potential Epidemiological Consequences | |
|---|---|---|---|
| Lighter drinking a | Heavier drinking b | ||
| Dilated Cardiomyopathy | Unrelated | One (of several) causes;? requires cofactors | ↑︎ risk of HF, AF, cardioembolic stroke and HS if on ACs |
| Systemic HTN | Little or none | Probably causal in susceptible persons | ↑︎ risk of HF, AF, IS, and HS |
| CAD | Protective | ? less protective or ↑︎ risk | ↑︎ risk of HF, cardioembolic stroke, and AF; t risk of HS if on ACs |
| Supraventricular arrhythmia | Little or none | Probably a causal factor, especially with binges | ↑︎ risk of cardioembolic stroke, and HS if on ACs |
| HS | ? unrelated or slight ↑︎ risk | ↑︎ risk | Disability and ↑︎ risk of VTE |
| IS | Protective | Probable ↑︎ risk; varies with subtype | Disability and ↑︎ risk of VTE |
| Heart failure | Indirectly protective | Varies with underlying CV condition | Disability and ↑︎ risk of VTE |
AC , Anticoagulant; AF , atrial fibrillation; CAD, coronary artery disease; HS , hemorrhagic stroke; HTN , hypertension;; IS , Ischemic stroke; VTE, venous thromboembolism; cv, cardiovascular; t, increase; 4, decrease;?, possibly.
Studies have linked moderate alcohol consumption (two drinks/day in men and one drink/day in women) with a reduced risk of cardiovascular disease. There is a strong biological plausibility that moderate wine consumption may have a positive effect on organs and systems. Whether the positive effect of wine on health is attributed to ethanol, to wine micro-constituents, or to their synergistic effect, is still unanswered. Low to moderate alcohol consumption decreases platelet aggregation, raises plasma levels of endogenous tissue plasminogen activator, and lowers insulin resistance and likely poses little cardiovascular risk.
Heavy alcohol consumption has a detrimental effect on those with preexisting CAD. It reduces exercise tolerance, induces coronary vasoconstriction, and raises heart rate and blood pressure. These patients also have a significantly higher incidence of peripheral arterial disease. The additive cardiovascular effects of ethanol and nicotine contribute to dysrhythmias and sudden death in patients with CAD.
Alcohol abuse is a known risk factor for the development of alcoholic cardiomyopathy which presents as a dilated cardiomyopathy that can lead to heart failure. , Heavy drinkers have increased odds of having a prolonged QTc interval and supraventricular dysrhythmias. Supraventricular (usually atrial fibrillation) and ventricular (usually transitory ventricular tachycardia) dysrhythmias, commonly referred to as “holiday heart,” have been documented in alcoholic patients who have been drinking heavily. Tachydysrhythmias as a result of episodic drinking commonly revert to sinus rhythm with abstinence and do not require immediate intervention if the patient is hemodynamically stable.
Pulmonary Effects
There is a clear and statistically significant relationship between alcohol consumption and the risk of community-acquired pneumonia (CAP). Consuming drinks that contain 10 to 20 g of alcohol per day is linked to an 8% increased risk of acquiring CAP. Pneumococcal pneumonia is the most common type of pneumonia in both healthy individuals and heavy alcohol users. In addition, Klebsiella pneumoniae also is increased in people with AUD and seems to cause disproportionate rates of lung infection and high mortality in this population.
For centuries, it has been known that people with AUD are more likely to have pulmonary infections such as pneumonia and tuberculosis. Over the past two decades, it has become clear that other conditions such as RSV and ARDS also are linked to high-risk alcohol consumption.
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