Alcohol-Related Disease: John T. Finnell

137
Alcohol-Related Disease
John T. Finnell
As eloquently stated by Paracelsus in the 16th century, “all substances Twenty-seven percent of the US population admits to alcohol mis-
are poisons; there is none which is not a poison. The right dose differ- use.5 Alcohol misuse accounts for more than 100,000 deaths in the
entiates a poison from a remedy.” 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.5,6 Alcoholism permeates all
KEY CONCEPTS levels of society. Studies reveal a complex association between alcohol
consumption and socioeconomic status (SES),7 where people of lower
• M oderate alcohol consumption is defined as one or two drinks/day for men
SES show greater susceptibility to the damaging effects of alcohol.
and one drink/day for women.
Alcohol use and misuse also have social and financial costs, with
• DSM–5 integrates alcohol abuse and alcohol dependence into a single
estimates of over $220 billion in societal costs in the United States
disorder called alcohol use disorder (AUD), with mild, moderate, and severe
annually.8 The literature refers to harmful, hazardous, and risky drink-
sub-classifications.
ing interchangeably as a pattern of drinking that increases the risk of
• Benzodiazepines are the main treatment of alcohol withdrawal and alcohol
harm for the person consuming alcohol or others. The International
withdrawal-induced seizures. Minor alcohol withdrawal occurs as early
Classification of Disease 10th Revision (ICD-10), draft ICD-11, and the
as 6 h and usually peaks at 24–36 h after the cessation of or significant
Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-
decrease in alcohol intake.
4) use the term “alcohol dependence.” Alcohol dependence is a result of
• Major alcohol withdrawal occurs after 24 h and usually peaks at 50 h (but
repeated use leading to a person having impaired control over the use
may take up to 5 days) after the decrease or termination of drinking.
of alcohol despite physical, psychological, and social harms. The fifth
• Delirium tremens is the extreme end of the alcohol withdrawal spectrum;
edition of the Diagnostic and Statistical Manual (DSM-5) combines
it consists of gross tremors, profound confusion, fever, incontinence, and
diagnostic criteria for alcohol abuse and dependence under the term
frightening visual hallucinations.
“alcohol use disorder,” with severity modifiers of “mild,” “moderate,” or
• Alcohol withdrawal seizures occur 6–48 h after the cessation of drinking,
“severe,” based on the number of criteria met. DSM-5 AUD of moder-
with 60% of patients experiencing multiple seizures within a 6-h period.
ate or greater severity is essentially equivalent to DSM-4 and ICD-10
• Alcohol withdrawal should be assessed and managed using a validated
criteria for alcohol dependence. DSM–5 integrates alcohol abuse and
scale, such as the CIWA-Ar scale.
alcohol dependence into a single disorder called alcohol use disorder
• Brief intervention and screening (SBIRT—screening, brief intervention,
(AUD), with mild, moderate, and severe sub-classifications.
and referral to treatment) can reduce alcohol consumption and is feasible
At least 24% to 31% of ED patients meet National Institute Alcohol
and effective in the emergency department.
Abuse and Alcoholism (NIAAA) criteria for “at-risk” or heavy drink-
ing. 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
FOUNDATIONS
years. (Table 137.1: Terms and Definitions of Unhealthy Alcohol Use.9)
Excess alcohol consumption places a significant burden on individ- Patients, their families, and society, in general, should be aware that
uals and society. Globally, alcohol consumption is the seventh lead- AUDs are not a result of any individual weakness or moral failing but
ing risk factor for both death and the burden of disease and injury. arise from a complex interaction of individual, social, cultural, and bio-
2016 data from the World Health Organization (WHO) state that logical factors. Most people with AUD are difficult to identify because
5.3% of all deaths globally were attributable to alcohol consump- they are likely to have jobs and families and to present with general
tion.1 The overall costs associated with alcohol use represent more complaints, such as malaise, insomnia, anxiety, sadness, or a range of
than 1% of the gross national product in high-and middle-income medical problems.
countries, with the costs of social harm (e.g., violence and road acci- In 2013, the US Preventive Services Task Force (USPSTF) recom-
dents) being far greater than health costs alone. In short, except for mended that clinicians screen adults 18 years or older for alcohol misuse
tobacco, alcohol accounts for a higher burden of disease than any and provide brief behavioral counseling interventions to those engaged in
other drug.2 risky or hazardous drinking behaviors.10 Of the available screening tools,
From 2002 to 2010,3 the rate of emergency department (ED) vis- the USPSTF determined that 1-item to 3-item screening instruments
its for alcohol-related diagnoses increased by 38%. In addition to the have the best accuracy for assessing unhealthy alcohol use in adults 18
number of visits, current National Hospital Ambulatory Care sur- years or older. These instruments include the abbreviated Alcohol Use
vey data indicates that the total time and the length of stay (LOS) for Disorders Identification Test–Consumption (AUDIT-C) and the NIAAA-
ethanol-related visits are increasing as well.4 recommended Single Alcohol Screening Questionnaire (SASQ).9 This high
1846
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CHAPTER 137 Alcohol-Related Disease 1847
TABLE 137.1 Terms and Definitions of Unhealthy Alcohol Use

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
For adolescents: NIAAA defines moderate-and high-risk use based on days of alcohol use in the past year, by age
group:
Moderate risk:
Ages 12–15 years: 1 day/year
Ages 16–17 years: 6 days/year
Age 18 years: 12 days/year
Highest risk:
Age 11 years: 1 day
Ages 12–15 years: 6 days
Age 16 years: 12 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:
1. Having times when the patient drank more, or longer, than intended
2. More than once wanted to cut down or stop, tried It, but could not
3. Spending a lot of time drinking or being sick/getting over the aftereffects of drinking
4. Wanting to drink so badly that they could not think of anything else
5. Found that drinking (or being sick from drinking) often interfered with taking care of home or family
responsibilities, caused problems at work, or caused problems at school
6. Continuing to drink even though it was causing trouble with family and friends
7. Given up or cut back on activities that were important or interesting ¡ท order to drink
8. More than once gotten into situations while or after drinking that increased the chances of getting hurt (e.g.,
driving, swimming, unsafe sexual behavior)
9. Continued to drink even though it was causing depression or anxiety, other health problems, or causing
memory blackouts
10. Having to drink much more than previously ¡ท order to get the desired effect, or finding that the usual number
of drinks had much less effect than previously
11. Experiencing the symptoms of withdrawal after the effects of alcohol were wearing off, such as trouble
sleeping, shakiness, restlessness, nausea, sweating, racing heart, or seizure
Severity is determined based on the number of symptoms present:
Mild: 2–3 symptoms
Moderate: 4–5 symptoms
Severe: ≥6 symptoms
(Continued)
1848 PART IV Environment and Toxicology
TABLE 137.1 Terms and Definitions of Unhealthy Alcohol Use—cont’d.

Term Source Definition
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
Episodes3 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- ≥3 of the following at some time during the previous year:
10-CM
A strong desire or sense of compulsion to take the substance
Difficulties in controlling substance-taking behavior in terms of its onset, termination, or levels of use
A physiological withdrawal state when substance use has ceased or been reduced, as evidenced by the
characteristic withdrawal syndrome for the substance; or use of the same (or a closely related) substance with
the intention of relieving or avoiding withdrawal symptoms
Evidence of tolerance, such that increased doses of the psychoactive substance are required ¡ท order to achieve
effects originally produced by lower doses (clear examples of this are found in alcohol-and opiate-dependent
individuals who may take daily doses sufficient to incapacitate or kill nontolerant users)
Progressive neglect of alternative pleasures or interests because of psychoactive substance use, increased
amount of time necessary to obtain or take the substance, or to recover from its effects
Persisting with substance use despite clear evidence of overtly harmful consequences, such as harm to the liver
through excessive drinking, depressive mood states consequent to periods of heavy substance use, or drug-
related impairment of cognitive functioning; efforts should be made to determine that the user was actually, or
could be expected to be, aware of the nature and extent of the harm
Abbreviations: ASAM. American Society of Alcoholism; SAMHSA. Substance Abuse and Mental Health Services Administration; WHO. World Health
Addiction Medicine; DSM-5. Diagnostic Organization.
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
aAccording to the American Society of Addiction Medicine, the preferred term; is “heavy drinking episode.”
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.
burden of alcohol-related injury and disease indicates a need to increase potentially faster production of acetaldehyde, which is rapidly metab-
awareness of AUD and its effective treatment options (see Box 137.3).11 olized by ALDH2. However, about 40% of Asian people (Japanese,
Chinese, and Koreans) have an inactive ALDH2 mutation that results
Metabolism of Alcohol in much higher acetaldehyde levels after drinking than normal.
While some alcohol is absorbed in the stomach, the vast majority is About 10% of people who are homozygous for this gene form can-
absorbed in the small intestine. It is distributed uniformly to all organ sys- not drink alcohol without becoming sick and have almost no risk of
tems, including the placenta. Although 2% to 10% of alcohol is excreted AUD, whereas those who are heterozygous have a relatively low rate
through the lungs, urine, and sweat, most is metabolized to acetaldehyde, of AUD.
primarily by alcohol dehydrogenase (ADH). The oxidation of alcohol is An alternative pathway, the microsomal ethanol-oxidizing system
a complex process involving three enzyme systems, all contained in the (MEOS), is induced by chronic alcohol exposure. The primary com-
hepatocyte. Acetaldehyde is then quickly converted to carbon dioxide ponent of the MEOS is the molecule cytochrome P450, which exists in
and water, primarily through aldehyde dehydrogenase (ALDH). The several variants. The variant most important for alcohol metabolism is
common forms of ADH decrease the alcohol concentration in blood by cytochrome P450 2E1 (CYP2E1). Many effects of alcoholism are pro-
about 4.5 mmol/L ethanol/h (the equivalent of about one drink/h): duced by the toxic byproducts (hydrogen, acetaldehyde), acceleration
of the metabolism of other drugs, and activation of hepatotoxic com-
Ethanol ADH Alcohol
 hydrogenase
NAD→NADH
→ pounds by these metabolic pathways.
Acetaldehyde ADH Alcohol
 dehydrogenase
→ Although the liver is the major site of ethanol metabolism, other tis-
NAD→NADH
sues contribute to its metabolism. ADH is found in the gastric mucosa,
Acetyl coenzyme A C
ritical acid

Cycle
→ CO2 + H2O but the gastric metabolism of alcohol is decreased in women and those
of Asian descent. This increased bioavailability of ethanol or decreased
where NAD is nicotinamide adenine dinucleotide and NADH is first-pass metabolism may explain the greater vulnerability of women
reduced nicotinamide adenine dinucleotide. to acute and chronic complications of alcohol.
At least two variations of ADH genes (ADH1B*2 and ADH1C*1) Alcohol metabolism has two elimination rates. The alcohol elimi-
produce a slightly more rapid breakdown of alcohol and therefore nation rate approximates zero-order kinetics (constant rate) for lower
TABLE 137.2 Physiologic Effects and Blood BOX 137.1 DSM-5 Criteria for Withdrawal
Ethanol Levels Delirium (Delirium Tremens)
Blood Ethanol Criteria for Alcohol Withdrawal
Concentration (mg/dL) Effectsa Cessation of or reduction in heavy and prolonged use of alcohol
20–50 Diminished fine motor control At least two of eight possible symptoms after reduced use of alcohol:
50–100 Impaired judgment, impaired coordination • Autonomic hyperactivity
• Hand tremor
100–150 Difficulty with gait and balance
• Insomnia
150–250 Lethargy, difficulty sitting upright without • Nausea or vomiting
assistance • Transient hallucinations or illusions
300 Coma in the novice drinker • Psychomotor agitation
400 Respiratory depression • Anxiety
aThese
• Generalized tonic-clonic seizures
effects are for the occasional drinker. Chronic drinkers can func-
tion at much higher alcohol concentrations because of tolerance. On the
Criteria for Delirium
other hand, patients may become comatose with low levels of alcohol
Decreased attention and awareness
in mixed alcohol-drug overdose.
Disturbance in attention, awareness, memory, orientation, language, visu-
ospatial ability, perception, or all these abilities change from the normal
ethanol levels and first-order kinetics (amount of drug removed over level and fluctuate in severity during the day
time is proportional to the concentration of the drug) for higher lev- No evidence of coma or other evolving neurocognitive disorders
els, especially in chronic alcoholics; most likely, through induction of
From the American Psychiatric Association. Diagnostic and Statistical
the MEOS pathway, the elimination rate is increased at higher blood
Manual of Mental Disorders. 5th ed. Washington DC: American
levels. Psychiatric Publishing; 2013.
The absorption and elimination rates of alcohol vary by individ-
ual and depend on many factors. There is enormous variation among
patients in the rate of elimination of ethanol from the blood, ranging vomiting, anxiety, coarse tremor, tachycardia, hypertension, hyperre-
from 9 to 36 mg/dL/h in published data. Although the clearance rate flexia, and sleep disturbances such as insomnia and vivid dreams.
may be as high as 36 mg/dL/h in some chronic drinkers, 20 mg/dL/h is The second symptom set includes additional neuronal excitation,
a reasonable rate to assume in a typical intoxicated ED patient. with epileptiform seizures and global confusion, usually occurring
Physiologic effects vary directly with the blood alcohol level (Table within 24 to 48 hours of abstinence and usually peaks at 50 hours after
137.2). Diminished fine motor control and impaired judgment appear cessation of or a significant decrease in alcohol intake but occasionally
with alcohol concentrations as low as 20 mg/dL (0.02 mg%), but wide takes up to 5 days. The syndrome is characterized by pronounced anx-
individual variability exists. Chronic alcoholics can exhibit impres- iety, insomnia, irritability, tremor, anorexia, tachycardia, hyperreflexia,
sive tolerance. The blood alcohol concentration of a person cannot be hypertension, fever, decreased seizure threshold, visual and auditory
accurately determined without quantitative testing. More than 50% of hallucinations, and finally delirium.
the adult population is obviously intoxicated with a level of 150 mg/ The third set of symptoms features delirium tremens or alcohol
dL (0.15 mg%). As the ethanol level rises, the patient’s level of con- withdrawal delirium (AWD). While only 5% of patients hospitalized
sciousness declines, eventually ending in a coma. Death is caused by for alcohol withdrawal have delirium tremens, this syndrome is a
aspiration or respiratory depression. life-threatening manifestation of alcohol withdrawal and consists of
gross tremor, frightening visual hallucinations, profound confusion,
CLINICAL FEATURES agitation, and a hyperadrenergic state characterized by a temperature
above 101°F (≈38.5°C), blood pressure higher than 140/90 mm Hg,
Alcohol Withdrawal Syndrome and tachycardia. It seldom appears before the third post abstinence
Alcohol is a central nervous system (CNS) depressant. Chronic alco- day.
hol use results in a down-regulation of γ-aminobutyric acid (GABA) The criteria for withdrawal delirium, as described in Box 137.1, are
receptor activity and disinhibition of the dopaminergic reward path- delirium and alcohol withdrawal. Alcohol withdrawal is the most com-
way.12 This down-regulation of GABA receptors is thought to lead mon alcohol-related illness that may require inpatient admission and
to an increase in the desirable effects of alcohol and vulnerability for is associated with adverse events such as uncontrolled agitation with
dependence due to the presence of increased synaptic GABA. The the potential for over-sedation, generalized seizures, and prolonged
hallmark of alcohol withdrawal is CNS excitation, with increased cere- hospital stay.3 Emergency clinicians should be familiar with the com-
brospinal fluid, plasma, and urinary catecholamine levels. Alcohol monly used withdrawal rating instrument known as the Clinical Insti-
withdrawal syndrome (AWS) is a continuum of syndromes that begins tute Withdrawal Assessment of Alcohol Scale, revised (CIWA-Ar). See
after a decrease in the amount of intake of ethanol. Therefore, only a Table 137.3.
reduction, not the abrupt cessation, of ethanol intake may result in
withdrawal. Alcohol-Related Seizures
AWS is often divided into three sets of symptoms. The first set con- Patients presenting to the ED with seizures should be questioned about
sists of autonomic hyperactivity, which appears within hours of the last alcohol intake (Box 137.2). Of seizure patients presenting to an ED,
drink and usually peaks within 24 hours. 20% to 40% will have their seizures related to alcohol use or abuse. The
Symptoms may occur as early as 6 hours after cessation of or a sig- primary consideration in the initial care of seizure patients who regu-
nificant decrease in alcohol intake and usually peaks at 24 to 36 hours. larly consume alcohol is the recognition of treatable, life-threatening
It is characterized by mild autonomic hyperactivity—anorexia, nausea, causes. Alcohol may act in one of several ways to produce seizures in
TABLE 137.3 Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA-Ar)
Components of Scale Most Severe Manifestations
Nine itemsa
• N
ausea or vomiting Constant nausea with vomiting
• T remor Severe tremor, even with arms extended
• P aroxysmal sweats Drenching sweats
• A
nxiety Acute panic
• T actile disturbances (e.g., itching, numbness, sensation of bugs crawling on or under the skin) Continuous hallucinations
• A
uditory disturbances (e.g., sensitivity to sound, hearing things that are not there) Continuous hallucinations
• V isual disturbances (e.g., sensitivity to brightness and color, seeing things that are not there) Continuous hallucinations
• H
eadache, sensation of a band around the head Extremely severe headache
• A
gitation Pacing during most of an interview with clinician or
thrashing about
One item—orientation and clouding of sensoriumb
aScoredon a scale ranging from 0 (no symptoms) to 7 (most severe symptoms).
bScoredon a scale ranging from 0 (no symptoms) to 4 (disoriented with respect to place or person).
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.
BOX 137.2 Differential Diagnosis tremens that presents at least 48 to 72 hours after abstinence. Hallu-
of Alcohol-Related Seizures cinations are typically visual, although tactile hallucinations have
been described. Alcoholic hallucinosis is also generally not associ-
Withdrawal (alcohol or drugs) ated with autonomic instability such as tachycardia, hypertension, or
Exacerbation of idiopathic or posttraumatic seizures hyperthermia.
Acute intoxication (e.g., amphetamines, anticholinergics, cocaine, isoniazid,
organophosphates, phenothiazines, tricyclic antidepressants, salicylates, Cardiovascular Effects
lithium) Acute and chronic ethanol consumption can affect the mechanical
Metabolic (e.g., hypoglycemia, hyponatremia, hypernatremia, hypocalcemia, function of the heart, produce dysrhythmias, and exacerbate coronary
hepatic failure) artery disease (CAD). It may alter myocardial function by direct toxic
Infectious (e.g., meningitis, encephalitis, brain abscess) effects, by associated hypertension, or indirectly by altering specific
Trauma (e.g., intracranial hemorrhage) electrolytes. Acute intoxication can decrease cardiac output in alco-
Cerebrovascular accident holic and nonalcoholic patients with preexisting cardiac disease (see
Sleep deprivation Table 137.4).13
Noncompliance with anticonvulsants Studies have linked moderate alcohol consumption (two drinks/
day in men and one drink/day in women) with a reduced risk of car-
diovascular disease.14–16 There is a strong biological plausibility that
patients by its partial or absolute withdrawal after a period of chronic moderate wine consumption may have a positive effect on organs and
intake by, an acute alcohol-related metabolic disorder (e.g., hypoglyce- systems. Whether the positive effect of wine on health is attributed to
mia, hyponatremia), an acute event leading to cerebral trauma, precip- ethanol, to wine micro-constituents, or to their synergistic effect, is still
itation of seizures in patients with idiopathic or posttraumatic epilepsy, unanswered.17 Low to moderate alcohol consumption decreases plate-
or lowering of the seizure threshold in patients with prior existing let aggregation, raises plasma levels of endogenous tissue plasminogen
intracerebral disease states. activator, and lowers insulin resistance and likely poses little cardiovas-
cular risk.14
Alcohol Withdrawal Seizures Heavy alcohol consumption has a detrimental effect on those
Withdrawal seizures may occur 6 to 48 hours after the cessation of with preexisting CAD. It reduces exercise tolerance, induces coro-
drinking. Of patients with seizures, 90% have one to six generalized nary vasoconstriction, and raises heart rate and blood pressure. These
tonic-clonic seizures, and 60% experience multiple seizures within a patients also have a significantly higher incidence of peripheral arte-
6-hour period. The incidence of partial seizures, common with post- rial disease.18 The additive cardiovascular effects of ethanol and nic-
traumatic epilepsy, is increased during alcohol withdrawal. The term otine contribute to dysrhythmias and sudden death in patients with
alcohol withdrawal seizure is reserved for seizures with these charac- CAD.19
teristics. The term alcohol-related seizure is used to refer to all seizures Alcohol abuse is a known risk factor for the development of alco-
in the aggregate associated with alcohol use, including this subset of holic cardiomyopathy which presents as a dilated cardiomyopathy that
alcohol withdrawal seizures. can lead to heart failure.14,20 Heavy drinkers have increased odds of
having a prolonged QTc interval and supraventricular dysrhythmias.21
Alcoholic Hallucinosis Supraventricular (usually atrial fibrillation) and ventricular (usually
Alcoholic hallucinosis is clinically distinct from delirium tremens and transitory ventricular tachycardia) dysrhythmias, commonly referred
is characterized by hallucinations presenting within 12 to 24 hours of to as “holiday heart,” have been documented in alcoholic patients who
abstinence and resolve within 24 to 48 hours, in contrast to delirium have been drinking heavily. Tachydysrhythmias as a result of episodic
TABLE 137.4 Cardiovascular Effects of Alcohol

Potential Epidemiological
Condition Probable Relationship With Alcohol Consequences
Lighter drinkinga Heavier drinkingb
Dilated Cardiomyopathy Unrelated One (of several) causes; ? requires ↑ risk of HF, AF, cardioembolic
cofactors 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 ↑ risk of cardioembolic stroke,
binges 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.
aLess than three standard-sized drinks per day; bThree or more standard-sized drinks per day.
Data from Klatsky AL. Alcohol and cardiovascular diseases: where do we stand today? J Intern Med. 2015;278(3):238-–250.
drinking commonly revert to sinus rhythm with abstinence and do for peptic ulcer disease. Peptic ulcer disease is the most common cause
not require immediate intervention if the patient is hemodynamically of bleeding in alcoholic patients with upper GI hemorrhage, as well as
stable. in those who do not regularly consume alcohol.
Pulmonary Effects Liver Damage

There is a clear and statistically significant relationship between alcohol Hepatic damage has been recognized for centuries as the hallmark of
consumption and the risk of community-acquired pneumonia (CAP). chronic alcohol abuse. Above a certain quantity, alcoholic consump-
Consuming drinks that contain 10 to 20 g of alcohol per day is linked tion can elicit a spectrum of liver lesions among which steatosis is pres-
to an 8% increased risk of acquiring CAP.22 Pneumococcal pneumo- ent in nearly all drinkers who consume in excess of 40 g/day regularly.24
nia is the most common type of pneumonia in both healthy individ- The activation of the immune system with the production of cytokines
uals and heavy alcohol users. In addition, Klebsiella pneumoniae also such as tumor necrosis factor-alpha is one of the earliest events in many
is increased in people with AUD and seems to cause disproportionate types of liver injury. This cascade stimulates Kupffer cells and the pro-
rates of lung infection and high mortality in this population.23 duction of other cytokines that together enlist inflammatory cells, kill
For centuries, it has been known that people with AUD are more hepatocytes, and initiate healing through fibrogenesis.
likely to have pulmonary infections such as pneumonia and tubercu- Alcoholic liver disease is the most common liver disorder in the
losis. Over the past two decades, it has become clear that other con- Western Hemisphere and, along with hepatitis C (HCV), is a leading
ditions such as RSV and ARDS also are linked to high-risk alcohol cause of liver transplantation. Alcohol use is associated with more per-
consumption.23 sistent HCV infection and more extensive liver damage than no alcohol
use because of interactions between alcohol use and HCV that affect
immune responses, cytotoxicity, and oxidative stress.2 No safe level of
Gastrointestinal and Hepatic Effects alcohol consumption has been determined for patients with HCV.2
Esophagus and Stomach
Alcoholic patients have a higher incidence of esophagitis, gastric can- Alcoholic Hepatitis
cer, and esophageal carcinoma than in the general population. Acute Alcoholic hepatitis is a pro-inflammatory chronic liver disease that is
alcohol ingestion also decreases lower esophageal sphincter pressure, associated with high short-term morbidity and mortality (25% to 35%
delays gastric emptying, and disrupts the normal gastric mucosal bar- in 1 month) in the setting of chronic alcohol use.25 It is a clinical syn-
rier. Alcohol consumption, because of its inherent toxicity, has been drome characterized by right upper quadrant pain, a tender enlarged
shown to eliminate infection of the gastric mucosa by Helicobacter liver, fever, jaundice, leukocytosis, and altered liver function test results.
pylori. Forceful or persistent emesis can lead to a Mallory-Weiss tear or aspartate transaminase (AST) levels are usually less than 400 IU/L, and
more severely, Boerhaave syndrome. ALT levels are typically less than half the AST level. It is associated with
profound immune dysfunction with a primed but ineffective immune
Gastrointestinal Bleeding response against pathogens.26
Alcohol is closely associated with gastrointestinal (GI) bleeding. Alcoholic hepatitis has a range of clinical manifestations from
Causes and contributing factors include Mallory-Weiss tears, esoph- mildly symptomatic hepatomegaly to fulminant hepatic failure. The
agitis, esophageal varices, acute and chronic gastritis, thrombocyto- severity of the disease can be estimated in the ED by a prolonged pro-
penia, portal hypertensive gastropathy, qualitative and quantitative thrombin time/international normalized ratio (INR) or with the use of
platelet disorders, and prolonged clotting times. Alcohol may exacer- the Maddrey discriminant factor. The ABIC (age, bilirubin, INR, cre-
bate gastric mucosal damage when it is combined with nonsteroidal atinine) score and model for end-stage liver disease (MELD) are also
antiinflammatory drugs (NSAIDs), but ethanol itself is not a risk factor helpful in predicting mortality in these patients.
Cirrhosis deficiencies, oculomotor abnormalities (nystagmus being the most

The causal association between alcohol intake and alcoholic liver dis- common), cerebellar dysfunction, and an altered mental state or mild
ease has been well documented, yet liver cirrhosis develops in only memory impairment. Mental abnormalities include lethargy, inatten-
10% to 20% of heavy drinkers.2 Cirrhosis is the disruption of the nor- tiveness, abulia, and impaired memory, progressing without treatment
mal architecture of the liver by scarring and regenerating nodules of to coma.
parenchyma. Alcoholism is the most common cause of cirrhosis in the Korsakoff psychosis or amnesic state also called an alcohol-induced
United States and is responsible for approximately 48% of all cirrhotic- persisting amnestic disorder, is a disorder with recent memory impair-
induced deaths.27 Alcoholic cirrhosis usually requires 10 to 15 years of ment, inability to learn new information or recall previously learned
chronic drinking, often punctuated by one or more episodes of acute information, apathy, and confabulation. Although it is common, con-
alcoholic hepatitis. The clinical outcome is determined by the develop- fabulation is not essential for the diagnosis. Whereas 80% of patients
ment of complications of portal hypertension and hepatic dysfunction. with acute Wernicke’s encephalopathy have Korsakoff syndrome, age
Alteration of the normal hepatic architecture by fibrosis and nodule older than 40 years and many years of heavy alcohol use are additional
formation may eventually lead to portal hypertension. Portal hyperten- risk factors.
sion may be complicated by ascites and esophageal varices. Although Treatment of WKS consists of abstinence, adequate diet, and thi-
cirrhosis is irreversible, its progression may be halted with abstinence. amine. The ophthalmoplegia and nystagmus usually have a good
response to thiamine administration within hours to days. The ataxia
Pancreatitis and Malabsorption and mental changes may take days to weeks to improve and usually have
The association of ethanol with acute and chronic pancreatitis is well a poorer prognosis. Less than 25% of patients show any real recovery,
established, but the exact pathogenesis is unclear. Hypotheses include 50% show some recovery, and the remainder show no response, despite
reflux of duodenal contents and bile into the pancreatic duct, obstruc- adequate thiamine replacement. Because magnesium is a cofactor for
tion by a plug of pancreatic juice rich in proteins, and a direct toxic this enzyme system, its serum levels should be corrected. Patients with
effect of ethanol. WKS require admission with thiamine and magnesium repletion.
The diagnosis of alcoholic pancreatitis can be difficult because
asymptomatic alcoholics may have an elevated amylase level. Con- Alcoholic Cerebellar Degeneration
versely, up to 30% of patients with acute alcoholic pancreatitis have an Characterized by ataxia of the extremities, cerebellar ataxia of alco-
amylase value within normal limits. The serum lipase level rises after holism results in a wide-based stance and uncoordinated gait. Lower
amylase, remains elevated longer, and is a more reliable indicator of extremity involvement predominates, although the arms may rarely be
alcoholic pancreatitis, especially when it is more than three times the involved. Pathologic changes consist of the degeneration of elements
normal range. in the cerebellum, especially the Purkinje cells. The diagnosis is based
on history, physical examination, and findings on magnetic resonance
Neurologic Effects imaging or computed tomography (CT), which shows severe cerebel-
Neuropathy. A symmetric sensorimotor polyneuropathy is lar atrophy. Treatment consists of abstinence, adequate nutrition, and
common with chronic alcohol abuse, usually in the lower extremities. It thiamine.
is thought to be a combination of nutritional deficiency with thiamine
or vitamin B12 deficit and a direct neurotoxic effect of alcohol. Burning Infectious Disease
pain and paresthesia are common complaints. Findings on physical Chronic alcohol exposure depresses the development and expression
examination include loss of light touch, decreased pinprick sensation, of cell-mediated immunity. This depression may contribute to the
and reduced lower extremity deep tendon reflexes. Distal muscle high incidence of head, neck, and upper GI cancers in alcoholics. The
weakness is a delayed finding. The neuropathy may lead to nonhealing suppression of macrophage function by alcohol reduces the reticulo-
ulcers on the feet. Treatment of alcoholic neuropathy is abstinence, endothelial system’s ability to clear particles. This may contribute to
adequate diet, and thiamine. Complete recovery is rare. spontaneous bacteremia, spontaneous bacterial peritonitis, pneumo-
So-called “Saturday night palsy” or “honeymooner’s syndrome” is nia, and tuberculosis.
a wrist drop caused by radial nerve compression. The patient usually The most common infection in alcoholism is pneumonia. Although
has spent the night with his or her arm drooped over the back of a alcoholic patients may contract a variety of bacterial pneumoniae,
chair, bench, or companion; compressing the radial nerve against the Streptococcus pneumoniae is still the most common organism. Periods
humerus producing neurapraxia. Loss of function due to radial nerve of alcoholic stupor with incomplete glottic closure and subsequent aspi-
neuropraxia usually returns after a few weeks to months. ration can lead to aspiration pneumonia or lung abscess. K. pneumo-
Wernicke-Korsakoff Syndrome. There are high rates of dementia niae, classically associated with alcoholism, is currently more common
reported in patients with AUD, and up to 25% when all types of in patients with cytotoxic chemotherapy, hematologic malignant dis-
severe cognitive impairment are considered. Previously, two main ease, and transplantation than in the chronic alcoholic. Chronic alco-
disorders were described: Wernicke-Korsakoff syndrome (WKS) and hol consumption increases the risk and severity of chronic infections
alcohol-related dementia (ARD). Now, the DSM-5 introduces major with HIV; hepatitis C virus (HCV); and Mycobacterium tuberculosis.29
neurocognitive disorder as an alternative term to dementia, with a
subtype related to substance or medication use. WKS and ARD could Endocrine Effects
be a direct result of alcohol neurotoxicity or the consequence of a Alcohol dependence adversely affects many endocrine systems.
concurrent underlying pathology (such as thiamine deficiency) or both Peripheral thyroid hormone dysfunction and central hypothalamic-
(neurotoxicity associated with nutritional deficiencies).28 pituitary-
thyroid axis deregulation are seen. Male hypogonadism
Although they are similar pathologically and are caused by thiamine and feminism are seen in chronic male alcoholics. Alcohol’s effects
deficiency, Wernicke and Korsakoff syndromes are clinically distinct. on the testes and hypothalamus decrease testosterone production
Wernicke encephalopathy, a medical emergency with a mortality rate in men. Alcohol may cause impotence by CNS sedation, secondary
of approximately 17%, remains a clinical diagnosis and is often unrec- depression, or decreased testosterone production. Decreased tes-
ognized. Contemporary criteria require two of these signs—dietary tosterone, increased estrogen (in patients with liver disease), and
increased prolactin levels can lead to decreased libido, feminization, Although chronic alcoholics who require admission often have
and gynecomastia in male alcoholics and to abnormalities in lactation potassium, magnesium, and phosphate depletion, empirical treatment
and menstruation in women. In female alcoholics, increased levels of with potassium and phosphate is discouraged. Serum levels and renal
testosterone and estrogen are found. Estrogen replacement therapy function should be determined first. Unintended hyperkalemia and
may increase hormonal levels threefold and thus increase the risk of hyperphosphatemia can produce significant morbidity, and phosphate
cholelithiasis and breast cancer. infusion exacerbates hypocalcemia if present. Because most magne-
sium is intracellular, a normal serum magnesium level does not rule
Metabolic Effects out decreased total-body magnesium stores. If the serum level is nor-
Carbohydrates mal, total-body levels may still be low. As long as renal function is ade-
Alcohol- induced hypoglycemia occurs in up to 4% of chronic quate, empiric magnesium treatment can be considered. Abstinence
alcoholics. Coma, seizures, hemiparesis, and a variety of other and a proper diet resolve electrolyte and nutritional deficiencies in the
neurologic signs have been described in patients presenting with alcoholic patient who is healthy enough to be treated as an outpatient.
alcohol-induced hypoglycemia. Starvation, depletion of liver glyco-
gen stores, decreased plasma cortisol levels, the impaired release of Alcoholic Ketoacidosis
growth hormone, and inhibition of gluconeogenesis contribute to Twenty-five percent of patients who are admitted to the hospital with
this phenomenon. an alcohol-related disorder develop alcoholic ketoacidosis.30 Alcoholic
Hyperglycemia and diabetes may be found in chronic alcoholism. ketoacidosis occurs most frequently in severe chronic alcoholics who
Alcohol abuse can lead to chronic pancreatitis, resulting in the under- have had a recent binge followed 1 to 3 days later by protracted vomit-
production of insulin by the damaged pancreatic cells. Alcohol also ing, decreased food intake, dehydration, and abstinence. Nausea, vom-
impairs peripheral glucose utilization, causing relative insulin resis- iting, and abdominal pain are common presenting complaints. Serum
tance (similar to type 2 diabetes). glucose levels are usually less than 200 mg/dL. Normal blood pH may
be found despite ketonemia because of coexisting respiratory alkalosis
Lipids and metabolic alkalosis.
Ethanol increases the hepatic synthesis of triglycerides. Abstinence Treatment of alcoholic ketosis consists of the administration of nor-
is necessary to reverse elevated triglyceride levels. Except for its rela- mal saline, glucose, and thiamine with correction of hypokalemia. This
tionship to fatty infiltration of the liver, the clinical significance of this can be accomplished with 5% dextrose in normal saline and 30 mEq of
hyperlipidemia is unknown. potassium chloride or 30 mEq of oral potassium. If no serious compli-
cating illness is present, ketosis is often reversed within 12 to 24 hours
Electrolytes of treatment.
Ethanol has numerous effects on electrolytes and mineral metabo-
lism, as summarized in Table 137.5. Hyponatremia and hypokale- Hematologic Effects
mia are common in active drinkers. Vomiting, diarrhea, magnesium Chronic alcohol use is associated with significant alterations in the
depletion, malnutrition, and metabolic alkalosis contribute to these immune system that predispose people to viral and bacterial infections
abnormalities. and cancer development. The alcoholic presents with myriad hemato-
Alcoholism is the most common cause of severe magnesium defi- logic abnormalities. The direct toxic effect of ethanol and its metabo-
ciency in adult outpatients. Magnesium deficiency is seen in 30% of lites, secondary nutritional deficiency, and hepatic disease, individually
alcoholics as a result of malabsorption, malnutrition, diarrhea, vom- or in combination, affect red blood cells, white blood cells, platelets,
iting, and increased urinary losses. Oral magnesium supplementation hemostasis, and the immune system.
in chronic alcoholics improves liver function test results, electrolyte
balance, and muscle strength. Anemia
Hypocalcemia is common in alcoholic patients with magnesium Several mechanisms cause anemia, which is common in the alcoholic.
depletion. The mechanism is related to diminished parathyroid hor- Megaloblastic anemia resulting from folate deficiency is the most com-
mone secretion, decreased tissue responsiveness to parathyroid hor- mon anemia in alcoholics. The mean corpuscular volume (MCV) is
mone, decreased vitamin D metabolism, and decreased calcium release typically increased but may be normal when iron deficiency coexists.
from bone, which is independent of parathyroid hormone. Correction Malnutrition, the inability of the cirrhotic liver to store folate, exces-
of magnesium depletion is necessary to restore calcium to normal lev- sive urinary loss, and malabsorption decrease folate stores. Alcohol
els. Hypoalbuminemia, pancreatitis, or vitamin D deficiency also con- accelerates the development of megaloblastic anemia in individuals
tribute to low serum calcium levels or low total-body stores of calcium with depleted folate stores (MCV > 100 fL) by less clearly defined
in alcoholic patients. mechanisms.
Hypophosphatemia is found in up to 50% of hospitalized patients Iron deficiency anemia is common and is usually a result of blood
with alcoholism. Phosphorus depletion results from malnutrition, loss from the GI tract. With iron deficiency anemia, the serum iron
vomiting, respiratory alkalosis, diarrhea, enhanced release of cal- level is decreased, total serum iron-binding capacity is elevated, and
citonin, phosphate-binding antacids, and urinary loss (related to serum ferritin level is decreased. Alcoholics frequently have chronic
vitamin D deficiency and secondary hyperparathyroidism). Hypo- inflammatory diseases that produce anemia of chronic disease.
phosphatemic patients often have low magnesium levels. Rehydra-
tion, carbohydrate repletion, and parenteral alimentation further Leukocyte Abnormalities
exacerbate phosphorus depletion. Glucose bolus and infusions have Leukopenia is common in alcoholic patients and has several possi-
been shown to produce a significant fall in serum inorganic phos- ble causes. Sepsis, folate deficiency, and hypersplenism all lead to a
phate levels. Severe hypophosphatemia (<1 mg/dL) has been asso- decreased white blood cell count. Alcohol has a direct toxic effect on
ciated with acute respiratory failure, myocardial depression, CNS white blood cell production in the bone marrow. Granulocyte mobi-
irritability, dysfunction of erythrocytes, leukocytes, and platelets, and lization (chemotaxis) and adherence are also impaired, resulting in
rhabdomyolysis. decreased inflammatory responses.
TABLE 137.5 Electrolyte Disturbances30

Disturbance Mechanism or Cause Comment Treatment
Acid-Base
Alcoholic ketoacidosis Anion-gap metabolic acidosis due to decrease in Increased NADH:NAD ratio favors Administer 5% dextrose in 0.9%
insulin: glucagon ratio formation of/3-hydroxybutyric acid (normal) saline and treat other
disorders if present
Lactic acidosis Increased NADH:NAD ratio due to ethanol Average lactate level 3 mmol/L consider Administer 5% dextrose in 0.9%
metabolism sepsis or thiamine deficiency with (normal) saline and treat other
higher levels disorders if present
Hyperchloremic normal- Indirect loss of bicarbonate due to loss of ketoacid Regeneration of bicarbonate by kidneys Provide conservative management
gap metabolic acidosis salts in urine repairs deficit
Metabolic alkalosis Vomiting Increase in anion gap greater than Restore volume of extracellular fluid
decrease in bicarbonate concentration with chloride-containing fluids, correct
when combined with alcoholic hypokalemia
ketoacidosis
Respiratory alkalosis Alcohol withdrawal, chronic liver disease, pain, Often the primary disorder in a mixed Administer benzodiazepines for alcohol
sepsis acid-base disturbance withdrawal; treat underlying disorders
Hypophosphatemia Alcohol-induced urinary loss, magnesium Muscle weakness, rhabdomyolysis, Oral supplements preferred; for
deficiency, acidemia, increased parathyroid tissue ischemia, hemolysis, cardiac complications, administer 42–67
hormone level, nutritional deficiency, decrease in dysfunction; urine phosphate mmol phosphate over 6 to 9 hr, not
gastrointestinal absorption, cellular shift due to excretion >100 mg/24 h r or fractional to exceed 90 mmol/day to avoid
insulin release, respiratory alkalosis, excretion ≥5% indicates renal decrease in calcium and magnesium
β2-adrenergic stimulation wasting levels
Hypomagnesemia Alcohol-induced urinary loss, phosphate deficiency, Persistent renal wasting can last Oral supplements preferred; intravenous
nutritional deficiency, decreased gastrointestinal several weeks, accounting for magnesium indicated in patients
absorption, cellular shift due to insulin release, recurrence of hypomagnesemia after with arrhythmias or neuromuscular
respiratory alkalosis, β2-adrenergic stimulation initial correction; urinary magnesium irritability
excretion >25 mg/ 24 h or fractional
excretion >2% indicates renal wasting
Hypocalcemia† Decrease in parathyroid hormone level and Correct for a low albumin concentration Correct the magnesium deficit; correct
resistance due to magnesium deficiency, alcohol- as follows: corrected calcium=serum the deficiency in vitamin D
induced urinary loss, vitamin D deficiency calcium in mg/dL + [0.8× (4.0-serum
albumin in g/dL)]; bicarbonate therapy
can decrease ionized fraction
Hypokalemia Urinary loss due to coupling of increased distal A low or normal potassium level Oral supplements preferred; for
sodium delivery and increased aldosterone level, in patients with rhabdomyolysis complications, administer intravenous
magnesium deficiency, diarrhea, cellular shift suggests a significant underlying potassium chloride at 10–20 mmol/h;
due to insulin release, correction of acidosis, total-body deficit of potassium; urinary administer potassium before
respiratory alkalosis, β2 adrenergic stimulation potassium >30 mmol/24 h or urinary Bicarbonate in patients with acidemia
potassium: creatinine ratio >13 (in
millimoles of potassium per gram of
creatinine) indicates renal wasting
Hyponatremia Increased release of vasopressin due to volume Increased risk of osmotic demyelination Restore volume and increase protein
depletion; decreased solute excretion in beer intake; limit rate of correction to
potomanía 6–8 mmol in first 24 hours, to slow
rate with 5% dextrose in water,
desmopressin, or both
Data from Palmer BF, Clegg DJ. Electrolyte Disturbances in Patients with Chronic Alcohol-Use Disorder. N Engl J Med. 2017;377(14):1368–1377.
Platelet Disorders Hemostasis

Thrombocytopenia can occur with folate deficiency, marrow suppres- Alcoholic patients have a bleeding diathesis for many reasons, includ-
sion, sepsis, disseminated intravascular coagulation, or splenic seques- ing thrombocytopenia, qualitative platelet disorders, deficient produc-
tration. The direct toxic effects of alcohol decrease measured survival tion of hepatic clotting factors, GI variceal formation, and vitamin K
time and impair the production of platelets in the bone marrow, but deficiency. Bleeding associated with coagulation abnormalities may
marrow toxicity rarely reduces the platelet count below 30,000/mm3. require fresh-frozen plasma for the immediate correction of coagu-
Qualitative platelet function is also impaired. Binge drinking is asso- lation factor depletion; vitamin K (10 mg IV) takes 6 to 10 hours to
ciated with a reactive thrombocytosis potentially responsible for acute reverse the vitamin K–dependent factors II, VII, IX, and X. Because
stroke and sudden death. of poor diet and impaired hepatobiliary function, alcoholics may have
insufficient vitamin K storage and benefit from vitamin K delivery. abdominal discomfort, diaphoresis, vertigo, palpitations, and confu-
However, alcoholic patients with profound liver failure are unable to sion. A severe reaction may produce hypotension, seizures, and dys-
produce the precoagulation factors II, VII, IX, X, and IV, so vitamin K rhythmias. The disulfiram-ethanol reaction is thought to occur by the
therapy is ineffective. Platelet transfusions should be started in the ED accumulation of acetaldehyde secondary to inhibition of the ALDH
for adult patients with active bleeding when the platelet count is less enzyme, which may be deficient in many Asians, or another unknown
than 50,000/mm3. toxic factor. The common ink cap mushroom (Coprinopsis atramenta-
tia), while nontoxic when ingested alone, causes a similar disulfiram
Oncologic Effects reaction if consumed with alcohol. Treatment for disulfiram reaction
While alcohol itself is not carcinogenic, its metabolite, acetaldehyde, is generally observation, cardiac monitoring, an antiemetic for symp-
has emerged as an important contributor; it can form stable DNA toms, and intravenous (IV) fluids.
adducts, trigger mutations in tumor suppressors and oncogenes, and
interfere with DNA repair. Over 5% of all new cancer occurrences and Other Considerations—Patient Groups Affected
6% of all cancer deaths worldwide were estimated to be attributable Adolescents. Excessive high school and college drinking continues
to alcohol.31,32. Alcohol consumption has been highly associated with to be prevalent and problematic. Approximately 1.2 million youths aged
specific oncological diseases such as oral, pharyngeal, laryngeal, esoph- 12 to 17 met the criteria for SUDs in 2015 (5% of this population).35
ageal, hepatic, colorectal, and breast cancers.31,32 Alcohol is by far the most commonly used substance among youth,
with 37% of 18-year-olds endorsing alcohol use and 24 % reporting
Hypothermia being drunk in the past month.36 Alcohol is the most commonly
Acute alcohol ingestion is one of the most common precipitating fac- used drug and is a common contributor to the leading cause of death,
tors for accidental hypothermia and occurs in 33% to 75% of patients unintentional injury, homicide, and suicide among adolescents (10 to
presenting with a core temperature below 35°C (95°F). Alcohol exac- 20 years old) in the United States.
erbates hypothermia of other causes, with depressed hypothalamic Adolescent onset of alcohol use has been associated with an
thermoregulation, peripheral vasodilation producing heat loss, CNS increased risk for developing an AUD later in life.37 Although under-
depression, sepsis, inability to shiver, hypoglycemia, and increased risk age youth may drink less often than adults, they typically drink in
of environmental exposure. Hypothermia may be the presentation of larger quantities than adults when they do drink, and often binge
Wernicke syndrome, possibly caused by lesions of the posterior hypo- drink.38 Binge drinking, as defined by the NIAAA, is a pattern of
thalamus, hypoglycemia, or sepsis. alcohol consumption that brings blood alcohol concentration to
.08 g/dL, which typically occurs following the intake of five or more
Psychiatric Effects standard alcohol drinks by men and four or more by women over
Depression and antisocial personality are the two most common psy- a period of approximately 2 hours. In 2011, the NIAAA produced
chiatric disorders that correlate with alcoholism, with a prevalence of a two-question Youth Alcohol Screening Tool which asks about the
30% to 60% in most studies. Of alcoholic men admitted to a psychiat- frequency of alcohol consumption and friends’ alcohol use in the past
ric ward, approximately 40% have another psychiatric disorder unre- year (Table 137.6).39
lated to substance abuse—in particular, antisocial personality disorder, Older Patients. Alcohol use is a growing public health concern for
schizophrenia, mood disorders, and anxiety disorders. elderly adults. Elderly patients, meaning patients ages 65 years and
Mental illness and substance use often co-occur and heavy alcohol older, comprise the fastest-growing portion of the US population. By
use and AUDs are known risk factors for violence.33 Secondary depres- 2040, the elderly will comprise more than 20% of the total population.
sion may be caused by alcoholism, or the primary affective disorder Compared with all other substances, alcohol is the most commonly used
may be present with secondary alcoholism. Mild depressive symptoms among the elderly, and thus, the risks of drinking by older individuals
are also common in alcohol withdrawal. Alcoholism, major depression, will undoubtedly become an increasing issue as this population rises
and antisocial personality all predispose to suicide, and interaction over the coming decades.40
among the three is particularly dangerous, but the acute risk on any Common screening tests (e.g., the CAGE questionnaire) tend to
given day is difficult to assess.34 Alcohol increases the lifetime risk of be less sensitive in this age group. Alcohol may exacerbate underlying
suicide, with over 15% of all alcoholics eventually dying by suicide. disease by masking anginal chest pain, worsening hypertension, and
inducing dysrhythmias. Older adults who consume low to moderate
Toxicologic Effects levels of alcohol, however, may have a decreased risk for the develop-
Alcohol has long been known to have additive or even synergistic ment of dementia and heart failure.
effects with several drugs including opioids and sedative hypnotic Older patients are more likely to have neuropsychiatric complica-
agents. Acute intoxication decreases the rate of drug metabolism, tions of alcoholism, such as sleep problems, anxiety, depression, and
which is partially explained by competition for the same enzymatic dementia. Alcohol is involved in one-third of suicides in older adults.
process in the liver. Ethanol increases aspirin-induced prolongation Older subjects also perform less well than younger subjects on tests of
of bleeding time and reduces the metabolism of warfarin, leading to perception and attention when under the influence at all blood alcohol
increased anticoagulant effects. There is an increased risk of upper GI levels. This may result in an increased risk of fractures from falling and
bleeding when alcohol is combined with NSAIDs. osteoporosis. However, evidence has suggested that compared with
abstinence, consumption of up to one drink/day is associated with a
Disulfiram and Similar Reactions decreased risk of osteoporotic hip fracture, and there is a beneficial
Most patients pretreated with disulfiram (Antabuse) who then con- effect of moderate alcohol consumption on bone density.
sume even small amounts of alcohol experience an extremely unpleas- Pregnant Women. There is no known safe level of alcohol
ant reaction. These patients have a hypersensitivity to ethanol and consumption during pregnancy. Alcohol is a known teratogen
experience a direct response within 15 minutes, lasting 30 minutes to that can impact fetal growth and development during all stages of
several hours. The reaction consists of skin flushing on the head that pregnancy. The current recommendation from the American College
spreads to the trunk, along with nausea, vomiting, headache, chest and of Obstetricians and Gynecologists, Center for Disease Control (CDC),
TABLE 137.6 The NIAAA Youth Alcohol Screening Tool

Age: First Question: Second Question:
Elementary School (ages 9–11) Friends: Any drinking? “Do you have any friends who Patient: Any drinking? “How about you —have you
drank beer, wine, or any drinking containing alcohol ever had more than a few sips of beer, wine, or any
in the past year?” drink containing alcohol?
Middle School (ages 11–14) Friends: Any drinking? “Do you have any friends who Patient: How many days? “How about you—in
drank beer, wine, or any drinking containing alcohol the past year, on how many days have you had
in the past year more than a few sips of beer, wine, or any drink
containing alcohol?”
High School (ages 14–18) Patient: How many days? in the past year, on how Friends: How much? “If your friends drink, how many
many days have you had more than a few sips of drinks do they usually drink on an occasion?”
beer, wine, or any drink containing alcohol?”
Surgeon General, and medical societies from other countries all for resuscitation. Alcohol-induced skin vasodilation may be accompa-
recommend complete abstinence during pregnancy.41 nied by an increase in skeletal muscle, mesenteric, and renal bed con-
Alcohol readily crosses the placenta with fetal blood alcohol levels striction and left ventricular stroke work. Thus, the overall effect on
approaching maternal levels within 2 hours of maternal intake. There systemic vascular resistance and blood pressure may be balanced.
are a wide variety of developmental defects that result from alcohol Intoxication renders the signs and symptoms of intra-abdominal
exposure, including brain abnormalities, CNS dysfunctions, and and retroperitoneal injury less reliable than usual. If the risk of an
growth deficiencies of developing organs and body systems. These intra-abdominal injury exists, further evaluation (e.g., diagnostic
adverse effects on the developing fetus are known collectively as fetal ultrasonography, CT imaging) should be considered. Alcohol intoxica-
alcohol spectrum disorders (FASDs).42 FASDs cause dysfunctions in tion predisposes to abdominal wall laxity and therefore less protection
learning, emotion, cognition, motor performance, and can lead to from blunt trauma. These patients are also likely to have full stomachs,
behavioral as well as social problems.42 FASDs are characterized by a increasing the risk of gastric injury after trauma and predisposing to
triad of CNS defects, including mild to moderate mental retardation, vomiting and aspiration, especially during acute airway management.
dysmorphology, involving mostly facial structures, and growth defi- The fatty liver changes in alcoholism can result in hepatomegaly.
ciencies, usually consisting of short stature and microcephaly. FASDs Portal hypertension in alcoholics may produce splenomegaly. These
are now considered the most common identifiable source of mental organs can become more vulnerable to the effects of trauma because of
retardation. Children exposed to prenatal alcohol exhibit increased their enlarged size, protrusion beneath the protection of the ribs, and
activity levels, cognitive and attention deficits, perseverative behavior, increased intracapsular pressure.
and language and motor problems, which persist into adulthood. The American College of Surgeons Committee on Trauma requires
Alcohol has the ability to freely pass through a lactating moth- screening for problem drinking for designation at a level I or II trauma
er’s milk and thus lactating mothers who decide to continue to drink center. In addition, level I trauma centers must provide intervention
should avoid breastfeeding 3 to 4 hours after moderate to high con- for identified problem drinkers. Although many institutions use blood
sumption of alcohol.41 alcohol levels to determine at-risk drinking in trauma patients, the
Alcohol Use Disorders Identification Test (AUDIT) offers a practical
Trauma alternative (Box 137.3).43
Injury is a leading cause of death in those between the ages of 1 and 44
years, accounting for more than 50 million injuries/year and approx-
DIFFERENTIAL DIAGNOSIS
imately 26,000 deaths/year. In the United States, alcohol is the major
risk factor for virtually all categories of intentional and unintentional Acute alcohol intoxication is a diagnosis of exclusion. Before it is
injury. In addition to increasing the frequency and severity of the assumed that a patient’s behavior is caused only by alcohol, other
injury, alcohol consumption significantly impacts the management of conditions should be considered, particularly co-ingestion of other
the trauma victim. Alcohol intoxication often complicates the initial substances and pharmaceutical agents, head trauma, and infection.
assessment of injury severity, resulting in an increased need for inva- Hypoglycemia, hypoxia, carbon dioxide narcosis, mixed alcohol-drug
sive diagnostic and therapeutic procedures (e.g., intubation and venti- overdose, ethylene glycol poisoning, isopropanol or methanol poison-
lation, CT imaging, intracranial pressure monitoring). ing, hepatic encephalopathy, psychosis, severe vertigo, postictal state,
Alcohol may diminish the patient’s capacity to respond to hem- and psychomotor seizures can be manifested in a manner similar to
orrhagic shock by altering hemodynamic effects and the acid-base that of ethanol intoxication.
balance. Volume depletion as a result of the diuretic effect of alcohol AWS can initially be confused with acute schizophrenia, encephali-
or vomiting can impair the reserve of the intoxicated trauma patient. tis, drug-induced psychosis, thyrotoxicosis, anticholinergic poisoning,
Peripheral vasodilation caused by alcohol may contribute to hypoten- and withdrawal from other sedative hypnotic agents. Alcohol with-
sion and hypothermia. Although these effects may be transient, they drawal and alcohol-induced hypoglycemia also present with similar
underscore the need for early and adequate fluid resuscitation in these clinical presentations.
patients. Intoxicated patients with severe non-neurologic trauma may
have lower blood pressures and carbon dioxide levels, indicative of
DIAGNOSTIC TESTING
compensatory hyperventilation, on hospital arrival compared with
sober patients. More importantly, a poorly understood cardiac depres- Determination of a blood ethanol level is not routinely necessary
sant effect also increases the depth of shock and volume requirements in caring for the intoxicated patient when there is clear evidence of
thrombin time, prothrombin time and INR, and partial thrombo-

BOX 137.3 AUDIT-C Questions
plastin time help evaluate episodes of significant alcohol disease-
1. How often did you have a drink containing alcohol in the past year? induced bleeding.
a. Never (0 points) Liver function tests are followed in a serial manner in cases of alco-
b. Monthly or less (1 point) holic hepatitis. An electrocardiogram (ECG) is indicated for tachydys-
c. Two to four times a month (2 points) rhythmias or chest pain (e.g., holiday heart, acute ischemia). A CT scan
d. Two to three times per week (3 points) of the head or cervical spine imaging may be indicated if head trauma
e. Four or more times a week (4 points) or seizures are suspected or confirmed or if the patient’s mental status
2. How many drinks containing alcohol did you have on a typical day when does not improve in step with the metabolism of alcohol. A chest radio-
you were drinking in the past year? graph is obtained to rule out cardiomyopathy, infectious pneumonia,
a. 0–2 (0 points) or aspiration pneumonitis.
b. 3–4(1 point)
c. 5–6 (2 points) Alcohol Screening Questionnaires
d. 7–9 (3 points) Detection of risky drinking behaviors can be through clinical history
e. 10 or more (4 points) or the administration of short alcohol screening tools in the ED setting.
3. How often did you have six or more drinks on one occasion in the past year? The screening tools with superior sensitivity and specificity are the
a. Never (0 points) SASQ, AUDIT, and AUDIT-Consumption (AUDIT-C), see Box 137.3.
b. Less than monthly (1 point) As part of the initial assessment and in alignment with national
c. Monthly (2 points) recommendations, computerized screening programs could be used as
d. Weekly (3 points) an effective method for detecting at-risk alcohol use in ED patients.
e. Daily or almost daily (4 points) Identification of AUD and brief, sentinel event advice in the ED can
be an effective and cost-effective method to reduce levels of alcohol
Adapted from Miller LB, Brennan-Cook J, Turner B, et al. Utilizing an
consumption and alcohol-related harm.
Evidence-Based Alcohol Screening Tool for Identification of Alcohol
The SASQ From the NIAAA can be used to streamline the screen-
Misuse. J Addict Nurs. 2018;29(2):90–95.
ing process—it includes only 1 question: “How many times in the past
year have you had x or more drinks in a day?” (where x is 5 for men
alcohol intake (e.g., confirmation by the patient). When the men- and 4 for women).
tal status is sufficiently altered that an adequate history cannot be
obtained, there is evidence of head trauma, or the patient fails to
improve (detoxify) as expected, a serum ethanol level or measure-
MANAGEMENT
ment by a breathalyzer should be determined. If the degree of obtun- Comatose or stuporous patients may require assisted ventilation and
dation is not commensurate with the measured (or breathalyzed) intubation. If the bedside serum glucose level identifies hypoglycemia,
level, and other laboratory test results (e.g., toxicology screen, elec- IV glucose, as D50W or an infusion of D5W, is indicated. Patients with
trolyte levels, metabolic profile) do not explain the altered mental evidence of poor nutrition should receive thiamine, 100 to 250 mg IM
status, a head CT scan is indicated. Adequate history from paramed- or IV once daily for 3 to 5 days. If an opioid overdose is suspected,
ics, patient, and family members, serial physical examinations (espe- naloxone may be diagnostic and therapeutic. Because magnesium is a
cially mental status), and bedside testing, such as serum glucose level necessary cofactor for thiamine metabolism, consider administering
and oximetry, can help clarify the clinical situation and guide further magnesium, 2 g IV. When possible, hypoglycemia should be docu-
testing. mented before the empirical administration of glucose. With the airway
Blood tests can be useful if the history is in doubt and can also help maintained and respirations supported, the patient’s liver eventually
patients recognize that alcohol has adversely affected their health. The metabolizes the alcohol, and most patients recover.
utilization of direct metabolites of ethanol is considered more accurate Intoxicated patients who do not appear capable of appropriate
biomarkers of recent alcohol consumption. Three of these biomarkers, decision making require evaluation and treatment in the ED, regard-
ethyl glucuronide (EtG), ethyl sulfate (EtS), and phosphatidylethanol less of their willingness to cooperate. It is incumbent on the emer-
(PEth), are gaining acceptance, although they are not currently avail- gency clinician to establish that the patient understands the nature
able for routine testing.5,44 of the problem, whether intoxication alone or intoxication in the
Tests of liver function that measure AST and ALT levels can identify context of acute illness or injury and is capable of making reasoned
heavy drinking and AUDs with sensitivities of 25% to 45% and spec- and responsible decisions about care. Inappropriate discharge and
ificities as high as 90%. A ratio of AST to alanine transaminase (ALT) failure to diagnose are two common areas of liability in the treatment
higher than 2 suggests that alcohol is the cause of liver injury. of the alcohol-dependent patient. Discharge can be considered when
a patient is clinically sober enough to be able to dress, walk, make
Laboratory Tests reasonable decisions, and function independently, as judged and well
In the apparently intoxicated patient with altered mental status, the documented by the treating emergency clinician. When possible, it is
serum glucose level, usually as a point of care test, should be mea- ideal to have another sober adult who is willing to take responsibility
sured to assess for hypoglycemia. In the alcoholic patient, electrolyte for and remain with the patient for the next 24 to 48 hours. Once clin-
levels and acid/base status should be determined to look for hypo- ically sober and cleared for discharge, patients should be reminded
magnesemia, hypophosphatemia, hyponatremia, and metabolic aci- not to drink and drive.
dosis. A complete blood count is obtained to evaluate for anemia,
leukopenia, and thrombocytopenia and a serum lipase level to eval- Alcohol Withdrawal Syndrome
uate for pancreatitis if the patient has severe upper abdominal pain Family, friends, bystanders, or paramedics often give more reliable
or tenderness, especially if accompanied by vomiting. A complete historical data than the patient does. Accurate vital signs are essential;
blood count, peripheral smear, platelet count, reticulocyte count, this may require a rectal temperature. Hyperthermia, hypothermia,
tachypnea, or tachycardia may suggest serious disorders that often The typical dose is 2 to 5 mg q4–8h prn; q1h may be required with
accompany the alcohol- dependent patient. A rapid and thorough acute agitation; but not to exceed 20 mg/day. Haloperidol has no
physical examination should be performed, with attention to the level anticonvulsant properties; however, extrapyramidal effects may be
of consciousness, signs of hepatic failure, or coagulopathy. Signs of seen. Caution should be used in patients who may be susceptible to
trauma are sought, as well as a thorough neurologic examination. a prolonged QTc interval. Droperidol has effects and risks similar to
The AWS should be promptly recognized and treated. The CIWA-Ar those of haloperidol and remains a safe and effective treatment for
is a validated tool for symptom-based prescribing of benzodiazepines for acutely agitated patients in the ED. The recommended adult dose is 2.5
alcohol withdrawal. Scores on the CIWA-Ar ranges from 0 to 67; scores mg IV/IM; additional doses of 1.25 mg may be given to a desired effect
lower than 8 indicate mild withdrawal symptoms that rarely require the if the clinical benefit outweighs the potential risk.
use of medications, scores from 8 to 15 indicate moderate withdrawal Other Agents. Patients being treated for major alcohol withdrawal
symptoms that are likely to respond to moderate doses of benzodiaze- may be given thiamine (100 mg IV) and magnesium (2 g IV). Although
pines, and scores higher than 15 indicate severe syndromes that require magnesium sulfate does not decrease the severity of withdrawal
close monitoring to avoid seizures and AWD (or delirium tremens). symptoms, the incidence of delirium, or seizures, it carries no
significant risk with adequate renal function. For patients who require
Pharmacologic Treatment intubation for refractory withdrawal or for other reasons, an infusion
Patients suffering from alcohol withdrawal should receive pharma- of propofol or a benzodiazepine should be initiated to treat the patient’s
cologic intervention along with supportive care. The ideal drug for alcohol withdrawal.
alcohol withdrawal should have a rapid onset, a wide margin of safety,
metabolism not dependent on liver function, and limited abuse poten- Neurologic Examination
tial. Although no one drug class meets all these requirements, benzodi- New-Onset Seizures
azepines are clearly the mainstay of treatment. Patients with new-onset, alcohol-related seizures should be thoroughly
Benzodiazepines. Benzodiazepines have anticonvulsant activity, evaluated. This includes alcoholics who claim to have had seizures but
dose-dependent respiratory and cardiovascular depressive effects, and for whom no documentation or appropriate evaluation is available.
and be given IV/IM if necessary. By interacting with receptors linked to Metabolic disorders, toxic ingestion, infection, and structural abnor-
the GABA-associated chloride ion channel, benzodiazepines substitute malities should also be considered.
for the withdrawal of the GABA-potentiating effect of alcohol and If the initial physical examination findings, imaging studies, and
abate withdrawal signs and symptoms. Numerous benzodiazepines laboratory test results are within normal limits, patients who remain
have been studied, but there is no evidence of the clear superiority of seizure-free and symptom-free, with no sign of withdrawal after 4 to
any one benzodiazepine. 6 hours of observation, may be discharged. It may be unclear whether
Lorazepam has good bioavailability with the oral, intramuscular, and the patient has had a pure alcohol withdrawal seizure or a new-onset
IV routes. It may be given via an IM injection in agitated patients with no seizure disorder in the setting of alcohol ingestion. Long-term treat-
IV access. The half-life of lorazepam is ~12 hours and it does not have any ment with antiepileptic drugs is not useful in unprovoked new-onset
active metabolites.. Excessive sedation, confusion, and ataxia are potential seizures that have resolved or when a clear relation to alcohol con-
complications of all benzodiazepines with prolonged half-lives. Lorazepam sumption can be identified.
is metabolized (conjugated) in the liver, yielding inactive products. Although Optimal outpatient treatment includes follow-up and referral to
the half-life of lorazepam increases in patients with cirrhosis or liver failure, a detoxification or rehabilitation program. Ideally, the assistance of a
it is much shorter than the increase with chlordiazepoxide. The elimination reliable family member or friend who is not a drinking partner and can
of lorazepam is only minimally altered in patients with renal failure and in remain with the patient for at least 1 or 2 days is helpful.
older adults. Lorazepam may be given IV in a dose of 1 to 4 mg, depending
on the severity of the withdrawal. Dosing can be repeated at 5 to 15-minute Prior History of Seizures During Withdrawal
intervals for patients in severe withdrawal. Although it is not ideal, an intra- The risk of seizure increases significantly in alcoholic patients with man-
muscular dose of 1 to 4 mg can be used every 30 to 60 minutes until the ifestations of alcohol withdrawal who relate a history of alcohol with-
patient is calm and then every hour, as needed, for light somnolence. drawal seizure. Detoxification with benzodiazepines reduces alcohol
Diazepam is another commonly used benzodiazepine to treat withdrawal seizures and should be initiated early because most seizures
patients with alcohol withdrawal. When given IV, it has a rapid onset occur within the first 24 hours after alcohol withdrawal. An initial dose
(1 to 3 mins) and a duration of 1 to 2 hours, though its half-life can be of 2 mg of lorazepam or 5 mg of diazepam can be given IV. These doses
increased significantly in patients with liver dysfunction. Since diaze- frequently need to be repeated, as noted in the Benzodiazepine section.
pam has a more rapid onset than lorazepam, its dosing interval can be
much shorter. One such dosing strategy involves giving diazepam 5 mg Abnormal Neurologic Examination
IV every 5 to 10 minutes for patients with major withdrawal symptoms. New-Onset Partial Seizures. Partial seizures account for up to
The dose can be repeated in 5 to 10 minutes. If the second dose of 5 mg 50% of alcohol-related seizures. Conversely, approximately 20% of
is not working, consider 10 mg for the third and fourth doses every 5 patients with partial alcohol-related seizures have structural lesions—
to 10 minutes. If this is not effective, consider 20 mg for the fifth and hematomas, tumors, vascular abnormalities, or stroke. These primary
subsequent dose until adequate sedation has been obtained. causes of partial alcohol-related seizure, such as prior head trauma,
Butyrophenones. Haloperidol, a dopamine antagonist, can be may be easily missed in the history taking. As a result, an emergent CT
considered in patients with major alcohol withdrawal or delirium scan of the head is indicated to evaluate new-onset partial seizures. The
tremens and acute agitation or behavioral issues not responding to patient with a history of a focal alcohol-related seizure who has been
IV benzodiazepines. However, antipsychotics should never be used previously evaluated does not require an emergency CT scan provided
alone or as a first-line treatment for alcohol withdrawal as they do not a return to baseline occurs promptly.
treat the underlying pathophysiology. Haloperidol has little effect on Patients Taking Anticonvulsants. A patient currently taking
myocardial function or respiratory drive, and its safety and efficacy antiepileptic drugs for an antecedent seizure disorder who presents
by the IV, intramuscular, or oral route in the ED has been established. with a seizure while intoxicated falls into a different category. Such
an episode could be an isolated event in a usually compliant patient of laboratory analysis are within normal limits may be released with
without a history of chronic alcohol abuse. In this patient, a seizure in appropriate medications and aftercare instructions. Nevertheless, the
the setting of a subtherapeutic antiepileptic drug level may represent patient can benefit from treatment for the underlying disease of alco-
the consequences of noncompliance with antiepileptic medication, co- holism and should be advised or referred accordingly.
ingestants, or sleep deprivation versus alcohol withdrawal seizure.
Seizures
The alcoholic patient with a first-time, alcohol-related seizure may be
DISPOSITION discharged to a suitable social situation in these situations: (1) when the
Most patients with acute alcohol intoxication are managed in the ED patient’s alcohol withdrawal is mild and controlled by supportive care
or observation unit and then discharged home. Patients who achieve or low-dose benzodiazepines; (2) the diagnostic evaluation, including a
sufficient sobriety to be ready for discharge are offered detoxification head CT scan, is unremarkable; (3) the patient has had fewer than two
or alcohol treatment programs. Most alcoholics suffer from a combi- seizures; and (4) the patient has been observed to be alert and oriented,
nation of medical, psychiatric, and social problems. Hospitalization with stable vital signs and physical examination findings, normalized
may be necessary to diagnose and treat these multiple problems. More- laboratory study results since the last seizure, and appropriate outpa-
over, with alcoholics who are no longer able to care for themselves, tient follow-up can be ensured.
hospitalization is often dictated for this reason alone. Unfortunately, Patients with a documented history of alcohol-related seizures can
many managed care and Medicaid plans limit or do not cover inpa- be discharged if they have had no more than two alcohol-related sei-
tient detoxification. In choosing medical versus psychiatric admission, zures during a 6-hour period, with a lucid interval between seizures,
a medical illness usually takes priority. Optimal outpatient therapy for and are observed to be seizure-free and at baseline mental and phys-
chronic alcoholics includes the involvement of concerned family or ical status for at least 6 hours after their last alcohol-related seizure.
friends to ensure that the patient takes his or her medications properly, Three to five brief, self-limited seizures may occur with alcohol with-
keeps follow-up appointments, abstains from alcohol, and maintains drawal seizures. We recommend prolonged observation in the ED or
an adequate diet. Alcoholic patients who undergo outpatient treat- observation unit for patients with two or more seizures because of the
ment need close supervision; therefore, a follow-up clinic appointment potential for deterioration to status epilepticus. Such patients should be
within 24 to 48 hours should be considered. observed until at least 6 hours have passed since their last seizure and
they have a normal mental status and neurologic examination.
Acute Intoxication Patients with partial seizures or focal neurologic findings on phys-
Acute intoxication alone seldom requires admission. However, a com- ical examination require admission unless these findings have been
bined alcohol-drug overdose or associated medical, psychiatric, or previously documented. Patients with seizures associated with head
social problems may require hospitalization. Acute alcohol intoxica- trauma or mixed alcohol-drug withdrawal are admitted. Status epilep-
tion is a diagnosis of exclusion reached after adequate observation to ticus or recurrent seizures during ED observation indicate a lack of
ensure that the altered mental status resolves and that the patient is seizure control and require further hospitalization, often in a critical
hemodynamically stable. care setting.
Alcohol levels that may be tolerated by an adult can be lethal in
children. It is prudent to admit young pediatric patients with acute Psychiatric and Social Problems
intoxication and ensure close psychosocial follow-up for adolescent Alcoholic patients requiring admission with acute intoxication,
patients. Children presenting with hypoglycemia or medical compli- alcohol-related seizure, alcohol withdrawal, or medical or surgical
cations should be admitted. Child abuse or neglect should always be disorders are usually best managed in acute care units rather than by
considered. a general psychiatric service. Some psychiatric and social conditions
in the alcoholic can be better handled on a general psychiatric unit—
Alcohol Withdrawal psychosis, exacerbation of schizophrenia, depression with suicidal
Outpatient treatment consists of lorazepam, 1 to 2 mg TID tapered tendencies, any patient who is a danger to self or others, or alcoholic
over 3 to 6 days, chlordiazepoxide, 25 to 100 mg TID tapered over 3 to hallucinosis with an otherwise clear sensorium.
6 days, or diazepam, 30 mg once daily tapered over 5 days, depending Patients who are no longer able to care for themselves may also
on the severity of symptoms. Adequate diet, abstinence, and participa- require admission. Although these patients’ ultimate destination is a
tion in a rehabilitation program in the community are also desirable. rehabilitation center or a border care program, hospitalization may be
Any patient requiring 300 mg of chlordiazepoxide or 60 mg of diaze- necessary to rule out medical or psychiatric illness and treat impending
pam/day to control withdrawal should be considered for admission. withdrawal symptoms. Patients who wish to stop drinking are usually
Patients with signs of major withdrawal (fever, hallucinations, con- referred to a detoxification unit for treatment of impending withdrawal.
fusion, extreme agitation) require admission for close monitoring, Psychosocial interventions are the basis of long-term treatment, but
serial neurological checks, and repeated medication dosing. Risk fac- medications are also often used. However, the data surrounding the
tors for clinical deterioration in patients with moderate to severe with- use of medications are weak.45 The FDA has approved three medica-
drawal include older patients who may be at greater risk for delirium tions for alcohol dependence in the United States: disulfiram, naltrex-
tremens and may not tolerate the systemic stress of major withdrawal. one, and acamprosate. A fourth drug, nalmefene (oral), is approved
Patients with delirium tremens generally require ICU admission. Cri- throughout the European Union and is taken on an “as needed” basis
teria for ICU admission may also include patients with hemodynamic prior to anticipated drinking occasions.
instability, electrolyte or acid-base disturbance, persistent hyper or Other medications for AUDs have shown limited efficacy, and
hypothermia, rhabdomyolysis, renal insufficiency, and co-morbid con- there is a high degree of variability in treatment response. Baclofen
ditions such as severe infection or pancreatitis. for the long-term treatment of alcohol dependence shows no clear-
Patients with mild alcohol withdrawal can be observed in the ED. cut evidence from randomized, double-blind studies.1,45 Gabapentin
After 4 to 6 hours of observation and treatment, the alert-oriented is used as monotherapy or as an add-on pharmacotherapy in out-
patient whose vital signs, physical examination findings, and results patient settings in the control of alcohol consumption and craving
and in helping patients achieve abstinence.46 Ondansetron may show than no intervention at all to reduce binge drinking among college-
benefit in early-onset but not in late-onset alcoholics. Risperidone aged students. The Internet could be an economic and acceptable form
for agitation has minimal effects on vital signs with or without a of delivering brief interventions and is a preferred approach to reach
benzodiazepine, suggesting that risperidone is a safe option for binge drinkers in college.50
patients presenting with acute agitation even in the setting of alcohol Most communities have an Alcoholics Anonymous (AA) chapter
intoxication.47 or treatment center for anyone who desires help with alcohol. Sober-
Brief intervention and screening (SBIRT—screening, brief inter- ing centers can have a prominent role in the care for those with acute
vention, and referral to treatment) can reduce alcohol consumption alcohol intoxication, particularly those individuals with chronic public
and is feasible and effective in the ED.48 An ultra-BI (less than 10 min- intoxication who are likewise homeless. In smaller communities, clergy
utes face-to-face time) or employing technology such as computers and or social workers can usually arrange rehabilitation. Psychosocial treat-
mobile phones reduces previously identified barriers to ED clinician ments such as brief counseling, motivational enhancement therapy, the
utilization.49 Internet-based interventions show promise for reduc- community reinforcement approach, guided self- change, behavior
ing alcohol consumption, especially among those meeting criteria for contracting, and social skills training were among the top ten most
hazardous or harmful drinking. Telephone contact after the ED visit effective interventions for AUDs, together with various pharmacolog-
may be another effective tool to screen injured patients for hazardous ical interventions.
drinking and offer a brief intervention while avoiding interruptions to The references for this chapter can be found online at ExpertConsult.
patient flow. Providing internet-based interventions is more effective com.

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1860.e1
1860.e2 PART IV Environment and Toxicology
C H A P T E R 1 3 7 : Q U E S T I O N S A N D A N S W E R S
1. A 56-year-old man presents with alcohol intoxication. He is drowsy 4. Given that brief intervention and screening (SBIRT—screening,
but arousable to painful stimuli. He is confused. Vital signs are brief intervention, and referral to treatment) can reduce alcohol
within normal limits, and there is no evidence of trauma. Routine consumption and is feasible and effective in the emergency depart-
testing should include which of the following first? ment, which of the following interventions are particularly effective
a. Basic metabolic panel and preferred for college students?
b. Glucose a. AA meetings
c. Serum blood ethanol level b. In-person counseling
d. Urine toxicology screen c. Internet-based interventions
Answer: b. Chronic alcoholics have decreased glycogen stores and fre- d. Pharmacologic-based interventions
quently experience hypoglycemia. While a basic metabolic panel could Answer: c. Studies show that providing internet-based interventions
provide you with additional information, the primary electrolyte of is more effective to reduce binge drinking among college students. The
interest is glucose. Serum blood ethanol and urine drug screens may be Internet could be an economic and acceptable form of delivering brief
helpful in the undifferentiated patient with altered mental status, but interventions and is a preferred approach to reach binge drinkers in
these patients still require a bedside glucose test first. college. AA Meetings, counseling, and pharmacologic treatment are
2. A 42-year-old woman presents with agitation, confusion, and fever. likely to occur later in the treatment process.
She is noted to experience visual hallucinations during your inter- 5. A 28-year-old man with alcohol use disorder presents with fever,
view. Her vital signs reveal hypertension, tachycardia, and fever. chills, and a productive cough. The x-ray reveals right lower lobe
Physical examination is otherwise unremarkable. Diagnostic stud- pneumonia. Which of the following is the most likely etiology of
ies (including head CT scan and lumbar puncture) are nonspecific. this infection?
Which diagnosis is most consistent with this patient’s presentation? a. Klebsiella pneumoniae
a. Acute schizophrenia b. Mycobacterium tuberculosis
b. Alcohol withdrawal c. Mycoplasma pneumoniae
c. Anticholinergic poisoning d. Streptococcus pneumoniae
d. Thyrotoxicosis Answer: d. Pneumococcal pneumonia is the most common type of
Answer: b. Patients are often confused and agitated and exhibit auto- pneumonia in both healthy individuals and heavy alcohol users. Other
nomic instability, resulting in hypertension, tachycardia, and, often, infections such as Klebsiella pneumoniae and Mycobacterium are also
fever. Hallucinations are typically visual. Schizophrenia typically increased in patients with alcohol use disorders and cause dispropor-
results in auditory hallucinations and, although patients are delu- tionate rates of lung infection, but not the most common. Klebsiella
sional, they are not typically confused. Patients with anticholinergic pneumoniae, classically associated with alcoholism, is currently more
poisoning typically present with confusion but also have dry mouth, common in patients with cytotoxic chemotherapy, hematologic malig-
dry eyes, dry skin, hypoactive bowel sounds, and urinary retention. nant disease, and transplantation than in the chronic alcoholic.
Thyrotoxicosis patients exhibit lid lag, tremor, and gastrointestinal
complaints.
3. In addition to altered mental status (AMS), which of the following
is a criterion for diagnosing Wernicke encephalopathy?
a. Alcohol intoxication
b. Fever
c. Oculomotor abnormalities
d. Seizure
Answer: c. Criteria to diagnoses Wernicke encephalopathy require two
of the following: (1) dietary deficiencies; (2) oculomotor abnormalities;
(3) cerebellar dysfunction; and (4) AMS or mild memory impairment.
Although it is most often diagnosed in alcoholics, alcohol consumption
is not required. Treatment is with replacement of dietary deficiencies,
particularly thiamine. Magnesium levels should be checked and treated
if low. Magnesium is a cofactor for thiamine and is often depleted in
chronic alcoholics.

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Alcohol-Related Disease: John T. Finnell

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137

TABLE 137.1 Terms and Definitions of Unhealthy Alcohol Use

TABLE 137.1 Terms and Definitions of Unhealthy Alcohol Use—cont’d.

TABLE 137.4 Cardiovascular Effects of Alcohol

Pulmonary Effects Liver Damage

Cirrhosis deficiencies, oculomotor abnormalities (nystagmus being the most

TABLE 137.5 Electrolyte Disturbances30

Platelet Disorders Hemostasis

TABLE 137.6 The NIAAA Youth Alcohol Screening Tool

thrombin time, prothrombin time and INR, and partial thrombo-

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