Alcohol related disorders

By Dr Yebeltal Yamlksira R1
November,2020
 Outline

 Introduction
 Epidemiology
 Effects of alcohol
 Etiology
 Clinical features and Diagnosis of Alcohol related disorders
 Differential Diagnosis
 Treatment
 introduction

 Alcohol use disorders (AUDs) have special relevance to psychiatry.

 Alcohol is a potent drug that causes both acute and chronic changes in
almost all neurochemical systems, with the result that heavy drinking can
produce serious temporary psychological symptoms including
 Depressions, anxiety, and psychoses.
 Several preexisting psychiatric diagnoses, including antisocial
personality, bipolar, and schizophrenic disorders, increase the risk for
later AUDs.
 DEFINITION AND COMPARATIVE NOSOLOGY

Alcohol Use Disorders

 In the DSM-5, an AUD is diagnosed as the repeated presence of at least
two of 11 major areas of life impairments related to alcohol that cluster
together in a syndrome over approximately the same 12-month period.
 The criteria are very similar to those listed for abuse and dependence in
DSM-IV, with the exception that
 One DSM-IV item was dropped (legal problems) and
 One new item was added (craving).
 In ICD-10 the diagnosis of alcohol dependence requires three or more
items clustering together.
 ICD-10 also lists a second potentially less severe diagnosis of harmful use,
defined as repeated interference with psychological and physical health
functioning.
 Persons with harmful use are not likely to meet criteria for DSM-5 AUD,
and vice versa.
Type 2 or type B alcoholism.
 a more severe early onset of an AUD, accompanied by criminality and
problems with other drugs,
 This approach reflects the fact that most early-onset medical and psychiatric
disorders have a more severe course.
 Much of the prognostic significance of type 2 or type B alcoholism rests with
concomitant conduct disorder and antisocial personality disorder in early
onset substance use disorders.
 An onset after age 40 tends to be associated with less severe social
difficulties and more subtle AUD signs and symptoms, but a greater
likelihood of medical problems.
 Severity and Remission

 AUD severity can be classified as

 Mild (two to three criteria endorsed)

 Moderate (with four to five criteria met), or

 Severe (with 6 or more of the 11 criteria)

 Remission criteria in DSM-5 are based on the fact that the highest risk for
relapse is in the first 3 to 12 months of recovery.
 Early remission occurs if none of the 11 AUD criteria (other than craving)
were experienced during the prior 3 months,
 Sustained remission indicates that no such problems were experienced for
at least 12 months.
 EPIDEMIOLOGY

 About 90 percent of Americans have consumed alcohol at some time in their

lives
 By the end of high school, 80 percent of students have imbibed alcohol, and
more than 60 percent have been intoxicated
 During any year,

 65 percent of men were drinkers

 a ratio of the proportions of men versus women who consumed alcohol of

approximately 1.3 men to 1.0 women.
 The highest drinking frequency and quantity usually occurs from the late
teens to the mid-20s.
 The lifetime risk for AUDs is approximately 15 percent for men and 10
percent for women, with 1-year prevalence rates of about 6 percent
 The peak ages of onset of an AUD are from the early 20s to about age 40
 One study done in ethiopia showed that
 The overall prevalence of lifetime alcohol consumption was 49.3%, and
 40.7% of the study participants reported consumption of alcohol in the
past 30 days, defined as current drinkers.
 Heavy episodic drinking was reported by 12.4% of the participants
(20.5% males and 2.7% females)
 According to the 2011 Demographic and Health Survey (DHS) report by
Central Statistics Authority (CSA) of Ethiopia, a national survey involving
a representative sample from the age group 15–49 year old,
 45 % of women and 53 % of men reported a history of alcohol
consumption in their life time
 48 % of women and 53 % men of ever drinkers reported consumption
of alcohol six or more days in the past month.
 Consumption rate was higher in urban areas, and the rates increased
with age for both men and women
 Prevalence Studies done in different parts of Ethiopia using the four-item
“CAGE” screening questionnaire have shown that hazardous alcohol
drinking was 3.7 % and 2.7 % in rural and urban areas respectively.
 In another study carried out in a semi-nomadic population in Southern
Ethiopia using a structured diagnostic interview, the Composite
International Diagnostic Interview (CIDI), the prevalence rate of alcohol
dependence was 1.6 %,
 More in men than women, 3.7 % and 0.1 % respectively

 Homemade alcoholic beverages include tella (local beer with alcohol

content 2-4 %), tej (honey wine with alcohol content 7-11 %)
and araqe (strong distilled liquor with alcohol content up to 45 %)
 Comorbid Conditions

 The psychiatric diagnoses most commonly associated with the alcohol-related

disorders are
 other substance-related disorders, antisocial personality disorder, mood
disorders, and anxiety disorders.
Antisocial Personality Disorder
 A relation between antisocial personality disorder and alcohol-related
disorders has frequently been reported.
 Some studies suggest that antisocial personality disorder is particularly
common in men with an alcohol-related disorder and can precede the
development of the alcohol-related disorder
Mood Disorders
 Up to 80 percent of men and women with AUDs report temporary symptoms of sadness
or anxiety during the course of their disorder.
 in at least 40 percent these temporary symptoms become intense and persistent enough to
meet criteria for major psychiatric conditions, such as major depressive episodes or
panic disorder,
 Depression is more common in women than in men with these disorders and is likely to
occur in patients with alcohol-related disorders who have a high daily consumption of
alcohol and a family history of alcohol abuse.
 These individuals are at great risk for attempting suicide.

 Some clinicians recommend antidepressant drug therapy for depressive symptoms that
remain after 2 to 3 weeks of sobriety.
 Patients with bipolar I disorder are thought to be at risk for developing an alcohol-related
disorder; they may use alcohol to self-medicate their manic episodes
Anxiety Disorders
 Many persons use alcohol for its efficacy in alleviating anxiety.

 25 to 50 percent of all persons with alcohol-related disorders also meet the diagnostic
criteria for an anxiety disorder.
 Phobias and panic disorder are particularly frequent comorbid diagnoses in these patients.

 Used in an attempt to self-medicate symptoms of agoraphobia or social phobia,

 Alcohol-related disorder is likely to precede the development of panic disorder or

generalized anxiety disorder.
Suicide
 Most estimates of the prevalence of suicide among persons with alcohol-related disorders
range from 10 to 15 percent,
 Factors that have been associated with suicide among persons with alcohol-related disorders
include
 The presence of MDE, weak psychosocial support systems, a serious coexisting
medical condition, unemployment, and living alone.
 ALCOHOL’S EFFECTS

 A standard alcoholic drink in the United States is defined as containing 10 to 12

g of ethanol, which is roughly the amount in
 12 oz of beer (containing ~3.6 percent ethanol), 5 oz of table wine (~12
percent ethanol), and about 1.5 oz of 80-proof spirits (~40 percent ethanol).
 For an average 70-kg (155-lb) person who has average body fat, one drink is
likely to raise the blood alcohol level by approximately 15 to 20 mg/dL (the
same as 0.015 to 0.020 g/dL), with roughly the same amount metabolized in
about an hour.
 Faster absorption from the digestive tract occurs on an empty stomach and if
alcohol is taken as a carbonated beverage.
Alcohol as a Depressant Drug
 Depressants are drugs that produce somnolence and decreased neuronal
activity, but are not powerful in attenuating pain.
 Thus, alcohol, benzodiazepines, barbiturates, and related drugs are
considered depressants and produce similar intoxications,
 Are potentially lethal in overdose (especially when multiple
depressants are taken together),
 Have cross-tolerance with other depressants, and can produce physical
dependence with similar withdrawal syndromes
Neurochemical Effects of Ethanol
 γ-aminobutyric acid (GABA) especially on the GABA-A receptor (GABAA),

 The most potent effects contributing to the sedating, sleep-inducing,

anticonvulsant, and muscle-relaxing properties of alcohol.
 Glutamate-gated ionophoric receptors, N- methyl-d-aspartate (NMDA)

 with dampened stimulatory effects during intoxication and heightened activity

during withdrawal.
 Dopamine and its metabolites,

 Alcohol acutely increases concentration and chronic drinking changes dopamine

receptor numbers and sensitivity, with related effects on intoxication and craving
 Alcohol also increases serotonin in the synapses and upregulates serotonin
receptors.
 alcohol acutely enhances the functioning of the opioid-related brain systems and
impacts adenosine, acetylcholine, and cannabinoid 1 (CB1) receptors
 Behavioral Effects

 At a level of 0.05 percent alcohol in the blood, thought, judgment, and restraint are loosened
and sometimes disrupted.
 At a concentration of 0.1 percent, voluntary motor actions usually become perceptibly clumsy.

 In most states, legal intoxication ranges from 0.1 to 0.15 percent blood alcohol level.

 At 0.2 percent, the function of the entire motor area of the brain is measurably depressed, and
the parts of the brain that control emotional behavior are also affected.
 At 0.3 percent, a person is commonly confused or may become stuporous

 At 0.4 to 0.5 percent, the person falls into a coma.

 At higher levels, the primitive centers of the brain that control breathing and heart rate are
affected, and death ensues secondary to direct respiratory depression or the aspiration of
vomitus.
 Tolerance
 In behavioral tolerance

 a person learns through practice how to perform tasks effectively while

experiencing the effects of alcohol.
 Pharmacokinetic tolerance

 involves adaptations of alcohol metabolizing systems to rid the body of

alcohol more rapidly.
 pharmacodynamic or cellular tolerance

 reflects an adaptation of the nervous system so that it can function

despite high blood alcohol concentrations by resisting the actions of
alcohol on the cell.
 Blackout

 A blackout is a memory impairment (anterograde amnesia) for the

period when a person was drinking heavily but remained awake.
 This phenomenon is the result of the ability of high doses of any brain
depressant (e.g., alcohol or benzodiazepines) to interfere with the
acquisition and solidification of memory.
 As many as 50 percent of drinkers have at some time had a blackout, and

 Repeated experiences of this effect of high doses of alcohol is a warning

sign that an AUD may be present.
 Sleep Impairment

 Alcohol can help a person fall asleep, but after two or more drinks, the sleep
pattern can be impaired.
 A heavy drinker is likely to awaken after several hours and have problems going
back to sleep.
 Alcohol suppresses rapid eye movements (REM) sleep, inhibits stage 4 sleep

 Is associated with frequent alternations between sleep stages (sleep

fragmentation), with more intense and disturbing dreams.
 in individuals with AUDs for whom sleep stages might not return to normal
until three or more months of abstinence.
 More sleep problems following abstinence are associated with a greater risk for
relapse.
 Cerebellar Degeneration

 Characterized by

 Unsteady gait

 Impaired standing steadiness, and

 Mild nystagmus,

 Cerebellar degeneration results from combinations of effects of ethanol,

acetaldehyde, and vitamin deficiencies.
 Treatment requires total abstinence and vitamin supplementation, although
complete recovery is not usual
 Effects on the Rest of the Body

 One to two drinks per day of any alcoholic beverage might decrease the
risks for myocardial infarction and thrombotic stroke
 Through decreasing platelet aggregation and enhancing high-density
lipoprotein (HDL) cholesterol levels
 An additional potential cardioprotective action, unique to red wine, may
occur through antioxidant flavonoids or the inhibition of a vasoconstrictor
(endothelin-1).
 Low doses of alcohol may also decrease the risks for some dementias,
peripheral arterial disease, and gallstones
 Peripheral Neuropathy

 Approximately 10 percent of people with AUDs develop a deterioration of

functioning of nerves to the hands and feet, called peripheral neuropathy.
 The symptoms include numbness of the hands and feet, often bilateral,
frequently accompanied by tingling and paresthesias.
 Although the condition is usually relatively mild and often improves with
abstinence, in some individuals the pain and numbness may be permanent.
 Gastrointestinal Problems
 Acute and potentially severe inflammation of the esophagus or stomach,
often accompanied by vomiting and bleeding.
 In the presence of dilated esophageal veins, as seen with cirrhosis, it can
induce a potentially lethal blood loss.
 produce a reversible swelling of the liver often described as a fatty liver.

 Inflammation of liver cells accompanied by increases in liver function tests is

called alcoholic hepatitis
 approximately 15 percent of patients with AUDs develop cirrhosis leading to
varices, ascites and hepatic encephalopathy
 Perhaps 10 percent of people with AUDs develop an inflammation of the
pancreas or acute pancreatitis
Cardiovascular Problems
 Heavy alcohol intake and associated withdrawal symptoms can increase blood
pressure and elevate both LDL cholesterol and triglycerides,
 enhancing the risk for myocardial infarction and thrombosis.

 Alcoholic cardiomyopathy)

 The leading cause of early deaths associated with AUDs is heart disease.

Blood-Producing Systems
 Consumption of four to eight drinks or more per day decreases the production
of white blood cells and impairs the ability of those cells to migrate to sites
of infection.
 Such drinking can also increasing the average size of red cells (the mean
corpuscular volume [MCV]), and can impair the production of blood platelets.
 Laboratory Tests.

 The adverse effects of alcohol appear in common laboratory tests, which can
be useful diagnostic aids in identifying persons with alcohol-related
disorders.
 The γ-glutamyl transpeptidase levels are high in about 80 percent of those
with alcohol-related disorders, and
 The mean corpuscular volume (MCV) is high in about 60 percent, more
so in women than in men.
 Other laboratory test values that may be high in association with alcohol
abuse are those of uric acid, triglycerides, aspartate aminotransferase
(AST), and alanine aminotransferase (ALT).
 Fetal Alcohol Effects

 Alcohol and acetaldehyde have deleterious effects on the developing fetus. Both substances
cross the placenta, and in high enough doses can produce fetal death and spontaneous
abortion.
 At least 5 percent of surviving infants of heavy-drinking mothers evidence mixtures of a fetal
alcohol syndrome that can include
 low IQ, a small head, low birth weight, facial abnormalities (e.g., flat bridge of the
nose, absent philtrum, and epicanthal eye folds), an atrial septal heart defect, and
syndactyly.
 None of these are reversible, and the cognitive defects remain throughout life.

 Additional less obvious problems are part of a range of fetal alcohol spectrum disorders
(FASD), including mild to moderate cognitive difficulties
 e.g., impaired executive functioning in attention and planning, problems in letter
and word fluency, difficulties with impulse control, and may carry an enhanced risk
for SUDs.
Cancer
 AUDs are associated with high rates of most cancers, especially tumors of
the head, neck, esophagus, stomach, liver, colon, lungs, and breast.
 cancer is the second cause of premature death in individuals with AUDs

Other Problems
 High doses of alcohol adversely affect almost all body systems, cutting a
decade or more off the lifespan even for people with higher
socioeconomic and educational status.
 Additional body effects related to AUDs include

 Testicular atrophy; bone fractures; a host of eye effects, including

cataracts; dental difficulties; skeletal muscle wasting; and greater
risk for accidents
 ETIOLOGY

 Series of genetic influences combine to explain approximately 60 percent

of the proportion of risk for alcoholism, with environment responsible for
the remaining proportion of the variance.
 The combination of a series of psychological, sociocultural, biological,
and other factors that are responsible for the development of severe,
repetitive alcohol-related life problems.
 Genetic Theories
 Four lines of evidence support the conclusion that alcoholism is genetically influenced.

1. 3-4 fold increased risk for severe alcohol problems is seen in close relatives of alcoholic
people.
 The rate of alcohol problems increases with the number of alcoholic relatives, the
severity of their illness, and the closeness of their genetic relationship to the person
under study.
2. The rate of similarity, or concordance, for severe alcohol-related problems is significantly
higher in identical twins of alcoholic individuals than in fraternal twins
3. The adoption-type studies have all revealed a significantly enhanced risk for alcoholism in
the offspring of alcoholic parents, even when the children had been separated from their
biological parents.
4. Finally, studies in animals support the importance of a variety of yet-to-be-identified genes
in the free-choice use of alcohol, subsequent levels of intoxication, and some consequences.
 Psychological Theories

 Alcohol can be used to

 Reduce tension

 Decrease the effects of psychological pain.

 Decreases feelings of nervousness and

 Helps cope with the day-to-day stresses of life.

 Enhanced feeling of well-being and an improved ease of interactions.

 To enhance feelings of being powerful and sexually attractive

 Add to the relief of withdrawal symptoms

 Psychodynamic Theories

 Perhaps related to the disinhibiting or anxiety-lowering effects of lower

doses of alcohol is the hypothesis that some people may use this drug to
help them deal with
 Self-punitive harsh superegos and
 To decrease unconscious stress levels.
 In addition, classic psychoanalytical theory hypothesizes that at least some
alcoholic people may have become fixated at the oral stage of
development and use alcohol to relieve their frustrations by taking the
substance by mouth
Behavioral Theories
 Expectations about the rewarding effects of drinking, cognitive attitudes
toward responsibility for one’s behavior, and subsequent reinforcement
after alcohol intake
 All contribute to the decision to drink again after the first experience with
alcohol and to continue to imbibe despite problems.

Sociocultural Theories
 Environmental events, presumably including cultural factors, account for as
much as 40 percent of the alcoholism risk.
 Social and psychological theories are probably highly relevant, because they
outline factors that contribute to the onset of drinking, the development of
temporary alcohol-related life difficulties, and even alcoholism.
 Environmental

 Environmental risk and prognostic factors may include

 Cultural attitudes toward drinking and intoxication

 The availability of alcohol (including price),

 Acquired personal experiences with alcohol, and stress levels.

 Additional potential mediators of how alcohol problems develop in

predisposed individuals include
 Heavier peer substance use

 Exaggerated positive expectations of the effects of alcohol, and

 Suboptimal ways of coping with stress.

 Gender-Related Diagnostic issues

 Males have higher rates of drinking and related disorders than females.
However, because
 Females generally weigh less than males

 Have more fat and less water in their bodies, and

 Metabolize less alcohol in their esophagus and stomach,

 They are likely to develop higher blood alcohol levels per drink than
males.
 Females who drink heavily may also be more vulnerable than males to
some of the physical consequences associated with alcohol, including
liver disease.
 Alcohol-Related Disorders

 Alcohol Use Disorder

 Alcohol Intoxication
 Alcohol Withdrawal
 Other Alcohol-induced Disorders
 Unspecified Alcohol-Related Disorder
Specify if:
 In early remission:
 After full criteria for alcohol use disorder were previously met, none of the
criteria for alcohol use disorder have been met for at least 3 months but for less
than 12 months (with the exception that Criterion A4, “Craving, or a strong
desire or urge to use alcohol,” may be met).
 In sustained remission:
 After full criteria for alcohol use disorder were previously met, none of the
criteria for alcohol use disorder have been met at any time during a period of 12
months or longer (with the exception that Criterion A4, “Craving, or a strong
desire or urge to use alcohol,” may be met).
Specify if:
 In a controlled environment:
 This additional specifier is used if the individual is in an environment where
access to alcohol is restricted.
 Development ,Course and prognosis

 The first episode of alcohol intoxication is likely to occur during the mid-teens.
 Alcohol related problems that do not meet full criteria for a use disorder or
isolated problems may occur prior to age 20 years
 The age at onset of an alcohol use disorder with two or more of the criteria
clustered together peaks in the late teens or early to mid 20s.
 alcohol-related disorders develop by their late 30s
 An earlier onset of alcohol use disorder is observed in adolescents with
preexisting conduct problems and those with an earlier onset of intoxication.
 An important development in at least 20 percent of people with AUDs is a
spontaneous remission.
 Such outcomes are most likely for those with

 Fewer alcohol-related problems, more social supports, jobs,

greater life stability, and no concomitant ASPD or SUD diagnoses.
 However, if drinking continues, the person potentially decreases their
lifespan by at least 10 years as a result of the alcohol-related pathologies
 This early death also reflects a 10 percent risk for suicide, usually during a
depressive episode.
 Fewer than half of people with AUDs ever receive treatment for their
disorder.
 However, once they complete a program, a majority do well and develop
long-term, often permanent, abstinence.
 Good outcomes are most likely in patients without ASPD, and in the
context of having a job and close family contacts.
 These attributes predict about a 60 percent chance for >1 year of
abstinence, with 1-year rates associated with a good chance for continued
abstinence over an extended period.
 Individuals with independent major psychiatric conditions, such as
ASPD, schizophrenia, and bipolar I disorder, are likely to run the course
of their independent psychiatric illness as well
 Functional Consequences of AUD

 Alcohol use disorder can impact major areas of life functioning likely to be
impaired including
 Driving and operating machinery, school and work

 Interpersonal relationships and communication, and health.

 Absenteeism from work, job-related accidents, and low employee

productivity.
 Homelessness

 Significant increase in the risk of accidents, violence, and suicide.

 It is estimated that one in five intensive care unit admissions in some
urban hospitals is related to alcohol
 40% of individuals in the United States experience an alcohol-related
adverse event at some time in their lives,
 Alcohol accounts for up to 55% of fatal driving events.

 Severe alcohol use disorder, especially in individuals with antisocial

personality disorder, is associated with the commission of criminal acts,
including homicide.
 Severe problematic alcohol use also contributes to disinhibition and
feelings of sadness and irritability, which contribute to suicide attempts
and completed suicides.
 In the United States, the average age at first intoxication is approximately
15 years, with the highest prevalence at approximately 18-25 years.
 Frequency and intensity usually decrease with further advancing age.
 The earlier the onset of regular intoxication, the greater the likelihood the
individual will go on to develop alcohol use disorder
 Withdrawal phenomena usually begin within about 8 hours of abstinence,
peak on the second or third day, and diminish by the fourth or fifth day.
 The symptoms persist in a more mild form for as long as 3 to 6 months as
part of a protracted withdrawal syndrome, the symptoms of which might
contribute to relapse.
 Alcohol withdrawal, even without delirium, can be serious; it can include
seizures and autonomic hyperactivity.
 Conditions that may predispose to, or aggravate, withdrawal symptoms
include fatigue, malnutrition, physical illness, and depression
 The classic sign of alcohol withdrawal is tremulousness, although the
spectrum of symptoms can expand to include psychotic and perceptual
symptoms (e.g., delusions and hallucinations), seizures, and the symptoms
of delirium tremens (DTs), called alcohol delirium in DSM-5.
 Tremulousness (commonly called the “shakes” or the “jitters”) develops 6
to 8 hours after the cessation of drinking, the psychotic
 Perceptual symptoms begin in 8 to 12 hours,

 Seizures in 12 to 24 hours, and DTs anytime during the first 72 hours,

 The syndrome of withdrawal sometimes skips the usual progression and,

for example, goes directly to DTs.
 Withdrawal Seizures.

 Seizures associated with alcohol withdrawal are stereotyped, generalized, and

tonic–clonic in character.
 Patients often have more than one seizure 3 to 6 hours after the first seizure.

 Status epilepticus is relatively rare and occurs in less than 3 percent of patients.

 Seizure activity in patients with known alcohol abuse histories should still
prompt clinicians to consider other causative factors, such as
 Head injuries, CNS infections, CNS neoplasms, other cerebrovascular
diseases; hypoglycemia, hyponatremia, and hypomagnesemia—all of
which can also be associated with seizures.
 Alcohol withdrawal delirium
(delirium tremens)
 The essential feature of the syndrome is delirium occurring within 1 week after a
person stops drinking or reduces the intake of alcohol
 Occur in the context of withdrawal and can include

 Agitated, confused state,

 fluctuating levels of psychomotor activity, ranging from hyperexcitability to

lethargy
 Disturbance of consciousness and cognition,

 Perceptual distortions, most frequently visual or tactile hallucinations; or

(rarely) auditory hallucinations.
 Autonomic hyperactivity such as tachycardia, diaphoresis, fever, anxiety,
Insomnia, and hypertension; and
 Alcohol withdrawal delirium is a medical emergency that can result in
significant morbidity and mortality.
 Patients with delirium are a danger to themselves and to others. Because of

 The unpredictability of their behavior, patients with delirium may be

assaultive or suicidal or may act on hallucinations or delusional thoughts
as if they were genuine dangers.
 Untreated, DTs has a mortality rate of 20 percent,

 It is likely that a clinically relevant medical condition may be present

 Liver failure, pneumonia, gastrointestinal bleeding

 Sequelae of head trauma, hypoglycemia, an electrolyte imbalance,

postoperative status.
 Alcohol-induced disorders

 These are diagnosed instead of alcohol intoxication or alcohol withdrawal

only when the symptoms are sufficiently severe to warrant independent
clinical attention.
 Are likely to improve without formal treatment in a matter of days to weeks
after cessation of severe intoxication and/or withdrawal.
 When symptoms are observed only during a delirium, they should be
considered part of the delirium and not diagnosed separately
 Consider the intake of substances of abuse in the context of a preexisting
mental disorder are likely to result in an intensification of the preexisting
independent syndrome
 all alcohol-induced syndromes other than alcohol induced neurocognitive
disorder, amnestic confabulatory type (alcohol-induced persisting
amnestic disorder),
 Regardless of the severity of the symptoms, are likely to improve relatively
quickly and unlikely to remain clinically relevant for more than 1 month
after cessation of severe intoxication and/or withdrawal
 Alcohol-Induced Psychiatric Disorders

 Are clinically meaningful (e.g., interfere with functioning and/or cause severe
distress) psychiatric syndromes (e.g., depression) that resemble independent
psychiatric disorders (e.g., major depressive disorders), and are in excess of
symptoms usually associated with alcohol intoxication or withdrawal.
 They develop during, or soon after, intoxication or withdrawal from alcohol.

 For men and women presenting with psychiatric symptoms (e.g., anxiety,
depression, or psychoses) with concomitant alcohol-related problems,
 the first step in establishing a diagnosis of an alcohol-induced disorder is to
obtain a chronological history of the conditions.
(1) The age of onset of alcohol problems severe and repetitive enough for a
diagnosis of an AUD

(2) Periods of abstinence of a month or more since the AUD onset to

determine if a full psychiatric syndrome ever occurred outside the context
of problematic alcohol use; and

(3) The ages when the patient met criteria for the major psychiatric disorder.

 If a review of the timeline reveals no evidence that the additional

psychiatric syndromes either clearly antedated the severe alcohol problems
or persisted for a month or more after abstinence, an AUD is the major
disorder
 Alcohol-Induced Depressive and Bipolar
Disorders
 This condition includes the same symptoms observed in major depressive
disorders, but the alcohol induced intense sadness markedly improves
within several days to 1 month of abstinence without antidepressant
medications.
 Eighty percent of people with AUDs report intense depressions, including
about 40 percent who were depressed for ≥2 weeks at a time, but only
about 15 percent of such men and women have ever had a depression that
meets the criteria for a major depressive disorder when they have not
been drinking heavily.
 In case of bipolar disorder criteria are basically the same as for mania, and,
similar to bipolar diagnoses in general.
 This diagnosis should not be made if the mania developed in the context of
an antidepressants or electroconvulsive therapy.
 It is best to limit this label to bipolar I diagnoses because hypomanic
behaviors are very similar to the usual symptoms and signs of repeated
intoxication and withdrawal.
 Alcohol-Induced Anxiety Disorders

 Almost 80 percent of people with AUDs report prominent anxiety during an acute
withdrawal episode, and their complaints can be intense enough for the clinician to
consider diagnosing
 a panic disorder, generalized anxiety disorders, social phobia, and other
anxiety conditions.
 However, when psychological or physiological symptoms of anxiety are observed in
people with AUDs only in the context of heavy drinking or within the first month
or so of abstinence, the symptoms are likely to diminish and subsequently
disappear with time alone.
 Only a few preexisting anxiety or stress disorders (e.g., panic disorder, social phobia
and posttraumatic stress disorder [PTSD]) have been clearly shown to modestly
increase the risk for later AUDs.
 Alcohol-Induced Psychotic Disorders

 About 3 percent of people with AUDs experience auditory hallucinations

and/or paranoid delusions in a clear sensorium that develop in the context
of heavy drinking or withdrawal.
 Many of the symptoms resemble those seen in schizophrenia, but when the
psychotic features develop only in the context of alcohol problems they are
likely to clear spontaneously within a few days to a month of
abstinence.
 The syndromes may recur if heavy alcohol intake resumes.
 Alcohol-Induced Major Neurocognitive Disorders, Amnestic
Confabulatory Type,
Persistent (Wernicke–Korsakoff Disorder

 In the past was referred to as an alcohol- induced persisting amnestic

disorder,
 Which is the result of a relatively severe CNS deficiency of thiamine.

(1) Wernicke encephalopathy

 acute encephalopathy characterized by mental confusion,
ophthalmoplegia, and gait ataxia
 an acute syndrome requiring emergent treatment to prevent death and
neurologic morbidity
 tends to reverse fairly rapidly with vitamin supplementation
(2) Korsakoff syndrome
 Permanent in at least a partial form in about 50 percent of the people affected.

 is characterized by a pronounced anterograde and retrograde amnesia along

with potential impairment in visuospatial, abstract, and other types of
learning.
 In most cases, the level of loss of recent memory is out of proportion to the
global level of cognitive impairment.
 500 s mg of thiamine iv, infused over 30 minutes, TID for two consecutive
days
 250 mg IV/IM once daily for an additional five days, then 100mg po BID for
5-7 days
 Administration of glucose without thiamine can precipitate or worsen WE; thus,
thiamine should be administered before glucose..
 Alcohol-Induced Major Neurocognitive
Disorders (Persisting Dementias)
 Global decreases in intellectual functioning, cognitive abilities, and
memory are observed.
 Brain functioning tends to improve with abstinence, but half of patients
have long-term and even permanent disabilities.
 More than 50 percent of these patients have increased brain ventricle sizes
and shrinkage of the cerebral sulci, although these changes are usually
reversible with abstinence.
 Approach to patients

 Several simple questionnaires can help screen for problems.

 The Alcohol Use Disorders Identification Test (AUDIT,) uses ten items to review the
pattern of life problems related to alcohol.
 More simple instruments, such as the CAGE are too short to be optimally sensitive or
specific.
 [need to] Cut down [on drinking],

 Annoyance when asked about drinking,

 Guilt [about drinking],

 [need for] Eye-openers the morning after heavy drinking

 Although the AUDIT is useful, such questionnaires do not diagnose an AUD, but only
highlight individuals who are especially appropriate for a more detailed clinical
interview.
 LABORATORY TESTS
 These state markers of heavy drinking reflect physiological alterations likely to be
occur after ingesting about five or more drinks a day over several weeks.
 γ-glutamyltransferase (GGT)

 With a sensitivity and specificity of about 60 percent is a level of at least 35

U/L of
 Enzyme levels are likely to return to normal after 2 to 4 weeks of abstinence,
after which further increases over 20 percent are useful in identifying a return
to drinking
 CDT deglycosylated form of the protein,mtransferrin.

 A value over 3 percent has sensitivities and specificities of 60 percent

 Biological half-life of about 16 days

 The combination of GGT and CDT is better than either test alone for
identification of heavy drinking and monitoring abstinence.
 MCV over 91 μm3 has a sensitivity of about 50 percent in identifying
heavy drinking
 The 120-day lifespan of red cells does not allow MCV to be useful as an
indicator of a return to drinking.
 Other indicators that can be helpful in identifying patients who are regularly
consuming heavy doses of alcohol include
 High normal values of uric acid (e.g., >6.4 mg/dL), and

 Elevations in the usual liver function tests.

 Useful physical findings include

 Modest elevations in blood pressure, frequent bruising, cancer of the

head, neck, or upper digestive tract, an enlarged liver, evidence of
cirrhosis, and pancreatitis.
 Differential Diagnosis
Nonpathological use of alcohol.
 The key element of alcohol use disorder is the use of heavy doses of alcohol with
resulting repeated and significant distress or impaired functioning.
 While most drinkers sometimes consume enough alcohol to feel intoxicated, only a
minority (less than 20%) ever develop alcohol use disorder.
 Therefore, drinking, even daily, in low doses and occasional intoxication do not by
themselves make this diagnosis.
Conduct disorder in childhood and adult antisocial personality disorder.
 Alcohol use disorder, along with other substance use disorders, is seen in the
majority of individuals with antisocial personality and preexisting conduct disorder.
 Because these diagnoses are associated with an early onset of alcohol use disorder
as well as a worse prognosis, it is important to establish both conditions.
Sedative, hypnotic, or anxiolytic use disorder.
 The signs and symptoms of alcohol use disorder are similar to those seen in
sedative, hypnotic, or anxiolytic use disorder.
 The two must be distinguished, however, because the course may be
different, especially in relation to medical problems.
 Intoxication with or withdrawal of these drugs or with other sedating
substances (e.g., antihistamines, anticholinergic drugs) can be mistaken for
alcohol intoxication or withdrawal.
 The differential requires

 observing alcohol on the breath, measuring blood or breath alcohol

levels, ordering a medical workup, and gathering a good history.
Other medical conditions.
 Several medical (e.g., diabetic acidosis) and
 Neurological conditions (e.g., cerebellar ataxia, multiple sclerosis) can
temporarily resemble alcohol intoxication.
 Essential tremor
 A disorder that frequently runs in families, may erroneously suggest
the tremulousness associated with alcohol withdrawal.
 TREATMENT

 The core of treatment for AUDs involves

 Maximizing motivation for abstinence
 Helping the person restructure a life without alcohol, and
 Minimizing relapse to substance-using behaviors.
 This CBT-based approach is similar to efforts appropriate for any long-
term disorder that requires changes in lifestyles, such as diabetes or
hypertension.
 Three general steps are involved in treating the person with an AUD:

 Intervention

 Detoxification and

 Rehabilitation, including relapse prevention.

 These approaches can begin after life-threatening medical conditions are

addressed and psychiatric emergencies treated.
 Thus, suicidal plans, psychotic features without insight, and alcohol
withdrawal delirium require inpatient hospitalizations until the patient is
stabilized enough to begin alcohol rehabilitation.
 Intervention

 The goal is to use the principles of motivational interviewing and brief

interventions to help patients recognize the adverse consequences likely to occur
if they do not stop drinking.
 It is summarized by the acronym FRAMES:

 G iving Feedback on alcohol risks

 Emphasizing a person’s Responsibility for change

 Offering Advice

 Giving a Menu of options to consider

 Employing Empathy; and

 Emphasizing Self-efficacy, or the ability to change

 The goal is to

 Establish an alliance with patients by

 Understanding of their viewpoint while

 Encouraging them to think through consequences associated with

alcohol
 Emphasizing the way that changing behaviors might yield benefits.

 Recognize the patient’s ambivalence toward abstinence and to

monitor the person’s readiness to change.
 Resistance is best handled through discussion and problem solving
rather than direct confrontation.
 Detoxification

 The essential first step in detoxification is a

 Thorough physical examination.
 In the absence of a serious medical disorder or a comorbid SUD,
severe alcohol withdrawal is unlikely.
 The second step is to offer
 Rest,
 Nutrition, and
 Oral multiple vitamins, including thiamine.
 We use the 10-question Clinical Institute Withdrawal Assessment from
Alcohol - Revised (CIWA-Ar) scale, which has been found to be valid
and reliable .
 CIWA-Ar scores, combined with a history of withdrawal seizures or
delirium tremens, are used to categorize a patient’s withdrawal as
 Very mild withdrawal – <10

 Mild withdrawal – 10 to 15

 Moderate withdrawal – 16 to 20

 Severe withdrawal – >20

 Indications for choosing Rx setting

Out paitent Inpatient

 Fever
 CIWA-Ar <15
 Disorientation
 No hx of delirium tremens
 Drenching sweats
 No hx Alcohol withdrawal seizures.
 Severe tachycardia
 Cognitively intact and motivated to
 Hypertension
avoid alcohol.
 Pregnancy
 Ability to take oral medications.
 Concurrent substance use (eg,
 Ability to commit to near daily
benzodiazepines)
medical visits.
 Markedly abnormal laboratory values
 Very mild withdrawal

 (CIWA-Ar <10) are typically treated using a symptom-triggered approach as

they may continue with minimal symptoms without progression..
 Symptom-triggered dosing schedules for the benzodiazepines chlordiazepoxide
and oxazepam for mild withdrawal :
 ●Longer-acting benzodiazepine – eg, chlordiazepoxide

 •Day 1 – 50 mg every 6 to 12 hours as needed

 •Days 2 to 5 – 25 mg every 6 hours as needed

 ●Shorter-acting benzodiazepine – eg, oxazepam

 •Day 1 – 30 mg every 6 hours as needed

 •Days 2 to 5 – 15 mg every 6 hours as needed

 Mild withdrawal

 Fixed dosing schedules for the benzodiazepines chlordiazepoxide and oxazepam for mild withdrawal are
shown below:
 Longer-acting benzodiazepine – eg, chlordiazepoxide
 Day 1 - 50 mg every 6 to 12 hours

 Day 2 - 25 mg every 6 hours

 Day 3 - 25 mg twice a day

 Day 4 - 25 mg at night

 Shorter-acting benzodiazepine – eg, oxazepam

 Day 1 - 30 mg every 6 hours

 Day 2 - 30 mg every 8 hours

 Day 3 - 30 mg every 12 hours

 Day 4 - 30 mg at night

 Withdrawal in some patients will progress at different rates and end before or after four days, requiring
some “as needed” flexibility in dosing.
 Moderate to Severe withdrawal

Ruling out alternative diagnoses

 This is particularly true when the presentation includes altered mental
status and fever
 Perform extensive testing, including lumbar puncture and cranial CT

 Conditions, such as infection (eg, meningitis), trauma (eg, intracranial

hemorrhage), metabolic derangements, drug overdose, hepatic failure,
and gastrointestinal bleeding, can mimic or coexist with alcohol
withdrawal
 A premature diagnosis of alcohol withdrawal can lead to inappropriate use
of sedatives, which can further delay accurate diagnosis
 Symptom control and supportive care

 Next step is alleviating symptoms and identifying and correcting metabolic

derangements.
 Benzodiazepines are used to control psychomotor agitation and prevent
progression to more severe withdrawal.
 Supportive care, including

 Intravenous fluids, nutritional supplementation, and frequent clinical

reassessment including vital signs, is important.
 Patients should be placed in a quiet, protective environment.

 Mechanical restraint may be necessary temporarily for patients suffering

from delirium tremens (DT) in order to protect both the patient and
caretakers
 Protracted Withdrawal

 Finally, regarding withdrawal, mild symptoms of anxiety, insomnia, and

autonomic overactivity are likely to continue for 2 to 6 months following
acute withdrawal.
 Although no pharmacological treatment for this syndrome has been
identified, a medication discussed below for the rehabilitation phase,
acamprosate (Campral), may diminish some of these symptoms.
 It is important to warn patients that some sleep problems or feelings of
nervousness might remain after acute withdrawal, and consider efforts to
help them feel more comfortable, because these protracted withdrawal
symptoms enhance the probability of relapse.
 Rehabilitation

 For most patients, rehabilitation includes three major components

(1) Continued efforts to increase and maintain high levels of motivation

for abstinence

(2) Work to help the patient readjust to a lifestyle free of alcohol; and

(3) Relapse prevention

 The treatment process in either inpatient or outpatient setting involves
intervention, optimizing physical and psychological functioning,
enhancing motivation, reaching out to family,
 the first 2 to 4 weeks of care as an intensive period of help.
 Those efforts must be followed by at least 3 to 6 months of less frequent
outpatient care.
 Outpatient care uses a combination of individual and group counseling,
judicious avoidance of psychotropic medications unless needed for
independent disorders, and involvement in such self-help groups as AA.
 Counseling.

 In the first several months should focus on day-to-day life issues to help
patients maintain a high level of motivation for abstinence and to enhance
their functioning
 Counseling or therapy can be carried out in an individual or group setting

 To optimize motivation, treatment sessions should explore

 The consequences of drinking

 The likely future course of alcohol-related life problems, and

 The marked improvement that can be expected with abstinence.

 Whether in an inpatient or an outpatient setting, individual or group
counseling is usually ordered a minimum of three times a week for the
first 2 to 4 weeks, followed by less intense efforts, perhaps once a week,
for the subsequent 3 to 6 months
 Much time in counseling deals with how to build a lifestyle free of
alcohol.
 The need for a sober peer group
 A plan for social and recreational events without drinking, and
 Approaches for reestablishing communication with family members
and friends.
 Relapse prevention

 First identifies situations in which the risk for relapse is high.

 Develop modes of coping to be used when the craving for alcohol increases
or when any event or emotional state makes a return to drinking likely.
 An important part of relapse prevention is reminding the patient about the
appropriate attitude toward slips.
 The efforts to achieve and maintain a sober lifestyle are not a game in which
all benefits are lost with that first sip.
 Recovery is a process of trial and error, and slips can be clues to help identify
high-risk situations and to develop more appropriate coping techniques.
 Importance of the Family

 Important aspect of recovery involves helping family and friends

understand more about AUDs and how rehabilitation is an ongoing
process.
 Counseling and support for spouses, offspring, and friends can help them
work to rebuild key relationships
 Learn how to avoid protecting the patient from the consequences of
drinking, a step likely to undercut the patients motivation to abstinence.
 Possible Medications for the AUD.

1. Acamprosate
 Antagonizes neuronal overactivity related to the excitatory
neurotransmitter glutamate
 Diminish mild anxiety, mood swings, and other sleep difficulties
 Dose is 2,000 mg divided into three doses per day, 666 mg TID
 in patients with significant liver faliure, excreted thru kidney
 Side effect might include diarrhea
 Check scr, CI in severe kidney disease
2. Naltrexone (ReVia)
 Long-acting opioid antagonist
 Is hypothesized to decrease the rewarding effects of a drink and to
diminish craving
 Dose is 50mg-100mg po daily or 380mg IM monthly (for non compliant
pts)
 Side effects are nausea, dizziness, vomiting , abdominal pain and diarrhea
 If a patient is taking opioids might lead to withdrawal
 If opioids are taken for pain relief might diminsh their effects
3. Disulfiram (Antabuse)
 Prescribed at 250 mg per day.

 The goal is to warn patients that drinking alcohol while taking disulfiram
precipitates nausea, vomiting, and changes in blood pressure
 Patients should not drink any alcohol at least 12 hours before starting
and reactions may last up to 14 days after discontinuation
 Side effects may include mood swings, rare instances of psychosis, a
possible increase in peripheral neuropathies, and a rare but potentially
fatal hepatitis.
 For patients who don’t respond to Naltrexone or acamprosate
 Although not approved for treatment of AUD topiramate and gabapentin
have showed promising results in treated individuals
 Decrease post withdrawal anxiety and low mood
 Reduce cravings and insomnia