Management of Moderate and Severe Alcohol Withdrawal Syndromes

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Management of moderate and severe alcohol withdrawal syndromes
Authors: Robert S Hoffman, MD, Gerald L Weinhouse, MD

Section Editor: Stephen J Traub, MD
Deputy Editor: Jonathan Grayzel, MD, FAAEM
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2017. | This topic last updated: Sep 27, 2017.
INTRODUCTION — Alcoholism is a common condition and most clinicians are forced to confront its
complications in some of their patients. There are an estimated 8 million alcohol dependent people in the United
States alone, and approximately 500,000 episodes of withdrawal severe enough to require pharmacologic
treatment occur each year [1].
The in-patient management of syndromes associated with moderate and severe alcohol withdrawal is reviewed
here. The ambulatory management of mild alcohol withdrawal, the initial diagnosis and treatment of alcohol
dependence, and specific conditions due to alcohol-related organ damage (eg, cirrhosis, pancreatitis) are
discussed elsewhere. (See "Medically supervised alcohol withdrawal in the ambulatory setting" and
"Psychosocial treatment of alcohol use disorder" and "Pharmacotherapy for alcohol use disorder" and "Clinical
manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis" and "Etiology and
pathogenesis of chronic pancreatitis in adults" and "Hematologic complications of alcohol use" and "Screening
for unhealthy use of alcohol and other drugs in primary care" and "Brief intervention for unhealthy alcohol and
other drug use".)
PATHOPHYSIOLOGY
Overview — It is not entirely clear why some individuals suffer from more severe withdrawal symptoms than
others, but genetic predisposition may play a role [2]. Experiments in 1955 demonstrated that alcohol-naive
volunteers given continual alcohol for longer periods developed more severe withdrawal than those who drank
for shorter periods [3]. These results imply that most people are vulnerable to the effects of the abrupt cessation
of prolonged, sustained ethanol intake. However, withdrawal usually does not occur in the general population
because most people drink in an episodic fashion that does not lead to the sustained high blood concentrations
of alcohol necessary to develop tolerance and withdrawal.
Symptoms of alcohol withdrawal occur because alcohol is a central nervous system depressant. Alcohol
simultaneously enhances inhibitory tone (via modulation of gamma-aminobutyric acid activity) and inhibits
excitatory tone (via modulation of excitatory amino acid activity). Only the constant presence of ethanol
preserves homeostasis. Abrupt cessation unmasks the adaptive responses to chronic ethanol use resulting in
overactivity of the central nervous system.
Gamma-aminobutyric acid — Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the
brain. Highly specific binding sites for ethanol are found on the GABA receptor complex [4]. Chronic ethanol use
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induces an insensitivity to GABA such that more inhibitor is required to maintain a constant inhibitory tone [5]. As
alcohol tolerance develops, the individual retains arousal at alcohol concentrations which would normally
produce lethargy or even coma in relatively alcohol naïve individuals. Cessation of alcohol or a reduction from
chronically elevated concentrations results in decreased inhibitory tone.
Excitatory amino acids — Glutamate is one of the major excitatory amino acids. When glutamate binds to the
N-methyl-D-aspartate (NMDA) receptor, calcium influx leads to neuronal excitation by binding to the glycine
receptor on the NMDA complex. Ethanol inhibits glutamate induced excitation [6,7]. Adaption occurs by
increasing the number of glutamate receptors in an attempt to maintain a normal state of arousal. Cessation of
alcohol or a reduction from chronically elevated concentrations results in unregulated excess excitation.
COMPLICATIONS OF ALCOHOL WITHDRAWAL
Minor withdrawal symptoms — Minor withdrawal symptoms are due to central nervous system hyperactivity,
and can include:
● Insomnia
● Tremulousness
● Mild anxiety
● Gastrointestinal upset; anorexia
● Headache
● Diaphoresis
● Palpitations
Symptoms are usually present within six hours of the cessation of drinking and often develop while patients still
have a significant blood alcohol concentration (table 1) [8]. If withdrawal does not progress, these findings
resolve within 24 to 48 hours. The specific minor withdrawal symptoms in a given patient typically are consistent
from one episode to the next. The ambulatory management of mild alcohol withdrawal, including criteria to
determine which patients are suitable for out-patient management, is discussed separately. (See "Medically
supervised alcohol withdrawal in the ambulatory setting".)
Withdrawal seizures — Withdrawal-associated seizures are generalized tonic-clonic convulsions that usually
occur within 12 to 48 hours after the last alcoholic drink, but may occur after only two hours of abstinence (table
1) [9]. The seizures occur predominantly in patients with a long history of chronic alcoholism, as evidenced by
their typical onset during the fourth and fifth decades of life.
Withdrawal seizures are usually singular or occur as a brief flurry of seizures over a short period. Recurrent or
prolonged seizures or status epilepticus are not consistent with withdrawal-associated seizures and should
prompt an investigation into possible structural or infectious etiologies, generally guided by the findings of cranial
computed tomography (CT) and/or lumbar puncture. Benzodiazepines, phenobarbital, and propofol can be used
to treat status epilepticus while investigations proceed. Several studies have demonstrated that phenytoin is
ineffective in the treatment of alcohol withdrawal seizures and the drug should not be used for this purpose [10-
12]. (See "Evaluation and management of the first seizure in adults".)
While some authors use other anticonvulsants such as carbamazepine and levetiracetam in the therapy of
alcohol withdrawal, the role of these medications in alcohol withdrawal related seizures is incompletely
evaluated.
Although seemingly benign, alcohol withdrawal seizures left untreated progress to delirium tremens in nearly
one-third of patients [9]. (See 'Delirium tremens (DT)' below.)
Alcoholic hallucinosis — Despite a tendency to equate alcoholic hallucinosis with delirium tremens, the two
terms are NOT synonymous. Alcoholic hallucinosis refers to hallucinations that develop within 12 to 24 hours of
abstinence and typically resolve within 24 to 48 hours (which is the earliest point at which delirium tremens
typically develops) (table 1) [13]. Hallucinations are usually visual, although auditory and tactile phenomena may
also occur. Patients are aware that they are hallucinating and often very distressed. However, in contrast to
delirium tremens, alcoholic hallucinosis is not associated with global clouding of the sensorium but only with
specific hallucinations, and vital signs are usually normal. (See "Approach to the patient with visual
hallucinations", section on 'Alcohol and drug use or withdrawal'.)
Delirium tremens (DT)
Clinical manifestations of severe withdrawal and DT — Approximately 5 percent of patients who undergo
withdrawal from alcohol suffer from DT. DT is defined by hallucinations, disorientation, tachycardia, hypertension,
hyperthermia, agitation, and diaphoresis in the setting of acute reduction or abstinence from alcohol. DT typically
begins between 48 and 96 hours after the last drink and lasts one to five days (table 1). DT and alcoholic
hallucinosis are NOT synonymous and symptoms that occur a few hours after the cessation of drinking, even if
severe, are usually not manifestations of DT. Virtually all patients who develop DT experience symptoms of
alcohol withdrawal prior to the onset of DT. (See 'Alcoholic hallucinosis' above.)
Patients with DT have significantly elevated cardiac indices, oxygen delivery, and oxygen consumption [14].
Arterial pH rises due to hyperventilation, which may be a rebound effect related to the respiratory depressant
properties of alcohol. Hyperventilation and consequent respiratory alkalosis in this setting result in a significant
decrease in cerebral blood flow [15]. There is a correlation between the length of the preceding alcohol binge,
the degree of clouding of the sensorium, and the size of the average decrease in cerebral hemispheric blood
flow, although there is no association between blood flow parameters and hallucinations or tremors [15].
Severe alcohol withdrawal is often associated with fluid and electrolyte status abnormalities. Almost all patients
in acute withdrawal are hypovolemic as a result of diaphoresis, hyperthermia, vomiting, tachypnea, and
decreased oral intake. Hypokalemia is common due to renal and extrarenal potassium losses, alterations in
aldosterone levels, and changes in potassium distribution across the cell membrane [16,17]. Hypomagnesemia
is common in patients with DT and may predispose to dysrhythmias and seizures [18]. Hypophosphatemia may
occur due to malnutrition, may be symptomatic, and if severe, may contribute to cardiac failure and
rhabdomyolysis.
Risk factors — Risk factors for the development of DT include [19-21]:
● A history of sustained drinking

● A history of previous DT
● Age greater than 30
● The presence of a concurrent illness
● The presence of significant alcohol withdrawal in the presence of an elevated alcohol level
● A longer period since the last drink (ie, patients who present with alcohol withdrawal more than two days
after their last drink are more likely to experience DT than those who present within two days)
Mortality — With early identification and current management strategies, mortality from DT is less than five
percent. This figure has diminished from the 37 percent mortality rate reported in the early 20th century, probably
as a result of earlier diagnosis, improvements in supportive and pharmacologic therapies, and improved
treatment of comorbid illnesses [2,22-26]. Death usually is due to arrhythmia, complicating illnesses, such as
pneumonia, or failure to identify an underlying problem that led to the cessation of alcohol use, such as
pancreatitis, hepatitis, or central nervous system injury or infection. Older age, preexisting cardio-pulmonary
disease, core body temperature greater than 40ºC (104ºF), and coexisting liver disease are associated with a
greater risk of mortality [27].
MANAGEMENT
Ruling out alternative diagnoses — Alcohol withdrawal remains a clinical diagnosis. It may be necessary to
perform extensive testing, including lumbar puncture and cranial CT, to rule out other diagnostic considerations
with confidence. This is particularly true when the presentation includes altered mental status and fever.
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 [28]. A
premature diagnosis of alcohol withdrawal can lead to inappropriate use of sedatives, which can further delay
accurate diagnosis [29].
Symptom control and supportive care — Once comorbid illnesses have been excluded or adequately treated,
the management of alcohol withdrawal is directed at 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. Clinicians must avoid complacency when treating
patients with alcohol withdrawal. (See 'Treatment of psychomotor agitation with benzodiazepines' below and
'Symptom-triggered therapy' below.)
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. Clinicians
should follow their facility's guidelines for documentation and implementation of physical restraints. Once
adequate chemical sedation is achieved, physical restraints should be removed, as resistance against restraints
can increase temperature, produce rhabdomyolysis, and cause physical injury.
Volume deficits can be calculated and replaced accordingly, or, if there are no contraindications, isotonic
intravenous fluid can be infused rapidly until patients are clinically euvolemic. Thiamine and glucose should be
administered in order to prevent or treat Wernicke's encephalopathy [30,31]. Multivitamins containing or
supplemented with folate should be given routinely, and deficiencies of glucose, potassium, magnesium, and
phosphate should be corrected as needed. Initially (first day or two), treatment should be intravenous as
gastrointestinal absorption is impaired in many patients who abuse alcohol chronically. The details of these
supportive treatments are discussed separately. (See "Wernicke encephalopathy", section on 'Treatment' and
"Overview of the chronic neurologic complications of alcohol" and "Clinical manifestations and treatment of
hypokalemia in adults" and "Evaluation and treatment of hypophosphatemia".)
Some clinicians treat alcohol withdrawal patients with an intravenous infusion of a combination of thiamine,
folate, and a multivitamin in isotonic saline with 5 percent dextrose. The multivitamin makes the fluid appear
yellow, and thus, this treatment combination is sometimes referred to as a “banana bag”. Use of this treatment
has not been well studied, and it may not meet the specific requirements for fluid, glucose, and other substrates
of many patients with alcohol withdrawal.
During the early phases of withdrawal alcoholic patients are often given nothing by mouth (ie, NPO) to prevent
aspiration [32]. However, nutritional support is essential as alcoholic patients are frequently malnourished and
have high metabolic needs due to their excited autonomic state. Initially, parenteral glucose supplementation is
sufficient, but additional nutrition may be needed for patients who remain unable to eat for more than a day or
two. Patients considered at high risk for complications should be monitored in an intensive care unit (table 2).
(See "Nutrition support in critically ill patients: An overview".)
Treatment of psychomotor agitation with benzodiazepines
Drug selection — Benzodiazepines are used to treat the psychomotor agitation most patients experience
during withdrawal and to prevent progression from minor withdrawal symptoms to major ones [22-25,28,32-35].
Diazepam (Valium), lorazepam (Ativan), and chlordiazepoxide (Librium) are used most frequently to treat or
prevent alcohol withdrawal, but other benzodiazepines may be used [36]. In general, long-acting
benzodiazepines with active metabolites (eg, diazepam or chlordiazepoxide) are preferred because they seem to
result in a smoother course with less chance of recurrent withdrawal or seizures. We recommend a symptom-
triggered approach to treatment with benzodiazepines. (See 'Symptom-triggered therapy' below.)
We prefer lorazepam (Ativan) or oxazepam (Serax) for the treatment of patients with advanced cirrhosis or acute
alcoholic hepatitis. The shorter half-life of lorazepam and the absence of active metabolites with oxazepam may
prevent prolonged effects if oversedation occurs. In contrast, chlordiazepoxide has a relatively long half-life and
may lead to oversedation in patients with severe liver disease. Treatment with agents available in parenteral form
(eg, lorazepam, diazepam) may be necessary in patients who cannot receive oral medications.
Given the recent trend of drug shortages, preferred agents may not always be available. A treatment algorithm
for clinicians managing moderate or severe alcohol withdrawal without access to diazepam is provided (algorithm
1).
Benzodiazepines exert their effect via stimulation of gamma-aminobutyric acid (GABA) receptors, causing a
decrease in neuronal activity and relative sedation. (See 'Gamma-aminobutyric acid' above.)
Route — All patients with seizures or DT require intravenous (IV) therapy with benzodiazepines. IV therapy is
appropriate for the initial management of most patients with tremulousness from alcohol withdrawal because of
guaranteed absorption and rapidity of onset. It is important to have IV access in all patients at risk of severe
withdrawal.
Intramuscular administration should be avoided because of variable drug absorption. Oral formulations are
preferred in most outpatient settings, for the prevention of withdrawal in asymptomatic patients known to be at
risk, and for those with mild and minimal symptoms. (See 'Prophylaxis' below and "Medically supervised alcohol
withdrawal in the ambulatory setting".)
Following IV administration, patients should be converted to oral dosing as soon as possible based on their
clinical response.
Dosing — Titration of medications should be based upon a given patient's risk factors for and ability to
tolerate DT. As an example, a patient younger than 45 years with no comorbid illnesses should be lightly sedated
to a degree that insures safety and comfort but does not obscure the neurologic examination. In contrast, an
older patient with preexisting cardiopulmonary disease may benefit from heavier sedation, but must be closely
monitored due to the greater risk imposed by the high systemic stress of major withdrawal or oversedation.
Explicit criteria for ICU admission are provided (table 2).
A variety of dosing schedules can be used. We generally give IV diazepam, 5 to 10 mg IV every 5 to 10 minutes,
until the appropriate level of sedation is achieved. Lorazepam, 2 to 4 mg IV every 15 to 20 minutes, can also be
used. Equivalent doses of oral chlordiazepoxide are on the order of 25 to 100 mg, which can be repeated hourly.
In severe withdrawal, select patients may require massive doses (>500 mg diazepam) to achieve initial control of
symptoms, and continued aggressive use of benzodiazepines thereafter (>2000 mg diazepam over 48 hours).
Fixed schedule therapy, in which a benzodiazepine is given at fixed intervals even if symptoms are absent, is
often administered despite evidence against this strategy [37-40]. A fixed dose schedule strategy is most useful
for preventing withdrawal in patients at risk, but asymptomatic or minimally symptomatic. The only advantage of
this strategy is for the provider, as frequent reassessment is not required.
Symptom-triggered therapy — We favor a symptom-triggered approach to the treatment of alcohol

withdrawal that involves providing medication only when a patient has symptoms.
To use this approach, a regular systematic assessment should be made of the patient's status using a validated
instrument, such as the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar), a measure of
withdrawal severity (table 3) [41], or some equivalent assessment. A calculator to determine the CIWA-Ar score
is provided (calculator 1). Evaluation intervals as frequent as every 10 to 15 minutes are appropriate for patients
with more severe symptoms being treated with IV benzodiazepines. Once severe symptoms are controlled,
hourly reassessment of such patients is reasonable. In contrast, an interval of four to six hours is reasonable for
stable patients with mild symptoms receiving oral benzodiazepines.
When the score is elevated, additional medication is given. For acute withdrawal, we give diazepam 5 to 10 mg
IV (or chlordiazepoxide 25 to 100 mg orally) for any score of 8 or greater on the CIWA-Ar.
In some patients with severe alcohol withdrawal, including those who require tracheal intubation and mechanical
ventilation, assessment scales such as the CIWA-Ar that rely upon patients being able to answer specific
questions cannot be used effectively. In these patients, we suggest using a sedation scale more appropriate for
the intensive care setting such as the Richmond Agitation-Sedation Scale (RASS) (table 4). We aim for a score
of 0 to -2 when using the RASS to manage such patients. (See "Sedative-analgesic medications in critically ill
adults: Selection, initiation, maintenance, and withdrawal", section on 'Monitoring'.)
Multiple randomized and observational studies support this simple concept of giving the patient the therapy they
need, only when they need it [37-40,42]. Taken collectively, these studies demonstrate that symptom-triggered
therapy achieves equivalent or superior clinical endpoints while requiring lower total doses of sedatives and
shorter periods of hospitalization.
In the landmark study of this approach, 101 patients admitted to an inpatient alcohol detoxification unit were
randomly assigned to treatment with chlordiazepoxide using a fixed schedule or a symptom-triggered therapy
[37]. Patients in the symptom-triggered group required less medication (median 100 versus 425 mg) and a
shorter treatment period (median 9 versus 68 hours), and had similar or better clinical outcomes.
Disposition and monitoring — Patients being treated for moderate or severe alcohol withdrawal must be
closely monitored and many require admission to an intensive care unit (ICU). A table of ICU admission criteria is
provided (table 2). Older patients are at greater risk for delirium tremens and may not tolerate the systemic stress
of major withdrawal. Standard monitoring includes continual assessment of vital signs, pulse oximetry, fluid
status, and neurological function. (See 'Delirium tremens (DT)' above.)
Refractory delirium tremens — Some patients have refractory delirium tremens (DT) despite treatment with
high-dose benzodiazepines, possibly because of low endogenous GABA levels or acquired conformational
changes in the GABA receptor [43,44]. Refractory DT is not clearly defined. It may be present if more than 50 mg
of diazepam or 10 mg of lorazepam is required to control the symptoms of severe withdrawal during the first hour
of treatment, or if doses greater than 200 mg of diazepam or 40 mg of lorazepam fail to adequately control
symptoms during the initial three to four hours of treatment [45]. As with any dangerous intoxication, we
recommend obtaining assistance from a medical toxicologist or poison control center in such instances. (See
'Additional resources' below.)
In patients with refractory DT, barbiturates (specifically phenobarbital) can be very effective when given with
benzodiazepines [45]. Benzodiazepines, which increase the frequency of GABA chloride channel opening, and
barbiturates, which increase the duration of channel opening, may work synergistically. We give phenobarbital
130 to 260 mg IV, repeated every 15 to 20 minutes, until symptoms are controlled. While one recent study
provides support for early use of phenobarbital, we feel that this study needs to be replicated before it can be
adopted into mainstream practice [46]. In addition, some preliminary evidence supports the use of
dexmedetomidine in refractory patients [47]. While this approach appears promising, we advise caution until well
performed controlled trials of safety and efficacy are available.
Another reasonable alternative treatment for refractory DT is propofol, which can act to open chloride channels in
the absence of GABA, and may also antagonize the excitatory amino acids that are upregulated during alcohol
withdrawal [48,49]. Endotracheal intubation and mechanical ventilation are frequently necessary if phenobarbital
or propofol are used.
Alternative and contraindicated agents — Drugs other than phenobarbital and propofol have been used with
benzodiazepines or, rarely, alone to treat alcohol withdrawal. These agents are less well studied than
benzodiazepines and may mask the hemodynamic signs of withdrawal, which can precede seizures. We believe
they should not be used routinely in the treatment of moderate or severe alcohol withdrawal. Such drugs include:
● Ethanol
● Antipsychotics (eg, haloperidol)
● Anticonvulsants (eg, carbamazepine)
● Centrally acting alpha-2 agonists (eg, clonidine, dexmedetomidine)
● Beta blockers (eg, propranolol)
● Baclofen
All of these agents can reduce the frequency and intensity of minor withdrawal symptoms, but more data support
the efficacy and safety of benzodiazepines in reducing the risk of seizures and delirium tremens.
● Ethanol – Ethanol should not be used as therapy in the setting of acute alcohol withdrawal. It is difficult to
titrate, associated with many adverse metabolic and end-organ effects, and clearly inferior to
benzodiazepines [50]. Of note, the metabolism and kinetics of ethanol have not been well studied in the
critically ill.
● Antipsychotics – Phenothiazines and butyrophenones (including haloperidol) lower the seizure threshold and
should not be used routinely in the withdrawing alcoholic [51]. These drugs may also interfere with heat
dissipation and do not exhibit cross-tolerance with ethanol.
Treatment with antipsychotics would only be appropriate when a decompensated thought disorder (such as
schizophrenia) coexists with ethanol withdrawal and any symptoms associated with ethanol withdrawal have
been definitively treated with benzodiazepines. In our experience, such occurrences are rare, even in
patients with known thought disorders.
If a clinician determines that antipsychotic therapy is indicated, we recommend an ECG to screen for QT
prolongation (a contraindication to many antipsychotic medications) and the correction of electrolyte
abnormalities (such as hypokalemia and hypomagnesemia, which are common in alcoholics) before any
medication is administered.
● Anticonvulsants – Sustained anticonvulsant therapy has no role in patients with isolated alcohol withdrawal
seizures. The overwhelming majority of seizures from withdrawal are self-limited and do not require
treatment with anticonvulsants. If status epilepticus ensues, phenobarbital or propofol may be used for short-
term management in conjunction with benzodiazepines, while an underlying cause is investigated. (See
'Withdrawal seizures' above.)
While carbamazepine may have a role in the outpatient management of mild alcohol withdrawal, convincing
evidence that the drug effectively treats patients with delirium tremens or other severe symptoms is lacking
[52]. (See "Medically supervised alcohol withdrawal in the ambulatory setting".)
● Centrally acting alpha-2 agonists ‒ Some clinicians report using centrally acting alpha-2 agonists (eg,
dexmedetomidine) as adjunct therapy for alcohol withdrawal, and these agents may reduce some symptoms
of withdrawal. However, there are no controlled trials showing that they prevent the development of seizures
or DT. Pending more convincing studies, we believe centrally acting alpha-2 agonists should not be used as
a primary treatment for acute severe alcohol withdrawal.
● Beta blockers – Beta blockers may reduce minor symptoms of withdrawal, but they have not been shown to
prevent the development of seizures or DT. We believe they should not be used for the treatment of acute
severe alcohol withdrawal. However, patients with known cardiovascular disease should be given their
maintenance medications after sedation and volume resuscitation, as sustained tachycardia and
hypertension may contribute to cardiovascular morbidity especially in the elderly.
● Baclofen – Baclofen, a selective agonist of the gamma-aminobutyric acid (GABA)-B receptor used to treat
reversible spasticity, has been studied as a therapy for acute alcohol withdrawal, but its effectiveness in
controlling severe symptoms remains unproven [53-56]. We believe baclofen should not be used for the
treatment of acute severe alcohol withdrawal.
PROPHYLAXIS — Patients with a history of seizures, delirium tremens, or prolonged, heavy alcohol
consumption, who are minimally symptomatic or asymptomatic and are admitted to the hospital for other
reasons, can be prophylactically treated with oral chlordiazepoxide. Should more severe symptoms develop, the
patients are managed in standard fashion. (See 'Management' above.)
For prophylaxis, we give 25 to 100 mg every six hours for one day, followed by 25 to 50 mg every six hours for
an additional two days. Monitoring is no different from patients in active withdrawal. Patients should be
reassessed frequently and additional 25 to 50 mg doses of chlordiazepoxide administered each hour if a score of
8 or greater is achieved on the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar) (table 3)
[41].
Asymptomatic or minimally symptomatic patients at lower risk for seizures or delirium tremens who are being
admitted to the hospital for other reasons should be closely monitored and may be treated with oral
chlordiazepoxide 25 to 50 mg every hour as needed when a score of 8 or greater is achieved on the CIWA-Ar.
After acute treatment, all patients should be screened for alcohol dependence and should be considered at risk
for recurrent episodes of withdrawal. In-hospital evaluation and long-term follow-up are recommended. (See
"Psychosocial treatment of alcohol use disorder".)
ADDITIONAL RESOURCES — Regional poison control centers in the United States are available at all times for
consultation on patients who are critically ill, require admission, or have clinical pictures that are unclear (1-800-
222-1222). In addition, some hospitals have clinical and/or medical toxicologists available for bedside
consultation and/or inpatient care. Whenever available, these are invaluable resources to help in the diagnosis
and management of ingestions or overdoses. The World Health Organization provides a listing of international
poison centers at its website: www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries
and regions around the world are provided separately. (See "Society guideline links: General measures for acute
poisoning treatment".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and
“Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
“patient info” and the keyword(s) of interest.)
● Basics topic (see "Patient education: Alcohol withdrawal (The Basics)")
SUMMARY AND RECOMMENDATIONS — A table summarizing the emergent management of alcohol

withdrawal is provided (table 5).
● Alcohol withdrawal remains a clinical diagnosis. It may be necessary to perform extensive testing (eg,
lumbar puncture and cranial CT) to rule out other diagnoses as many patients with alcoholism do not stop
drinking spontaneously and present with overt withdrawal symptoms that may mask other disorders.
Conditions such as infection, trauma, metabolic derangements, drug overdose, hepatic failure, and
gastrointestinal bleeding can mimic or coexist with alcohol withdrawal. (See 'Ruling out alternative
diagnoses' above.)
● Alcohol withdrawal syndromes encompass symptoms ranging from mild tremulousness to life-threatening
delirium tremens. A table summarizing the timing of withdrawal symptoms is provided (table 1). (See 'Minor
withdrawal symptoms' above and 'Withdrawal seizures' above and 'Alcoholic hallucinosis' above and
'Delirium tremens (DT)' above.)
● Delirium tremens (DT) is a syndrome characterized by agitation, disorientation, hallucinations, and

autonomic instability (tachycardia, hypertension, hyperthermia, and diaphoresis) in the setting of acute
reduction or abstinence from alcohol. DT is associated with a mortality rate of up to 5 percent, but the rate
can be substantially higher if the condition goes untreated. Alcoholic hallucinosis and DT are distinct clinical
entities. Patients at risk and those who fail to respond appropriately to initial doses of sedatives should be
monitored closely and treated aggressively (table 2). (See 'Delirium tremens (DT)' above.)
● Risk factors for delirium tremens include:
• A history of sustained drinking
• A history of previous DT
• Age greater than 30
• The presence of a concurrent illness
• The presence of significant alcohol withdrawal in the presence of an elevated ethanol level
• A longer period (more than two days) between the last drink and the onset of withdrawal
● Patients in alcohol withdrawal require medical treatment and observation. We suggest that patients who
present with signs and symptoms of moderate or severe alcohol withdrawal be treated with benzodiazepines
(Grade 2B). We give diazepam 5 to 10 mg IV, repeated every 5 to 10 minutes until symptoms are controlled.
Lorazepam may also be used (2 to 4 mg IV, repeated every 15 to 20 minutes). The general goal of sedation
is a calm but alert state. Patients at greater risk for adverse outcomes may need heavier sedation. IV
benzodiazepines should be continued until it is clear that the patient is no longer delirious and at high risk for
aspiration, and that absorption from the gut is reliable. (See 'Treatment of psychomotor agitation with
benzodiazepines' above.)
● We recommend that benzodiazepines be dosed and administered using a validated assessment tool, such
as the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar) (table 3) (Grade 1A). This
requires formally assessing patients at regular intervals. Evaluation intervals as frequent as every 10 to 15
minutes are appropriate for patients with severe symptoms; an interval of four to six hours is reasonable for
stable patients with mild symptoms. For acute withdrawal, we give diazepam 5 to 10 mg IV (or
chlordiazepoxide 25 to 100 mg orally) for any score of 8 or greater on the CIWA-Ar. (See 'Symptom-
triggered therapy' above.)
● Patients with moderate or severe alcohol withdrawal need close monitoring, some in an intensive care
setting (table 2). (See 'Disposition and monitoring' above.)
● For delirium tremens refractory to aggressive treatment with high-dose benzodiazepines, we suggest
treatment with phenobarbital or propofol (Grade 2C). Patients receiving these agents require ICU admission
and will likely require mechanical ventilation (table 5). (See 'Refractory delirium tremens' above.)
● Asymptomatic or minimally symptomatic patients at risk for alcohol withdrawal, but admitted to the hospital
for other reasons, should be closely monitored and may be treated prophylactically with oral
benzodiazepines. We use chlordiazepoxide. (See 'Prophylaxis' above.)
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Topic 323 Version 33.0
GRAPHICS
Timing of alcohol withdrawal syndromes
Onset after last

Syndrome Clinical findings
drink
Minor Tremulousness, mild anxiety, headache, diaphoresis, palpitations, anorexia, GI 6 to 36 hours

withdrawal upset; Normal mental status
Seizures Single or brief flurry of generalized, tonic-clonic seizures, short post-ictal 6 to 48 hours
period; Status epilepticus rare
Alcoholic Visual, auditory, and/or tactile hallucinations with intact orientation and normal 12 to 48 hours
hallucinosis vital signs
Delirium Delirium, agitation, tachycardia, hypertension, fever, diaphoresis 48 to 96 hours

tremens
Graphic 75499 Version 1.0
Suggested criteria for ICU admission of patients with alcohol withdrawal
Age >40
Cardiac disease (heart failure, arrhythmia, angina, myocardial ischemia, recent myocardial infarction)
Hemodynamic instability
Marked acid-base disturbances
Severe electrolyte abnormalities (hypokalemia, hypophosphatemia, hypomagnesemia, hypocalcemia)
Respiratory insufficiency (hypoxemia, hypercapnia, severe hypocapnia, pneumonia, asthma, COPD)
Potentially serious infections (wounds, pneumonia, trauma, urinary tract infection)
Signs of gastrointestinal pathology (pancreatitis, GI bleeding, hepatic insufficiency, suspected peritonitis)
Persistent hyperthermia (T >39°C [103°F])
Evidence of rhabdomyolysis
Renal insufficiency or increased fluid requirements
History of prior alcohol withdrawal complications (eg, delirium tremens, alcohol withdrawal seizures)
Need for frequent or high doses of sedatives or an intravenous infusion to control symptoms
Withdrawal despite an elevated ethanol concentration
COPD: Chronic obstructive pulmonary disease; GI: Gastrointestinal; ICU: Intensive care unit
Adapted from Carlson, RW, Keske, B, Cortez, D, J Crit Illness 1998; 13:311.
Treatment of severe alcohol withdrawal when IV diazepam is not

available*
AWS: alcohol withdrawal syndrome; CIWA: clinical institute withdrawal assessment for alcohol scale; RASS:
richmond agitation sedation scale.
* Doses are for adults. Medications and doses may need adjustment based upon comorbities (eg, liver
disease), patient age, or other factors (eg, coadministered medications).
¶ Lorazepam infusion is titrated to effect, and additional symptom-based bolus doses, 2-4 mg IV, are given
when titrating the infusion up.
Courtesy of Robert S. Hoffman, MD.
Clinical Institute Withdrawal Assessment Scale for Alcohol, revised (CIWA-Ar)
Nausea and vomiting Headache

0 No nausea or vomiting 0 Not present
1 1 Very mild
2 2 Mild
3 3 Moderate
4 Intermittent nausea with dry heaves 4 Moderately severe
5 5 Severe
6 6 Very severe
7 Constant nausea, frequent dry heaves and vomiting 7 Extremely severe
Paroxysmal sweats Auditory disturbances

0 No sweats visible 0 Not present
1 Barely perceptible sweating, palms moist 1 Very mild harshness or ability to frighten
2 2 Mild harshness or ability to frighten
3 3 Moderate harshness or ability to frighten
4 Beads of sweat obvious on forehead 4 Moderately severe hallucinations
5 5 Severe hallucinations
6 6 Extremely severe hallucinations
7 Drenching sweats 7 Continuous hallucinations
Anxiety Visual disturbances

0 No anxiety, at ease 0 Not present
1 1 Very mild photosensitivity
2 2 Mild photosensitivity
3 3 Moderate photosensitivity
4 Moderately anxious, guarded 4 Moderately severe visual hallucinations
5 5 Severe visual hallucinations
6 6 Extremely severe visual hallucinations
7 Acute panic state, consistent with severe delirium or 7 Continuous visual hallucinations
acute schizophrenia
Tactile disturbances
Agitation
0 None
0 Normal activity
1 Very mild paresthesias
1 Somewhat more than normal activity
2 Mild paresthesias
2
3 Moderate paresthesias
3
4 Moderately severe hallucinations
4 Moderately fidgety and restless
5 Severe hallucinations
5
6 Extremely severe hallucinations
6
7 Continuous hallucinations
7 Paces back and forth during most of the interview or
constantly thrashes about Orientation and clouding of sensorium
0 Oriented and can do serial additions
Tremor
1 Cannot do serial additions
0 No tremor
1 Not visible, but can be felt at fingertips 2 Disoriented for date by no more than 2 calendar days
2 3 Disoriented for date by more than 2 calendar days
3 4 Disoriented for place and/or patient
4 Moderate when patient's hands extended Total score is a simple sum of each item score
(maximum score is 67).
5
Score:
6
<10: Very mild withdrawal
7 Severe, even with arms not extended
10-15: Mild withdrawal
16-20: Modest withdrawal
>20: Severe withdrawal
Adapted from Sullivan JT, Skyora K, Schneiderman J, et al. Br J Addict 1989; 84:1353.
Richmond agitation-sedation scale (RASS)
Score Term Description
+4 Combative Overtly combative or violent, immediate danger to staff
+3 Very agitated Pulls on or removes tubes or catheters, aggressive behavior toward staff
+2 Agitated Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1 Restless Anxious or apprehensive but movements not aggressive or vigorous
0 Alert and calm
-1 Drowsy Not fully alert, sustained (>10 seconds) awakening, eye contact to voice
-2 Light sedation Briefly (<10 seconds) awakens with eye contact to voice
-3 Moderate sedation Any movement (but no eye contact) to voice
-4 Deep sedation No response to voice, any movement to physical stimulation
-5 Unarousable No response to voice or physical stimulation
Procedure
1. Observe patient. Is patient alert and calm (score 0)?
2. Does patient have behavior that is consistent with restlessness or agitation?
Assign score +1 to +4 using the criteria listed above.
3. If patient is not alert, in a loud speaking voice state patient's name and direct patient to open eyes and look
at speaker. Repeat once if necessary. Can prompt patient to continue looking at speaker.
Patient has eye opening and eye contact, which is sustained for more than 10 seconds (score -1).
Patient has eye opening and eye contact, but this is not sustained for 10 seconds (score -2).
Patient has any movement in response to voice, excluding eye contact (score -3).
4. If patient does not respond to voice, physically stimulate patient by shaking shoulder and then rubbing
sternum if there is no response.
Patient has any movement to physical stimulation (score -4).
Patient has no response to voice or physical stimulation (score -5).
Reproduced with permission from: Sessler, C, Gosnell, M, Grap, MJ, et al. The Richmond agitation-sedation scale. Validity and
reliability in adult intensive care unit patients. Am J Respir Crit Care Med 2002; 166:1338. Copyright © 2002 American
Thoracic Society.
Moderate and severe alcohol withdrawal: Rapid overview
To obtain emergent consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-222-
1222, or access the World Health Organization's list of international poison centers
(www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html).
Syndromes
Alcohol tremulousness - occurs early, characterized by hypertension, tachycardia, tremors, and anxiety, with normal
mental status
Alcohol withdrawal seizures - occurs early, usually single or brief flurry of seizures with short post-ictal period
Alcoholic hallucinosis - occurs early, no evidence of autonomic instability
Delirium tremens - occurs late, characterized by delirium and autonomic instability
History
Pattern of alcohol use, history of withdrawal symptoms; inquire about reasons for cessation of alcohol
Physical examination
Vital signs, mental status, presence of tremor; examine for signs of trauma, abdominal tenderness, other findings
consistent with complications of chronic alcohol use
Laboratory testing
No test truly assesses withdrawal; ancillary data (eg, serum ethanol concentration, lumbar puncture (CSF), head CT,
lipase) frequently needed to assess patient and rule out coexistent illness
Treatment
Benzodiazepines
First line therapy for ALL alcohol withdrawal syndromes
Most patients with symptoms require IV therapy initially
Give:
Diazepam, 5 to 10 mg IV, repeat every 5 to 10 minutes, OR
Lorazepam, 2 to 4 mg IV, repeat every 15 to 20 minutes
Massive doses (>2000 mg diazepam in 48 hours) may be required
Clinically stable patients with minimal symptoms may be treated with oral medications
Barbiturates
Synergistic with benzodiazepines; give if patient refractory to high-dose benzodiazepines
Phenobarbital 130 to 260 mg IV, repeat every 15 to 20 minutes
Intubation frequently required with concurrent benzodiazepine and barbiturate use
ALL patients requiring barbiturates are monitored in an intensive care unit
Propofol
Excellent agent if patient refractory to benzodiazepines and barbiturates
Intubation almost always required
1 mg/kg IV push as induction agent for intubation; titrate continuous infusion for sedation
Supportive care
Assure adequate fluid and electrolyte replacement
Give parenteral thiamine 100 mg and glucose daily
Give multivitamin supplements
Ensure adequate caloric support

Contributor Disclosures
Robert S Hoffman, MD Nothing to disclose Gerald L Weinhouse, MD Nothing to disclose Stephen J Traub,
MD Nothing to disclose Jonathan Grayzel, MD, FAAEM Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
Conflict of interest policy

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2/11/2017 Management of moderate and severe alcohol withdrawal syndromes - UpToDate

Official reprint from UpToDate®

Authors: Robert S Hoffman, MD, Gerald L Weinhouse, MD

COMPLICATIONS OF ALCOHOL WITHDRAWAL

Delirium tremens (DT)

Risk factors — Risk factors for the development of DT include [19-21]:

● A history of sustained drinking

Treatment of psychomotor agitation with benzodiazepines

Symptom-triggered therapy — We favor a symptom-triggered approach to the treatment of alcohol

● Basics topic (see "Patient education: Alcohol withdrawal (The Basics)")

SUMMARY AND RECOMMENDATIONS — A table summarizing the emergent management of alcohol

● Delirium tremens (DT) is a syndrome characterized by agitation, disorientation, hallucinations, and

● Risk factors for delirium tremens include:

• A history of sustained drinking

• Age greater than 30

• The presence of a concurrent illness

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 323 Version 33.0

Timing of alcohol withdrawal syndromes

Onset after last

Minor Tremulousness, mild anxiety, headache, diaphoresis, palpitations, anorexia, GI 6 to 36 hours

Delirium Delirium, agitation, tachycardia, hypertension, fever, diaphoresis 48 to 96 hours

Graphic 75499 Version 1.0

Suggested criteria for ICU admission of patients with alcohol withdrawal

Marked acid-base disturbances

Severe electrolyte abnormalities (hypokalemia, hypophosphatemia, hypomagnesemia, hypocalcemia)

Respiratory insufficiency (hypoxemia, hypercapnia, severe hypocapnia, pneumonia, asthma, COPD)

Potentially serious infections (wounds, pneumonia, trauma, urinary tract infection)

Signs of gastrointestinal pathology (pancreatitis, GI bleeding, hepatic insufficiency, suspected peritonitis)

Persistent hyperthermia (T >39°C [103°F])

Renal insufficiency or increased fluid requirements

Withdrawal despite an elevated ethanol concentration

Graphic 73377 Version 2.0

Treatment of severe alcohol withdrawal when IV diazepam is not

Courtesy of Robert S. Hoffman, MD.

Graphic 53322 Version 2.0

Clinical Institute Withdrawal Assessment Scale for Alcohol, revised (CIWA-Ar)

Nausea and vomiting Headache

4 Intermittent nausea with dry heaves 4 Moderately severe

7 Constant nausea, frequent dry heaves and vomiting 7 Extremely severe

Paroxysmal sweats Auditory disturbances

2 2 Mild harshness or ability to frighten

3 3 Moderate harshness or ability to frighten

4 Beads of sweat obvious on forehead 4 Moderately severe hallucinations

6 6 Extremely severe hallucinations

7 Drenching sweats 7 Continuous hallucinations

Anxiety Visual disturbances

1 1 Very mild photosensitivity

4 Moderately anxious, guarded 4 Moderately severe visual hallucinations

5 5 Severe visual hallucinations

6 6 Extremely severe visual hallucinations

2 3 Disoriented for date by more than 2 calendar days

3 4 Disoriented for place and/or patient

16-20: Modest withdrawal

>20: Severe withdrawal

Graphic 64835 Version 2.0

Richmond agitation-sedation scale (RASS)

Score Term Description