ALCOHOL WITHDRAWAL: PATHOPHYSIOLOGY, DIAGNOSIS
ANDTREATMENT
Carlos A. Hernandez-Avila,M.D.
Department of PsychiatryUniversity of Connecticut School of Medicine
Alcohol Medical ScholarsProgram
Prepared: April 2005
I. INTRODUCTION
Slide1
Slide2
A. Alcohol Dependence (AD), major cause of mortality and morbidity
B. More than 2/3 of AD patients in clinical settings have Alcohol Withdrawal (AW)
C. AW often presents as anxiety and insomnia. Misdiagnosis can be deadly
D. Topics to be covered:
Epidemiology
Pathophysiology
Clinical Picture and Diagnosis
Treatment
II. EPIDEMIOLOGY
A. Epidemiology of Alcohol Use Disorders (AUD):1
Slide3
15.3 million have alcohol abuse or dependence
13 % of men and4 % of women over age 18
More frequent among European-Americans
15-30% of primary care and hospitalized patients
40% trauma patients have blood alcohol levels (BAL) 100 mg/dl
B. Alcohol Use Disorders (AUDs) can bedefined:2
a.
Slide4
1. Alcohol Abuse:
b. Significant impairment/distress in a 12-month period
c. Diagnosis requires 1+ of following:
d.
i. Failure to fulfill major obligations
e.
ii.Hazardous activities during intoxication
f.
iii.Legal problems
iv.Social/interpersonal problems
2. Alcohol Dependence (AD):
g. Significant impairment/distress in a 12-month period
h. Diagnosis requires 3+ of following:
i.
i. Tolerance
j.
ii. Withdrawal
k.
iii.Larger amounts for longer period than intended
l.
iv.Persistent desire and unsuccessful attempts to cut down
m.
v. Excessive time spent drinking alcohol
n.
vi. Activities given up due to drinking
o.
vii. Continued use despite problems
C. Epidemiology of Alcohol Withdrawal (AW):3,4,5,6
AW symptoms affect up to 70 % of AD patients
Slide5
More frequent in the elderly
No gender or ethnic differences
85% of patients with AW experience mild-to-moderate symptoms
15% severe symptoms with complicating conditions:
a.Seizures, 10% of the cases
b.Delirium Tremens, 5%
i.In the past, mortality rate was 15-25%
ii.Currently  1%
III. PATHOPHYSIOLOGY OF ALCOHOLWITHDRAWAL
A. Alcohol effects in the brain:7
Slide6
1. Variable effects as a function of duration of administration
2. No single site of action
3. Affects multiple neurotransmitter systems:
a. Glutamate and aspartate
b. GABA
c. Dopamine
d. Noradrenaline
e. Corticotropin-releasing-factor
B. Excitatory neurotransmitter systems and AW:8
Slide7
Glutamate:
Main excitatory neurotransmitter
ActivateNMDA receptors and voltage-operating channels:
Calcium influx neuronal excitability
Excessive activation seizures, neurotoxicity and cell death
Effects of drinking on excitatory neurotransmission: 8
Alcohol antagonizes NMDA receptors
Chronic drinking and tolerance to alcohol are associated with
compensatory:
NMDA receptors number
Calcium (Ca) channels
3.Excitatory neurotransmission during AW: 8
Slide8
a. Rodents show glutamate / aspartate in brain regions related to:
i.Reward (e.g. Striatum and Nucleus Accumbens [NAC])
ii. Alcoholcognitive disturbances and AW seizures (e.g.
Hippocampus)
b. Patients show Glutamate in cerebrospinal fluid (CSF)
c. In summary:During AW there is excitatory neurotransmission
C. Inhibitoryneurotransmission and AW: 9
Slide9
GABA:
a. Maininhibitory neurotransmitter
b. Activatesreceptor-operated öCL channels
i. Membranehyper-polarization (stability)
ii.Neuronal excitability
Effects of drinking on GABA: 9
a. Acute alcohol   GABAA receptorfunction
bChronic drinking GABAA receptor sensitivity  tolerance
3. GABA and AW:9
a. During AW GABAAreceptor remains impaired
b. Repeated AWfurther impairs GABAA receptor  neuronal
excitability(e.g. neuronal ãkindlingä)  AW seizures and delirium
c. In summary,changes in GABA neurotransmission during AW translate:
i. Impairment ofneuronal inhibitory mechanisms
ii. Anxiety,sympatheticactivity and seizures
E. Dopamine (DA):10
Slide10
Mainneurotransmitter mediating reward:
a. Released bythe Ventrotegmental area (VTA) into the NAC
b. Occurs inanticipation and during rewarding stimuli (i.e., food, sex)
Effects of drinking on DA: 10
a. Acute alcohol  DA in NAC
b. Chronic drinking and tolerance   DAin NAC
3. DA and AW: 10
Slide11
i. DAdeficit in NAC
ii. Negativemoods (i.e., dysphoria, anhedonia or loss of ability to
enjoy previously rewardingactivities)
ii. Reassumingdrinking reverses DA deficit
iv. Drinkingrelieves negative moods (i.e., negative reinforcing).
4. When AW iscomplicated with delirium and hallucinations:
i.DAand homovanilic acid in CSF
ii.GABAactivity leads to DA
5. In summary,during AW:
i. DA deficit inthe NAC mediates negative mood states
ii. However,delirium and hallucinations are associated with  DA
F. OtherNeurotransmitter Systems:
Slide12
1. Norepinephrine and methoxy-4-hydroxyphenilglycol (MHPG):11
a.  Plasma concentrations correlate with BP, pulse, tremors and
diaphoresis
b. 2-adrenoreceptor regulation of norepinephrine release
2. Corticotropin-releasing-factor (CRF): 12, 13
a. Long lasting CRF levels in CSF and amygdale
b. CRFR1 receptor sensitivity
i. Anxiogenic-likeresponse
ii. CRFR1antagonists block this effect
iii. Stress sensitivity even after acute AW symptoms subside
AWPathophysiology: Key Issues:7
Slide13
Brainhomeostasis reflects a balance between:
Excitatory
Inhibitory neurotransmission
Neuroadaptation:
Chronic drinking  neuroadaptation to maintain homeostasis
Allows brain functioning while disturbed by alcohol
During AW neuroadaptive mechanisms are out of balance:
Neuronal overexcitation  autonomic hyperactivityand seizures
Reward deficit  negative mood states and urges to drink
G. Genetics of Alcohol Withdrawal:Association Studies:
Slide14
1. AD patients differ in AWpredisposition even drinking similar amounts14
2. There is a predisposition tocomplications of heavy drinking (e.g., alcoholic liver
disease) independentfrom genes predisposing to AD15,16
3. Evidence of genetic factorsconferring predisposition to AW:
a.Genetic lines of rodents prone to AW seizures17
b.Human gene variants (e.g., alleles) associated with AW seizures and delirium:
i. A9 allele ofDA transporter, DA clearance DA18
ii. Short alleleof 5-HT transporter,  5-HT clearance14
iii. A1 allele ofthe DRD2, DRD2 density depression during AW19
IV. DIAGNOSIS AND EVALUATION
A. AW DiagnosticCriteria (DSM-IV):2
Slide15
1. Severity may bevariable: mild to life threatening
2. Begins a fewhours or days (1-2) after cessation or reduction of prolonged
drinking
3. Symptoms causesignificant distress or impairment
4. Is not due toanother medical or mental disorder
5. Diagnosis: 2+of:
a.Autonomic hyperactivity (e.g., sweating or pulse > 100)
b.Hand tremor
c. Insomnia
d. Nausea orvomiting
e. Transientvisual, tactile or auditory hallucinations or illusions
f. Agitation
g. Anxiety
h. Grand malseizures
B. OptimalAssessment of AW requires:
Slide16
Completehistory, physical, and mental status exam
Laboratorytest
Standardizedassessments
C. History andPhysical:
1. Predictors ofAW severity:
a. Older age
b. Severityof drinking and high tolerance
c. Number of AW episodes and detoxifications
d. History ofprevious AW seizures of delirium tremens
e. Presence of AW symptoms despite high BAL
f. Major medical or surgical problems
g. Concomitantsedative/hypnotic use
2. Physical and mental status exam:
a.Signs suggestive of chronic alcohol drinking:
i.General: Underweight, chronic fatigue
Slide17
ii. GI:Dyspepsia, gastritis, hepatitis or liver cirrhosis stigmata
(jaundice, bleeding time, ascitis, GI bleeding, spider angiomas,
bruises)
iii.Immunological: Opportunistic infections
iv.Cardiovascular: Hypertension, cardiomyopathy, arrhythmia
v. Osteoporosisand pathological fractures
vi.Neuropsychiatric: Neuropathy, seizures, delirium,
encephalopathy and/ordementia, mood, anxiety and psychotic
symptoms
b. However,average alcoholic may present with a relatively normal
appearance.
D. LaboratoryTests:20
Slide18
No AW specific test. Lab testing identifies acute and/or heavy drinking
(>5drinks/day).
BloodAlcohol Levels (BAL):
Doesnot detect heavy drinking but identifies acute
intake (~ 12-18 hours)
Poorprognosis when AW occurs with intoxicating BAL
(0.08-0.10 g/dl)
Gamma-glutamyltransferase(GGTP):
Alcoholenzymatic induction GGTP
Normalizationafter 2-3 weeks of abstinence
Sensitivity:40-60%, specificity: 80% if value >35 IU/L
CarbohydrateDeficient Transferrin (CDT):21
Heavydrinking induces deglycosylation of transferring
Normalizesin 1-2 weeks
Sensitivity: 60-80%, specificity:80-90% if value >20
IU/L
CDT + GGTP best diagnosticcombination
Erythrocytemean corpuscular volume (MCV):
Alcohol/acetaldehydeinterfere with nuclear maturation
of red blood cells  macrocytosis
Folicacid or B12 deficiency also  macrocytosis(MCV
>91.5 3)
Upto a third of heavy drinkers
Sensitivity:30-40%, specificity: 80%
StandardizedEvaluation: The Clinical InstituteWithdrawal Assessment,
revised (CIWA-Ar [Appendix 1]). 22
Slide19
1. Validated indetoxification, psychiatric and medical/surgical units
2. Severity scaleranging from 0 to 7, items include:
Agitation
Anxiety
Auditorydisturbances
Cloudingof sensorium
Headache
Nausea/vomiting
Paroxysmalsweats
Tactiledisturbances
Tremor
Visual disturbances
3. InitialCIWA-Ar severity and need of medication:
Score8-10 (mild), usually some nausea,anxiety and
headache no need for pharmacological treatment
Score10-15 (moderate) marked autonomic activity
Score> 15 (severe) impending deliriumtremens and
urgency of pharmacological treatment
4. Subsequentassessments:
Every4-8 hours to assess effectiveness of treatment
Untilscore < 8-10 for 24 hours
F. Natural courseof AW symptoms:
Slide20
1. Progressioncan be divided in 4 stages (not everyone has all four):
a.Stage 1 (24 ö 48 hours):
i. 6-8 hours: anxiety, tremor, nausea andvomiting, heart
rate and blood pressure
ii. Insomnia,illusion and hallucinations
ii. Peak severity occurs after 36 hours
iii. 90% of AWseizures occur in this stage
iv. Most AW casesare self-limited to this stage
b. Stage 2 (48 ö72 hours):
Intensified stage 1 symptoms
Severe tremors
Psychomotor agitation
Hallucinations
c. Stage 3 (72 ö105 hours): ãDelirium Tremens:ä
i.Confusion and disorientation
ii.Psychomotor agitation
iii.Visual and auditory hallucinations
iv. Severe autonomic hyperactivity
Admission to an ICU may be warranted
d. Stage 4 ( > 7 days): Not typically recognized asa part of the AW natural
history. Also known as protracted withdrawal:
i. Last 2 ö 4+weeks. Some symptoms last months
ii. Anxiety,chronic fatigue, depression, sleep disturbances
and headache
iii. Symptomscontribute to relapse
V. TREATMENT of AW
A. Treatment Setting: Ambulatory orInpatient?
Slide21
1. Outpatient(O/P) treatment overview:23
a. 80% can betreated
b. AW severity:
i.CIWA <8
ii.Some cases with CIWA 8 ö15
iii.No hx. of AW seizures or delirium
iv.No serious medical/surgical problems
v.No serious comorbid psychiatric or drug problems
vi.Has social support
vii.Supervision and housing available
2. Inpatient (I/P) treatment29
a. 10 -20% ofpatients:
Baseline CIWA > 15
CIWA 8 ö15 plus other admission criteria
Multiple episodes of AW and detoxifications
High AW severity during previous episodes
History of AW seizures and/or delirium tremens
Major medical or surgical problems
Slide22
Major psychiatric and/or drug problems
Poor family/social support, homelessness
Pregnancy
B. Benzodiazepines and AW: 30
Slide23
1.Benzodiazepines: First line oftreatment. Provide the best combination of
efficacy, safety and cost
2. Six prospectivetrials involving 5 different agents
a.GABAAreceptor function
b.Greater efficacy than placebo
i.Seizure: ~ 90%
ii. Delirium: ~ 70%
c.Greater efficacy and safety than other sedative-hypnotics
3. Choice of abenzodiazepine:
Slide24
Allbenzodiazepines are effective
Longerhalf-life benzodiazepines (e.g., chlordiazepoxide [Librium],
diazepam [Valium])
More effective than shorter half life in seizures: ~ 58%
Smoother AW
Shorterhalf-life agents (e.g., lorazepam [Ativan], oxazepam [Serax])
Less oversedation
Indicated in the elderly and liver impairment
4. Fixed scheduletherapy: 30
Slide25
a. A typical benzodiazepine regimen consists:On day 1, one of the
following Q 6 h:
i.Chlorodiazepoxide, 50 ö 100 mg
ii. Diazepam, 10ö 20 mg
iii. Lorazepam, 2ö 4 mg
iv. When symptomsnot controlled (or CIWA > 8 ö10) provide
additional dose
v.Dose 20% each day
5. However infixed standardized therapy with benzodiazepines:
a.Dose to control AW symptoms vary greatly
b. Fixed regimensfrequently do not properly treat AW (i.e., undermedicate
or overmedicate)
c.Treatment should allow
i.Individualization
ii.Rapid appropriate dosing
6.Symptom-triggered therapy: 30,31
Slide26
a.Allows objective titration to individual needs:
i. CIWA-Ar assessmentand monitoring
ii. Medicationadministration triggered by a severity threshold
b.Two controlled clinical trials:
i.Comparable efficacy to fixed schedule treatment
ii.Less medication, less side effects, and shorter treatment
ii. No seizures episodes
c.One of these agents every hour when CIWA is  8-10:
i. Chlorodiazepoxide,50-100 mg
ii. Diazepam, 10 ö20 mg
iii. Lorazepam, 2-4 mg
C. Anticonvulsantsand AW
1. Carbamazepine(CBZ) and Valproate (VPA): 27, 28, 30, 3 2
Slide
27
a. CBZ: 6controlled trials, VPA: 1 controlled trial:
i.Both better than placebo in mild to moderate AW
ii. CBZ similarthan oxazepam and lorazepam but greater reduction
of distress and faster returnto work
ii. CBZ also protracted AW symptoms (i.e., insomnia, anxiety,
psychological distress)
ii. Both, CBZ andVPA prevent AW seizures in animals, limited
human data
iii.Anti-kindling effect so may  future AW severity
iv.Do not potentiate alcohol CNS and respiratory depression
v.No impairment of psychomotor abilities or cognition
vi. No abusepotential
vii.Limited data on prevention/treatment of delirium
viii. Nohematological or hepatic toxic effects when used for 7 days
b.CBZ and VPA limitations
i.In general not better than benzodiazepines
ii.Side effects and potential toxicity
iii.5 ö 10 times greater cost
D.Other Agents: 30
Slide28
1. Antipsychotics
a. Phenotiazines andbutyrophenones
b. Less effective thanbenzodiazepines preventing delirium
ii.  seizurerisk
iii. Mayhelp controlling agitation
2. -Adrenergicantagonist (propanolol [Inderal]) and α-adrenergic agonist
(clonidine[Catapres])
a.  Autonomic activity
b. May hide impending seizures
3. Magnesium
a.  Levels during AW
b. Supplementation does not  AWseverity
4. Ethyl Alcohol
a.No evidence of efficacy
b.Toxic, expensive and risk of tissue damage
3.Nonpharmacological treatment:
Slide29
a.Quiet environment to  sensory stimulation
b. Nutrition andhydration
i. Oral thiamine(before glucose administration) and folic acid.
Prevents Wernicke-Korsakoffsyndrome
ii.Does not prevent seizures or delirium
iii. Oral fluidsand electrolytes if necessary (magnesium, calcium
and phosphates)
c. Orientation toreality
d. Supportivebrief interventions: Motivate to change
e. Referral to AAand relapse prevention treatment
F. Conclusions:
1. AW is a common problem inclinical settings
Slide30
2. AW pathophysiology characterizedby:
a. Imbalance ofneuroadaptive mechanism
b. Excitatoryneuronal activity
3. Clinicians mustactively screen for AD and potential AW
4. If untreated can be deadly
5. Benzodiazepines are the mosteffective and safest treatment
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Appendix 1. Addiction Research Foundation Clinical InstituteWithdrawal Assessment
Appendix 1
CIWA-Ar
Patient:__________________________ Date: ________________ Time: _______________.(24 hour clock,
midnight = 00:00)
Pulse or heart rate, taken for one minute:_________________________ Blood pressure:______
NAUSEA AND VOMITING -- Ask "Do you
feel sick to your stomach? Have you vomited?"
Observation.
0 no nausea and no vomiting
1 mild nausea with no vomiting
2
3
4 intermittent nausea with dry heaves
5
6
7 constant nausea, frequent dry heaves and
vomiting
TACTILE DISTURBANCES -- Ask "Have you any itching,
pins and needles sensations, any burning, any numbness, or do
you feel bugs crawling on or under your skin?" Observation.
0 none
1 very mild itching, pins and needles, burning or numbness
2 mild itching, pins and needles, burning or numbness
3 moderate itching, pins and needles, burning or numbness
4 moderately severe hallucinations
5 severe hallucinations
6 extremely severe hallucinations
7 continuous hallucinations
TREMOR -- Arms extended and fingers spread
apart. Observation.
0 no tremor
1 not visible, but can be felt fingertip to fingertip
2
3
4 moderate, with patient's arms extended
5
6
7 severe, even with arms not extended
AUDITORY DISTURBANCES -- Ask "Are you more aware of
sounds around you? Are they harsh? Do they frighten you? Are
you hearing anything that is disturbing to you? Are you hearing
things you know are not there?" Observation.
0 not present
1 very mild harshness or ability to frighten
2 mild harshness or ability to frighten
3 moderate harshness or ability to frighten
4 moderately severe hallucinations
5 severe hallucinations
6 extremely severe hallucinations
7 continuous hallucinations
PAROXYSMAL SWEATS -- Observation.
0 no sweat visible
1 barely perceptible sweating, palms moist
2
3
4 beads of sweat obvious on forehead
5
6
VISUAL DISTURBANCES -- Ask "Does the light appear to be
too bright? Is its color different? Does it hurt your eyes? Are you
seeing anything that is disturbing to you? Are you seeing things
you know are not there?" Observation.
0 not present
1 very mild sensitivity
2 mild sensitivity
3 moderate sensitivity
7 drenching sweats
4 moderately severe hallucinations
5 severe hallucinations
6 extremely severe hallucinations
7 continuous hallucinations
ANXIETY -- Ask "Do you feel nervous?"
Observation.
0 no anxiety, at ease
1 mild anxious
2
3
4 moderately anxious, or guarded, so anxiety is
inferred
5
6
7 equivalent to acute panic states as seen in
severe
delirium or acute schizophrenic reactions
HEADACHE, FULLNESS IN HEAD -- Ask "Does your head
feel different? Does it feel like there is a band around your head?"
Do not rate for dizziness or lightheadedness. Otherwise, rate
severity.
0 not present
1 very mild
2 mild
3 moderate
4 moderately severe
5 severe
6 very severe
7 extremely severe
AGITATION -- Observation.
0 normal activity
1 somewhat more than normal activity
2
3
4 moderately fidgety and restless
5
6
7 paces back and forth during most of the
interview,
or constantly thrashes about
ORIENTATION AND CLOUDING OF SENSORIUM -- Ask
"What day is this? Where are you? Who am I?"
0 oriented and can do serial additions
1 cannot do serial additions or is uncertain about date
2 disoriented for date by no more than 2 calendar days
3 disoriented for date by more than 2 calendar days
4 disoriented for place/or person
Total CIWA-Ar Score ______
Rater's Initials ______
Maximum Possible Score 67