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 Slide1
I. INTRODUCTION Slide2
1. Epidemiology
2. Pathophysiology
3. Clinical Picture and Diagnosis
4. Treatment
II. EPIDEMIOLOGY
A. Epidemiology of Alcohol Use Disorders (AUD):1 Slide3
1.
15.3 million
have alcohol abuse or dependence
2.
13 % of men
and4 % of women over age 18
3.
More frequent
among European-Americans
4.
15-30% of
primary care and hospitalized patients
5.
40% trauma
patients have blood alcohol levels (BAL) Ò100 mg/dl
B. Alcohol Use Disorders (AUDs) can bedefined:2
Slide4
iv.Social/interpersonal problems
2. Alcohol
Dependence (AD):
C. Epidemiology
of Alcohol Withdrawal (AW):3,4,5,6
Slide5
1.
AW symptoms
affect up to 70 % of AD patients
2.
More frequent
in the elderly
3.
No gender or
ethnic differences
4.
85% of patients
with AW experience mild-to-moderate symptoms
5.
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
1. Glutamate:
a. Main excitatory neurotransmitter
b. ActivateNMDA receptors and voltage-operating channels:
ÐCalcium influx ¨neuronal excitability
c. Excessive activation ¨seizures, neurotoxicity and cell death
2. Effects of drinking on excitatory neurotransmission: 8
a. Alcohol antagonizes NMDA receptors
b. Chronic drinking and tolerance to alcohol are associated with compensatory:
i. ÐNMDA receptors number
ii. ÐCalcium (Ca) channels
3.Excitatory neurotransmission during AW: 8 Slide8
a. Rodents show Ðglutamate / 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 ÐGlutamate in cerebrospinal fluid (CSF)
c. In summary:During AW there is Ðexcitatory neurotransmission
C.
Inhibitoryneurotransmission and AW: 9
Slide9
1. GABA:
a. Maininhibitory neurotransmitter
b. Activatesreceptor-operated öCL channels
i. Membranehyper-polarization (Ðstability)
ii.øNeuronal excitability
2. Effects of drinking on GABA: 9
a. Acute alcohol ¨ Ð GABAA receptorfunction
bChronic drinking ¨øGABAA 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) ¨ ÐAW seizures and delirium
c. In summary,changes in GABA neurotransmission during AW translate:
i. Impairment ofneuronal inhibitory mechanisms
ii.Ð Anxiety,Ðsympatheticactivity and seizures
E. Dopamine (DA):10 Slide10
1. Mainneurotransmitter mediating reward:
a. Released bythe Ventrotegmental area (VTA) into the NAC
b. Occurs inanticipation and during rewarding stimuli (i.e., food, sex)
2. Effects of drinking on DA: 10
a. Acute alcohol ¨Ð DA in NAC
b. Chronic drinking and tolerance ¨ ø DAin NAC
3. DA and AW: 10 Slide11
i. ÐDAdeficit 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.ÐDAand homovanilic acid in CSF
ii.øGABAactivity leads to ÐDA
5. In summary,during AW:
i. DA deficit inthe NAC mediates negative mood states
ii. However,delirium and hallucinations are associated with Ð DA
F. OtherNeurotransmitter
Systems:
Slide12
i. Anxiogenic-likeresponse
ii. CRFR1antagonists block this effect
iii. ÐStress sensitivity even after acute AW symptoms subside
AWPathophysiology: Key Issues:7 Slide13
1. Brainhomeostasis reflects a balance between:
a. Excitatory
b. Inhibitory neurotransmission
2. Neuroadaptation:
a. Chronic drinking ¨ neuroadaptation to maintain homeostasis
b. Allows brain functioning while disturbed by alcohol
c. During AW neuroadaptive mechanisms are out of balance:
i. Neuronal overexcitation ¨ autonomic hyperactivityand seizures
ii. 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, øDA clearance ¨ÐDA18
ii. Short
alleleof 5-HT transporter, ø 5-HT clearance14
iii. A1 allele ofthe DRD2, øDRD2 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
1. Completehistory, physical, and mental status exam
2. Laboratorytest
3. Standardizedassessments
C. History andPhysical: Slide17
1. Predictors ofAW
severity:
a. Older age
b. ÐSeverityof drinking and high tolerance
c. ÐNumber 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
ii. GI:Dyspepsia, gastritis, hepatitis or liver cirrhosis stigmata (jaundice, Ðbleeding 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).
1. BloodAlcohol Levels (BAL):
a. Doesnot detect heavy drinking but identifies acute intake (~ 12-18 hours)
b. Poorprognosis when AW occurs with intoxicating BAL (0.08-0.10 g/dl)
2. Gamma-glutamyltransferase(GGTP):
a. Alcoholenzymatic induction ÐGGTP
b. Normalizationafter 2-3 weeks of abstinence
c. Sensitivity:40-60%, specificity: 80% if value >35 IU/L
3. CarbohydrateDeficient Transferrin (CDT):21
a. Heavydrinking induces deglycosylation of transferring
b. Normalizesin 1-2 weeks
c.
Sensitivity: 60-80%,
specificity:80-90% if value >20 IU/L
d.
CDT + GGTP best
diagnosticcombination
4. Erythrocytemean corpuscular volume (MCV):
a. Alcohol/acetaldehydeinterfere with nuclear maturation of red blood cells ¨ macrocytosis
b. Folicacid or B12 deficiency also ¨ macrocytosis(MCV >91.5 m3)
c. Upto a third of heavy drinkers
d. 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:
a. Agitation
b. Anxiety
c. Auditorydisturbances
d. Cloudingof sensorium
e. Headache
f. Nausea/vomiting
g. Paroxysmalsweats
h. Tactiledisturbances
i. Tremor
j. Visual disturbances
3. InitialCIWA-Ar severity and need of medication:
a. Score8-10 (mild), usually some nausea,anxiety and headache no need for pharmacological treatment
b. Score10-15 (moderate) marked autonomic activity
c. Score> 15 (severe) impending deliriumtremens and urgency of pharmacological treatment
4. Subsequentassessments:
a. Every4-8 hours to assess effectiveness of treatment
b. 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, Ðheart 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):
i. Intensified stage 1 symptoms
ii. Severe tremors
iii. Psychomotor agitation
iv. Hallucinations
c. Stage 3 (72 ö105 hours): ãDelirium Tremens:ä
i.Confusion and disorientation
ii.Psychomotor agitation
iii.ÐVisual and auditory hallucinations
iv. Severe autonomic hyperactivity
v. 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 Slide22
a. 10 -20% ofpatients:
i. Baseline CIWA > 15
ii. CIWA 8 ö15 plus other admission criteria
iii. Multiple episodes of AW and detoxifications
iv. High AW severity during previous episodes
v. History of AW seizures and/or delirium tremens
vi. Major medical or surgical problems
vii. Major psychiatric and/or drug problems
viii. Poor family/social support, homelessness
ix. 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.ÐGABAAreceptor function
b.Greater efficacy than placebo
i.øSeizure: ~ 90%
ii. øDelirium: ~ 70%
c.Greater efficacy and safety than other sedative-hypnotics
3. Choice of abenzodiazepine: Slide24
a. Allbenzodiazepines are effective
b. Longerhalf-life benzodiazepines (e.g., chlordiazepoxide [Librium], diazepam [Valium])
i. More effective than shorter half life in øseizures: ~ 58%
ii. Smoother AW
c. Shorterhalf-life agents (e.g., lorazepam [Ativan], oxazepam [Serax])
i. Less oversedation
ii. 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.øDose 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 Ò 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 øprotracted 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 ø 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.ÐSide 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. Ð seizurerisk
iii. Mayhelp controlling agitation
2. b-Adrenergicantagonist (propanolol [Inderal]) and α-adrenergic agonist (clonidine[Catapres])
a. ø Autonomic activity
b. May hide impending seizures
3. Magnesium
a. ø Levels during AW
b. Supplementation does not ø 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 ø 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: Slide30
1. AW is a common problem inclinical settings
2. AW pathophysiology characterizedby:
a. Imbalance ofneuroadaptive mechanism
b. ÐExcitatoryneuronal activity
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
|
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. |
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 |
|
TREMOR -- Arms extended and fingers spread apart.
Observation. |
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. |
|
PAROXYSMAL SWEATS -- Observation. |
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. |
|
ANXIETY -- Ask "Do you feel nervous?"
Observation. |
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. |
|
AGITATION -- Observation. |
ORIENTATION AND CLOUDING OF SENSORIUM -- Ask
"What day is this? Where are you? Who am I?" |
|
|
Total CIWA-Ar
Score ______ |