Alcohol Use Disorder Assessment & Treatment Strategies - PowerPoint Presentation

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Alcohol Use DisorderAssessment & Treatment Strategies

Sharon Vipler

MD, CCFP,

dipl.ABAMSlide2

St. Pauls’ Hospital Addiction Medicine Consult Team

Medical Lead, Creekside Withdrawal Management Centre (Inpatient unit and RAAC)

Surrey Memorial Hospital Addiction Medicine Consult Liaison team Quibble Creek Opioid Agonist Therapy ClinicBCCSU Clinical Expert DisclosuresNo financial or commercial conflicts of interest and no identified mitigating biases. Slide3

ObjectivesDiagnosis of Alcohol Withdrawal

Understand the neurobiology of acute alcohol withdrawal and develop an approach to the management of acute withdrawal

Explore the pharmacological options for relapse preventionSlide4

But first…Slide5

What’s being used? Slide6

Who’s using Alcohol Slide7
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Alcohol and the Brain

Alcohol is a central nervous system depressant

It simultaneously enhances inhibitory tone (via GABA) and inhibits excitatory tone (via glutamate)Constant presence of ethanol = new homeostasis Abrupt cessation = Reveals adaptive responses to chronic ethanol use Results in over activity of central nervous system

Management of Moderate and Severe Alcohol Withdrawal Syndromes --

UpToDateSlide13

GABA (gamma aminobutyric

acid)

Major inhibitory neurotransmitter in the brainHighly specific binding sites for ethanol on GABA receptor complex.Constant etoh = insensitivity to GABA = more inhibitor required to maintain constant inhibitory toneAs

etoh

tolerance develops – Arousal is maintained at alcohol concentrations normally producing lethargy in relatively alcohol

na

ï

ve

patients.

Cessation (or reduction) of alcohol = decreased inhibitory tone. Slide14

Excitatory Amino Acids(Glutamate)

Glutamate is one of the major excitatory amino acids.

Binds to NMDA receptor = calcium influx, leading to neuronal excitation.Ethanol inhibits glutamate induced excitation. Adaptation occurs by increasing number of glutamate receptors in an attempt to maintain a normal state of arousal.Cessation (reduction) of alcohol results in unregulated excess excitation. Slide15

Acute Withdrawal Slide16

Minor Withdrawal Symptoms

Insomnia

TremulousnessMild anxietyGastrointestinal upset; anorexia HeadacheDiaphoresisPalpitationsSymptoms usually present

within 6 hours

of cessation of drinking.

Can develop while patient still has a significant blood alcohol concentration

If no further progression of withdrawal, symptoms can

resolve within 24 to 48

hoursSlide17

Withdrawal Seizures

Generalized tonic

clonic convulsionsUsually singular or a brief flurry of seizures over a short periodUsually occur within 12-48 hours after the last drinkSlide18

Alcoholic Hallucinosis

NOT synonymous with delirium tremens

Usually visual hallucinationsAuditory and tactile hallucinations may also occurNo associated global clouding of sensorium and vital signs usually normalDevelop within 12-24 hours of abstinence Typically resolve within 24-48 hours (earliest development of DTs is around the 24 hour mark)Slide19

Delirium Tremens (DTs)

Synonymous to severe alcohol withdrawal in most texts

Hallucinations, disorientation, tachycardia, hypertension, hyperthermia, agitation and diaphoresis, in the setting of acute reduction or abstinence from alcohol. Symptoms typically persist up to 7 days (in absence of complications)Approximately 5-10% of patients in alcohol withdrawal develop DTs.Associated with a mortality rate of up to 5 percent.

Previously (early 20

th

century) mortality rate approached 40%. Improvement likely result of earlier diagnosis, improvements in supportive and pharmacological therapies and improved management of comorbid illness.Slide20

“Kindling” Effectin Alcohol Withdrawal

The term “kindling” was first introduced by Goddard et al (1969) to explain a phenomenon noted after repeated weak electrical stimulation of the brain. Initial stimulation resulted in no seizure activity.

After repeated periodic application, the same stimulus induced full motor seizures. The brain had become sensitized to the stimulation. Later, it was shown that sensitization could occur in the setting of electrical or chemical stimulation.Goddard et al. A permanent change in brain function resulting from daily electrical stimulation. Experimental Neurology 25: 295-330, 1969. Slide21

Kindling

For kindling to occur, the stimulus needs to be administered in a repeated and intermittent fashion.

Researchers have postulated that each withdrawal-induced episode of CNS hyperexcitability may serve as a stimulus that supports a kindling process.

Kindling in Alcohol Withdrawal, Becker. Alcohol Health and Research World

Vol

22, No.1, 1998.Slide22

Acute Withdrawal

…

.managementSlide23

CIWA-Ar

Most widely used clinical tool for management of AWS

Based on patient report and observer ratingValidated only in mild-to-moderate WDDoes not incorporate vital sign assessment (can be important in recognizing severe AWS)Not a prediction tool – tool to recognize severity of withdrawal as it is occurring. Maldonado et al (2014) Slide24

CIWA-Ar

Additionally, initiating CIWA in certain patient populations is not without risk….

Care needs to be taken when initiating CIWA protocols Ensure that alcohol withdrawal is truly the cause of the patient’s presentationProviding benzodiazepines to a patient who has evolving delirium for reasons other than alcohol withdrawal is very risky and can create situations exceedingly difficult to manage. Slide25

Management of

Alcohol Withdrawal:

BarbituratesBenzodiazepinesFixed dosing vs symptom triggered dosingSlide26

Relapse prevention

pharmacological optionsSlide27

Disulfiram

FDA approved 1951

Aversive agentBlocks aldehyde dehydrogenase = build up of acetylaldehydeFlushing, tachy, sob, N/V, HA, etc Serious potential SELow adherencePossible utility in highly motivated, specific situationsSlide28

Naltrexone

FDA approved 1994

Opioid antagonist less pleasure derived from drinking Reduces relapse to heavy drinking (NNT = 11)Target dose = 50mg OD (titrate up to target dose)Avoid in patients with depression or hepatic dysfunction or opioid req’ment.HA/dizziness (12%) and nausea (14%) most common SE

ACP

Journal

Club; 10/1/2014, Vol. 161

Issue

8, p6-6Slide29

Acamprosate

FDA approved 2004

Inhibitor of glutamate and modulator of GABA (“gaba-ergic”)Reduces chronic withdrawal symptomsCan help maintain abstinence (NNT = 11)Dose 666mg TID (333mg TID in moderate renal impairment) avoid in severe renal impairmentDiarrhea/other GI (17%) most common SE

ACP Journal Club. 2011

Rösner

S, et alSlide30

Gabapentin

Off label use

Another “gaba-ergic” agentUnique in that can be initiated during acute withdrawal (acts as bzd sparing agent)Can be continued for relapse prevention Improves rates of abstinence and no heavy drinking days (NNT 8)Target dose 600mg tid Slide31

Other considerationsSlide32
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If the patient be in the prime of life and from drinking he has trembling hands, it may be well to announce beforehand either delirium or convulsion

--Hippocrates