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Alcohol Misuse

Dr. Adel Alzayed


Kuwait University – medical college

 Background of alcohol and substance misuse




 Alcohol Dependency Syndrome
 Alcohol Intoxication
 Alcohol withdrawal
 Alcohol delirium
 Alcohol persisting dementia
 Alcohol persisting amnestic disorder
 Alcohol psychotic disorders
 Alcohol mood disorders
 Alcohol anxiety disorders
 Alcohol sexual dysfunction
 Alcohol sleep disorder
 Alcohol induced psychotic syndromes

Background

Alcohol is the most commonly abused drug


Consequences related to:


 Pharmacology
 Hazards inherent to route of admin
 Dose and frequency of use
 Personality of user
20-30% of males and 5-10% of f admissions were deemed
to be
 “problem drinkers”

Alcohol d/o = for 10% (first) - 20% psychiatric admissions

DSM IV criteria met in 16% of males and 3% of females



Prevalence of alcohol related problems is linked to alcohol
consumed per capita

Rise in consumption since 1950@ 60%

 Mortality rates from alcohol related cancers increasing over 10 yrs


 Risk of cirrhosis increases along with increasing consumption starting at
 6 units per day (f) and 8 units per day(m).
 12 units/day risk increased 14 fold(m)


 Admissions due to medical complications begins to rise at 21 units /week
 CVA begins at 42 units/wk

 Male Female
 Hazardous drinking 21u/wk 14 u/wk
 Safe use <“ <“

Intoxication

 A transient condition following the administration of alcohol or other

psychoactive substance, resulting in disturbance in level of consciousness,


cognition, perception, affect or behaviour or other psychophysiological
functions and responses

 Related to drug level(some exceptions)

 Recovery is complete

 Symptoms need not always reflect the primary actions of the substance. Effects of

substances such as cannabis+ hallucinogens may be unpredictable

 Ddx. Acute head injury / hypoglycaemia / mixed substance abuse


Acute Intoxication(Alcohol)


 Initial action on the reticular formation activation
 Later toxic effects on cortical neuronesInebriation
(exhilarationI excitementI loquacitIIIIIIII
I I I mgI I I I ml
 Reduced psIchological efficiencI at variance with
subI ective superioritI and sI ill
 Thinking superficial + slowed with poverty of associations + impaired judgement, reasoning, learning, conc

 Slowed motor control + reaction time  ataxia and in coordination


 Imotions of self pitII sadnessI irritabilitI and hostilitI
or hilarity may gain the upper hand coma
 IlacIouts
 III pupils dilated or constricted and tendon reflexes weaI
 Iaradoxical reactions


Alcohol Dependency Syndrome
A cluster of physiological, behavioural, and cognitive
phenomena in which the use of a substance or a class of
substances takes on a much higher priority for a given
individual than other behaviours that had a higher value
 +3 of
q Desire
q Difficulty controlling substance taking behaviour
q A physiological withdrawal state when substance reduced
or d/c or use of the same substance to relieve or avoid
withdrawal symptoms (200-300g/day/yrs)
q Tolerance
q Neglect of alternate pleasures
q Persistence despite harmful consequences


ADS : Edwards and Gross 1976

Stereotyped pattern of drinking


Prominence of drink seeking behaviour
Increased tolerance
Repeated withdrawl symptoms
Relief or avoidance of withdrawls by further
drinking
Subjective awareness of compulsion to drink
Rapid reinstatement after abstinence(within 72 hrs
if severely dependent)
 14% lifetime prevalence
 M:F 4:1
 47% meet criteria for another d/o Odds Ratio
 Antisocial pd 21
 Drug dependence 11.2
 Mania 6.2
 Schizophrenia 4.0
 Panic d/o 2.4
 Major Depression 1.7

 Onset: males late teens/20’s Insidious course: later for females, more likely
to drink alone and have higher rates of co-morbid depression, stronger
genetic predisposition and more physical complications
 Higher in urban, divorced, separated, lowest in middle social groups
High risk groups: manufacture or sell alcohol,
commercial travellers, entertainers, doctors,
journalists

Permissive factors: job mobility, absence of
restraining structures/ supervision,
availability of alcohol


Aeitology: Multi factorial

Family stuudies: 7 fold increase in first degree rels


Twin Studies: 70%:43% for males…Prikens 91
 47%:32% for females….Kendler 92
Adoption studies:Danish, Sweedish,US
 sons of alcoholics 4 times more likely to have ADS
 high rates of conduct d/o in male offspring of
 alcoholics
 ADS and anti-social pd are genetically independent

 BIOCHEMISTRY

 DA: Alcohol stimulates Da release in nuclues accumbens. Increased DA


craving

 5HT Alcohol potentiates effect of 5HT at 5HT3 receptors. Recent reports of 5HT
Agonists reducing craving


PSYCHOLOGICAL

 no evidence of an alcoholic personality



Modelling may explain familial association
 Operant conditioning: Relief of withdrawl symptoms promotes further abuse

 SOCIOCULTURAL

CNS Effects: Withdrawl state

 A group of variable symptoms occurring on absolute or relative withdrawal


of a substance

 Tremulousness, anxiety, irritability, dysphoria, retching, sweating, mood
change, hyperacusis, tinnitus, muscle cramps, sleep abnormalities,
perceptual distortions hallucinations(4-24 hrs)

 Fits occur 12-36 hrs after d/c may occur up to 12 days

 5% dts
 34% tremulousness
 11% hallucinations = tremor
 2% a hallucinations
 12% fits
 3% Wernicke Korsakoff syndrome

EEG show slowing during intoxication,
normalisation,16-33 hours later the alpha
wave diminishes with random spike and
bursts of slow wave activity.

Alcoholdecreases RIII
I ithdrawlexcess of RI I


DETOXIFICATION

 Treatment of minor withdrawls



 Inpt v opd Rx.

 Treat in hospital if previous hx. of DT’s or seizures, or suicidal or other
significant psychopathology
In hospital:

 Chlordiazepoxide (a benzodiazepine)
 reducing dose eg initially 40 mg QID
 + Thiamine 300mg od
 Ensure hydration
 Titrate dose with symptoms
 Regular nursing obs
 Clonidine adrenergic blocker : useful
Delerium Tremens

 Full syndrome of DT’s 3-4 days after d/c (risk begins


12u/day)..typically at night time

 Hallucinations, +/- delusions, confusion, disorientation,
tremulousness, increased psychomotor activity,
fearfulness,signs of autonomic disturbance

NB. Remember infxn and trauma (present in 50%),

wernickes encephalopathy, metabolic disturbances,


hypoglycaemia, head injury
Treatment of Delerium Tremens

Prevention
Rx in hospital. Medical emergency
 I/2 hrly temp, pr, bp, intake/output
 Fluids(6 L/day of which 1.5L n saline)
 Check mg and k and glucose
 Sedation(up to 400mg /day of chlordiazepoxide)
 High potency vitamin preparation
 Phenytoin or carbamazepine if seizures
Wernickes Encephaolpathy

 ACUTE NEUROPSYCHIATRIC REACTION TO SEVERE THIAMINE DEFICIENC



 *Nystagmus, .....................................96%
 *Ataxia of gait …………………………....87%
 *Global confusionalstate..90%(disorientation, apathy and derangement of memory) +/-
confabulation
 *+/-Peripheral neuropathy ……………………48%

 Nutritional deficiency..84%, Liver d/o: 33%
 Rx.: Medical emergency Thiamine 50 mg im/parentrovite im/iv..if not respnoding check mg
 General mx. ie. Rx. infxn, electrolytes, dehydration
 Prognosis confusion clears:1-2 months,
 50%84% amnseic syn
 Pathology degenerative changes: thalamus, hypothalamus, mamillary bodies, Hippocampus, 3 +4th
ventricles
Korsakoff syndrome and Dementia
 Korsakoff syndrome:
 Inability to form new memories and retrorgade amnesia for
years
 Confabulation ie. Apparent recollection of imaginary events
 Perseveration of other functions and clear consciousness
 Peripheral neuropathy
 Only 20% improve with thiamine

 Dementia
 Mild cognitive deficits but reversible with abstinence
 Females may be more at risk
 Rare< 40 years
 CT/MRI: ATROPHY
CNS

 Seizures
 Myopathy
 Optic atrophy
 Cerebellar degeneration
 Marchifava-Bignami disease
 Ientral Iontine IIelinolIsis
IsIchiatric

 Co-morbidities
 Suicide and DSH 56% of men and 23% of women who comit suicide are alcoholics…………….Kessel 1965
 Homicide
 Sexual difficulties
Respiratory

Cardiovascular
Gastrointestinal

Liver damage.. After 10 years of abuse .Cirrhosis 10% of alcoholics


Haematological
Neoplasm

FAS
Social/Occupation

Accidents: 80% of fatal car accidents involve alcohol/ Crime



Hallucinations

B9, transient, while person still drinking


Usually auditory
In the absence of confusion

Sensory disturbances eg tinnitus often reported b/f the
hallucinations develop eg tinnitus

Withdrawl of alcohol usually results in resolution of
symptoms………………………………...Bendetti

Aloholic hallucinosis ?schizophrenia?organic psychosis?
Thiamine deficiency
Othello Syndrome: Pathological Jealousy

Delusions of infidelity
Alcoholic Convulsions


 within 12-48 hrs of d/c or reduction of alcohol

 Usually grand mal



 Several years of addiction

 Not a latent epileptic process brought to life

Alcohol abuse

 Difficult pt often evasive/rationalise alcohol intake. High index


of suspicion warranted

 CAGE Questionnaire

 Use a problem orientated approach

 Ask about last 7/7 activities + amt. of alcohol consumed

 Lab’s: mcv, ggt

 Involve family realtionship is an important predictor of o/c


 Goal orientated treatment plan
Alcohol Dependency Treatment

 Detox

 Aversive treatment: Disulfiram “antabuse” 200-
400mg/day…consumption of alcohol 
tachI cardiaI flushingI
laboured breathing and
hypotension…
 sfx: tiredness, headache, halitosis, reduced libido, dermatitis,
neuritis,and confusional states
 CI: suicidal pt, psychosis, heart disease, hypotensive drugs,
intoxicated
 can be disipensed by partner as pt of a contract or by (proven
benefit.) an employer

 Acamprosate ”Camparal EC” GABA analogue….reduces


craving

Specialist Services

Pyschosocial intervention:

 Inpt for 6-8 weeks eg..Tabor Lodge, Matt Talbot House.



 No clear adv of inpt. over opd mx.

 OPD Mx.Counselling services eg. Arbour House St. Finbars Hospital
 Social skills training: id. social cues, teach skills eg refuse
drinks, buying non alcoholic drinks, avoid rounds, go to pub
late, being firm, learning new ways to cope
 Group therapy…rationalisations and misperceptions are
revealed
 Conjoint and family therapy ..enable pts of the family to have
their views heard in a controlled manner..

 AA and ALAnon
Outcome

 Dependent upon social and marital stability



 Severity of dependency

 Involvement of spouse, community reinforcement strategies

 Social skill training and follow up

 Poor if: brain damage/ comorbid psych illness esp anti-social
pd/criminal hx./low IQ/poor support/low motivation

 10 year follow up: 61% in remission for 3 years