Alcohol dependence
D E FI N I T ION
Alcohol dependence is characterized by three or more of:
. Withdrawal on cessation of alcohol.
. Tolerance.
. Compulsion to drink, difficulty controlling termination or the levels of use.
. Persistent desire to cut down or control use.
. Time is spent obtaining, using, or recovering from alcohol.
. Neglect of other interests (social, occupational, or recreational).
. Continued use despite physical and psychological problems.
Recommended limits for , and < are 14 and 21 units/week, respectively. (1 unit¼8 g alcohol –
1 glass wine or 0.5 pint of beer.)
AE T IOLOGY
Genetic factors suggested by twin studies and family history ( 1 in 3 have
a parent with alcohol-related problem).
Environmental factors include cultural, parental and peer group influences, availability of
alcohol, occupation (e.g. " risk in publicans, doctors, lawyers).
Patients with depressive and anxiety states are at risk.
Alcohol withdrawal: Alcohol enhances inhibitory GABA activity and inhibits excitatory
glutamate neurotransmission. Chronic alcohol exposure results in a compensatory
reduction in GABA receptor function and upregulation of the glutamate NMDA receptors.
Abrupt alcohol cessation leads to overactivation of the excitatory NMDA system
relative to the GABA system.
E P IDEMIOLOGY
The prevalence of alcohol dependence in primary care populations in the
United States was reported as 2–9% in 2004.
H ISTORY
Alcohol history: A drinking diary is useful to record how much, what, when and with whom
alcohol is taken.
CAGE screening questions:
Cut-down: ‘... felt that you should cut-down on intake?
Annoyed: ‘... felt annoyed by criticism of your drinking?
Guilt: ‘... felt guilty about how much you drink?
Eye-opener:‘... feel that you need a drink when you wake up?
Evaluate for associated comorbidities including smoking, other substance abuse, depression,
anxiety and panic attacks.
Acute intoxication: Amnesia, ataxia, dysarthria, disorientation, palpitations, flushing and
coma.
Symptoms of withdrawal: Nausea, sweating and tremor, restlessness, agitation, visual
hallucination, confusion, seizures.
EXAMINA T I ON
Signs suggestive of chronic alcohol misuse: Dupuytren’s contracture, palmar erythema,
bruising, spider naevi, telangiectasia, facial mooning, bilateral parotid enlargement,
gynaecomastia, smell of alcohol.
Signs ofcomplications: (See Complications below and also Alcoholic hepatitis and Liver failure.)
INVE S T I G A T IONS
Blood: Commonly used markers are MCV ("), GGT ("), transaminases ("). Other less specific
markers include " uric acid, " triglycerides or markers of end organ damage (e.g. bilirubin,
albumin, PT in liver).
Acute overdose: Blood alcohol, glucose, ABG (risk of ketoacidosis or lactic acidosis), U&E,
toxic screen (e.g. barbiturates, paracetamol).
Alcohol dependence (continued)
MANAGEMENT
Acute intoxication: Monitor and support of airway, breathing, circulation. Intubation and
ventilation if severe respiratory depression, IV fluids and careful monitoring of urine
output, blood glucose (as may #), U&E and blood gases.
Withdrawal: IV vitamin B complex (Pabrinex) and reducing doses of chlordiazepoxide. Close
attention to dehydration, electrolyte imbalances and infections. Nutritional support
important as often malnourished. Lactulose and phosphate enemas may help any
encephalopathy.
Advice and intervention: Motivational interviewing techniques, counselling and community-
based services, self-help groups (e.g. AA), alcohol treatment units for those with
established problems, detoxification period is necessary for those physically dependent.
Medical: Acamprosate reduces craving. Naltrexone (opioid receptor antagonist) may be
given to patients who need additional support to maintain abstinence (contraindicated in
patients with underlying liver disease, and liver function tests should be monitored).
Disulfiram (an aldehyde dehydrogenase inhibitor) causes patient to develop vasomotor
symptoms, nausea, abdominal pain when drinking alcohol.
COMPL I C A T IONS
GI: Oesophagitis, Mallory–Weiss tears, varices, gastritis, peptic ulcers, acute or chronic
pancreatitis.
Liver: Fatty change, alcoholic hepatitis, cirrhosis.
Neurological: Acute intoxication.
Withdrawal: Fits, delirium tremens (48–72 h after cessation – coarse tremor, agitation,
fever, tachycardia, confusion, delusions and hallucinations). Chronic complications
include cerebral atrophy and dementia, cerebellar degeneration, optic atrophy, peripheral
neuropathy, myopathy. Indirect effects include hepatic encephalopathy, thiamine
deficiency, causing Wernicke’s encephalopathy1 or Korsakoff’s psychosis.2
Haematological: Anaemia (vitamin B12 or folate deficiency, iron deficiency in patients with
GI bleeding), thrombocytopaenia (due to enlarged spleen in patient with cirrhosis or direct
toxic effect on megakaryocytes), abnormal platelet function.
Respiratory: Depression, inhalation of vomitus.
Cardiac: Hypertension, cardiomyopathy, arrhythmias.
Drug interactions: E.g. oral contraceptive pills (alcohol is a liver enzyme-inhibitor acutely,
but chronic abuse induces liver enzymes.)
Teratogenicity: Foetal alcohol syndrome.
Psychosocial: Depression, anxiety, deliberate self-harm. Domestic, employment and financial
problems.
P ROGNOS I S
Depends on complications. Alcoholic fatty liver is reversible on abstinence
from alcohol. In general, 5-year survival rates in those with alcoholic cirrhosis who stop
drinking are 60–75%, but < 40% in those who continue.
2 Korsakoff’s psychosis is characterized by profound impairment of retrograde and anterograde memory
with confabulation, as a result of damage to the mammillary bodies and the hippocampus. Irreversible.
1 Wernicke’s encephalopathy is nystagmus, ophthalmoplaegia and ataxia, together with apathy,
disorientation and disturbed memory. Treat urgently with thiamine or may progress to Korsakoff’s
psychosis.
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