ALCOHOL USE DISORDERS
A. Gastrointestinal System
i. Fatty liver, cirrhosis of liver, hepatitis, liver cell carcinoma, liver failure
ii. Gastritis, refl ux oesophagitis, oesophageal vari ces, Mallory-Weiss syndrome, achlorhydria, peptic ulcer, carcinoma stomach and oeso phagus iii. Malabsorption syndrome, protein-losing
enter-opathy
iv. Pancreatitis: acute, chronic, and relapsing B. Central Nervous System
i. Peripheral neuropathy ii. Delirium tremens
iii. Rum fi ts (Alcohol withdrawal seizures) iv. Alcoholic hallucinosis
v. Alcoholic jealousy
vi. Wernicke-Korsakoff psychosis vii. Marchiafava-Bignami disease viii. Alcoholic dementia
ix. Suicide
x. Cerebellar degeneration xi. Central pontine myelinosis xii. Head injury and fractures.
C. Miscellaneous
i. Acne rosacea, palmar erythema, rhinophyma, spider naevi, ascitis, parotid enlargement
ii. Foetal alcohol syndrome (craniofacial ano malies, growth retardation, major organ system malfor-mations)
iii. Alcoholic hypoglycaemia and ketoacidosis iv. Cardiomyopathy, cardiac beri-beri v. Alcoholic myopathy
vi. Anaemia, thrombocytopenia, Vitamin K factor defi ciency, haemolytic anaemia
vii. Accidental hypothermia
viii. Pseudo-Cushing’s syndrome, hypogonadism, gynaecomastia (in men), amenorrhoea, infer tility, decreased testosterone and increa sed LH levels ix. Risk for coronary artery disease
x. Malnutrition, pellagra
xi. Decreased immune function and proneness to infections such as tuberculosis
xii. Sexual dysfunction II. Social Complications i. Accidents
ii. Marital disharmony iii. Divorce
iv. Occupational problems, with loss of pro ductive man-hours
v. Increased incidence of drug dependence vi. Criminality
vii. Financial diffi culties.
Table 4.6: Body Fluid Alcohol Levels BAC* (mg%) Behavioural Correlates 25-100 Excitement
80 Legal limit for driving (in UK)**
100-200 Serious intoxication, slurred speech,
incoordination, nystagmus
200-300 Dangerous
300-350 Hypothermia, dysarthria, cold sweats 350-400 Coma, respiratory depression
>400 Death may occur
Urinary Diagnostic Equivalent BAC
Alcohol (mg%) Use (mg%)
>120 Suggestive 80
>200 Diagnostic 150
*BAC - Blood Alcohol Concentration
**30 mg/100 ml in India (Section 185 of the Motor Vehicle Act, 1988)
Table 4.5: CAGE Questionnaire
The CAGE questionnaire basically consists of four questions:
i. Have you ever had to Cut down on alcohol (amount)?
ii. Have you ever been Annoyed by people’s criticism of alcoholism?
iii. Have you ever felt Guilty about drinking?
iv. Have you ever needed an Eye opener drink (early morning drink)?
A score of 2 or more identifi es problem drinkers.
Clinically, Korsakoff’s psychosis presents as an organic amnestic syndrome, characterised by gross memory disturbances, with confabulation. Insight is often impaired. The neuropathological lesion is usually wide-spread, but the most consistent changes are seen in bilateral dorsomedial nuclei of thalamus
and mammillary bodies. The changes are also seen in periventricular and periaqueductal grey matter, cerebellum and parts of brain stem.
The underlying cause is believed to be usually severe untreated thiamine defi ciency secondary to chronic alcohol use.
Marchiafava-Bignami disease
This is a rare disorder characterised by disorien tation, epilepsy, ataxia, dysarthria, hallucina tions, spastic limb paralysis, and deterioration of personality and intellectual functioning. There is a widespread demy-elination of corpus callosum, optic tracts and cerebel-lar peduncles. The cause is probably an alcohol-related nutri tional defi ciency.
Other Complications These include:
i. Alcoholic dementia.
ii. Cerebellar degeneration.
iii. Peripheral neuropathy.
iv. Central pontine myelinosis.
Treatment
Before starting any treatment, it is important to follow these steps:
i. Ruling out (or diagnosing) any physical disorder.
ii. Ruling out (or diagnosing) any psychiatric disorder and/or co-morbid substance use disorder.
iii. Assessment of motivation for treatment.
iv. Assessment of social support system.
v. Assessment of personality characteristics of the patient.
vi. Assessment of current and past social, interper-sonal and occupational functioning.
The treatment can be broadly divided into two categories which are often interlinked. These are detoxifi cation and treatment of alcohol depen dence.
Detoxifi cation
Detoxifi cation is the treatment of alcohol withdrawal symptoms, i.e. symptoms produced by the removal of the ‘toxin’ (alcohol). The best way to stop alcohol (or any other drug of dependence) is to stop it suddenly
unless the risks of acute discontinuation are felt to be high by the treating team. This decision is often based on several factors including chronicity of alcohol dependence, daily amount consumed, past history of alcohol withdrawal complications, level of general health and the patient’s wishes.
The usual duration of uncomp licated withdrawal syn drome is 7-14 days. The aim of detoxifi cation is sympto matic management of emergent withdrawal symptoms.
The drugs of choice for detoxifi cation are usually benzodiazepines. Chlordiazepoxide (80-200 mg/day in divided doses) and diazepam (40-80 mg/day in divi ded doses) are the most frequently used benzo diazepines.
The higher limit of the normal dose range is used in delirium tremens.
A typical dose of Chlordiazepoxide in moderate alcohol dependence is 20 mg QID (four times a day) on day 1, 15 mg QID on day 2, 10 mg QID on day 3, 5 mg QID on day 4, 5 mg BD on day 5 and none on day 6. However, in more severe dependence, higher doses are needed for longer periods (up to 10 days).
These drugs are used in a standardised protocol, with the dosage steadily decreasing everyday before being stopped, usually on the tenth day. Clormethia zole (1-2 g/day) and carbamaze pine (600-1600 mg/day) are experimental drugs and should not be used routinely for detoxifi cation.
In addition, vitamins should also be adminis tered.
In patients suffering from (or likely to suffer from) delirium tremens, peripheral neuropathy, Wernicke-Korsakoff syndrome, and/or with other signs of vita-min B defi ciency (especially thiavita-mine and nicotinic acid), a preparation of vitamin B containing 100 mg of thiamine (vitamin B1) should be administered parente rally, twice everyday for 3-5 days. This should be followed by oral adminis tration of vitamin B1 for at least 6 months.
Care of hydration is another important step; it is extremely important not to administer 5% dextrose (or any carbohydrate) in delirium tremens (or even in uncomplicated alcohol withdrawal syndrome) without thiamine.
Although detoxifi cation can be achieved on an outpatient (OPD) basis, some patients do require hospitalisation. These patients may present with:
i. Signs of impending delirium tremens (tremor, autonomic hyperactivity, disorientation, or per-ceptual abnormali ties), or
ii. Psychiatric symptoms (psychotic disorder, mood disorder, suicidal ideation or attempts, alcohol-induced neuro psy chiatric disorders), or
iii. Physical illness (caused by chronic alcohol use or incidentally present), or
iv. Inability to stop alcohol in the home setting.
Detoxifi cation is the fi rst step in the treatment of alcohol dependence.
Treatment of Alcohol Dependence
After the step of detoxifi cation is over, there are sev-eral methods to choose from, for further management.
Some of these important methods include:
i. Behaviour therapy
The most commonly used behaviour therapy in the past has been aversion therapy, using either a sub-threshold electric shock or an emetic such as apomor-phine. Many other methods ( covert sensitisation, relaxation techniques, assertiveness training, self-control skills, and positive reinforcement) have been used alone or in combination with aversion therapy.
Currently, in most settings, it is considered unethical to use aversion therapy for the treatment of alcohol dependence.
ii. Psychotherapy
Both group and individual psychotherapy have been used. The patient should be educated about the risks of continuing alcohol use, asked to resume personal respon sibility for change and be given a choice of options for change. Motivational enhancement therapy with or without cognitive behaviour therapy and life-style modifi cation is often useful, if available.
iii. Group therapy
Of particular importance is the voluntary self-help group known as AA ( Alcoholics Anonymous), with branches all over the world and a membership in hun-dreds of thousands. Although the approach is partly
religious in nature, many patients derive benefi ts from the group meetings which are non-professional in nature.
iv. Deterrent agents
The deterrent agents are also known as alcohol sen-sitising drugs.
Disulfi ram (tetraethyl thiuram disulfi de) was dis-covered in 1930s, when it was observed that workers in the rubber industry developed unpleasant reactions to alcohol intake, due to accidental absorption of antioxidant disul fi ram. The mechanism of action of disulfi ram is summarised in Figure 4.1.
When alcohol is ingested by a person who is on disulfi ram, alcohol-derived acetal de hyde cannot be oxidised to acetate and this leads to an accumulation of acetaldehyde in blood. This causes the important disulfiram-ethanol reaction (DER) characterised by fl ush ing, tachycardia, hypotension, tachypnoea, palpitations, headache, sweating, nausea, vomi ting, giddiness and a sense of impending doom associated with severe anxiety.
The onset of the reaction occurs within 30 minutes, becomes full blown within 1 hour, and subsides usu-ally within 2 hours of ingestion of alcohol. In sensitive patients or in those who have ingested a large amount of alcohol, DER can be very severe and life threatening due to one or more of the following: shock, myo cardial infarction, convulsions, hypoxia, confusion and coma.
Therefore, treatment with disulfi ram is usually begun in an inpatient hospital setting, usually after a challenge test with alcohol to demonstrate that unpleasant and dangerous side-effects occur, if either alcohol or alcohol-containing eatable/drink is con-sumed whilst treatment is continued with disulfi ram.
The usual dose of disulfi ram is 250-500 mg/day (taken before bedtime to avoid drowsi ness in daytime) in the fi rst week and 250 mg/day subsequently for the maintenance treatment. The effect begins within 12 hours of fi rst dose and remains for 7-10 days after the last dose. The patient should carry a warning card detailing the forbidden alcohol-containing articles, the possible effects and their emergency treatment, along with patient identifi cation details.
The contraindications of disulfi ram use are fi rst trimester of pregnancy, coronary artery disease, liver failure, chronic renal failure, peripheral neuropathy, muscle disease and psychotic symptoms presently or in the past.
In selected patients (such as an older age group, good motivation, good social support, absent under-lying psychopathology and good treatment concord-ance), the response can be dramatic. In addition to oral prepara tions, subcu taneous disulfi ram implants are also now available. However, they provide unpre-dictable blood levels of disulfi ram.
Other deterrent agents
1. Citrated calcium carbimide (CCC): The mecha-nism of action is similar to disulfi ram but onset of action occurs within 1 hour and is reversible. The usual dosage is 100 mg/d in two divided doses.
2. Metronidazole.
3. Animal charcoal, a fungus (Coprinus atra men -tarius), sulfonylureas and certain cephalos porins also cause a disulfi ram like action.
v. Anti-craving agents
Acamprosate, naltrexone and SSRIs (such as fl uoxet-ine) are among the medications tried as anti-craving agents in alcohol dependence.
Acamprosate (the Ca++ salt of N-acetyl-homo taurinate) interacts with NMDA recep tor-mediated glutamater-gic neurotransmission in the various brain regions and reduces Ca++ fl uxes through voltage-operated channels.
Naltrexone (oral opioid receptor antagonist) prob-ably interferes with alcohol-induced reinfor cement by blocking opioid receptors. Fluoxetine (and other SSRIs) have been occasionally used as anti-craving agents in their usual antidepressant doses.
vi. Other medications
A variety of other medicines such as benzodia-zepines, antidepressants, antipsychotics, lithium, carbamazepine, and even narcotics have been tried.
These should be used only if there is a special indi-cation for their use (for example, antidepressants for underlying depression).
vii. Psychosocial rehabilitation
Rehabilitation is an integral part of the multi-modal treatment of alcohol dependence.