Continuation to the previous post, pharmacological therapy should ideally come after lifestyle modifications have failed. Potential of drug abuse is a major challenge for most physicians and therapists .
The therapy can be divided into two broad categories :
Symptom – triggered Therapy – As it sounds, the medication is given only when there is a symptom. This will result in a treatment that is shorter, potentially avoiding over use of sedatives, and allows more focus on specific targets. There is also a scale used called, Clinical Institute Withdrawal Assessment- Alcohol.
Fixed Schedule therapy– Meds given at regular intervals at a fixed dosing have been used for alcohol withdrawal. Major problem with this approach is underdosing, and especially for the class of benzodiazepines. Cross tolerance can happen too. Additional medications can be given too when the symptoms are indicated.
Alcohol Withdrawal Seizures:- Anticonvulsants are not needed for treatment of seizures induced because of habitual consumption. By the time medications are administered seizures get over. Supportive therapy is more required than drugs in this case. Phenytoin which is not cross-tolerant to alcohol, does not prevent or treat withdrawal seizures. Increase in the dosage or tapering schedule of benzodiazepine can be used in detoxification, or a one time injection. Patients with a history of withdrawal seizures can be predicted to experience severe withdrawal syndromes.
Alcoholics often have electrolyte imbalances because of inadequate nutrition and fluid volume related to antidiuretic hormone inhibition. Excessive hydration is not needed since the vasopressin levels will be already high.
Oral Potassium supplements are used for Hypokalemia (low K+ levels). Renal functions have to be good though, if potassium supplements are started. Hypomagnesemia also is seen in patients, but supplementation is not needed unless the symptoms are present of low magnesium.
One important syndrome which is seen is Wenicke Korsikoff syndrome ( mental confusion, eye movement, disorders, and ataxia – poor motor coordination), so to prevent this Vitamin B complex syrups can be used.
In practice thiamine supplementation is given orally once daily , 100 mg for 1 to 4 weeks. Intamuscularly or Intravenously is also adminsitered for 3-4 weeks. Thiamine is given before dextrose administration, since it is helpful for glucose metabolism.
Alcohol hypoglycemia- usually occurs even if there is no liver disease. It is more likely if the patient is more sensitive to alcohol or if the patient is working out or fasting. What actually happens is , that the pathway to gluconeogenesis is stopped, while glycogenolysis remain. When glycogen stores are over, the patient will undergo hypoglycemia, because liver will not be able to metabolize glucose from gluconeogenesis. Substrate used for gluconeogenesis are Lactate and Pyruvate, and energy is diverted and used for metabolizing alcohol.
Deters a patient from drinking by producing an aversion reaction, so in the absence of alcohol dilsufiram has minimal effects.
Its effects comes from its blocking mechanism of the enzyme aldehyde dehydrogenase in the biochemical pathway for alcohol metabolism, allowing acetaldehyde to accumulate. The resulting increases causes severe facial flushing, throbbing headache, nausea, vomiting, chest pain, palpitations, tachycardia, weakness, dizziness, blurred vision, confusion, and hypotension.
Because of the above symptoms, severe reactions including myocardial infarction, congestive heart failure, cardiac arrythmia, respiratory depressionn, convulsions, and death can also occur in vulnerable individuals.
Liver functions should be checked since idiosyncratic hepatotoxicity can occur. An ideal testing time can be 2 weeks, 3 months, 6 months, twice yearly thereafter.
Dosing- 250 mg/day, and 500 mg/day, however 250 mg seems to produce lesser side effects and the problem is that higher doses are needed to reliably show aversive reactions.
An opiate antagonist that has been available in the USA since 1984. It got approved in 1994, and is thought to attenuate (reduce) the reinforcing effects of alcohol. Patients report less intoxicated while taking alcohol during naltraxone treatment, and craving is less.
It has a dose dependent hepatotoxicity and it generally occurs at doses higher than recommended, so this would mean it will be contraindicated in patients with hepatitis or liver failure. Nausea is most common side effect of naltrexone, occurring in approximately 10% of the patients.
Additionally it can cause headache, dizziness, nervousness, fatigue, insomnia, vomiting, anxiety and somnolence ( intense desire to sleep)
Dosing – 50 mg per day is sufficient to effectively block the receptor. A new depot formulation helps in better adherence and compliance, usual effective dose is 380 mg IM each month.
Its a recent drug compared to others mentioned above. It was available in Europe for many years, and was approved in US in the summer 2004. Patients treated with Acamprosate are more successful in maintaining abstinence from alcohol versus placebo ( having no physiological benefit).
Gastrointestinal adverse effects are more common, some studies also indicate mood disorders , and some show that the drug is not very promising with its mechanism hitting on serotonergic receptors.
Dosing – 1000 mg to 2000 mg per day, and the tablets available are of 333 mg or higher.