Clonidine for Treatment of Alcohol Withdrawal | Karine Wong, Pharm.D. | RxEconsult
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Clonidine for Treatment of Alcohol Withdrawal Category: Addiction by - January 16, 2014 | Views: 10777 | Likes: 1 | Comment: 0  

Clonidine for alcohol withdrawal

A medical resident wrote an order for “clonidine 0.1 mg PO every 6 hours PRN alcohol withdrawal.” Wow. The pharmacy resident and nurse had no idea how to clarify this order. To best educate the resident, I felt that it was best to research the topic and see what the medical resident had in mind.

After alcohol consumption, alcohol adheres to receptors in the brain. Alcohol blocks the receptors’ actions. Receptors have their own function. Initially, alcohol blocks glutamate, which makes you feel “free” and “uninhibited”. Feelings of inhibition can lead to inappropriate legal and moral choices. Alcohol worsens the situation by releasing dopamine, the hormone responsible for the “buzzed” feeling. At this point, the drinker will not care about their choices and consequences because they feel buzzed. With more alcohol consumed, receptors responsible for speech, walking, and motor coordination will be inhibited. Shortly, the drinker will become inebriated or drunk.

As time wears on and alcohol is cleared from the system, the receptors that were blocked by alcohol become hypersensitive. Consequently, people suffering from withdrawals are at risk for irritability, insomnia, hallucinations, fast heart rate, high blood pressure, and seizures. At the same time, receptors that were facilitated by alcohol become slower to turn back on and thus, tolerance to alcohol develops. As a result, chronic drinkers will have to consume more alcohol to achieve the initial effects of euphoria or “buzz”. This is called physiologic tolerance. The vicious cycle of alcoholism begins here.

When drinkers become hospital patients, they are usually in the acute phase of the alcohol withdrawal and suffering from severe symptoms such as tremors, agitation, delirium, tachycardia, hypertension, seizures, hallucinations, or even coma (after large doses of alcohol). At this time, there is no treatment for alcohol intoxication. Physicians are merely treating the symptoms of withdrawal. Ultimately, the best treatment for alcohol intoxication is abstinence, which should be managed on an outpatient basis.

Delirium/anxiety

  1. Treatment with benzodiazepines; hold for over-sedation
    1. Librium 25 mg (or 50 mg) orally every 6 hours x 8 doses OR
    2. Lorazepam 2 mg (or 4 mg) orally every 6 hours x 8 hours then reduce to 1 mg (or 2 mg) orally every 6 hours x 8 hours
  2. In studies, clonidine was slightly effective in reducing delirium symptoms if used with a benzodiazepine. Oral dosing was clonidine 0.1 mg to 0.3 mg every 6 hours (not PRN). Withdrawal symptoms of tachycardia and hypertension were significantly reduced in patients taking clonidine.  

Dehydration

  1. Treatment: IV fluids with normal saline or D5W (appropriate if BP is elevated).

Thiamine deficiency (secondary to malnutrition) and a severe form of thiamine deficiency called the Wernicke–Korsakoff syndrome. Patients can suffer from encephalopathy then followed by long-term psychosis.

  1. Treatment: Add IV multivitamin, thiamine 100 mg, and folic acid 1 mg to one liter of IV fluid, to be given daily.

Status Epilepticus

  1. Initial treatment
    1. Lorazepam 0.1 mg/kg slow IV push (max rate of 2 mg/min), may repeat in 10 to 15 minutes OR
    2. Diazepam 0.15 mg/kg IV push over 5 minutes, may repeat in 10 to 20 minutes
  2. Full review of seizure treatment is beyond the scope of this article.

In conclusion, the resident did know about the off-label use of clonidine for alcohol withdrawal. However, the dosing was incorrect and there was no concurrent use of a scheduled benzodiazepine. The patient did suffer from hypertension, which he was given clonidine from a previous PRN order for BP above 180/110. To prevent future medication errors, the resident was educated on the correct use of clonidine in this setting.

References

  1. Lobo IA, Harris RA. GABAA Receptors and Alcohol. Pharmcol Biochem Behav. 2008 July; 90(1): 90-94.
  1. Martin D. The role of GABAA Receptors in Mediating the Effects of Alcohol in the Central Nervous System. J Psychiatry Neurosci. 2003 July; 28(4): 263–274.
  1. Muzyk J, Fowler JA, Norwood DK et al. Role of α2-agonists in the Treatment of Acute Alcohol Withdrawal. The Annals of Pharmacotherapy. 2011;45(5):649-657. 
  1. www.pharmacistsletter.com (accessed 1/14/14)
  1. www.medscape.com (accessed 1/14/14)
About the Author

Dr. Karine Wong has a 10 year history of working in hospital management and 2 years as a hospital pharmacist and outpatient pharmacist. She recently published a children's book called Don't Sit on Her.

 
The material on this site is for information only and is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider.
 

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