Preventing and Treating Wernicke’s Encephalopathy

All people with heavy or chronic alcohol use should be considered at risk of developing Wernicke’s encephalopathy. Given that so many patients with Wernicke’s encephalopathy are undiagnosed and thiamine is safe and costs little, all patients undergoing alcohol withdrawal should be treated with thiamine to prevent Wernicke’s encephalopathy (see above). And given the major clinical repercussions of not treating Wernicke’s encephalopathy, all patients with any features of Wernicke’s encephalopathy should be treated as though Wernicke’s encephalopathy is established.

In patients showing no clinical features of Wernicke’s encephalopathy or memory impairment, thiamine is recommended as a prophylactic measure. 

• As well-controlled trials have provided limited evidence to guide therapy, significant uncertainty exists about the required dose and duration of therapy. Modelling of thiamine entry to the brain suggests that high doses are required. There is clinical consensus that it is important to recommend high doses of thiamine to ensure enough is being given to prevent serious neurological disease. 
• Healthy patients with good dietary intake may be administered oral thiamine 300 mg per day (for example, 100 mg three times daily) for 3 to 5 days, and maintained on 100 mg oral thiamine for a further 4 to 9 days (total of 1 to 2 weeks of oral thiamine). 
• Patients with chronic alcohol use with poor dietary intake and general poor nutritional state should be administered parenteral thiamine doses (due to poor intestinal absorption of oral thiamine supplements). The recommended dose of thiamine 300 mg intramuscularly or intravenously per day for 3 to 5 days, and subsequent oral thiamine doses of 300 mg per day for several weeks.  
• Correct any electrolyte disturbances, including hypomagnesaemia. 
• Alcohol is associated with coagulopathy that may render intramuscular injection unsafe. 
• Where practical, thiamine should be given before any carbohydrate load (such as intravenous glucose) as carbohydrates can cause rapid utilisation of thiamine and precipitate Wernicke’s encephalopathy. 

It is imperative that treatment is initiated early as delays in treatment may worsen the patient’s prognosis. All people with heavy alcohol use displaying any features of Wernicke’s encephalopathy (such as confusion, ataxia, eye signs, coma, memory impairment, hypothermia with hypotension, or delirium tremens) should be treated as though Wernicke’s encephalopathy is established (even if intoxicated). 

• Thiamine should be given before any carbohydrate load (for example, intravenous glucose) or as soon as possible thereafter. 
• Parenteral doses of at least 500 mg per day thiamine (intramuscular or intravenous diluted in saline over 30 minutes) should be administered daily for at least 3 to 5 days, and subsequent doses of at least 300 mg (oral or parenteral) and up to 1000mg per day for 1 to 2 weeks. The intramuscular route should not be used for patients with coagulopathy. 
• Correct any electrolyte disturbances, including hypomagnesaemia.

Oral thiamine (for example, 100 mg daily) should be maintained until long-term abstinence has been achieved. People who have persistent alcohol use should be maintained on oral thiamine supplements.