What is included in the emergency department (ED) care for Wernicke encephalopathy (WE)?

Updated: Nov 20, 2018
  • Author: Philip N Salen, MD; Chief Editor: Andrew K Chang, MD, MS  more...
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Answer

Although as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat WE in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally, intravenous is preferred to intramuscular administration. 

Thiamine has a short half-life so multiple daily administrations may be necessary to replete levels and allow for optimal blood-brain diffusions. [5] Thiamine solution should be fresh, since old solutions may be inactive. Oral preparations have been shown to vary in bioavailability, but in hospital practice, thiamine is usually administered parenterally to patients thought to be at high risk of WKS. Parenteral administration is associated with some risk of anaphylaxis.

Treat all malnourished patients with large doses of parenteral thiamine, particularly if intravenous glucose administration is necessary, even in the absence of symptoms and signs of WE. Administering dextrose to an individual in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes. [11]

Start thiamine prior to or concurrently with treatment of intravenous glucose solutions, and continue until the patient resumes a normal diet. The administration of dextrose or other carbohydrates in this setting has the potential for harm, because glucose oxidation is a thiamine-intensive process that may drive the last reserves of circulating vitamin B-1 toward the intracellular compartment, thereby aggravating neurologic damage. [3]

Magnesium deficiency could also contribute to the poor recovery from WE in alcoholics. [1]  Patients with WE are likely hypomagnesemic and should be treated empirically with parenteral magnesium sulfate, as they may be unresponsive to parenteral thiamine in the presence of hypomagnesemia. [6] After correction of hypomagnesemia in conjunction with thiamine repletion, the blood transketolase activity can return to normal and clearing of the clinical signs of WE may occur.

There is evidence that suggests thiamine treatment brings about rapid resolution of the ataxia and ophthalmoplegia and slow but significant improvement in the severity of nystagmus. The global confusional state also appears to improve rapidly within hours of thiamine treatment, but other issues remain unresolved. Impairment of memory and learning responds more slowly and often incompletely, suggesting a different mechanism of effect. [6]


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