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    Wernicke’s Encephalopathy Diagnosis and Treatment

    Metabolic / Endocrine

    Last Updated Jun 05, 2021
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    By Kerry Walker, Manjot Kahlon


    Wernicke’s encephalopathy is a life-threatening neurological condition caused by a deficiency of thiamine (vitamin B1).

    • Substantial morbidity and mortality yet remain underdiagnosed.
      • Left untreated, there’s mortality in ~20% of patients with acute Wernicke’s encephalopathy and ~80% develop irreversible memory loss consistent with Korsakoff syndrome with only ~16% making full recovery.
    • Alcoholics and chronically malnourished individuals.
    • Compromised absorption (ex. hyperemesis gravidarum, intestinal obstruction, chemotherapy), with increased metabolism (ex. sepsis, malignancy), with increased carbohydrate intake (iatrogenic), secondary to liver disease or post-bariatric surgery.

    Diagnostic Process

    Consider in any patient presenting with at least two of the following:

    1. Dietary/nutritional deficiency.
    2. Ocular abnormalities.
    3. Cerebellar dysfunction.
    4. Altered mental status or mild memory impairment.
    • This diagnosis is made clinically.

    Common findings:

    • CN III or VI palsies, upbeat nystagmus, sluggish pupillary response, anisocoria, ataxia or gait instability, and peripheral neuropathy.
    • MRI may show hyperintense signals in the dorsomedial thalamic nuclei, periaqueductal grey matter, third or fourth ventricles, and the cerebral aqueduct. This is due to variable degrees of acidosis in the brain, wherein the absence of thiamine, glucose is metabolized anaerobically to lactic acid and induces tissue injury.

    Clinical Pitfalls:

    • Failure to recognize that alcohol consumption is not required for the diagnosis of Wernicke’s encephalopathy.
    • Mistake Wernicke’s encephalopathy for cerebellar infarction because both conditions tend to present with the classic triad of ophthalmoplegia, gait ataxia, and changes in mental status.
    • Failure to check for hypomagnesemia in the context of thiamine deficiency which may cause resistance to any administration of thiamine.
    • Failure to keep a high index of suspicion for Wernicke’s encephalopathy in vulnerable populations.

    Recommended Treatment

    Goal of treatment is rapid correction of thiamine deficiency, particularly in the brain.

      • The traditional recommendation is immediate replacement with 100mg IV thiamine followed by additional doses as needed, until symptoms improve; however, this is not based on randomized control trials.
      • The European Federation of Neurological Societies guideline recommends an IV infusion of 200mg thiamine diluted in 100mL normal saline or 5% dextrose, given over 30 min and 3x daily until symptoms resolve

    Magnesium levels should be checked and treated if low.

    Quality Of Evidence?


    Low – Although thiamine replacement therapy is the recommended treatment for Wernicke’s encephalopathy, randomized control trials have not provided sufficient evidence to suggest an optimal dose, frequency, route or duration of treatment.


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