Wernicke Encephalopathy Treatment & Management

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

Rapid correction of brain thiamine deficiency is the goal of therapy. [4]  WE must be viewed as a medical emergency, even if other, competing diagnoses of CNS processes are being considered. Because the condition is potentially reversible, institution of treatment is indicated in patients exhibiting any combination of symptoms and signs, particularly if the patient is in a high-risk population. Onset of the disease may be acute, subacute, or chronic. Administration of thiamine improves the patient’s condition to some degree in almost all cases; however, persistent neurologic dysfunction is common. [5]  Oral absorption is unreliable in patients at risk of Wernicke encephalopathy, which emphasizes the importance of parenteral treatment. [4]

Prehospital care

Because patients with WE present with altered mental status in the prehospital setting, focus prehospital care on stabilizing the airway, ensuring oxygenation, ruling out hypoglycemia, and maintaining blood pressure and euvolemia.


Emergency Department Care

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]



Inpatient and Outpatient Care

Inpatient care

Depending on mental status and the ability to protect his or her airway, admit a patient with suspected or confirmed WE to an inpatient internal medicine or neurology service.

Admission ensures that the patient receives continued intravenous thiamine and magnesium administration, observation for possible development of WKS, and evaluation for possible cardiovascular beriberi.

Inpatient therapy for infants with thiamine deficiency involves administration of high-dose, parenteral thiamine 50 mg/day for 2 weeks. [3]

Outpatient care

Patients who are malnourished, whether from alcohol or other causes, should continue to receive thiamine supplementation on an outpatient basis.

Alcohol also appears to significantly increase the amount of thiamine required to treat the patient successfully compared with individuals in whom thiamine deficiency has a predominantly nutritional cause. [6]


Consultations, Monitoring, and Prevention

An internist and/or metabolic specialist can evaluate the encephalopathic patient for metabolic causes of acute mental status abnormalities. Consult a neurologist for further evaluation and treatment of altered mental status or other focal neurologic deficits. A psychiatrist may be helpful in evaluating comorbid psychiatric conditions. Refer patients with alcoholism to alcohol-cessation programs and monitor them for signs of alcohol withdrawal.

Patients who have been treated for WE should be advised to avoid alcohol consumption and other behaviors that predispose to thiamine deficiency.

In the United States, many foods (but not alcoholic beverages) are supplemented with multiple vitamins and minerals. Some health policy experts have hypothesized that fortifying alcoholic beverages with thiamine would lower healthcare costs.



In addition, the administration of dextrose in the setting of thiamine deficiency can be harmful because glucose oxidation is a thiamine-intensive process that may drive the insufficient circulating vitamin B-1 intracellularly, thereby precipitating neurologic injury. [3]