Which clinical history findings are characteristic of Wernicke encephalopathy (WE)?

Updated: Nov 20, 2018
  • Author: Philip N Salen, MD; Chief Editor: Andrew K Chang, MD, MS  more...
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The three components of the classic triad of WE are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. However, a complicating factor of WE identification is that its presentation may not be associated with the classical clinical triad in up to 90% of patients.

Consideration for WE should be given to patients with any evidence of long-term alcohol abuse or malnutrition and any of the following: acute confusion, delirium, ataxia, ophthalmoplegia, memory disturbance, hypothermia with hypotension, and delirium tremens.

A high proportion of patients with acute WE who survive develop WKS, characterized by potentially irreversible retrograde amnesia (inability to recall information) and anterograde amnesia (inability to assimilate new information), with varying degrees of other cognitive deficits. [13]

Consider WE when any patient with long-term malnutrition presents with confusion or altered metal status. Significant overlap exists between WE and Korsakoff psychosis. For this reason, the two entities are often described together as WKS.

Alcohol abuse, AIDS, malignancy, hyperemesis gravidarum, prolonged total parenteral nutrition, iatrogenic glucose loading in a thiamine deficient patient, and other disorders associated with grossly impaired nutritional status are associated with WKS.

Bariatric surgery, of which there are more than 100,000 weight-loss procedures performed annually in the United States, has been associated with both malnutrition and WE. [7] Post–bariatric surgery patients have a limited capacity for food intake during the initial weeks after a bariatric procedure and a body's reserves of thiamine can be depleted after only 20 days of inadequate supply. Paradoxically, post–bariatric surgery patients may still be frankly obese when presenting with WE symptoms caused by thiamine deficiency. [7]

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