Abstract

Wernicke’s Encephalopathy (WE) is a neurological condition characterized by ophthalmoplegia, ataxic gait, and altered mental status. It is an underdiagnosed yet severely limiting disease process precipitated by thiamine deficiency. Often times, it can occur in conjunction with other disease states like refeeding syndrome in which the underlying etiology is prolonged periods of malnutrition. We present a unique case of non-alcoholic WE in a middle-aged male who initially presented with gallstone pancreatitis complicated with severe metabolic derangements. This ultimately resulted in the development of non-alcoholic WE. Prevention of this condition is a clinical challenge for most physicians as the classic features associated with thiamine deficiency lack diagnostic sensitivity and specificity in critically ill patients. As a result, early recognition and prompt management of this can dramatically decrease morbidity and mortality. Our case highlights and emphasizes the importance of maintaining a high index of suspicion for WE and refeeding syndrome in the setting of altered sensorium and metabolic derangements.

Highlights

  • Wernicke's encephalopathy (WE) is precipitated by thiamine deficiency and is more commonly seen in alcoholics [1]; it can be seen in patients with malnutrition

  • Wernicke’s Encephalopathy (WE) is a neurological condition characterized by ophthalmoplegia, ataxic gait, and altered mental status

  • We present a unique case of non-alcoholic WE in a middle-aged male who initially presented with gallstone pancreatitis complicated with severe metabolic derangements

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Summary

Introduction

Wernicke's encephalopathy (WE) is precipitated by thiamine deficiency and is more commonly seen in alcoholics [1]; it can be seen in patients with malnutrition. It was unclear at this time what could have caused him to have changes in his mental status, but he appeared stable Another CT scan of the abdomen was done which showed interval improvement of pancreatitis with a decrease in size of pseudocyst with drains and stents in place appropriately. This was deemed to be an appropriate window of time to perform PEJ tube placement. Multiple CT scans of the brain were done which all were inconclusive Due to his labile condition and high-risk hemodynamic instability, the PEJ placement was canceled and he was instead started on total parenteral nutrition (TPN) administered through a central line catheter. The improvement was gradual, it was clear that he was responding to the thiamine replacement therapy and eventually, his ophthalmoplegia improved as well

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