A Case Report published in BMCNeurol presents a case of Wernicke encephalopathy caused by thiamine deficiency in a nonalcoholic liver cirrhosis patient who presented with acute bilateral deafness and bilateral blindness.
]. We report a case of Wernicke encephalopathy in a nonalcoholic liver cirrhosis patient who presented with acute bilateral deafness and bilateral blindness.A 60-year-old Chinese man presented with a history of bilateral blindness and bilateral hypoacousia for 3 days. He had a history of liver cirrhosis and chronic hepatitis C virus infection and did not have a habit of alcohol consumption.
Subsequently, the plasma ammonium level returned to a normal level and was accompanied by an increase in serum sodium to 130 mmol/L. However, the patient’s clinical symptoms worsened into a slight coma rather than improving. He was immediately administered 100 mg of intravenous thiamine owing to the high suspicion index for Wernicke encephalopathy The patient soon regained consciousness but still had blindness and deafness.
Visual loss and hearing loss are less common findings in WE. Visual loss in WE results from a metabolic aetiology related to bilateral optic disc swelling or impairment of visual pathways []. Bilateral blindness has been observed to occur in WE, while bilateral deafness has rarely been reported. The pathogenesis of hearing loss in patients with WE is not clear.
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