Alcoholic cirrhosis with Wernicke encephalopathy: Clinical case report

Early differentiation between hepatic encephalopathy and Wernicke encephalopathy (WE) is clinically critical in patients with decompensated alcoholic cirrhosis, as vitamin B1 deficiency can produce overlapping neurological symptoms that obscure the correct diagnosis and delay life-saving treatment.

A 55-year-old male with a 2-year history of alcoholic cirrhosis was admitted to the hospital due to progressively worsening abdominal distension, diarrhea, and fatigue over the month prior to presentation.

WE was established based on the classic clinical triad of ocular motor dysfunction, ataxia, and mental confusion, supported by characteristic magnetic resonance imaging findings showing symmetric abnormal signals in the periaqueductal region of the midbrain.

Initial management comprised comprehensive ascites therapy addressing diarrhea, hyperlactatemia, hypokalemia, and hypoproteinemia. However, on the third hospital day, the patient acutely developed dysarthria, recent memory loss, hand tremors, unsteady gait, and strabismus, which prompted the immediate administration of high-dose intravenous vitamin B1, supplemented with intramuscular and oral B-complex vitamins.

Following targeted thiamine repletion, the patient's neurological symptoms showed significant and rapid improvement.

To our knowledge, this represents a rare case of WE in a critically ill alcoholic cirrhosis patient complicated by hepatic encephalopathy, in the absence of hepatocellular carcinoma or surgical intervention. This case strongly reinforces the need for clinicians to maintain a high index of suspicion for WE in such complex settings to enable timely diagnosis and intervention.