Case Presentation: A 29 year old female presents with one week of sudden onset double vision. She reports accompanying dark spots in her vision, photosensitivity, and some unsteadiness with walking. The patient’s friend noted that her eyes were “crossed” the morning of admission. Past medical history is significant for alcohol abuse and anxiety with a prior admission for alcohol withdrawal seizure several years ago. Eye exam reveals the loss of abduction bilaterally and impaired adduction, upward, and downward gaze in the right eye with dilated eye exam concerning for disc edema bilaterally. Romberg testing is significant for a slight sway without falling and gait was noted to be wide based. Laboratory work-up was notable for AST 185 U/L, ALT 66 U/L, total bilirubin 6.5 mg/dL, and a lactate of 11 mmol/L. Abdominal ultrasound noted hepatic steatosis and hepatomegaly without evidence of cirrhosis. Acute hepatitis panel was non-reactive. MRI Brain with venography and MRI orbits were within normal limits. B12, TSH, treponemal antibody, and HIV were negative. Empiric high dose thiamine was initiated with progressive clinical improvement and lactate levels improved with fluids. Several days after admission a whole vitamin B1 level resulted at 53 nmol/L (70-180 nmol/L) consistent with thiamine deficiency and helping to confirm the diagnosis of Wernicke encephalopathy with ophthalmoplegia.

Discussion: Vision changes are commonly evaluated by hospitalists who should be readily able to perform at least the initial work-up and treatment for patients with abnormal eye exams. Wernicke encephalopathy is an uncommon but well-known cause of ophthalmoplegia caused by thiamine (vitamin B1) deficiency and classically presenting in a triad of confusion, ataxia, and ophthalmoplegia. It is often but not exclusively seen in patients with a history of alcohol use disorder. Because the complete triad is seen in only 20% of patients and the presentation can be confused with alcohol intoxication or withdrawal, the diagnosis of Wernicke encephalopathy can be missed in as many as 75-80% of cases requiring providers to have a high index of suspicion for the disease (1). The mainstay of treatment is high dose intravenous thiamine administration. The overall safety profile for thiamine is good and treatment should be given without delay when the clinician suspects this diagnosis to prevent permanent neurologic deficits and the dreaded Korsakoff syndrome.While new ophthalmoplegia in a patient with alcohol use disorder is suspicious for Wernicke encephalopathy, clinicians should maintain a broad differential and rule out other dangerous causes of oculomotor dysfunction including demyelinating diseases, intracranial mass, infection, cavernous venous sinus thrombosis, and inflammatory diseases. Most patients with new onset oculomotor deficits such as this patient should undergo MRI of the brain and orbits with consideration of a lumbar puncture while empiric IV thiamine administration is started.

Conclusions: Wernicke encephalopathy is an uncommon cause of acute ophthalmoplegia and a diagnosis that is frequently missed by admitting providers. Clinicians should perform a broad initial work-up for oculomotor deficits with early administration of high dose IV thiamine while other causes are ruled out.