Case Presentation: A 46 year old African American woman presented with one week of worsening hearing loss along with 3 days of vision changes, confusion, visual hallucinations, and difficulty ambulating. She had history of invasive ductal cell carcinoma status-post mastectomy and chemotherapy. Additional history included hemorrhoids for which she underwent hemorrhoidectomy due to excessive bleeding while on chemotherapy.Vital signs were within normal limits other than tachycardia with heart rate to 110 beats per minute. The initial physical examination was notable for a reasonably well-nourished appearing woman although her BMI had dropped from 27 to 22 within the previous 18 months. She spoke very loudly and complained of difficulty hearing questions or reading written questions. Responses were inappropriate at times, which could have been attributable to misunderstanding questions asked. She was alert, intermittently oriented, and also complained of visual hallucinations. Neurologic examination was notable for end-gaze horizontal nystagmus, dysmetria as measured with finger-to-nose exam, decreased visual acuity and decreased hearing bilaterally. Laboratory evaluation was significant for WBC count 14.4 x 10^3uL, AST 106 U/L, and ALT 15 U/L. The patient was initiated on broad spectrum antibiotics for suspicion of meningitis. CT of brain and MRI of brain were normal. Lumbar puncture was performed and showed grossly normal CSF studies with negative cultures and PCR studies. Wernicke encephalopathy was suspected, and intravenous thiamine supplementation was initiated with subsequent improvement of auditory and visual disturbances, confusion and ataxia. Serum thiamine level returned undetectable and she later admitted to significantly more alcohol intake than the “occasional use” reported at admission.

Discussion: Wernicke encephalopathy is a condition of thiamine deficiency commonly affecting those with alcohol use disorder or gastric bypass history. Though traditionally associated with encephalopathy, ophthalmoplegia, and ataxia, it can rarely be associated with auditory deficits as well.  Wernicke encephalopathy should be suspected in any patient presenting with altered mentation and alcohol intake history, but also in those with auditory deficits. Recovery of deficits is possible with prompt diagnosis and treatment, and mortality from untreated disease is high.

Conclusions: Wernicke encephalopathy classically presents with the triad of encephalopathy, oculomotor dysfunction, and ataxia, but only one-third of patients have the full triad. Other less common findings include vestibular dysfunction, peripheral neuropathy, hypothermia, protein calorie malnutrition, and rarely hearing loss. It is imperative that hospitalists consider this entity in the differential diagnosis even when classic findings are not present in order to provide prompt treatment, prevent morbidity, although residual deficits are common.