Case Presentation: Patient is a 47-year-old female with a past medical history of uncontrolled type 2 diabetes, hypertension, and stage 3 chronic kidney disease. She was admitted to the hospital on 10/14/22 with intractable nausea/vomiting (N/V) and diarrhea. She had been in and out of the hospital for the past few months with these symptoms. On admission, she reported abdominal pain, N/V five times daily, lightheadedness, poor balance, and blurry vision for the past week. Labs were notable for potassium 3 mmol/L, glucose 349 mg/dL, Cr 2.17 (baseline ~1.5), and QTc 478 ms. On exam, she was ill-appearing, afebrile, and tachycardic. Abdomen was diffusely tender to palpation with hypoactive bowel sounds and left pupil was minimally responsive to light.She was consulted by neurology on 10/17 for an episode of unresponsiveness. CT head w/o contrast showed no acute intracranial abnormality. CT angio head/neck showed no large vessel occlusion or rate-limiting stenosis. Given her negative imaging, she was set for discharge on 10/18 but her exam that day was notable for ophthalmoplegia, gait disturbance, and confusion despite electrolyte and fluid repletion. Brain MRI w/ contrast was ordered, and thiamine levels were drawn followed by immediate IV thiamine repletion. Thiamine level was 46.2 nmol/L (ref 66.5-200) and brain MRI showed subtle signs of thiamine deficiency (hyperintensities around the third ventricles on T2 flair) and signs of subacute ischemic stroke in bilateral cerebellar hemispheres and left basal ganglia.
Discussion: Wernicke’s encephalopathy (WE) occurs in 1-2% of the general population in the US. This condition is thought to be underdiagnosed since the symptomology can mimic other conditions, such as acute alcohol intoxication. WE is defined by the clinical triad of ophthalmoplegia, ataxia, and confusion, but only 10% of patients exhibit all three symptoms. WE is reversible if treated immediately but if left untreated, roughly 80-90% of patients will develop Korsakoff syndrome, an irreversible condition defined by short-term memory loss and confabulation. In the US, most cases of WE are related to alcohol abuse, but this case presents a patient whose thiamine deficiency developed as a result of an uncontrolled chronic metabolic condition. This patient’s case was unique because her clinical exam was notable for the clinical triad leading us to a working diagnosis of WE. Her condition was likely due to uncontrolled diabetes causing gastroparesis leading to chronic refractory N/V and thus, thiamine deficiency. While it is possible that her subacute ischemic stroke might have contributed to or even exacerbated her symptoms, her history of persistent N/V and laboratory findings on admission made a strong case for thiamine deficiency and hence, WE.
Conclusions: During her stay, her N/V was eventually controlled with prochlorperazine, metoclopramide, and scopolamine. Her thiamine was replaced over time with notable improvement in her ophthalmoplegia, ataxia, and cognition. The patient had been independent for self-care and mobility prior to admission, but she was discharged on 11/02/22 to an inpatient rehab due to a decline in functional status. She planned to follow up with outpatient neurology and gastroenterology. This case emphasizes the importance of a thorough history and physical when faced with nonspecific symptoms, especially in patients with multiple comorbidities. It also shows how poor management of chronic conditions can result in acute processes with potentially irreversible effects.