Case Presentation: A 31-year-old female with history of generalized anxiety disorder (GAD), morbid obesity, and eight weeks status-post sleeve gastrectomy presented with 50-pound weight loss and mental status changes. Other symptoms included nausea, vomiting, and poor oral intake. Days to weeks prior to admission she developed generalized weakness, gait disturbance, diplopia, vertigo, and slowed mentation with confusion. Physical exam was significant for ophthalmoplegia and diminished strength in the lower extremities. Patient was alert and oriented to place and person only. Mental status exam was remarkable for indifferent demeanor, avoidant and hesitant eye contact, and latent speech with limited articulation and superficial responses. Thought process was goal-directed with no apparent delusions/paranoia/hallucinations, mood was restricted with blunted and neutral affect, facial expressions were incongruent to context with inappropriate smiling, and insight into illness was very limited.
The diagnosis of Wernicke’s encephalopathy (WE) was presumed given the clinical presentation and context. Treatment was initiated with high-dose intravenous thiamine, which over several days resulted in resolution of ophthalmoplegia, generalized weakness, confusion, and abnormal speech pattern. She also had a marked improvement in affect, while still demonstrating some signs of her underlying GAD.
Discussion: Morbid obesity is a curable systemic disease with increasing prevalence. Bariatric surgery has become a more common therapy for morbidly obese patients who have failed dietary, exercise, behavioral, and pharmacologic interventions. However, the current popularity of these procedures underplays the numerous associated complications, in particular deficiency of various micronutrients including thiamine. Classic WE presents with ophthalmoplegia, ataxia, and confusion although a wide range of neuropsychiatric symptoms can develop. WE after bariatric surgery typically occurs 4-12 weeks post-operatively. This patient’s GAD could easily have masked a diagnosis of WE, as certain symptoms overlapped with her psychiatric comorbidities.
Conclusions: WE is a challenging but grossly clinical diagnosis. Early detection and treatment with high-dose thiamine may prevent clinical deterioration and neuropsychiatric sequelae. Most patients with adequate treatment recover completely, but residual neurologic defects may persist, including memory impairment, ataxia, and nystagmus. It is essential that both hospital-based and outpatient physicians remain alert for patients at risk for WE, particularly those undergoing bariatric surgery or with other reasons for decreased oral intake with or without vomiting, and recognize that psychiatric manifestations are not uncommon.