Case 1 is a 57‐year‐old African American female patient with morbid obesity, type 2 DM, HTN. and CKD stage 3 who was admitted for DKA. She had undergone Roux‐en‐Y gastric bypass surgery 2 months prior complicated by intractable vomiting requiring repealed hospitalizations accompanied by weight loss > 50 pounds. Upper endoscopy revealed a distal anastomotic ulcer. Several weeks after admission, the patient was noted to be confused and staring. Neurologic consultation confirmed a contused state with disorientation; ophthalmoplegia with nystagmus on attempted horizontal and vertical gaze was present. A clinical diagnosis of Wernicke's encephalopathy was made. MRI of the brain was unremarkable. IV thiamine was given, and within 12 hours her mental status improved and eye movement returned. Prelrealment B1 level returned at < 20 ug/L (reference range 25‐75 fjg/L). Case 2 is a 30‐year‐old African American female s/p Roux‐en‐Y gastric bypass surgery for morbid obesity 18 months prior was hospitalized for nausea and vomiting. Review of systems revealed eye twitching, urinary incontinence, and bilateral lower‐extremity paresthesias. Pertinent physical exam findings included cachexia, horizontal and vertical nystagmus, bilateral upper and lower‐extremity weakness with impaired vibration sense Further neurological testing revealed ataxia and impaired short term memory. Brain imaging with CT scan and MRI was unremarkable Wernicke's encephalopathy was suspected, and therapy was instituted with intravenous thiamine. At discharge, her mental status was remarkably improved, although mild nystagmus persisted
Obesity is a growing epidemic in the United States, with an estimated 34‐% Americans affected. Bariatric surgery has become the treatment of choice for mortid obesity but may be accompanied by serious complications. Wernicke's encephalopathy resulting from thiamine deficiency may follow all types of bariatric surgery and classically presents with a triad of ophthalmoplegia, ataxia, and confusion. Wernicke's encephalopathy has been reported to typically emerge 4‐8 weeks after surgery given the 10‐ to 12‐day half life of thiamine. The threshold for suspecting Wernicke's encephalopathy after bariatric surgery should be low, particularly in patients with recurrent vomiting. Prompt treatment with intravenous thiamine is associated with favorable outcomes. Although it is widely appreciated that bariatric surgery patients be supplemented with thiamine postoperatively, the severity and timing of neurologic complications may not be fully comprehended and require physician and patient reinforcement.
Nutritional deficiencies are common after bariatric surgery, one of which is thiamine deficiency. A high index of suspicion is important for early diagnosis, as a delay in diagnosis and treatment may lead to death or permanent neurologic deficits
F. Ayele, none; M. Parker, none.
To cite this abstract:Ayele F, Parker M. Wernicke's Encephalopathy after Bariatric Surgery: A Case Series. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 212. Journal of Hospital Medicine. 2010; 5 (suppl 1). https://www.shmabstracts.com/abstract/wernickes-encephalopathy-after-bariatric-surgery-a-case-series/. Accessed November 20, 2019.