Objective: To review the clinical essentials of Wernicke encephalopathy (WE) after bariatric surgery.
Summary Background Data: An estimated 205,000 bariatric surgical procedures were performed in the United States in 2007. Such procedures may potentially lead to severe nutritional complications.
Methods: Literature searches were performed in Medline, Embase, and abstract collections. Inclusion criteria were WE after bariatric surgery, diagnosed by the presence of two or more of the following signs: mental status changes, eye movement abnormalities, cerebellar dysfunction, and dietary deficiency.
Results: Of 104 reported cases of WE after bariatric surgery, 84 cases were included. Gastric bypass or a restrictive procedure had been performed in 80 cases (95%). Admission to hospital for WE occurred within 6 months of surgery in 79 cases (94%). Frequent vomiting was a risk factor in 76 cases (90%) and had lasted for a median of 21 days at admission. Intravenous glucose administration without thiamine was a risk factor in 15 cases (18%). Brain magnetic resonance imaging identified lesions characteristic of WE in 14 of 30 cases (47%). Incomplete recovery was observed in 41 cases (49%); memory deficits and gait difficulties were frequent sequela. The recent increase in the use of bariatric surgery in the United States was associated with an increase in reported WE cases.
Conclusions: The number of WE cases after bariatric surgery is substantially higher than previously reported. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and symptoms to prevent and optimize the management of this condition.
Wernicke encephalopathy is a medical emergency that may occur as a complication of bariatric surgery. This systematic review summarizes the key clinical aspects in 84 such cases, including presentation, results of clinical and supplementary examinations, and patient outcomes.
From the Department of Medicine, Aker University Hospital and Faculty Division Aker University Hospital, University of Oslo, Oslo, Norway.
Supported by a research fellowship grant from Eastern Norway Regional Health Authority.
The author has received lecture fees from Johnson & Johnson, but all honoraria were donated directly to charity so that he received neither income nor a tax deduction.
Reprints: Erlend Tuseth Aasheim, Hormone Laboratory, Department of Endocrinology, Aker University Hospital, Trondheimsveien 235, 0514 Oslo, Norway. E-mail: firstname.lastname@example.org.