Obesity Surgery, 17, 704-706
Case Report
Wernicke’s Syndrome after Sleeve Gastrectomy Wojciech Makarewicz, MD, PhD; Lukasz Kaska, MD, PhD; Jarek Kobiela, MD; Tomasz Stefaniak, MD, PhD; Jacek Krajewski, MD; Marta Stankiewicz, MD1; Magdalena A. Wujtewicz, MD2; Andrzej J. Lachinski, MD, PhD; Zbigniew Sledzinski, MD, PhD Department of General, Endocrine and Transplant Surgery, Medical University of Gdansk, 1 Department of Clinical Nutrition, Medical University of Gdansk; 2Department of Anaestesiology and Intensive Care, Medical University of Gdansk, Poland We report a case of Wernicke’s encephalopathy after sleeve gastrectomy, which had been complicated by stomach wall edema and aggravated by dietary noncompliance. Despite intense parenteral nutrition, thiamine deficiency became clinically evident. It suggests that nutritional preparations used were unable to cover the increased thiamine requirement. After intense thiamine supplementation, gradual improvement occurred during the 6 months after the diagnosis, without permanent cognitive impairment. Clinicians involved in postoperative management of bariatric surgery patients must consider Wernicke’s syndrome in hyper-emetic patients, who show unclear neurological deterioration. Early diagnosis and treatment can instantly improve the patient’s condition without permanent sequelae.
(BMI >60) is a two-stage procedure. During the first stage, laparoscopic sleeve gastrectomy is performed to obtain initial weight reduction and co-morbidity reduction by restriction of food capacity, which simplifies fulfilling the dietary restrictions.4 It is followed about 1 year later by a malabsorptive stage, e.g. laparoscopic duodenal switch, laparoscopic Roux-en Y gastric bypass, laparoscopic mini gastric bypass. Laparoscopic mini-gastric bypass is advocated by some surgeons as an efficient, technically uncomplicated and, therefore, safe procedure.5
Case Report Key words: Morbid obesity, bariatric surgery, sleeve gastrectomy, Wernicke’s syndrome, mini-gastric bypass
Introduction Surgical treatment of morbid obesity has become wide spread in developed countries because of disappointing results of conservative methods of weight reduction, especially in patients with BMI >40.1-3 A surgical option for super-super-obesity Correspondence to: Prof. Zbigniew Sledzinski, MD, PhD, Department of General, Endocrine and Transplant Surgery, Medical University of Gdansk, Poland. Fax: +48 58 3492410; e-mail:
[email protected]
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Obesity Surgery, 17, 2007
A 38-year-old morbidly obese female was admitted to the Department of General, Endocrine and Transplant Surgery, for bariatric surgery. Previous history included heavy smoking and two caesarian sections 21 and 9 years ago. Co-morbidities included hypertension (controlled by 0.5 mg of trandolapril daily), type 2 diabetes (on oral hypoglycemic drugs) and bilateral knee arthropathy. Psychological evaluation did not reveal abnormalies despite a borderline result in the Illness Perception Questionnaire.6 With a BMI of 62 kg/m2, she was accepted for a two-stage procedure, with initial weight reduction by sleeve gastrectomy. The laparoscopic sleeve gastrectomy was performed uneventfully. On hospital discharge, © Springer Science + Business Media, Inc.
Wernicke’s Syndrome after Sleeve Gastrectomy
40 mg of omeprazole proton-pump inhibitor (PPI) was prescribed daily and detailed dietary instructions, including strict prohibition of early solid food consumption, were reinforced. The patient presented at the Emergency Department 1 week after discharge with generalized weakness, nausea, vomiting and dehydration, and was re-admitted. Serum potassium was 2.2 mg/dl, and thus electrolytes were supplemented. Parenteral nutrition and electrolyte fluids were instituted. Gastroscopy was performed to exclude obstruction to passage through the stomach. No pathology except edema of the gastric wall was identified. There was suspicion that the patient had been consuming solid foods at home. PPI and cisapride were prescribed. The patient was discharged 1 week later in good condition. She presented again 5 days after the last discharge with recurrence of the previous symptoms. Severe electrolyte depletion was found, and I.V. replacement was instituted. Neurological examination revealed aberrations in consciousness, hypokineses, diplopia with impaired eye movements, and finally complete loss of logical verbal contact. Because of progression of the neurological symptoms, MRI and angio-MR of the brain were performed. No abnormalities were found, and vascular and degenerative changes were ruled out. Functional stenosis of the stomach had been identified on gastroscopy; however, the endoscope could pass readily through stenotic region. Retention of gastric contents and delayed emptying were observed on dynamic upper GI radiological examination. Again, the family admitted moderate non-compliance of the patient in terms of consuming copious solid foods. The second-stage procedure which would improve emptying was considered necessary. Laparoscopic gastrojejunostomy was performed as a brief procedure, and completed the mini-gastric bypass. Postoperatively, the patient developed convergent squint. Temporary losses of consciousness with no logical verbal contact were observed. Paresis of the left tibial nerve appeared, with cessation of foot movement and loss of sensation. Concomitant vertical nystagmus developed. The evolution of symptoms suggested vitamin B1 deficiency with acute presentation of Wernicke’s encephalopathy. I.V. 50 mg of vitamin B1 Q.I.D. with wide spectrum multivitamin and mineral preparations and aminoacid/fatty acid supplementation were immediately initiated. Within a few hours
after vitamin B1 supplementation, nystagmus decreased and diplopia resolved. Nevertheless, left tibial nerve deficit remained, with foot-drop and loss of sensation on the lateral side of the shin. On neurologic examination 3 days after initiation of the intense supplementation, eye movements were normal. The patient remained conscious, with satisfactory logical verbal contact, but slight dementia. Neuroconductive studies of the left tibial nerve now revealed good conduction but lowered amplitude of M2 response. Mild hypoproteinemia and calcium deficiency were treated. The patient was discharged with a carefully planned diet and vitamin/mineral supplementation. On follow-up visits, no permanent damage was observed clinically. The BMI at 6 months had fallen to 44 and at 12 months to 33. The co-morbidities had resolved.
Discussion Development of intense and persistent vomiting can lead to vitamin, mineral and protein deficiencies in a short period of time.7 Disturbances may include thiamine deficiency, but folate, iron, copper, niacin, vitamin D or B12 deficiencies may also co-exist.7-9 Thiamine (vitamin B1) is a water-soluble vitamin whic acts as a co-enzyme in carbohydrate metabolism. Because thiamine pyrophosphate is essential for glucose metabolism, deficiency symptoms will present during high metabolic demands, refeeding or I.V. glucose administration (without thiamine). Thiamine is absorbed in the small intestine. Tissue storage (liver) is limited to
