Surgery for Obesity and Related Diseases 10 (2014) 992–994
Case report
Wernicke’s encephalopathy three weeks after sleeve gastrectomy Rawan Saab, M.D.a, Mansour El Khoury, M.D.b, Said Farhat, M.D.c,* a
Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon b Department of Surgery, Division of General Surgery, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon c Department of Internal Medicine, Division of Gastroenterology and Hepatology, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon
Abstract
Following bariatric surgeries for management of morbid obesity, less nutrients are absorbed, giving rise to complications due to vitamin deficiencies with frequently dramatic consequences. Neurologic complications resulting from folate, vitamin B12, and thiamine deficiencies have been estimated to occur in up to 16% of cases and present within weeks to months following bariatric surgery. Among bariatric surgeries, Roux-en-Y gastric bypass has been the most associated with such deficiencies due to both restrictive and malabsorptive components. Complications are less seen with restrictive surgeries. We report a case of rapid Wernicke’s encephalopathy due to a thiamine deficiency in a young female patient following Sleeve gastrectomy (SG). (Surg Obes Relat Dis 2014;10:992– 994.) r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved.
Case presentation A 27-year-old female presented to the emergency department with a 2-hour history of progressive alteration of her general status. She had undergone SG for management of morbid obesity 3 weeks before her admission. She was oriented to name only and able to follow simple commands. She was lethargic, somnolent but easily arousable. Upon questioning, she denied any respiratory, gastroenterological, or urinary symptoms and had no history of drug intake or recent trauma. In particular, she denied any recent vomiting following her surgery. Physical examination revealed an illlooking lady, afebrile, normotensive, regular heart rate and normal oxygen saturation. Skin examination showed no lesions, petechiae or ecchymoses, and her surgical wounds were well healed. Cardiac, lung, abdominal and extremity examination was unremarkable. Given her recent bariatric surgery and high index of suspicion, a quick neurologic examination was done, demonstrating a left direction-changing horizontal nystagmus, normal visual fields and no diplopia. She had short*
Correspondence: Said Farhat, M.D., St. George Hospital University Medical Center, Balamand University, P.O. Box 166, 378 Achrafieh Beirut 11 00 2807. E-mail: [email protected]
term memory loss, and was poorly cooperative with the sensory examination. There was weakness in all extremities with a decreased knee-jerk reflex bilaterally and a normal plantar reflex. A chest x-ray was done, showing clear lung fields, and a capillary blood glucose level was within reference range. Laboratory workup ruled out anemia, infection, and thrombocytopenia. Liver function tests were within normal limits. There were no electrolyte abnormalities and no acidosis. A brain computed tomography was obtained, which was normal for her age. Given the pertinent history of recent bariatric surgery, current presentation, and abnormal neurologic findings, Wernicke’s encephalopathy was suspected due to a thiamine deficiency. An intravenous line was inserted, and hydration with normal saline was started. Thiamine hydrochloride was empirically administered as a 100 mg bolus; she was transferred to the floor and closely monitored. Approximately 4 hours after admission to the ward, her status markedly improved with resolution of lethargy, regaining of muscular strength, and full memory capacity. A neurologic exam showed normal ocular reflexes and no nystagmus. Thiamine levels, drawn upon admission to the emergency department, were found later to be low, at a value of 43 nmol/ L (normal: 70-180 nmol/L).
1550-7289/14/$ – see front matter r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved. http://dx.doi.org/10.1016/j.soard.2013.11.016
Wernicke’s Encephalopathy After Gastrectomy / Surgery for Obesity and Related Diseases 10 (2014) 992–994
Discussion Thiamine (vitamin B1) is a water-soluble vitamin essential in carbohydrate metabolism, namely in the Krebs cycle and the pentose phosphate pathway, including alphaketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase [1]. Cerebral metabolism is highly dependent on thiamine, and deficiency may result in brain injury, particularly in regions with higher metabolic demands, including primarily the cerebellar vermis, dorsomedial thalamic nuclei, periaqueductal gray matter, and mamillary bodies [2,3]. As thiamine cannot be produced by animals and humans, it should be obtained from exogenous sources, namely vegetables, whole grain, and supplemented foods. Human storage of thiamine is about 25 mg to 30 mg with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys; thus, thiamine can be depleted within 2 to 3 weeks after deficient diet or malabsorption [4]. In 1881, a triad of acute mental confusion, ataxia, and ophthalmoplegia was described by Dr. Carl Wernicke as a manifestation of vitamin B1 deficiency with serious consequences if untreated. Only 16% of patients present the classic triad of Wernicke’s encephalopathy [5,6], while in up to 29%, ocular anomalies may be the only presenting signs, including nystagmus, conjugate-gaze palsies, and symmetric or asymmetric palsies of both lateral recti or other ocular muscles [5,6]. Most cases of Wernicke’s encephalopathy are due to chronic alcoholism, with 30% to 80% of alcoholics having signs or laboratory studies compatible with thiamine deficiency [7,8]. Thiamine is initially released in the duodenum by the action of the mucosal enzymes, phosphatase and pyrophosphatase, where some absorption occurs. Greater absorption takes place in the jejunum and ileum [9]. Non-alcohol-related conditions also predispose to thiamine deficiency, as demonstrated in gastrointestinal surgical procedures for morbid obesity, which gave rise to the term “bariatric beriberi.” They have been associated with peripheral polyneuropathy, however, not invariably [10]. In other surgeries, namely Bilroth procedures for gastric neoplasia, vitamin B1 malabsorption has also been described, due to resection of gastric folds [11], and thiamine deficiency has been directly proportional to the amount of gastric mucosa resected. Among extensive bariatric surgeries, Roux-en-Y gastric bypass has been most associated with thiamine deficiency as a direct consequence of the resection of greater intestinal tract portions and decrease in the area of gastric and mucosal folds, necessary for absorption as well as postoperative nausea, subsequent vomiting, and inadequate intake of thiamine. A recent systematic review [12] showed the occurrence of Wernicke’s encephalopathy occurring 4 to 12 weeks post bariatric surgery, especially in young women
993
with vomiting; the review also highlighted the frequency of atypical neurologic symptoms. Few cases report the manifestation of thiamine deficiency as early as 2 weeks postoperatively and as late as 20 years following gastrectomy [13,14]. Early manifestation may be due to unbalanced parenteral nutrition without thiamine supplementation, while late manifestation may be due to long-standing latent deficiency precipitated by minor dietary changes. Following surgery, thiamine deficiency is brought on by vomiting, poor dietary compliance, limited food ingestion, digestion, and consequent malabsorption. The authors recently published a report of a young woman developing Wernicke’s encephalopathy following Roux-En-Y gastric bypass and intractable vomiting [15]. In their current case, the patient did not experience any postoperative incidence of vomiting, which makes her thiamine deficiency unrelated to hyperemesis. Wernicke’s encephalopathy remains a diagnosis based on clinical findings, requiring a high index of suspicion. Confirmation may be obtained by measuring blood thiamine concentrations, or measuring the red blood cell transketolase activity. However, these tests are limited due to technical difficulty and lack of specificity [16]. Despite its low sensitivity of 53%, MRI is now considered confirmatory for Wernicke’s encephalopathy, as it has a 93% specificity to rule out the disorder [17,18]. Increased T2 signal bilateral and symmetric lesions can be seen in the paraventricular regions of the thalamus, mamillary bodies, periaqueductal region, the floor of the fourth ventricle, and the midline cerebellum. However, these typical patterns are observed in only 58% of patients [19]; given these limitations, the diagnosis is supported by the response and resolution of neurologic signs with administration of parenteral thiamine. In the authors’ case, they opted for prompt management of the presumed diagnosis based on a high index of suspicion and clinical history, both compatible with the manifestations of the disease in this young patient. A cerebral MRI was obtained a day later with the absence of abnormal findings. Several treatment regimens were studied by Cook and Thompson et al. [20,21] in patients highly suspected of suffering from Wernicke’s encephalopathy. Empirical treatment with 500 mg of thiamine hydrochloride infused over 30 minutes, 3 times a day for 2 to 3 days should be administered. When no clinical response is demonstrated, the infusion should be discontinued. Thiamine infusion does not replete stores; hence, prophylactic thiamine administration in patients at risk, specifically alcoholics, pregnant women, and patients with compromised absorption should be undertaken. If vitamin absorption is restored, the patient may be shifted to highpotency oral B-vitamin complex supplementation and maintained until deficiency factors are eliminated. In the patient case the authors presented, treatment was started with intravenous injections of 100 mg of thiamine
994
R. Saab et al. / Surgery for Obesity and Related Diseases 10 (2014) 992–994
hydrochloride infused over 30 minutes, 3 times a day for 3 days, after which she was started on Neurobion tablets (containing 100 mg of Vitamin B1, 200 mg of Vitamin B6, and 200 micrograms of Vitamin B12), one tablet a day, for life. To the authors’ knowledge, their case report is the fourth to pertain to Wernicke’s encephalopathy precipitated by thiamine deficiency following SG [22–24]. In the first case by Makarewicz et al. [22], a 38-year-old morbidly obese patient underwent SG, complicated by gastric wall edema, dietary noncompliance and recurrent vomiting; in addition to the restrictive nature of her surgery, these factors precipitated Wernicke’s encephalopathy 1 month after her surgery. Thiamine supplementation was administered, with gradual improvement over 6 months after the diagnosis. No permanent cognitive impairment was reported. The second case reported by Jeong et al. [23] described the manifestations of diplopia and dysarthria in a 24-yearold man who presented 4 months after SG. He had been experiencing these symptoms for 3 months after surgery but failed to report them to his physician. His symptoms partially improved with thiamine treatment; however, mild gait disturbances and dysarthria failed to completely resolve. In 2012, Moizé et al. [24] published a case of a 35-yearold obese female presenting to the emergency department 2.5 months after SG, complaining of repeated vomiting and 11.3% weight loss compared with her preoperative status. As workup failed to demonstrate an etiology, she was diagnosed with anxiety and discharged home only to be readmitted a month later with visual disturbances. A nystagmus was elicited by neurologic exam, and a thiamine level confirmed the diagnosis of Wernicke’s encephalopathy. Conclusion As thiamine cannot be produced and stores rely on exogenous sources, the authors recommend supplementing candidates for bariatric surgery with the vitamin before the procedure as well as lifelong prophylactic replacement. References [1] Donnino MW, Vega J, Miller J, et al. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Ann Emerg Med 2007;50:715–21. [2] Cirignotta F, Manconi M, Mondini S, Buzzi G, Ambrosetto P. Wernicke-Korsakoff encephalopathy and polyneuropathy after gastroplasty for morbid obesity: report of a case. Arch Neurol 2000;57: 1356–9.
[3] Toth C, Voll C. Wernicke’s encephalopathy following gastroplasty for morbid obesity. Can J N Sci 2001;28:89–92. [4] Baek JH, Sohn SK, Kim DH, et al. Wernicke’s encephalopathy after allogeneic stem cell transplantation. Bone Marrow Transplant 2005;35:829–30. [5] Victor M. The Wernicke-Korsakoff syndrome. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 28, part II. Amsterdam: North-Holland Publishing Company, 1976:243–70. [6] Naidoo DP, Bramdev A, Cooper K. Wernicke’s encephalopathy and alcohol-related disease. Postgrad Med J 1991;67:978–81. [7] Harper C, Fornes P, Duyckaerts C, Lecomte D, Hauw JJ. An international perspective on the prevalence of the WernickeKorsakoff syndrome. Metab Brain Dis 1995;10:17–24. [8] Darnton-Hill I, Truswell AS. Thiamine status of a sample of homeless clinic attenders in Sydney. Med _7 Aust 1990;152:5–9. [9] Angstadt JD, Bodziner RA. Peripheral polyneuropathy from thiamine deficiency following laparoscopic Roux-en-Y gastric bypass. Obes Surg 2005;15:890–2. [10] Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg 2002;12: 309–11. [11] Kumar N, McEvoy K, Ahlskog E. Arch Neurol 2003;60:1782–5. [12] Singh S, Kumar A. Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 2007;68:807–11. [13] Al-Fahad T, Ismael A, Soliman MO, Khoursheed M. Very early onset Wernicke’s encephalopathy after gastric bypass. Obes Surg 2006;16: 671–2. [14] Shimomura T, Mori E, Hirono N, Imamura T, Yamashita H. Development of Wernicke-Korsakoff syndrome after long intervals following gastrectomy. Arch Neurol 1998;55:1242–5. [15] Saab R, El Khoury M, Jabbour R. Wernicke encephalopathy After Roux-en-Y gastric bypass and hyperemesis gravidarum. Surg Obes Relat Dis 2013 May 22. pii: S1550–7289(13)00164-0. http://dx.doi. org/10.1016/j.soard.2013.05.002. [Epub ahead of print]. [16] Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff syndrome (WKS) and related neurologic disorders due to alcoholism and malnutrition, 2nd ed. Philadelphia: FA Davie, 1989:61–110. [17] Chung SP, Kim SW, Yoo IS, Lim YS, Lee G. Magnetic resonance imaging as a diagnostic adjunct to Wernicke’s encephalopathy in the ED. Am J Emerg Med 2003;21:497–502. [18] Antunez E, Estruch R, Cardenal C, Nicolas JM, Fernandez-Sola J, Urbano-Marquez A. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke’s encephalopathy. AJR Am J Roentgenol 1998;171:1131–7. [19] Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. Wernicke’s encephalopathy: MR findings and clinical presentation. Eur Radiol 2003;13:1001–9. [20] Cook CC. Prevention and treatment of Wernicke-Korsakoff Syndrome. Alcohol Alcohol Suppl 2000;35:19–20. [21] Hope LC, Cook CCH, Thomson AD. A survey of the current clinical practice in the UK concerning vitamin supplementation for chronic alcohol misusers. Alcohol Suppl 1999;34:862–7. [22] Makarewicz W, Kaska L, Kobiela J, et al. Wernicke’s syndrome after sleeve gastrectomy. Obes Surg 2007;17:704–6. [23] Jeong HJ, Park JW, Kim YJ, Lee YG, Jang YW, Seo JW. Wernicke’s encephalopathy after sleeve gastrectomy for morbid obesity. Ann Rehabil Med 2011;35:583–6. [24] Moizé V, Ibarzabal A, Sanchez Dalmau B, et al. Nystagmus: an uncommon neurological manifestation of thiamine deficiency as a serious complication of sleeve gastrectomy. Nutr Clin Pract 2012; 27:788.
Case report
Wernicke’s encephalopathy three weeks after sleeve gastrectomy Rawan Saab, M.D.a, Mansour El Khoury, M.D.b, Said Farhat, M.D.c,* a
Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon b Department of Surgery, Division of General Surgery, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon c Department of Internal Medicine, Division of Gastroenterology and Hepatology, Saint George University Medical Center, University of Balamand, Al-Kurah, North Lebanon
Abstract
Following bariatric surgeries for management of morbid obesity, less nutrients are absorbed, giving rise to complications due to vitamin deficiencies with frequently dramatic consequences. Neurologic complications resulting from folate, vitamin B12, and thiamine deficiencies have been estimated to occur in up to 16% of cases and present within weeks to months following bariatric surgery. Among bariatric surgeries, Roux-en-Y gastric bypass has been the most associated with such deficiencies due to both restrictive and malabsorptive components. Complications are less seen with restrictive surgeries. We report a case of rapid Wernicke’s encephalopathy due to a thiamine deficiency in a young female patient following Sleeve gastrectomy (SG). (Surg Obes Relat Dis 2014;10:992– 994.) r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved.
Case presentation A 27-year-old female presented to the emergency department with a 2-hour history of progressive alteration of her general status. She had undergone SG for management of morbid obesity 3 weeks before her admission. She was oriented to name only and able to follow simple commands. She was lethargic, somnolent but easily arousable. Upon questioning, she denied any respiratory, gastroenterological, or urinary symptoms and had no history of drug intake or recent trauma. In particular, she denied any recent vomiting following her surgery. Physical examination revealed an illlooking lady, afebrile, normotensive, regular heart rate and normal oxygen saturation. Skin examination showed no lesions, petechiae or ecchymoses, and her surgical wounds were well healed. Cardiac, lung, abdominal and extremity examination was unremarkable. Given her recent bariatric surgery and high index of suspicion, a quick neurologic examination was done, demonstrating a left direction-changing horizontal nystagmus, normal visual fields and no diplopia. She had short*
Correspondence: Said Farhat, M.D., St. George Hospital University Medical Center, Balamand University, P.O. Box 166, 378 Achrafieh Beirut 11 00 2807. E-mail: [email protected]
term memory loss, and was poorly cooperative with the sensory examination. There was weakness in all extremities with a decreased knee-jerk reflex bilaterally and a normal plantar reflex. A chest x-ray was done, showing clear lung fields, and a capillary blood glucose level was within reference range. Laboratory workup ruled out anemia, infection, and thrombocytopenia. Liver function tests were within normal limits. There were no electrolyte abnormalities and no acidosis. A brain computed tomography was obtained, which was normal for her age. Given the pertinent history of recent bariatric surgery, current presentation, and abnormal neurologic findings, Wernicke’s encephalopathy was suspected due to a thiamine deficiency. An intravenous line was inserted, and hydration with normal saline was started. Thiamine hydrochloride was empirically administered as a 100 mg bolus; she was transferred to the floor and closely monitored. Approximately 4 hours after admission to the ward, her status markedly improved with resolution of lethargy, regaining of muscular strength, and full memory capacity. A neurologic exam showed normal ocular reflexes and no nystagmus. Thiamine levels, drawn upon admission to the emergency department, were found later to be low, at a value of 43 nmol/ L (normal: 70-180 nmol/L).
1550-7289/14/$ – see front matter r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved. http://dx.doi.org/10.1016/j.soard.2013.11.016
Wernicke’s Encephalopathy After Gastrectomy / Surgery for Obesity and Related Diseases 10 (2014) 992–994
Discussion Thiamine (vitamin B1) is a water-soluble vitamin essential in carbohydrate metabolism, namely in the Krebs cycle and the pentose phosphate pathway, including alphaketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase [1]. Cerebral metabolism is highly dependent on thiamine, and deficiency may result in brain injury, particularly in regions with higher metabolic demands, including primarily the cerebellar vermis, dorsomedial thalamic nuclei, periaqueductal gray matter, and mamillary bodies [2,3]. As thiamine cannot be produced by animals and humans, it should be obtained from exogenous sources, namely vegetables, whole grain, and supplemented foods. Human storage of thiamine is about 25 mg to 30 mg with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys; thus, thiamine can be depleted within 2 to 3 weeks after deficient diet or malabsorption [4]. In 1881, a triad of acute mental confusion, ataxia, and ophthalmoplegia was described by Dr. Carl Wernicke as a manifestation of vitamin B1 deficiency with serious consequences if untreated. Only 16% of patients present the classic triad of Wernicke’s encephalopathy [5,6], while in up to 29%, ocular anomalies may be the only presenting signs, including nystagmus, conjugate-gaze palsies, and symmetric or asymmetric palsies of both lateral recti or other ocular muscles [5,6]. Most cases of Wernicke’s encephalopathy are due to chronic alcoholism, with 30% to 80% of alcoholics having signs or laboratory studies compatible with thiamine deficiency [7,8]. Thiamine is initially released in the duodenum by the action of the mucosal enzymes, phosphatase and pyrophosphatase, where some absorption occurs. Greater absorption takes place in the jejunum and ileum [9]. Non-alcohol-related conditions also predispose to thiamine deficiency, as demonstrated in gastrointestinal surgical procedures for morbid obesity, which gave rise to the term “bariatric beriberi.” They have been associated with peripheral polyneuropathy, however, not invariably [10]. In other surgeries, namely Bilroth procedures for gastric neoplasia, vitamin B1 malabsorption has also been described, due to resection of gastric folds [11], and thiamine deficiency has been directly proportional to the amount of gastric mucosa resected. Among extensive bariatric surgeries, Roux-en-Y gastric bypass has been most associated with thiamine deficiency as a direct consequence of the resection of greater intestinal tract portions and decrease in the area of gastric and mucosal folds, necessary for absorption as well as postoperative nausea, subsequent vomiting, and inadequate intake of thiamine. A recent systematic review [12] showed the occurrence of Wernicke’s encephalopathy occurring 4 to 12 weeks post bariatric surgery, especially in young women
993
with vomiting; the review also highlighted the frequency of atypical neurologic symptoms. Few cases report the manifestation of thiamine deficiency as early as 2 weeks postoperatively and as late as 20 years following gastrectomy [13,14]. Early manifestation may be due to unbalanced parenteral nutrition without thiamine supplementation, while late manifestation may be due to long-standing latent deficiency precipitated by minor dietary changes. Following surgery, thiamine deficiency is brought on by vomiting, poor dietary compliance, limited food ingestion, digestion, and consequent malabsorption. The authors recently published a report of a young woman developing Wernicke’s encephalopathy following Roux-En-Y gastric bypass and intractable vomiting [15]. In their current case, the patient did not experience any postoperative incidence of vomiting, which makes her thiamine deficiency unrelated to hyperemesis. Wernicke’s encephalopathy remains a diagnosis based on clinical findings, requiring a high index of suspicion. Confirmation may be obtained by measuring blood thiamine concentrations, or measuring the red blood cell transketolase activity. However, these tests are limited due to technical difficulty and lack of specificity [16]. Despite its low sensitivity of 53%, MRI is now considered confirmatory for Wernicke’s encephalopathy, as it has a 93% specificity to rule out the disorder [17,18]. Increased T2 signal bilateral and symmetric lesions can be seen in the paraventricular regions of the thalamus, mamillary bodies, periaqueductal region, the floor of the fourth ventricle, and the midline cerebellum. However, these typical patterns are observed in only 58% of patients [19]; given these limitations, the diagnosis is supported by the response and resolution of neurologic signs with administration of parenteral thiamine. In the authors’ case, they opted for prompt management of the presumed diagnosis based on a high index of suspicion and clinical history, both compatible with the manifestations of the disease in this young patient. A cerebral MRI was obtained a day later with the absence of abnormal findings. Several treatment regimens were studied by Cook and Thompson et al. [20,21] in patients highly suspected of suffering from Wernicke’s encephalopathy. Empirical treatment with 500 mg of thiamine hydrochloride infused over 30 minutes, 3 times a day for 2 to 3 days should be administered. When no clinical response is demonstrated, the infusion should be discontinued. Thiamine infusion does not replete stores; hence, prophylactic thiamine administration in patients at risk, specifically alcoholics, pregnant women, and patients with compromised absorption should be undertaken. If vitamin absorption is restored, the patient may be shifted to highpotency oral B-vitamin complex supplementation and maintained until deficiency factors are eliminated. In the patient case the authors presented, treatment was started with intravenous injections of 100 mg of thiamine
994
R. Saab et al. / Surgery for Obesity and Related Diseases 10 (2014) 992–994
hydrochloride infused over 30 minutes, 3 times a day for 3 days, after which she was started on Neurobion tablets (containing 100 mg of Vitamin B1, 200 mg of Vitamin B6, and 200 micrograms of Vitamin B12), one tablet a day, for life. To the authors’ knowledge, their case report is the fourth to pertain to Wernicke’s encephalopathy precipitated by thiamine deficiency following SG [22–24]. In the first case by Makarewicz et al. [22], a 38-year-old morbidly obese patient underwent SG, complicated by gastric wall edema, dietary noncompliance and recurrent vomiting; in addition to the restrictive nature of her surgery, these factors precipitated Wernicke’s encephalopathy 1 month after her surgery. Thiamine supplementation was administered, with gradual improvement over 6 months after the diagnosis. No permanent cognitive impairment was reported. The second case reported by Jeong et al. [23] described the manifestations of diplopia and dysarthria in a 24-yearold man who presented 4 months after SG. He had been experiencing these symptoms for 3 months after surgery but failed to report them to his physician. His symptoms partially improved with thiamine treatment; however, mild gait disturbances and dysarthria failed to completely resolve. In 2012, Moizé et al. [24] published a case of a 35-yearold obese female presenting to the emergency department 2.5 months after SG, complaining of repeated vomiting and 11.3% weight loss compared with her preoperative status. As workup failed to demonstrate an etiology, she was diagnosed with anxiety and discharged home only to be readmitted a month later with visual disturbances. A nystagmus was elicited by neurologic exam, and a thiamine level confirmed the diagnosis of Wernicke’s encephalopathy. Conclusion As thiamine cannot be produced and stores rely on exogenous sources, the authors recommend supplementing candidates for bariatric surgery with the vitamin before the procedure as well as lifelong prophylactic replacement. References [1] Donnino MW, Vega J, Miller J, et al. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Ann Emerg Med 2007;50:715–21. [2] Cirignotta F, Manconi M, Mondini S, Buzzi G, Ambrosetto P. Wernicke-Korsakoff encephalopathy and polyneuropathy after gastroplasty for morbid obesity: report of a case. Arch Neurol 2000;57: 1356–9.
[3] Toth C, Voll C. Wernicke’s encephalopathy following gastroplasty for morbid obesity. Can J N Sci 2001;28:89–92. [4] Baek JH, Sohn SK, Kim DH, et al. Wernicke’s encephalopathy after allogeneic stem cell transplantation. Bone Marrow Transplant 2005;35:829–30. [5] Victor M. The Wernicke-Korsakoff syndrome. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 28, part II. Amsterdam: North-Holland Publishing Company, 1976:243–70. [6] Naidoo DP, Bramdev A, Cooper K. Wernicke’s encephalopathy and alcohol-related disease. Postgrad Med J 1991;67:978–81. [7] Harper C, Fornes P, Duyckaerts C, Lecomte D, Hauw JJ. An international perspective on the prevalence of the WernickeKorsakoff syndrome. Metab Brain Dis 1995;10:17–24. [8] Darnton-Hill I, Truswell AS. Thiamine status of a sample of homeless clinic attenders in Sydney. Med _7 Aust 1990;152:5–9. [9] Angstadt JD, Bodziner RA. Peripheral polyneuropathy from thiamine deficiency following laparoscopic Roux-en-Y gastric bypass. Obes Surg 2005;15:890–2. [10] Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg 2002;12: 309–11. [11] Kumar N, McEvoy K, Ahlskog E. Arch Neurol 2003;60:1782–5. [12] Singh S, Kumar A. Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 2007;68:807–11. [13] Al-Fahad T, Ismael A, Soliman MO, Khoursheed M. Very early onset Wernicke’s encephalopathy after gastric bypass. Obes Surg 2006;16: 671–2. [14] Shimomura T, Mori E, Hirono N, Imamura T, Yamashita H. Development of Wernicke-Korsakoff syndrome after long intervals following gastrectomy. Arch Neurol 1998;55:1242–5. [15] Saab R, El Khoury M, Jabbour R. Wernicke encephalopathy After Roux-en-Y gastric bypass and hyperemesis gravidarum. Surg Obes Relat Dis 2013 May 22. pii: S1550–7289(13)00164-0. http://dx.doi. org/10.1016/j.soard.2013.05.002. [Epub ahead of print]. [16] Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff syndrome (WKS) and related neurologic disorders due to alcoholism and malnutrition, 2nd ed. Philadelphia: FA Davie, 1989:61–110. [17] Chung SP, Kim SW, Yoo IS, Lim YS, Lee G. Magnetic resonance imaging as a diagnostic adjunct to Wernicke’s encephalopathy in the ED. Am J Emerg Med 2003;21:497–502. [18] Antunez E, Estruch R, Cardenal C, Nicolas JM, Fernandez-Sola J, Urbano-Marquez A. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke’s encephalopathy. AJR Am J Roentgenol 1998;171:1131–7. [19] Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. Wernicke’s encephalopathy: MR findings and clinical presentation. Eur Radiol 2003;13:1001–9. [20] Cook CC. Prevention and treatment of Wernicke-Korsakoff Syndrome. Alcohol Alcohol Suppl 2000;35:19–20. [21] Hope LC, Cook CCH, Thomson AD. A survey of the current clinical practice in the UK concerning vitamin supplementation for chronic alcohol misusers. Alcohol Suppl 1999;34:862–7. [22] Makarewicz W, Kaska L, Kobiela J, et al. Wernicke’s syndrome after sleeve gastrectomy. Obes Surg 2007;17:704–6. [23] Jeong HJ, Park JW, Kim YJ, Lee YG, Jang YW, Seo JW. Wernicke’s encephalopathy after sleeve gastrectomy for morbid obesity. Ann Rehabil Med 2011;35:583–6. [24] Moizé V, Ibarzabal A, Sanchez Dalmau B, et al. Nystagmus: an uncommon neurological manifestation of thiamine deficiency as a serious complication of sleeve gastrectomy. Nutr Clin Pract 2012; 27:788.
