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October 1 here. Getting scared...liquid diet is getting old.........Surgeon chastised me for only losing 19 lbs since April...what??! He said someone of your size should have lost more and is accusing me of cheating. grr.. I'm part of a whole fancy program at a local hospital and they are strict......I'm afraid of blood clots now....., and just 2nd guessing everything. Found out I will have 6 incisions....as opposed to 5..not sure why that's bugging me but it is lol. I think I'm just a nervous nelly....not packing much...iphone and chargers, and my flip flops. figure i'll wear their gowns.... my cough has now subsided and barely there but dr did say he would cancel the surgery if I had a cough....i even went to a fancy vitamin lounge yesterday and paid for a high dose of vitamin C. Sorry..just all over the place. I go from being excited and elated to doom and gloom.

I go in for the, gastro sleeve on Oct 14 2019 I am on my , liver shrinking diet Sent from my LGL164VL using BariatricPal mobile app

I'm happy to have this over 50 group. I'm 61 years old, scheduled for sleeve 11/7/19 surgery, going alone, no one knows except my daughter who just had sleeve surgery and having a very difficult time. I'm getting cold feet, feeling alone and did I mention I have HIV and can't find anyone else with HIV willing to share their experiences. Help! Sent from my LG-H872 using BariatricPal mobile app

Surgery date July 15,2019 Beginning weight 315 Current weight 267 I feel wonderful the best decision I could have ever made Sent from my SM-G950U using BariatricPal mobile app

I also had surgery on 9/3/19. I had rou-en-y. Sent from my moto e5 plus using BariatricPal mobile app

Obesity Surgery Springer Preventing Wernicke Encephalopathy After Bariatric Surgery Erik Oudman, Jan W. Wijnia, [...], and Albert Postma Additional article information Abstract Half a million bariatric procedures are performed annually worldwide. Our aim was to review the signs and symptoms of Wernicke’s encephalopathy (WE) after bariatric surgery. We included 118 WE cases. Descriptions involved gastric bypass (52%), but also newer procedures like the gastric sleeve. Bariatric WE patients were younger (median = 33 years) than those in a recent meta-analysis of medical procedures (mean = 39.5 years), and often presented with vomiting (87.3%), ataxia (84.7%), altered mental status (76.3%), and eye movement disorder (73.7%). Younger age seemed to protect against mental alterations and higher BMI against eye movement disorders. The WE treatment was often insufficient, specifically ignoring low parenteral thiamine levels (77.2%). In case of suspicion, thiamine levels should be tested and treated adequately with parenteral thiamine supplementation. Keywords: Clinical nutrition, Dietary, Bariatric, Gastric, Obesity, Wernicke’s encephalopathy, Thiamine Introduction The prevalence of morbid obesity has risen to global epidemic proportions and bariatric surgery has been shown to be the most effective treatment to achieve substantial and long-lasting weight loss for morbid obesity [1–3]. In the past decades, the number of bariatric procedures performed has increased exponentially. Currently, laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy are the most commonly performed bariatric procedures with more than 500,000 interventions worldwide per year [4–6]. Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from malnutrition and a possible adverse complication from bariatric operations. WE is characterized by the classic triad of ataxia, eye movement disorders, and mental status change. The prevalence rate of WE is 0.6–2% of the population, but the condition is often only discovered at autopsy [7]. Current guidelines for bariatric surgery suggest preventive thiamine suppletion (12 mg) in multivitamin treatment for all patients undergoing surgery, but higher doses for patients with suspicion for deficiency [8]. The aim of this paper is to review the clinical characteristics of WE after bariatric surgery, also referred to as “bariatric beriberi” [9] and to raise the clinician’s index of suspicion about this neuropsychiatric diagnosis and its preventability. Methods We searched MEDLINE, EMBASE, and Google Scholar, using MeSH terms (WE, Korsakoff syndrome, beriberi, restrictive weight loss surgery, gastrectomy). There were no language restrictions. Studies published from 1985 to 2017 on bariatric surgery with a diagnosis of WE were included. We reviewed the title and abstract of these articles, and indexed the data for year of publication, age, sex, BMI, onset duration and progression of symptoms, radiographic findings, treatment, and follow-up. All included studies were either case reports or case series, since information on the course of illness and symptomatology was often lacking in all group studies. The maximum number of represented case descriptions in one study was five [10]. One study reviewed four cases [11], three studies reviewed three cases [12–14], and eight cases reviewed two cases [15–23]. Cases were excluded if too little information was available to confirm a diagnosis of WE or no clinical characteristics regarding the patient or course of illness were available. Since the collected data is not a random sample of cases, and not likely to be normally distributed, nonparametric statistical procedures were applied (Mann-Whitney U test for comparison of two independent means, chi-square test for multiple means). The recorded data are either number of patients (percentage) or median (range) as appropriate. Results General Overview We identified 118 case descriptions in the published literature [9–101]. The most common bariatric procedure was Roux-en-Y gastric bypass [9–13, 15–18, 24–63], followed by sleeve gastrectomy [19, 64–85] (see Fig. 1 for an overview on the characteristics of the identified bariatric cases that subsequently developed WE). [https://www] Fig. 1 Bariatric procedure case descriptions (n = 118) leading to Wernicke’s encephalopathy (left), gender and age distribution of case descriptions on Wernicke’s encephalopathy after bariatric surgery (right, n = 113) ... Importantly, new cases of WE have continuously been published since the early beginning of weight loss surgery, and the total number of reported bariatric WE cases is growing per 2-year period (Fig. 2), suggesting that it is still relevant to review this differential diagnosis. Also, the total number of bariatric interventions (NHDS and NSAS databases (1993–2006) [102] and ASMBS database (2011–2016) [103]) has been rising each year [5], resulting in a relative decrease of WE cases per intervention (Fig. ​(Fig.22). [https://www] Fig. 2 Reported bariatric WE cases by 2-year period (left) and relative reported WE cases by 2-year period compared to general reference information from NHDS and NSAS databases (1993–2006) [23] and ASMBS (2011–2016) [102]. The red dotted line ... Descriptions of sleeve gastrectomy [19, 64–85] had a more recent publishing date (median 2014) than papers on Roux-en-Y gastric bypass [9–13, 15–18, 24–63] (median 2006) (U (85) = 301.5, p  [https://www] Fig. 3 Months after bariatric procedure, Wernicke’s encephalopathy was diagnosed per surgical procedure (n = 115) Vomiting We further analyzed the symptomatology in all case descriptions. Vomiting was the most frequently described presenting symptom (103 cases, 87.3%) and could be seen as the most relevant precursor of WE. From the literature, it is known that vomiting can also be a major complication in bariatric surgery and is one of the most frequent causes of postoperative readmissions [104]. Severe vomiting is not a normal situation after bariatric surgery and therefore further investigation in cases with frequent vomiting is indicated. In the present sample, non-vomiting cases were distributed throughout all onsets post-surgery, but only 5 out of 15 case descriptions were after the first year, suggesting that other causes than vomiting are likely to cause WE later post-surgery. Alcohol abuse (2 cases), a malabsorptive bariatric procedure (2 cases), and a new operation for hernia (1 case) could explain the late onset in non-vomiting WE presentations, suggesting other factors that negatively affected vitamin B1 storage. Importantly, severe infections, such as postoperative intra-abdominal abscesses leading to thiamine deficiency [78], are also a common presenting feature of WE and are likely to relate to an adverse outcome of WE [105]. Wernicke Encephalopathy: Presenting Characteristics The most profound characteristic of WE in the reviewed case descriptions was ataxia (84.7%, 100 cases), presenting itself as gait abnormalities up to the full inability to walk or move. The second characteristic was an altered mental status (76.3%, 90 cases), presenting itself as delirium, confusion, and problems in alertness or cognition. The third characteristic was eye movement disorders (73.7%, 87 cases), such as nystagmus and ophthalmoplegia, resulting from extraocular muscle weakness. The full triad was present in 54.2% (64 cases), a percentage much higher than the originally reported 16% of patients that present themselves with the full triad in literature in post-mortem case descriptions of WE in alcoholics [105]. Post hoc analysis in the reviewed sample shows that patients presenting themselves with mental status change were older (median 36 years) than patients without mental status change (median 25.5 years) (U (66) = 262, p Moreover, patients with eye movement disorders had a lower BMI (median 45.6 kg/m2) than patients without eye movement disorders (median 52.1 kg/m2), suggesting that a higher BMI can protect against this symptom of WE in bariatric cases. Male patients that did not present themselves with eye movement disorders had a later onset of symptoms (median 24.0) than male patients that did have eye movement disorders (median 3.5) (U (33) = 49, p  Imaging CT scans of the brain did not reveal any significant radiological finding in all cases undergoing this procedure (13 cases), suggesting that CT imaging is not the most suitable imaging technique to detect WE. In 65.6% of the case descriptions where an MRI was performed (40 cases) the procedure revealed radiological alterations. This percentage is somewhat higher than the reported sensitivity of 53% in an earlier study on WE [106]. Of interest, positive MRI results were more frequently associated with mental status change (χ2 (1) = 3.9, p  Treatment: Too Little Too Late According to the European Federation of Neurological Societies and the Royal College of Physicians, 500 mg of parenteral thiamine should be given three times daily until symptoms of acute WE resolute. The treatment is lifesaving and has the potential to reverse this acute neuropsychiatric syndrome [107]. A total of 57 (47.5%) case descriptions were reported in detail on the treatment of WE symptoms. Suboptimal treatment, with relatively low doses of parenteral thiamine (Importantly, a progressive clinical course was visible in 31.6% of the patients (37 cases), resulting in post-acute deterioration of neuropsychiatric and neurological symptoms. This suggests that the diagnosis was easily missed, resulting in a lower likelihood of full recovery. Moreover, the detrimental effect of not treating WE promptly is visible in Fig. 4 showing that many of the patients who developed more than one acute symptom later progressed into chronic Korsakoff’s syndrome. This neuropsychiatric disorder is characterized by severe amnesia, executive problems, and confabulations, leading to lifelong impairment [108]. Patients that developed Korsakoff’s syndrome had significantly more acute symptoms (median 3 symptoms) than patients that did not develop Korsakoff’s syndrome (median 2 symptoms) (U (99) = 703.5, p  [https://www] Fig. 4 Long-term cognitive outcome related to number of acute symptoms (left), MRI outcome (middle, n = 55), and too low levels of thiamine treatment (right, n = 52) Although this finding was not significant, in the group that presented themselves with acute MRI abnormalities, more cases later developed Korsakoff’s syndrome (Fig. ​(Fig.4).4). Also, too low dose of a dose of thiamine suppletion therapy resulted in more cases of KS despite the lack of significance. Non-compliance Of interest, in 10.3% of the case descriptions (12 cases), non-compliance to the medication and follow-up medical regimen was reported. A lack of insight into a given situation is a relatively common sign of the acute and chronic phase of WE [105]. The patients did not follow their follow-up, did not take prescribed drugs, or discharged themselves from the hospital against advice, leading to adverse outcomes. Because of the severity of the syndrome, this aspect requires specific attention in the treatment of WE patients, and at risk bariatric patients. Discussion Persistent vomiting is a common symptom suggesting a complication after bariatric surgery [109]. Nausea, vomiting, and a loss of appetite are also common, non-specific symptoms of thiamine deficiency [8]. Ultimately, vomiting and a loss of appetite are also a preventable cause of thiamine deficiency [110], leading to Wernicke’s encephalopathy (WE) in the majority of bariatric case reports. Adequate, timely, prophylactic, and substantial thiamine treatment in all patients undergoing bariatric surgery is required to prevent the development of WE, which is a rare but severe complication. The present review highlights that current treatment was neither prophylactic, adequate, timely, nor substantial in the majority of cases, leading to worsening of WE symptoms, the development of additional WE symptoms, and ultimately chronic Korsakoff’s syndrome. One of the most remarkable findings in the present review is that the initial symptoms of WE are often not recognized as such, leading to a prolonged state of emergent WE. In 31.6% of the cases, the initial symptoms progressed into more severe symptoms, ultimately leading to chronic Korsakoff’s syndrome. Prompt treatment of the first symptoms suggestive of WE with high doses of parenteral thiamine replacement therapy is necessary to prevent further damage [110]. According to the European Federation of Neurological Societies and the Royal College of Physicians, 500 mg of parenteral thiamine should be given three times daily until symptoms of acute WE resolve [107]. Interestingly, guidelines for treating WE suggest that patients suspected of WE should already be treated as such [107, 111]. Additionally, prophylaxis of WE following early signs and symptoms is only achieved by use of parenteral vitamin supplements, since oral supplements are not absorbed in significant amounts [111]. Moreover, in bariatric surgery, it is always relevant to give prophylactic vitamin therapy, according to international guidelines, to prevent patients from WE. Of interest, newer methods for bariatric surgery such as sleeve gastrectomy and intragastric ballooning still can lead to WE, despite their relative benefits for the patient. Recently, Armstrong–Javors (2016) pointed out that new techniques lead to the primary risk factor of WE, namely vomiting, despite a theoretical advantage by reducing the stomach volume without bypassing the duodenum [112]. Suspicion for WE should therefore be equally high in more traditional surgical procedures and newer procedures. Also, the risk of developing WE due to vitamin B1 deficiency is not restricted to the first half year after surgery but appears to be lifelong, given other factors such as new infections, insufficient meals, or alcohol consumption [110, 113, 114]. Preventive education on the necessity of sufficient vitamin intake should be given before bariatric surgery is performed and is relevant in long-term follow-up. Bariatric patients in their teens or twenties are likely to be more protected for mental status change in the course of WE than patients in their thirties or older, as reflected in a younger age of non-mental status change patients. This finding is in line with earlier reports showing that age is the strongest predictor for postoperative delirium [115, 116]. Importantly, pediatric patients and young adults undergoing bariatric surgery therefore require more attention for sensorimotor problems, such as ataxia and eye movement disorders, besides prophylactic parenteral thiamine treatment. In this specific group, more attention to lifestyle training should be an essential element of treatment, since non-compliance is relatively higher [50]. Relatively more cognitive reserve in combination with non-compliance can leave symptoms of WE unnoticed for a longer period. Although eye movement disorders such as nystagmus and ophthalmoplegia were much more common in bariatric cases than those in the general WE population [113], a higher preoperational BMI was predictive for fewer eye movement disorders. Additionally, male subjects with longer post-bariatric onsets often had no eye movement disorders as a presenting characteristic of WE. It is likely that eye movement disorders represent the most severe form of thiamine deficiency, since it is also the least common phenomenon of the WE triad. Moreover, females are at greater risk for full thiamine depletion than males [8]. A possible mechanism of action explaining the protective effect of higher weight is a greater storing reserve of thiamine in severely obese patients in comparison with less severely obese patients. This mechanism of action has been referred to as “preferential intracellular thiamine recycling” [116], leading to relatively less thiamine depletion in patients with higher body weight. Often, cases with WE following anorexia nervosa present themselves first with eye movement disorders [117], suggesting that this symptom is likely to be the result of full thiamine depletion. This suggests that both patients with lower body weight, and female patients are at greater risk for developing WE, and should guide clinicians in preventive thiamine therapy [1–4, 118]. Radiologic imaging can be employed to support the diagnosis of WE, but is not always sensitive to WE symptomatology. Often, hyperintensities were visible in the thalamic region, the mammillary bodies, and the region around the third and fourth ventricle, in line with previous research on WE [7]. Our results show that MRI alterations are frequently associated with mental status change, but not the motoric aspects of WE. This finding is relevant, because it suggests that specifically in bariatric patients with motoric problems, such as ataxia or eye movement disorders, WE should be treated despite the outcome of an MRI. Non-compliance is common in WE patients following bariatric surgery (10.3%) and could be viewed as a more discrete symptom of the disorder. Patients with WE lack insight into their situation, due to the severity of the neurological problems [108, 110]. Education on the direct adverse consequences of malnourishment should be incorporated into the provision of information before surgery. After surgery, more automated checks on vomiting are relevant. A limitation of the present review is that we only reviewed case descriptions. Therefore, predictive information regarding prevalence rates and incidence rates is limited. Despite this limitation, the level of detail in the reviewed case studies leads to new insights into WE following bariatric surgery. Recently published studies on treatment perspectives of WE in general and psychiatric hospitals are alarming: European as well as American studies demonstrated that most patients did not receive thiamine at all or only received it orally in low doses [119, 120]. Both types of treatment lead to unnecessary cases of chronic Korsakoff’s syndrome characterized by severe amnesia, executive problems, and confabulations, leading to lifelong impairment [108]. It is therefore important to highlight the clinical signs of symptoms in this specific condition. In conclusion, there is a growing number of bariatric patients worldwide. Malnourishment-related WE is a rare but severe and preventable consequence of bariatric surgery that warrants attention given its rapid onset and detrimental course. All bariatric procedures can lead to deficiencies and therefore to WE. WE can be fully prevented by supplying prophylactic thiamine given either parenterally in vomiting patients or orally in non-vomiting patients. Mental confusion, eye movement disorders, and ataxia are often missed as crucial symptoms of WE. After the initial onset of symptoms, rapid treatment with high doses of thiamine is still a life-saving measure, directly ameliorating the core symptoms of WE. The large distribution of WE onsets suggests that bariatric patients remain more vulnerable to vitamin B1 deficiency for life, and therefore require lifelong routine follow-up on their B1 status. Acknowledgements We thank Topcare for supporting excellence of long-term care. We also thank Misha Oey for her advice, and textual suggestions. Compliance with Ethical Standards This review was conducted in compliance with the ethical standards. Conflict of Interest The authors declare that they have no conflict of interest. Ethical Approval Statement This article does not contain any studies with human participants or animals performed by the authors. Informed Consent Statement Informed Consent statement does not apply. Article information Obes Surg. 2018; 28(7): 2060–2068. Published online 2018 Apr 24. doi: 10.1007/s11695-018-3262-4 PMCID: PMC6018594 PMID: 29693218 Erik Oudman,[https://www]1,2 Jan W. Wijnia,1,2 Mirjam van Dam,1,2 Laser Ulas Biter,3 and Albert Postma1,2 1Experimental Psychology, Helmholtz Institute, Utrecht University, Heidelberglaan 1, 3584 CS Utrecht, The Netherlands 2Korsakoff Center Slingedael, Lelie Care Group, Rotterdam, The Netherlands 3Department of Bariatric Surgery, Franciscus Gasthuis, Rotterdam, The Netherlands Erik Oudman, Email: ln.uu@namduo.a.f. [https://www]Corresponding author. Copyright [emoji767] The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. References 1. Sjostrom L, Narbro K, Sjostrom CD, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741–752. [PubMed] [Google Scholar] 2. Colquitt JL, Picot J, Loveman E, Clegg AJ. Surgery for obesity. Cochrane Database Syst Rev 2009 (2):CD003641. [PubMed] 3. Buchwald H, Estok R, Fahrbach K, Banel D, Jensen MD, Pories WJ, Bantle JP, Sledge I. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009;122(3):248–256.e5. [PubMed] [Google Scholar] 4. Alqahtani A, Alamri H, Elahmedi M, Mohammed R. Laparoscopic sleeve gastrectomy in adult and pediatric obese patients: a comparative study. Surg Endosc Other Interv Technol. 2012;26(11):3094–3100. [PubMed] [Google Scholar] 5. Gadiot RPM, Biter LU, Zengerink HJF, de Vos tot Nederveen Cappel RJ, Elte JWF, Castro Cabezas M, Mannaerts GHH. Laparoscopic sleeve gastrectomy with an extensive posterior mobilization: technique and preliminary results. Obes Surg. 2012;22(2):320–329. [PubMed] [Google Scholar] 6. Nguyen NT, Goldman C, Rosenquist CJ, et al. Laparoscopic versus open gastric bypass: a randomized study of outcomes, quality of life, and costs. Ann Surg. 2001;234(3):279–289. [PMC free article] [PubMed] [Google Scholar] 7. Sechi G, Serra A. Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol. 2007;6(5):442–455. [PubMed] [Google Scholar] 8. Zafar A. Wernicke’s encephalopathy following roux en Y gastric bypass surgery. Saudi Med J. 2015;36(12):1493–1495. [PMC free article] [PubMed] [Google Scholar] 9. Moore CE, Sherman V. Effectiveness of B vitamin supplementation following bariatric surgery: rapid increases of serum vitamin B12. Obes Surg. 2015;25(4):694–699. [PubMed] [Google Scholar] 10. Chaves LC, Faintuch J, Kahwage S, Alencar Fde A. A cluster of polyneuropathy and Wernicke-Korsakoff syndrome in a bariatric unit. Obes Surg. 2002;12(3):328–334. [PubMed] [Google Scholar] 11. Bétry C, Disse E, Chambrier C, Barnoud D, Gelas P, Baubet S, Laville M, Pelascini E, Robert M. Need for intensive nutrition care after bariatric surgery. JPEN J Parenter Enteral Nutr. 2017;41(2):258–262. [PubMed] [Google Scholar] 12. Towbin A, Inge TH, Garcia VF, Roehrig HR, Clements RH, Harmon CM, Daniels SR. Beriberi after gastric bypass surgery in adolescence. J Pediatr. 2004;145(2):263–267. [PubMed] [Google Scholar] 13. Sullivan J, Hamilton R, Hurford M, Galetta SL, Liu GT. Neuro-ophthalmic findings in Wernicke’s encephalopathy after gastric bypass surgery. Neuro-Opthalmology. 2006;30:85–89. [Google Scholar] 14. Primavera A, Brusa G, Novello P. Wernicke-Korsakoff encephalopathy following biliopancreatic diversion. Obes Surg. 1993;3(2):175–177. [PubMed] [Google Scholar] 15. Salas-Salvadó J, García-Lorda P, Cuatrecasas G, et al. Wernicke’s syndrome after bariatric surgery. Clin Nutr. 2000;19(5):371–373. [PubMed] [Google Scholar] 16. Nakamura K, Roberson ED, Reilly LG, et al. Polyneuropathy following gastric bypass surgery. Am J Med. 2003;115(8):679–680. [PubMed] [Google Scholar] 17. Alves LF, Gonçalves RM, Cordeiro GV, Lauria MW, Ramos AV. Beriberi after bariatric surgery: not an unusual complication. Report of two cases and literature review. [article in Portuguese] Arq Bras Endocrinol Metabol. 2006;50(3):564–568. [PubMed] [Google Scholar] 18. Abarbanel JM, Berginer VM, Osimani A, Solomon H, Charuzi I. Neurologic complications after gastric restriction surgery for morbid obesity. Neurology. 1987;37(2):196–200. [PubMed] [Google Scholar] 19. Tabbara M, Carandina S, Bossi M, Polliand C, Genser L, Barrat C. Rare neurological complications after sleeve gastrectomy. Obes Surg. 2016;26(12):2843–2848. [PubMed] [Google Scholar] 20. Seehra H, MacDermott N, Lascelles RG, Taylor TV. Wernicke’s encephalopathy after vertical banded gastroplasty for morbid obesity. BMJ. 1996;312(7028):434. [PMC free article] [PubMed] [Google Scholar] 21. Shimomura T, Mori E, Hirono N, Imamura T, Yamashita H. Development of Wernicke-Korsakoff syndrome after long intervals following gastrectomy. Arch Neurol. 1998;55(9):1242–1245. [PubMed] [Google Scholar] 22. Rothkopf MM. Reversible neurologic dysfunction caused by severe vitamin deficiency after malabsorptive bariatric surgery. Surg Obes Relat Dis. 2006;2(6):656–660. [PubMed] [Google Scholar] 23. Kim MH, Baek JM, Sung GY, et al. Wernicke’s encephalopathy following gastrectomy in patients with gastric cancer [in Korean] J Korean Surg Soc. 2006;70:218–222. [Google Scholar] 24. Worden RW, Allen HM. Wernicke’s encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report. Curr Surg. 2006;63(2):114–116. [PubMed] [Google Scholar] 25. Walker J, Kepner A. Wernicke’s encephalopathy presenting as acute psychosis after gastric bypass. J Emerg Med. 2012;43(5):811–814. [PubMed] [Google Scholar] 26. Tozzo P, Caenazzo L, Rodriguez D, Bolcato M. Delayed diagnosis of Wernicke encephalopathy with irreversible neural damage after subtotal gastrectomy for gastric cancer: a case of medical liability? Int J Surg Case Rep. 2017;30:76–80. [PMC free article] [PubMed] [Google Scholar] 27. Stenerson M, Renaud D, Dufendach K, Swain J, Zarroug A, Homme J, Kumar S. Recurrent Wernicke encephalopathy in an adolescent female following laparoscopic gastric bypass surgery. Clin Pediatr. 2013;52(11):1067–1069. [PubMed] [Google Scholar] 28. Bhardwaj A, Watanabe M, Shah JR. A 46-yr-old woman with ataxia and blurred vision 3 months after bariatric surgery. Am J Gastroenterol. 2008;103(6):1575–1577. [PubMed] [Google Scholar] 29. Schroeder M, Troëng T, Brattström L, Navne T. Early complication following bariatric surgery. Wernicke encephalopathy in a 23-year old woman within three months after surgery [Article in Swedish] Lakartidningen. 2009;106(36):2216–2217. [PubMed] [Google Scholar] 30. Saab R, El Khoury MI, Jabbour RA. Wernicke encephalopathy after Roux-en-Y gastric bypass and hyperemesis gravidarum. Surg Obes Relat Dis. 2013;9(6):e105–e107. [PubMed] [Google Scholar] 31. Penders GEM, Daey Ouwens IM, van der Heijden FM. Wernicke encephalopathy and dry beriberi; late complications after bariatric surgery performed on a patient with a psychiatric history [article in Dutch] Tijdschr Psychiatr. 2017;59(2):116–120. [PubMed] [Google Scholar] 32. Nautiyal A, Singh S, Alaimo DJ. Wernicke encephalopathy—an emerging trend after bariatric surgery. Am J Med. 2004;117(10):804–805. [PubMed] [Google Scholar] 33. Longmuir R, Lee AG, Rouleau J. Visual loss due to Wernicke syndrome following gastric bypass. Semin Ophthalmol. 2007;22(1):13–19. [PubMed] [Google Scholar] 34. Loh Y, Watson WD, Verma A, Chang ST, Stocker DJ, Labutta RJ. Acute Wernicke’s encephalopathy following bariatric surgery: clinical course and MRI correlation. Obes Surg. 2004;14(1):129–132. [PubMed] [Google Scholar] 35. Lawton AW, Frisard NE. Visual loss, retinal hemorrhages, and optic disc edema resulting from thiamine deficiency following bariatric surgery complicated by prolonged vomiting. Ochsner J. 2017;17(1):112–114. [PMC free article] [PubMed] [Google Scholar] 36. Kushner R. Managing the obese patient after bariatric surgery: a case report of severe malnutrition and review of the literature. JPEN J Parenter Enteral Nutr. 2000;24(2):126–132. [PubMed] [Google Scholar] 37. Kulkarni S, Lee AG, Holstein SA, Warner JE. You are what you eat. Surv Ophthalmol. 2005;50(4):389–393. [PubMed] [Google Scholar] 38. Kramer LD, Locke GE. Wernicke’s encephalopathy. Complication of gastric plication. J Clin Gastroenterol. 1987;9(5):549–552. [PubMed] [Google Scholar] 39. Jethava A, Dasanu CA. Acute Wernicke encephalopathy and sensorineural hearing loss complicating bariatric surgery. Conn Med. 2012;76(10):603–605. [PubMed] [Google Scholar] 40. Jiang W, Gagliardi JP, Raj YP, Silvertooth EJ, Christopher EJ, Krishnan KR. Acute psychotic disorder after gastric bypass surgery: differential diagnosis and treatment. Am J Psychiatry. 2006;163(1):15–19. [PubMed] [Google Scholar] 41. Jenkins PF. Wernicke encephalopathy. Am Orthopt J. 2015;65:104–108. [PubMed] [Google Scholar] 42. Iannelli A, Addeo P, Novellas S, Gugenheim J. Wernicke’s encephalopathy after laparoscopic Roux-en-Y gastric bypass: a misdiagnosed complication. Obes Surg. 2010;20(11):1594–1596. [PubMed] [Google Scholar] 43. Grace DM, Alfieri MA, Leung FY. Alcohol and poor compliance as factors in Wernicke’s encephalopathy diagnosed 13 years after gastric bypass. Can J Surg. 1998;41(5):389–392. [PMC free article] [PubMed] [Google Scholar] 44. Fried RT, Levy M, Leibowitz AB, Bronster DJ, Iberti TJ. Wernicke’s encephalopathy in the intensive care patient. Crit Care Med. 1990;18(7):779–780. [PubMed] [Google Scholar] 45. Foster D, Falah M, Kadom N, Mandler R. Wernicke encephalopathy after bariatric surgery: losing more than just weight. Neurology. 2005;65(12):1987. [PubMed] [Google Scholar] 46. Fandiño JN, Benchimol AK, Fandiño LN, Barroso FL, Coutinho WF, Appolinário JC. Eating avoidance disorder and Wernicke-Korsakoff syndrome following gastric bypass: an under-diagnosed association. Obes Surg. 2005;15(8):1207–1210. [PubMed] [ Sent from my SM-N960U using BariatricPal mobile app

Hey all, I had gastric sleeve surgery on 9/24 as well. My doctor said 7 to 10 days on full liquid. I'll see him on Monday and will let you all know if he says I can switch. After training myself on the liquids I'm looking forward to the pureed food. I think I'm going to start with baby food. Are you keeping your liquids down comfortably? Sent from my SM-N950U using BariatricPal mobile app

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Hi all. I’m 55 and will be getting VSG on 10/15/19. I start pre op diet on Tuesday.

I'm scheduled for the sleeve on 10/21 with a 2 week liquid diet beginning on 10/7!

10/29 here, hopefully depending on insurance

Let me tell you a tale. lol. 9/21/19 - I wake up and immediately experience sharp, stabbing pain in my abdomen. It extends from my stomach down in a straight line. Soon after, I develop severe muscle soreness in my back. The pain is superficial; clearly muscular. It is tender to the touch. I decide MAYBE it is related to the gastric so I spend a few hours trying to go about my day. By 3PM I decide I need to go to the ER. I go to the closest ER to where I am. After 5 hours, they tell me they can't treat me because I complained of abdominal pain and they "don't treat bariatric patients". They have me transferred to the hospital that did my gastric bypass. - Cue $150 copay for no reason. 9/21/19 - Different ER. I get several doses of Dilaudid, to no effect. They do a CT scan and see my pouch and organs all look fine. Again, I express I have severe BACK pain and superficial abdominal pain. They call the bariatric surgeon on-call (not my surgeon) who says it's an ulcer. They do no diagnostics to confirm it's an ulcer. They discharge me with $100 in ulcer medicine and "a shot of Dilaudid to get me to my bed, at least". Cue 100$ in meds and $150 copay. 9/23/19 - I call my bariatric office and they fit me in as an emergency visit. The NP says it's definitely not an ulcer. DUH. He orders a back xray and abdominal xray. He prescribes me prescription NSAIDs and says to keep taking the ulcer medicine "anyways". Cue $50 copay. 9/24/19 - The bariatric office says no one is around to read my xrays. I have to sick my mother on them. LOL. They call me back immediately and say "they don't know what's wrong" and I could schedule an endoscopy to rule out bariatric issues. I tell them that is idiotic because I already have all the ulcer medicine. They agree. 9/25/19 - I attempt to go to work. I end up bursting into tears from the back pain. My PCP fits me in in the afternoon. She looks at my xrays and says I have degenerative disc disease from osteoarthritis and a thoracic hairline fracture, which may be more noticeable in an xray performed a week out from the injury. I do not need ulcer medicine. She sends me for a back brace, prescribes a strong muscle relaxer, and prednisone. 9/27/19 - I am back at work with no abdominal pain, but still excruciating back pain. I notice I have a gigantic red bruise straight down my spine and numerous purple bruises. No one has even looked at my back until I did this morning, so no doctor has even seen this. I call my PCP just to give her a status update. She is, of course, out of the office today. I continue to be in pain. BACK. PAIN. It is concluded that I likely injured myself with weight lifting at the gym on the 20th. None of this is bariatric-related, and I was pigeon-holed into a diagnosis without ANY diagnostics being completed because I happened to mention associated abdominal pain which was MUSCULAR but since I said "abdomen" no one wanted to touch me with a 10 foot pole because I am a bypass patient. I spent $500 for literally no reason, and had multiple hospitals and practitioners insist this was somehow bariatric related despite nothing lining up with any bariatric issue. Completely absurd. I should have insisted other diagnostics but I was in SO much pain for this past week, I wasn't even in the mindframe to argue. At first I thought MAYBE this was some freak ulcer thing, despite having ulcers before and knowing this ain't it. Anyways, I guess this is something to look out for in the future - that any remote mention of abdominal pain will trigger a complete shutdown of all common sense from medical providers that, hey, this isn't necessarily because this patient had gastric bypass and COULD be a f**king SPINAL FRACTURE.

10/15 here 😀

I’m still 10/15 but just found out that my surgeon wants to do VSG instead of RNY due to Gout that is genetic and not diet caused. Time to check out the VSG boards...

Due to gout problems that are genetic, (Not diet related), my surgeon wants to do VSG instead of RNY because of the malabsorption and he believes my gout could become worse after RNY. So I guess I have a lot of reading to do as I have been researching RNY non stop. I’m glad they didn’t cancel or delay my surgery. I was worried because i had to go on prednisone again due to a very bad gout attack. So my date is still 10/15 and my diet starts on Tuesday. I hope all my RNY friends the best and I’ll still be around... Be well!

Anyone else experience weight gain years after Gastric-Sleeve? I'm almost 200 lbs again and very frustrated. I know a few things I'm doing wrong - not getting enough nutrient dense foods, too many non- nutrients rich foods/calories - not enough water *I hate drinking water - not enough exercise - Depression and stress have taken their toll. Now I need to 'start over'. WIth a busy life - 4 children ages 10-30 and 2 3 yo grandchildren - 3 part time jobs - volunteer positions at church - it's hard to focus on self-care. I need help, encouragement, focus and answers to reverse the effects of it all. Hoping to get some practical advise here to help me get my life back on track. I want to live a long healthy life and just struggle with the enormity of variety and choices in the diet and health world...

This is so upsetting to see. I had surgery on Sept 4th (no pre op diet) required except for all liquids the day before and I have only lost 13lbs. I cant for the life of me figure out what is wrong with me. I get in 80oz- a gallon of water a day. And i always get my protein in between 65- even 100 a couple of days and my calories are in the 600 ish range. Of the 13 lbs, 10 i lost the first week and then since then just 1.5 a week! Im afraid that I went through all of this for it not t work... I could use some serious advice and calming words because I am desperately freaking out.

Hi, I am also on my pre-op diet (surgery 10/3). Are you on a clear liquid diet 7 days prior to surgery? My doctor has me on one and it is very hard. I think it is to prep me for post surgery and the diet needed after along with shrinking my liver. I find keeping fluids with me 24/7 will help but I am only on day 2. I did have some small slips last week with my low carb diet but felt I had to just do better and I did.

I struggled with pills the first week or so after surgery, it hurt. I broke my multivitamin up into small chunks at first and was told three quarters was fine until I could work my way up to a whole one. I think I did 10 days with the quarters then was able to take a whole one but only along with food. I just got switched to capsules today so yay for that! You just have to be careful that you aren't taking iron and calcium together or within 2 hours of each other as they will cancel each other out. I haven't had any problems with low blood sugar but I am just not hungry, at all. I have been focusing on high protein when I do eat because the protein shakes are getting to me. My doc is more concerned with me getting my protein, water, and vitamins in at this point. I'm focusing on that and then going to work on adding food in.

I had gastric sleeve 6 years ago but I cannot get this to change any of my information and it has me as pre-op I am 5 ft 9 in and I lost 133 lbs and just stopped... I got to 200lbs I’m taller so it was ok-ish but now I’ve gained 20 lbs and I’m getting scared bc I never really got to where I was wanting. I do not have loose skin, I kinda look like a small fat person... I wear a size 9/10 in women’s clothes BUT naked I look like miss piggy. I never got the loose skin, I still have thicker fat on my abdomen area and lower belly hangs but it’s thick. I need help, I’ve went to the gym, I’ve walked, I’ve ran... I don’t know what to do.

For a couple of years now there have been reports of the danger of heartburn drugs/PPI blockers like zantac that are commonly used to help with the side effects of gastric surgery. Today Canada officially recalled these drugs due to their link to cancer. Personally, I am completely dependent on these drugs due to the acid reflux side effect of my gastric sleeve. If you use these prescriptions daily, I strongly urge you to contact your doctor or pharmacist as soon as possible. https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2019/70989a-eng.php?utm_source=hs_email&utm_medium=email&utm_content=77363999&_hsenc=p2ANqtz-8zLyVDfQD8I8hCu3-XeY7Fh97rFTkpD6v27F37TI29RzLKaNdKiDz_TiM1BKOzRo_NfiS6IqmuYpTuPc_HRfMUlmpaxA&_hsmi=77363999 image-0.00596046447753906.jpg

For a couple of years now there have been reports of the danger of heartburn drugs/PPI blockers like zantac that are commonly used to help with the side effects of gastric surgery. Today Canada officially recalled these drugs due to their link to cancer. Personally, I am completely dependent on these drugs due to the acid reflux side effect of my gastric sleeve. If you use these prescriptions daily, I strongly urge you to contact your doctor or pharmacist as soon as possible. https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2019/70989a-eng.php?utm_source=hs_email&utm_medium=email&utm_content=77363999&_hsenc=p2ANqtz-8zLyVDfQD8I8hCu3-XeY7Fh97rFTkpD6v27F37TI29RzLKaNdKiDz_TiM1BKOzRo_NfiS6IqmuYpTuPc_HRfMUlmpaxA&_hsmi=77363999 image-0.00596046447753906.jpg

For a couple of years now there have been reports of the danger of heartburn drugs/PPI blockers like zantac that are commonly used to help with the side effects of gastric surgery. Today Canada officially recalled these drugs due to their link to cancer. Personally, I am completely dependent on these drugs due to the acid reflux side effect of my gastric sleeve. If you use these prescriptions daily, I strongly urge you to contact your doctor or pharmacist as soon as possible. https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2019/70989a-eng.php?utm_source=hs_email&utm_medium=email&utm_content=77363999&_hsenc=p2ANqtz-8zLyVDfQD8I8hCu3-XeY7Fh97rFTkpD6v27F37TI29RzLKaNdKiDz_TiM1BKOzRo_NfiS6IqmuYpTuPc_HRfMUlmpaxA&_hsmi=77363999 image-0.00596046447753906.jpg

For a couple of years now there have been reports of the danger of heartburn drugs/PPI blockers like zantac that are commonly used to help with the side effects of gastric surgery. Today Canada officially recalled these drugs due to their link to cancer. Personally, I am completely dependent on these drugs due to the acid reflux side effect of my gastric sleeve. If you use these prescriptions daily, I strongly urge you to contact your doctor or pharmacist as soon as possible. https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2019/70989a-eng.php?utm_source=hs_email&utm_medium=email&utm_content=77363999&_hsenc=p2ANqtz-8zLyVDfQD8I8hCu3-XeY7Fh97rFTkpD6v27F37TI29RzLKaNdKiDz_TiM1BKOzRo_NfiS6IqmuYpTuPc_HRfMUlmpaxA&_hsmi=77363999 image-0.00596046447753906.jpg

For a couple of years now there have been reports of the danger of heartburn drugs/PPI blockers like zantac that are commonly used to help with the side effects of gastric surgery. Today Canada officially recalled these drugs due to their link to cancer. Personally, I am completely dependent on these drugs due to the acid reflux side effect of my gastric sleeve. If you use these prescriptions daily, I strongly urge you to contact your doctor or pharmacist as soon as possible. https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2019/70989a-eng.php?utm_source=hs_email&utm_medium=email&utm_content=77363999&_hsenc=p2ANqtz-8zLyVDfQD8I8hCu3-XeY7Fh97rFTkpD6v27F37TI29RzLKaNdKiDz_TiM1BKOzRo_NfiS6IqmuYpTuPc_HRfMUlmpaxA&_hsmi=77363999 image-0.00596046447753906.jpg