Search the Community

No problem! I am glad I was able to help. As a side note, I also recommend watching Dr. Duc C. Vuong's video's. He is a bariatric surgeon that has a lot of videos that I found really helpful. Here is a link to his youtube channel: https://www.youtube.com/user/DoctorVuong

I’ve been taking things in stride as best I can but am rather miffed at doctors and events today so I am just going to rant even though I need to be trying to sleep. Prior to my gastric bypass surgery and gallbladder removal My gastroenterologist insisted I have a colonoscopy due to the fact that previous ct scan had shown severe narrowing of my colon and a recent ct showed possible colitis. But the colonoscopy had to wait until after my surgery. I went through three days of clear liquids and hellish prep trying to swallow the required liquids. While the nurse was great I was literally the last patient and they were already starting to close down the facility before my procedure started. I had an unusually hard time waking up from the sedation and just wanted to close my eyes but they were in a hurry to get me out, I was barely awake and told to get dressed and get in the car to go even though I was stumbling and could hardly walk. I didn’t get answers from the colonoscopy. I don’t know if endometriosis can be confused for colitis. But why would a ct scan show something but not a colonoscopy. It showed melanosis in the colon usually caused by chronic laxative use which I refuse to use laxatives on a regular basis so rarely take it. Also diverticulosis of the sigmoid colon which has been there some years now and the last doctor just said well you have to wait until you end up in the Er with an emergency to even do anything. Like ok. But no biopsy was taken of the darkened spots of my colon. And no explanation of my symptoms. My bariatric surgeon said My gastroenterologist could do the endoscopy since he is closer to where I live, and he got all my information and everything. I had previously had a balloon dilation of a very narrow stricture. They saw the stricture during this procedure (so I guess the previous dilation didn’t do anything) but my endoscopy report reads: “ge junction with mucosal tear from hiccup during dilation” I didn’t speak to the doctor, I wasn’t alert enough. He made it out like nothing to my mom. They didn’t take any biopsy from either tests. And I have a mucosal tear but not what to do about all the pain? Im just tired and frustrated. I can only manage so much when I don’t have clear answers. I have to have another procedure this time a surgery in two weeks to do with the endometriosis. Not even sure the doctor will be able to find where it is since it can be anywhere and the main reason is my ovary has to come out. All my long rambling, sorry. Has anyone had a tear happen during a balloon dilation? From what I see dilation isn’t a cure just a treatment or temporary fix. I know you don’t want the stoma too big but too small is not good either. I’ve been having spasms in my left side, crushing chest pain, nausea and difficulty with purée and other symptoms. I’m the end I just shut up and deal with it. Im not regretting RNY because with my nonexistent metabolism I would not have lost nearly 63lbs. And I knew it would take its toll on my chronic illness but so much at once has me exhausted. end of rant.

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

TGIF!!!!!!![emoji119][emoji119][emoji119] This was a helluva week!!!🥵 Day 24, 25 and 26 Hubby and I did date night last weekend. It was lovely! I'm not on any social media other than Bariatric pal by choice! So nothing to unfollow. I definitely said no to writing a blog for work. I'm typically the go to person for the blogs but I was TRULY swamped this week so it was a "HECK NO"!! Moment when I was asked! No guilt too!! Day 27: I'm using my phone as we speak so hard for it to be a phone free night. I may drop it when I'm done writing this[emoji2].....but then again, I'm on call tonight so no can't do. Squats!! Was happy for rest day! From day 25 onwards, squats have been done in 2 events![emoji28] I'll complete the rest of my 95 later tonight. B side: My older sister is my absolute girl crush!! I 🧡 her!! She's admirable, courageous and FIERCE!!! Did I say TGIF??? Yay!! Sent from my SM-N960U using BariatricPal mobile app

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.

30 is also rare among those of us "normal" bariatric patients. It happens, but it's the exception rather than the rule. You see that more among the "600 lb Life" crowd, since they're starting at a much higher BMI than most of us are. You are doing fine!!

I am still pre-op but I have also looked into loose skin. Loose skin after weight loss surgery is common because your skin does not have the time to adjust to the rapid weight loss. Although everyone is different, you will MOST LIKELY have loose skin and the only true way to completely resolve that issue is through plastic surgery. Based on some Youtubers that are bariatric patients, compression clothing can really help with minimizing the visibility of loose skin. I do recall a Youtuber suggesting that you buy quality compression clothing because it can make all the difference. I am sorry this isn't coming from personal experience but this is the best I know of it so far. You can look on Youtube for first hand experiences from real patients.

That’s really interesting. I never had metabolic syndrome, even when I was 300lbs. My blood sugar levels were always fine. I did have cravings for sweets, etc. And I overate in general. Now I can eat in moderation. I can have a bit of carbs without it turning into a need for more. Yesterday I had a few bites of pasta. It was no big deal, and I’ve not felt the desire or need to have anything carby today. That’s been my experience post-surgery, My dietician is fine with it, she is interested in patterns and trends. In fact, some of the work I’ve done with her and with the bariatric psych was to accept moderation, and not panic every time I eat part of a cookie. I think it’s really neat how different everyone is.

Congrats on your surgery and your smooth recovery. It seems like you are doing well. This website has menus/food/recipes in the Food and Nutrition section of the forums. Also, these websites are helpful with menus/recipes labeled by the stage of food that you're eating: https://www.bariatriccookery.com/ https://www.bariatriceating.com/bariatric-recipes.html And an important tip: Not only do you not have to live on grilled chicken and broccoli forever, but grilled chicken will probably be one of the last proteins that you can comfortably eat! For many of us, it was many, many months before we could handle grilled chicken! Hope this helps and good luck on your journey!

Ok, so now I'm approaching the chaffel bandwagon. I love them made with egg whites rather than whole egg. No eggy aftertaste to contend with. I also used Daisy 2% cottage cheese as part of the cheese and added a spoon of protein powder to up the protein even more and add to the crispness. Even though I overcooked these (should have been closer to 4 mins rather than 5), the turkey club sandwich was the closest I've come to an honest to God sandwich since a year before surgery! AND, go run and immediately buy these Twin Peaks Protein Puffs from Alex in the Bariatric Pal Store. Cuz I kid you not...the ingredients aren't crazy bad AND they taste and feel so much like miniature "cheesy poofs" aka UTZ cheeseballs that I feel like I should confess being bad. But the whole meal was less than 300cals and less than 8g net carbs, and had 37g of protein. Lemme repeat that in case you missed it...37g of protein. I feel like I'm yelling. Am I yelling? I ate the whole damn thing. It wasn't really a trigger meal. But I absently continued to eat cuz it tasted so great and was so exciting to eat as a sandwich with cheesy poofs. Can I just say, I heart the crap outta maintenance? Here's the MFP info. The order of the macros is: cals; protein; fat; carb (whole); fiber; sugar And here are the Twin Peaks Protein Puffs I ordered from Bariatric Pal Store. I'm so STOKED about these. TOTES worth the $25. Seriously. A serving size is 1 cup and there are 10 servings. But I only served 6g of protein puffs with my meal and it was PLENTY! These are not very sliderish cuz of the protein content. So I felt replete from them. So I should get about 50 servings per container. Bargain! (I love these enough, that I'm racing to leave a review and I rarely review things!) I can't wait to order the other flavors!

Hey guys, new video up on Bariatric Strong, the show all about bariatric fitness and nutrition. Today we discuss the wonderful world of Chipotle (can be a really good choice for macros and performance). Just click here --> Bariatric Strong Channel to be taken to the channel!

So I had my first consultation this week, the system is very different in Australia to what I have read about the surgery elsewhere. Things went very well, loved the team I spoke to, the Dr I saw was not the surgeon, but a very good bariatric physician, and after our consultation it would appear that I have the choice of; Signing up for top Health insurance, paying premiums for a year and then getting the surgery. Approx $5-7k AUD out of pocket and $5-8k in premiums for the 12 months Going through a semi subsidised model which would be in about 6 months Approx $10k AUD Paying for the surgery myself which would be in a matter of weeks. Appox $22k AUD Good news is I can do any of the above, am healthy and a good candidate, there is little requirements to do a lot of the pre-surgery requirements that other country/systems have, so I guess I now just have to decide.

Hello my lovely bariatric family! I'm now in Onederland and I'm happy! I'm down to 198 which puts me down 38 lbs since surgery (which im kind of disappointed with tbh) but I'm down 95 lbs total. I'm falling off the wagon a little this last week by drinking flat diet dr pepper and eating a few things that aren't the best for me. In going to try to get myself in check. How is everyone?!

Hey @JerseyNJ im the 11th im getting excited now . Im taking off 2 weeks and I haven't told anyone the type of surgery im having I just told HR I would be having surgery nov 11th they sent me forms for me and my surgeon and he did not go into what type of surgery (HIPPA) laws prevent that . If they want to be nosey they could google his name and find out he a bariatric surgeon but I don't care.This is about me not other's opinions . I am in Jersey too . Where are you? nice to have a almost surgery twin!!!

It’s like a corset you wear around your waist. It’s not tight tight like to shape your waist, but firm like those belts guys use for heavy lifting. It supports your tummy and keeps it from jiggling around which causes pain. It’s very comfortable and reduces pain significantly. I got mine from amazon a couple of days after surgery and it’s helped a lot. Here is a link: https://www.amazon.com/Everyday-Medical-Abdominal-Binder-Surgery/dp/B07G4N752D I highly recommend. I got the suggestion from someone else here on Bariatric Pal.

So 4-1/2 years ago, I had the sleeve. Within 3 months, I dropped 60 of the 100 pounds I wanted to lose. I was off all blood pressure meds (and still am). Within the year following my sleeve, I developed abdominal hernias that my bariatric surgeon repaired. At that point, my weight loss stopped and I never reached "goal". Also at the time, I was working a 12 hour, physically demanding (not with heavy lifting but with a lot of walking), night shift 7p-730a which was one of my first saboteurs to my weight loss success -- I wasn't getting enough sleep. I also didn't exercise at all because of my physically demanding job. I decided to leave my night shift job, which I loved very much, for a "day job" but there was a 1 hour commute each way to this job. Exercising was now an even bigger challenge, but I got a gym membership near my home and I would drive my hour commute to the gym, work out and by the time I got home it was 8 p.m. 3 nights a week. Then I was eating dinner late. Enter REFLUX. I started with 20 mg of omeprazole, which didn't quite do the trick with my symptoms. Moving on to 40 mg was better but as time went on even the 40 mg of omeprazole wasn't cutting it so I supplemented with OTC omeprazole 20 mg for a total of 60 mg a day. That's where I am now. A recent EGD revealed I have yet another hernia. Lessons Learned: 1) Lifestyle matters. Prepare a lifestyle to accommodate your surgery so that you can take care of you. I didn't do this. I tried to be superwoman. I am humbled. 2) Follow up with your doctor's office more frequently than your program requires. Accountability is everything. Don't wander off and think you don't need follow up because you most certainly do. 3) Bloodwork. I can't emphasize this enough. I always keep my bloodwork in check -- I didn't want to lose my hair -- and I didn't. 4) Get plenty of sleep. Sleep needs to be as necessary as water to your well being. With these lessons learned, I will be getting the Roux-en-Y revision surgery to end my GERD and hopefully put me back on track with the 70 pounds I want to lose. I have created a lifestyle now that allows me to take care of me. I have a gym membership that includes a pool. I work a day job that allows me to work at home one day a week. I finally realized that being good to me is not a selfish thing, but a necessary thing.

Hey all, was hoping for some help as my bariatric team hasn’t been much help. I’m 5 weeks PO and have constant nausea, vomiting, dizziness, cramping in my belly. I’m getting in about 10oz of fluids and about 2oz of soft foods a day. I’m constantly sick to my stomach regardless of what I put in it. I take Prilosec 40mg in the morning and Pepcid 40mg at night with nausea medicine throughout the day. I’m not able to take any vitamins as I get super sick and I’m feeling run down, weak, fatigue and starting to get cramps, numbness and tingling in my arms and legs. I don't have any leaks, I had a KUB study that said it’s from acid reflux which must surgeon says is normal and to just keep trying to intake more. Mind you I have, I’ve been trying to get them to help me with no luck, I’ve had to go to ER twice for fluids and I’m just in need of advice, opinions or even ideas on how to fight this feeling. Any and all advice is appreciated.

I think the important thing here to ask is how many calories people are taking in during their eating window. As a Bariatric Power Lifter, I am taking in about 3400 calories on heavy lifting days. With my restriction, it would be near impossible to get that in during an 8 hour window. In order to eat for athletic performance, IF does not work for me. If you eat less calories, I can see the appeal.

You're in Utah...so am I. Best way to find the information you need is to check in with two groups that are the best at Duodenal Switch in Utah. Rocky Mountain Associated Physicians holds regular bariatric seminars at St. Marks Hospital. The one I went to was conducted by Dr. Rodrick McKinlay. I have other co-morbidity issues (not CHF). Much of the session is open question and answer with an actual bariatric surgeon. The other group that seems to have some really good information is BMI Institute of Utah (Dr. Cottam). What I appreciate about this group is that they can send you a "self-pay" price list for Duodenal Switch. The average cost of a DS in Utah is between $22K to $25K. BMI has a partial outpatient DS that runs around $16K (if you have health insurance that won't pay for bariatric surgery). I was sad to learn that SelectHealth doesn't often cover these surgeries. I would highly recommend that you talk to both Dr. McKinlay and Dr. Cottam to get some advice on how they would handle working with someone who has CHF. All the best,

So, the VA referred me to plastic surgery to have a cyst removed from my knee. The surgeon said I qualified for skin removal because of the amount of my weight loss. I had no idea they would cover this, because they don’t cover Bariatric surgery unless you are on tri-care. The nurse practitioner said he is a good surgeon and that she would let him do work on her. I requested the referral and my Dr. put it in. We met and he said he could do the tummy tuck with liposuction and even make fake abs if I want them. He said the skin on my thighs isn’t as bad but that he could liposuction my inner thighs during the same operation. He also said the fat could be injected into my breast. I already met my deductible because of my gallbladder surgery, so I scheduled for December. I can do all of this or nothing. Still not sure what I want to do with my belly button either. I always had an outie, but when they did my gallbladder surgery they “repaired my hernia” which means they chopped off my belly button. 😂 I like to make phantom belly button pain jokes. the ladies at the gym say I should get the abs. I have been flat chested my whole life. I bought bra’s in the kids section and couldn’t get a nursing bra in my size when I breast fed. This should be interesting. I am 49 now do I really need to do this? Probably not, but I think I am going to because if I am getting one thing done might as well go for it and do all the pain at once. Hubby is worried about another major surgery but is supportive of what ever I decide. has anyone had all three of these procedures done? The tummy tuck would involve muscle reconstruction and liposuction on sides. What should I do with my belly button? I feel like it is already missing. 😂

This article discusses a very rare and extreme example of liver disease post-op (this patient died of a hospital infection, and not from anything related to her liver disease, btw). This may not be relevant to your daughter's case, but I'm sharing it in case you want to bring it to the doctors' attention. It's also a wake-up call for me because one of the reason's I'm getting VSG is to be an eligible liver or kidney donor for my sister. It's a reminder to us all that we must be diligent about taking vitamins. http://article.scholarena.co/Liver-Failure-after-Bariatric-Surgery-Clinical-Case-and-Literature-Review.pdf

This is a myth. Dietary ketosis is COMPLETELY different than metabolic acidosis. The body is a very resilient organism. It will maintain (in the absence of acute and overwhelming diseases or difficiences) a pH balance in blood and tissues within a VERY narrow margin. That is part of why they test CO2 and O2 and K (electrolytes) and Ca, balance in the blood. It shows what state your blood pH is in (in an average). And it regulates the pH balance primarily through the kidneys and lungs--keeping your blood from going into metabolic acidosis or even respiratory acidosis. Both of these states are an extremely critical emergency situation--like you are dying. Osteopenia can be caused from many different things. We as bariatric pts take a crap ton of calcium. But taking calcium out of balance (which we do) CAN contribute to osteopenia--as can quick weight loss. ADEK and K2 (metabolites) are necessary to build bones by sending the calcium to the bones rather than the soft tissues or pulling minerals from the bone. I've been low carb (in and out of ketosis) for the better part of 20 years. I do not have osteopenia. I also am on Femara which can also cause osteopenia/porosis. So...I would tend to really look at the studies that are "proving" acidity because of ketosis. Just my 2cents. Sorry you are dealing with osteopenia girl!!!

Dont get me wrong i will grab a shrimp - or small bite of some sort of soft salad but my main focus is on keeping the vitamins and nutrients balanced. Trust me i would take down a whole pizza or pound of carbs at any moment - We a group who did this together found it way easy to "Screw Food" once you get everything balanced. I have talked to a few people who say they have no pain eating also, See i thing the bariatric Gods know if i have no pain i will begin to eat wrong again. Who knows its a life journey but sure glad it did it

I'm still figuring it out.. like the wonderslim ones...basically a cheaper version of medifast. bariatric pal has them too. They get branded several ways and are all made by the Rolbard corporation If you find a box that comes with 7 shake packets and it's a pudding and/or a shake you know you have the right ones. Love them. you can spend anywhere between $11 for the box I've seen it for $18. for just 7 shakes but they are good and can be mixed with water. Add a scoop of unflavored GenePro powder then well on the way to hitting 60 gram protein goal.

I'm new here and new to the wls world lol. I have wanted bariatric surgery for as long as I can remember but was never a possibility because of the cost. Earlier this year I found out that it's covered by my health insurance so I decided to research it and have made the decision to start the process! This coming Thursday (the 26th) I'm going to the weight loss seminar that's mandatory for the program and am so excited! They gave me a huge packet of paperwork to turn in at the seminar. My question to any of you that have gone to a similar seminar is about how long after the seminar did the ball actually start rolling for the process? I have heard that we have to do an 8 week weight management class as part of the insurance requirement. Any advice or suggestions you can offer would be sooo helpful!!! Thanks in advance! Sent from my SM-N960U using BariatricPal mobile app