Jump to content
×
Are you looking for the BariatricPal Store? Go now!

Weirdest things you are looking forward to after surgery



Recommended Posts

Hi I sae this thread and thought id jump in.. the weirdest thing im looking fwd to is riding a roller coaster I havent been to the amusement park since 2004 and I cant wait im planning a big trip for next Summer to Six flags... Cant wait!!!

Share this post


Link to post
Share on other sites

I hear ya sister! That's my curse, no buy...it's no find. However, by my birthday in April, I will have probably changed my mind about what I really want. Hell, I may do so well the choices will be endless. Hmmm....then what? I guess I visit my 2 best friends, Ms. Visa & Mr. Mastercard.

Share this post


Link to post
Share on other sites

Headlines:

Last Updated: Jun 12, 2009 - 3:53:09 PM

Obesity surgery can lead to memory loss, other problems
American Academy of Neurology
Mar 14, 2007 - 7:41:20 AM
Email this article
Printer friendly page

ST. PAUL, Minn -- Weight loss surgery, such as gastric bypass surgery, can lead to a Vitamin deficiency that can cause memory loss and confusion, inability to coordinate movement, and other problems, according to a study published in the March 13, 2007, issue of Neurology, the scientific journal of the American Academy of Neurology.

The syndrome, called Wernicke encephalopathy, affects the brain and nervous system when the body doesn’t get enough vitamin B1, or thiamine. It can also cause vision problems, such as rapid eye movements.

The study found that the syndrome occurs most often in people who have frequent vomiting after the surgery. It usually occurs within one to three months after the surgery, although one case occurred 18 months after surgery.

The study reviewed the scientific literature for all reported cases of the syndrome occurring after obesity surgery. A total of 32 cases had been reported. Many of the people also had neurological symptoms that are not typical of Wernicke encephalopathy, such as seizures, deafness, psychosis, muscle weakness, and pain or numbness in the feet or hands.

"When people who have had weight loss surgery start experiencing any of these symptoms, they need to see a doctor right away," said study author Sonal Singh, MD, of Wake Forest University School of Medicine in Winston-Salem, North Carolina. "Doctors should consider vitamin B1 deficiency and Wernicke encephalopathy when they see patients with these types of neurological complications after weight loss surgery. If treated promptly, the outlook is usually good."

For treatment, patients are given vitamin B1 through an IV or injection. Of the 32 people, 13 made a full recovery. Many people continued to have problems, such as memory problems, weakness, or difficulty coordinating movement.

Singh said more studies are needed to determine how often the syndrome occurs after weight loss surgery. He said some doctors prescribe thiamine supplementation for their patients after weight loss surgery, but recommends that national standards be set for all doctors to follow.

Share this post


Link to post
Share on other sites

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 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

Share this post


Link to post
Share on other sites

OMG, Really? You can just provide the links to these. And for God's sake...Leave off the references. Those are easy enough to find on Google.

Share this post


Link to post
Share on other sites

Wow. What does thiamine deficiency have to do with the topic of this thread? That’s an awful lot of medical jargon mixed with scare tactics of posting it in a thread that has nothing to do with Vitamin deficiency.

I have complex lifelong chronic illness which includes neuroimmune/immunodeficiency. Basically it effects every aspect of my body. I also have neurological symptoms starting long before surgery. I take a series of gummy vitamins. My last bloodwork by my bariatric surgeon my thiamine aka B1 was within the normal range.

Just take the right Vitamins that have good bioavailability (whole food based, chewable or liquid form) and have regular bloodwork and there is no need to panic about vitamin levels. Besides an issue with Iron and some bloodwork that could indicate anemia (which I’ve had issue with before surgery) my blood vitamin levels have been fine so far. Even my extremely low Vitamin D is in normal range now.

Low thiamene isn’t going to instantly cause some life threatening neurological disease. If your doctor says it’s low, take the vitamin. Or just take a good food based b complex as prevention.

I e studied holistic heath, nutrition and vitamins. Do I remember everything. No my memory sucks but it’s crazy to post a long medical research report and not even on the appropriate topic. Sorry if I’m rather touchy today.

Taking a basic Multivitamin isn’t enough especially tablets like Centrum or any tablet that might not get properly utilized by the body is probably not enough. One of the things about gastric bypass surgery is an investment in our health and making sure to get the right vitamins and nutrition.

But I’ll shut up. I got flack because I said I take Gummy vitamins and too many. Just do your best and don’t worry about thiamene deficiency unless your doctor says it’s low and it’s easy enough to get a natures way alive b complex vitamin at the grocery store.

Share this post


Link to post
Share on other sites

Wow. What does thiamine deficiency have to do with the topic of this thread? That’s an awful lot of medical jargon mixed with scare tactics of posting it in a thread that has nothing to do with Vitamin deficiency.
I have complex lifelong chronic illness which includes neuroimmune/immunodeficiency. Basically it effects every aspect of my body. I also have neurological symptoms starting long before surgery. I take a series of gummy vitamins. My last bloodwork by my bariatric surgeon my thiamine aka B1 was within the normal range.
Just take the right Vitamins that have good bioavailability (whole food based, chewable or liquid form) and have regular bloodwork and there is no need to panic about Vitamin levels. Besides an issue with Iron and some bloodwork that could indicate anemia (which I’ve had issue with before surgery) my blood vitamin levels have been fine so far. Even my extremely low Vitamin D is in normal range now.
Low thiamene isn’t going to instantly cause some life threatening neurological disease. If your doctor says it’s low, take the vitamin. Or just take a good food based b complex as prevention.
I e studied holistic heath, nutrition and Vitamins. Do I remember everything. No my memory sucks but it’s crazy to post a long medical research report and not even on the appropriate topic. Sorry if I’m rather touchy today.
Taking a basic Multivitamin isn’t enough especially tablets like Centrum or any tablet that might not get properly utilized by the body is probably not enough. One of the things about gastric bypass surgery is an investment in our health and making sure to get the right vitamins and nutrition.
But I’ll shut up. I got flack because I said I take Gummy vitamins and too many. Just do your best and don’t worry about thiamene deficiency unless your doctor says it’s low and it’s easy enough to get a natures way alive b complex vitamin at the grocery store.

Someone posted a study from 2007 on this thread and I wanted to give a better study with a longer period of research. I just wanted to be upto date just incase someone freaked out about it.

Sent from my SM-N960U using BariatricPal mobile app

Share this post


Link to post
Share on other sites

Yes thanks for posting that.
Don’t care how many outdated and obscure studies get posted, because I promise that for every person who suffers from some completely rare Vitamin deficiency, morbid obesity is MORE dangerous to your health.

We have to choose our hard.
I’ll choose to be careful with my nutrition and take my Vitamins and live without the extra 100 pounds.

Share this post


Link to post
Share on other sites

Yes thanks for posting that.
Don’t care how many outdated and obscure studies get posted, because I promise that for every person who suffers from some completely rare Vitamin deficiency, morbid obesity is MORE dangerous to your health.

We have to choose our hard.
I’ll choose to be careful with my nutrition and take my Vitamins and live without the extra 100 pounds.
I was just providing updated information ... I am 3 weeks post-op I understand ... I just didn't want people going off the 2007 study so they dont get freaked out of having surgery.

Sent from my SM-N960U using BariatricPal mobile app

Share this post


Link to post
Share on other sites

On 09/28/2019 at 22:19, nikkilee72 said:


I was just providing updated information ... I am 3 weeks post-op I understand ... I just didn't want people going off the 2007 study so they dont get freaked out of having surgery.

Sent from my SM-N960U using BariatricPal mobile app

Congrats on being 3 weeks PO! You’ve officially gotten through the worst of it.

One thing I did today was 3 hours worth tough gardening. It’s in the 90’s still here and I was able to get through all of the bending, squatting, lifting, raking, and clean up without wanting to die.

This week I hit 100 pounds lost (from pre-surgery weight) and it feels AMAZING now to move in my own body. Still have 10-15 pounds to go and I can’t imagine how much better yet that will feel

Share this post


Link to post
Share on other sites

Congrats on being 3 weeks PO! You’ve officially gotten through the worst of it.

One thing I did today was 3 hours worth tough gardening. It’s in the 90’s still here and I was able to get through all of the bending, squatting, lifting, raking, and clean up without wanting to die.

This week I hit 100 pounds lost (from pre-surgery weight) and it feels AMAZING now to move in my own body. Still have 10-15 pounds to go and I can’t imagine how much better yet that will feel
That is incredible. I've lost 20lbs so far. And I am in shock everytime I get on the scale. I'm glad to know things get better. You'll get that last 10lbs before you know it!

Sent from my SM-N960U using BariatricPal mobile app

Share this post


Link to post
Share on other sites

I posted that "2007 " report because my cousin whom I had a group chat n chew dinner last night with some people who have had this surgery gathered and by the way I had to pick her up cause she did not : 'remember " where I lived as many times she has been to my house this is 2019 and she had the sleeve 18 months ago so this is real , she didn't know who my aunt(her mother) the "kids" in the house( her nieces and nephews) the conductor on the train she takes to work she didn't even remember she wanted to break up with her boyfriend it was her best friend who told her when he broke up with her "girl you was gonna break up with him anyway but just did not know how....So no don't down play this cause the article is "old" she thew up a lot when she got sleeved and went back to the ER .its only to say if you have or do throw up a lot at the beginning look into it to make sure your Vitamin B12 as well as others are not immediately rendered powerless and the brain is not defiecient which is was causes the memory loss...… My aunt and brothers took her to the hospital and this is what "They " said she didn't even remember she had surgery and one morning after looking in the mirror was terrified and asked her mother was she sick and dying because she lost so much weight . she had to be reminded so its real ... but hey im having my surgery November the 11th and this is in no way meant to be a scare tactic or deterent its just facts I was trying to pass on to my family here

God Bless

Edited by november11

Share this post


Link to post
Share on other sites

Oh i'm doing this do not get it twisted …..I am having my surgery .it outweighs many many things ..I just want the people who have not had the surgery yet as well as some who may have thrown up a lot when they were sleeved to be mindful...

its definitely on!!!!!!!

Edited by november11

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

  • Trending Products

  • Trending Topics

  • Recent Status Updates

    • cryoder22

      Day 1 of pre-op liquid diet (3 weeks) and I'm having a hard time already. I feel hungry and just want to eat. I got the protein and supplements recommend by my program and having a hard time getting 1 down. My doctor / nutritionist has me on the following:
      1 protein shake (bariatric advantage chocolate) with 8 oz of fat free milk 1 snack = 1 unjury protein shake (root beer) 1 protein shake (bariatric advantage orange cream) 1 snack = 1 unjury protein bar 1 protein shake (bariatric advantace orange cream or chocolate) 1 snack = 1 unjury protein soup (chicken) 3 servings of sugar free jello and popsicles throughout the day. 64 oz of water (I have flavor packets). Hot tea and coffee with splenda has been approved as well. Does anyone recommend anything for the next 3 weeks?
      · 1 reply
      1. NickelChip

        All I can tell you is that for me, it got easier after the first week. The hunger pains got less intense and I kind of got used to it and gave up torturing myself by thinking about food. But if you can, get anything tempting out of the house and avoid being around people who are eating. I sent my kids to my parents' house for two weeks so I wouldn't have to prepare meals I couldn't eat. After surgery, the hunger was totally gone.

    • buildabetteranna

      I have my final approval from my insurance, only thing holding up things is one last x-ray needed, which I have scheduled for the fourth of next month, which is my birthday.

      · 0 replies
      1. This update has no replies.
    • BetterLeah

      Woohoo! I have 7 more days till surgery, So far I am already down a total of 20lbs since I started this journey. 
      · 1 reply
      1. NeonRaven8919

        Well done! I'm 9 days away from surgery! Keep us updated!

    • Ladiva04

      Hello,
      I had my surgery on the 25th of June of this year. Starting off at 117 kilos.😒
      · 1 reply
      1. NeonRaven8919

        Congrats on the surgery!

    • Sandra Austin Tx

      I’m 6 days post op as of today. I had the gastric bypass 
      · 0 replies
      1. This update has no replies.
  • Recent Topics

  • Hot Products

  • Sign Up For
    Our Newsletter

    Follow us for the latest news
    and special product offers!
  • Together, we have lost...
      lbs

    PatchAid Vitamin Patches

    ×