Yay for math?

On January 19, 2010, in Uncategorized, by Andrea

I admit, I like studies.  Studies make Andrea’s brain happy.  Studies have hard numbers that make sense.  Andrea likes black and white things — these are good things for a g33k (and don’t ever let it escape you — Andrea is a g33k — one who seems to be speaking in the 3rd person today — this is not a good sign).

But sometimes, studies, especially when done by a mathematical computation are not-so-cool.  Like this one that states an average 42 y.o RNY patient with a BMI of 45 would only gain close to 3 years of life by having WLS?  First off, I think that’s off.  Cause if someone is suffering from co-morbidities, those WILL shorten your life expectancy.

The numbers get even more screwbally when looking at younger patients — I apparantly gained more than 5 years.  We don’t know for certain because the numbers were for 35 year olds and I was 25 when I got my guts rearranged.  But we can construe that I got at least the five years.  Yay, me.

I really think patients gain more than a few years.  But then again, I’m not a computer.

Of course, this doesn’t measure the QUALITY of one’s life gained – but of course a computer can’t measure that.

From medpagetoday.com:

Gastric Bypass Extends Life for Most Patients

By John Gever, Senior Editor, MedPage Today
Published: January 18, 2010
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

For most patients in most categories, bariatric surgery increases life expectancy, according to a new mathematical model.Only when short-term mortality following bariatric surgery is expected to be high or the likelihood of success is low will the procedure fail to improve life expectancy, researchers reported in the January Archives of Surgery.

Computer modeling predicted that a hypothetical “base case” patient — a 42-year-old woman with a body mass index of 45 — would gain 2.95 years of additional survival following bariatric surgery, according to Daniel P. Schauer, MD, of the University of Cincinnati, and colleagues.

Surgery failed to be beneficial in the model only when 30-day mortality reached 9.5% or the likelihood that surgery would not add life-years was 2% or less, they found.

Baseline 30-day mortality in the model was 0.2%, and the baseline efficacy of surgery in extending life expectancy was 53%.

“While not all patients are guaranteed a good outcome, our model indicates that gastric bypass increases life expectancy for most patient subgroups,” they concluded.

Their analysis was based on a Markov decision model using published data to estimate 30-day mortality following bariatric surgery and the efficacy of surgery in reducing long-term death rates.

The latter had two components: reduction in excess mortality associated with obesity, and research data on long-term mortality following bariatric surgery.

Excess mortality estimates came from National Health Interview Survey data on some 400,000 participants from 1991 to 1996 linked to the National Death Index. Inputs on surgery efficacy were derived from a 2007 study of nearly 8,000 patients who had undergone gastric bypass and the same number of medically treated or untreated obese controls.

That study found that the procedure cut death rates by half during about seven years of follow-up. (See Missing Link Found: Bariatric Surgery Reduces Mortality)

Schauer and colleagues obtained rates of inhospital mortality following bariatric surgery from the 2005 National Inpatient Survey, then multiplied them by three to estimate 30-day mortality.

The researchers explained that according to earlier research, inhospital death rates typically underestimate 30-day mortality by a factor of two to three.

Their threefold correction factor represents “a conservative estimate that biases the model against gastric bypass surgery,” they wrote.

Schauer and colleagues tested this correction factor and other aspects of the model in sensitivity analyses.

The biggest gains in life expectancy occurred in younger women with relatively high BMI values, the model showed.

The age effect was less important than BMI at the time of surgery. A 35-year-old woman with BMI of 45 would gain about 3.2 years of extra life, whereas at 55, a similarly obese woman would gain about 2.5 extra years.

But a 35-year-old woman with BMI of 55 could expect to live five more years with surgery, the model indicated.

Men in general derived less survival benefit from bariatric surgery, particularly with advancing age at the time of the procedure.

At 35, the difference in life expectancy gained was roughly 10%, but by age 75 it had grown to about 50%.

The sensitivity analyses found that relatively large changes in most parameters used in the model did not affect the overall results substantially.

The effect of 30-day mortality on whether or not surgery was beneficial for long-term survival was related to BMI and gender.

For women with a BMI of 40, 30-day mortality of more than 5% would mean surgery was not helpful, but short-term mortality had to exceed 15% for surgery not to be preferable for those with BMI of 55 or more. These thresholds were about 10% higher for men.

The efficacy of surgery in reducing mortality was less important for older men, the analysis also showed. A 75-year-man with a BMI of 35 could expect only a very slight gain in life span — perhaps one or two months.

“Younger patients have lower surgical risk and more time over which to realize the benefits of surgery. For older patients, the gain is smaller, and for some, gastric bypass surgery will decrease life expectancy,” Schauer and colleagues wrote.

However, they identified several potentially serious limitations to the analysis.

The study of long-term mortality following bariatric surgery was conducted at a single center and was not randomized. Additionally, long-term complications, such as need for repeat surgery, were not addressed in the model. Certain other risks that might be heightened after bariatric surgery were excluded as well, and quality of life was not modeled.

“The decision analysis presented here is a step forward in understanding optimal patient selection but also highlights some of the areas for which better data are needed,” the researchers wrote.

The National Institute of Diabetes and Digestive and Kidney Diseases funded the study.

No potential conflicts of interest were reported.

Update: Medscape has included their take:

Gastric Bypass Surgery May Prolong Lives of Morbidly Obese

Nancy Fowler Larson

January 19, 2010 — Morbidly obese Americans could live up to 3 years longer after undergoing gastric bypass surgery, the most popular bariatric surgical procedure, according to a computerized model-based study published in the January issue of the Archives of Surgery.

“While no large-scale randomized controlled trials have compared bariatric surgery with intensive medical management for the morbidly obese, there is evidence from large controlled trials and numerous case series that bariatric surgery is currently the only effective therapy for promoting clinically significant weight loss and improving obesity-associated conditions among adults with a body mass index (BMI) of 40 or higher (calculated as weight in kilograms divided by height in meters squared),” write Daniel P. Schauer, MD, MSc, from the University of Cincinnati Academic Health Center, Ohio, and colleagues. “Several retrospective cohort studies and 1 prospective study suggest that bariatric surgery also improves survival.”

The study sought to weigh the benefits of gastric bypass surgery against its risks in the morbidly obese, who make up 5.1% of the US population.

The researchers created a decision analytic Markov state transition model with multiple logistic regression as inputs to analyze the differences between having gastric bypass, the leading surgery (>65% of all patients who receive bariatric surgery) for the morbidly obese in the United States, vs undergoing no surgery. A 42-year-old woman and 44-year-old man, both with BMIs of 45 kg/m2, were chosen for the researchers’ base case analysis.

To determine in-hospital mortality risk, the authors used 23,281 cases from the 2005 National Inpatient Interview Survey and then adjusted the data for 30-day mortality. During each such cycle, patients’ risk for death was calculated using their BMI, surgical status, age, and sex.

Data from more than 399,000 participants from the 1991 to 1996 National Health Interview Survey were used to calculate excess mortality’s relationship with obesity. Bariatric surgery’s effect on mortality was assumed only in connection with excess deaths associated with obesity. Information about the surgery’s effectiveness was gathered from a recently conducted, substantial observational trial.

Younger, Higher-BMI Participants Had Best Results

The ultimate multivariable logistic regression model used 7 factors — BMI, BMI2, age, age2, sex, sex × BMI, and age × sex — to predict mortality, with a good fit to the data (Hosmer-Lemeshow goodness-of-fit, P > .05; c statistic, 0.83).

The computerized model showed that the 42-year-old female model lived 2.95 years longer (35.03 vs 32.08 years) after undergoing surgery. When 30-day surgical mortality increased to more than 9.5% (baseline 30-day mortality, 0.2%) or when surgical efficacy declined to 2% or less (baseline efficacy, 53%), surgery was not preferred.

The 44-year-old male model would live 2.57 years longer (26.82 vs 24.25 years) after undergoing surgery, according to the model. Surgical treatment was not preferred when 30-day surgical mortality rose above 8.6% (baseline 30-day mortality, 0.55%) or when the effectiveness of the surgery fell to 3% or less (baseline efficacy, 53%).

In both sexes, those who were younger and had a higher BMI had the largest life expectancy increases. In men, the increase was slightly lower for all ages and subgroups.

“The optimal decision for individual patients varies depending on the balance of risks between perioperative mortality, excess annual mortality associated with increasing BMI, and the efficacy of surgery; however, for the average morbidly obese patient, gastric bypass surgery increases life expectancy,” the authors write.

Multiple Study Limitations

The authors noted several limitations to their assessments:

  • Available data do not include BMI and other clinical variables.
  • All data for calculating surgery efficacy are from a single state (Utah).
  • The authors did not model long-term, postsurgical complications, including any necessary revision.
  • Life expectancy was the sole outcome metric, as there are no longitudinal studies exploring quality-of-life improvements.

Acknowledging that not all gastric bypass surgeries produce good results, the study authors concluded that their findings of longer life spans for most subjects will help physicians determine which patients are the best candidates.

“We believe results of this analysis can be used to better inform both patients’ and physicians’ decisions regarding gastric bypass surgery,” the authors write.

The National Institute of Diabetes and Digestive and Kidney Diseases supported the study. The study authors have disclosed no relevant financial relationships.

Arch Surg. 2010;145:57-62.

Controversial surgical center for teens

On January 15, 2010, in Uncategorized, by Andrea

I’m of two minds of this.

At 17, I would not have been ready for a life-altering event like this.  At times, I don’t think I was really ready at 25.  At 17, I would not have been ready for the responsibility of the vitamin regimen for RNY.  Maybe a non-malabsorptive surgical option like VSG or AGB — but not DS or RNY.  But I know there has to be an option for those that ARE.

From the Denver Post:

Surgical hope for obese teens

Rose opens the first bariatric program for youths in Colorado — amid controversy

Kat Borst tried low-carb and no-carb and South Beach and Weight Watchers and so many other diets she “can’t even list them all.” None worked.

So at 17 years old and 280 pounds, Borst underwent surgery to squeeze her stomach smaller. She’s lost 54 pounds since June and now hits the gym with her dad, even though she couldn’t climb a flight of stairs without wheezing before.

Borst’s weight loss, and the success of other teens who’ve had Lap-Band or gastric-bypass surgery at Rose Medical Center in Denver, have led the hospital to open a new bariatric program for teens — the first of its kind in Colorado.

The new center comes as childhood obesity has reached epic levels — about 17 percent of American children and teens are considered obese — but also as controversy looms about the safety of bariatric surgery for adolescents.

The program at Rose is tailored to teens, with several weeks of pre- and post-surgery sessions on nutrition, psychology and behavioral changes.

“Being 17 is really hard,” said Dr. Michael A. Snyder, a bariatric surgeon who will direct the center. “Being a teen with bariatric surgery is very difficult. Being a morbidly obese teen is a total nightmare.”

Snyder, who has done more than 2,800 bariatric surgeries and developed a special high-nutrition food for his patients, said he makes sure teens “are ready for a life-long commitment” before he performs surgery, which costs about $9,500 and is only sometimes covered by insurance. For most adolescents, Snyder places a Lap-Band, which is gradually tightened to reduce stomach capacity to about 10 to 20 percent of its original space.

It should take about 4 ounces of protein — a chicken breast about as big as a computer mouse, for example — to make a patient with a Lap-Band feel “Thanksgiving full” for two or three hours, Snyder said. The bariatric center counsels teens not to waste calories on frappachinos or sodas or really anything without protein — otherwise they don’t lose the weight and could suffer from malnutrition.

Doctors disagree on rules

Snyder, one of few bariatric surgeons in the state who will operate on people younger than 18, said the ideal patient is at least 100 pounds overweight and has tried dieting and exercise without success. The doctor cites studies showing a less than 3 percent chance that a morbidly obese person will lose the excess weight and keep it off on their own.

“It’s the safest bet in Vegas,” he said. “If you are morbidly obese, the rules are different for you.”

But other physicians argue Lap-Band and gastric-bypass surgery on adolescents is irresponsible and unsafe.

“I am so disgusted with this,” said Dr. Wendy Scinta, a pediatric bariatrician on the board of the American Society of Bariatric Physicians. “In children, it’s still considered experimental.”

Scinta, who runs a medical weight-loss clinic for children and teens in Syracuse, N.Y., said adolescents who have bariatric surgery could end up with severe vitamin deficiencies and require surgery later to remove “elephant skin,” the kind that hangs off the body when weight loss happens too quickly without maintaining muscle mass.

“It’s kind of young to be going through something so drastic,” she said. “We’re at the point where the obesity epidemic is happening faster than we can get our arms around it, but especially with children, we do

have some time. We need to give them a shot at doing something less aggressive at first.”At Scinta’s clinic, kids take medication to control their insulin levels, they learn — with their parents — to change the family diet to five small meals per day, and they are hooked up with pedometers and an exercise program. Childhood obesity often is caused by family or medical problems, Scinta said.

“Kids are easy,” she said. “You really give them their life back or give them a life if they have never had one.”

Scinta said she would recommend bariatric surgery — and she never has for a child or teen — only for a kid who weighed 600 or 700 pounds, couldn’t get out of bed and was “truly on death’s door.”

Doctors said it’s often difficult to discern the parents’ desires from the child’s when considering bariatric surgery for an adolescent.

“The hardest thing in the pediatric population is determining who is deciding they should have surgery,” said Dr. Scott Fisher, director of bariatrics at Penrose-St. Francis Health Services in Colorado Springs. “Is it society? Is it the parents who are embarrassed of their child’s weight? For 40-year-olds, it is because they are choosing themselves to make themselves healthier.”

The Penrose bariatric surgery center has operated on only 10 to 15 teens in the last eight years, Fisher said.

Diet still a challenge

Borst, who is 18 now and working toward her goal weight of 145 pounds, wishes she would have had her Lap-Band surgery sooner in life. She struggled with her weight since age 4, was ridiculed throughout elementary school and left high school for an online program because of all the teasing.

Now she’s planning on college next fall.

“I’m getting more confident,” she said. “It’s not fully built up yet because I’m still pretty big.”

Still, Borst’s life is different now. Before her surgery she “was feeling like absolute death.” Now she enjoys hopping on a treadmill or stationary bike and playing badminton. Her clothes, she said, are “falling off.”

Changing her diet has been the biggest challenge.

“I’m not going to lie; I have a lot of spells where I lose my determination,” she said. “I get disappointed in myself. Every teenager that goes into this has to know it’s not easy.”

Jennifer Brown: 303-954-1593 or jenbrown@denverpost.com

RNY relieves GERD

On January 11, 2010, in Uncategorized, by Andrea

Filing under the “duh” category for the medical community…  I would like to state, though, that my GERD has come back somewhat.  I still get heartburn, but never to the degree I once had.  I just wanna make it clear, though, despite being told otherwise, it is not because I’ve stretched my pouch out beyond repair or because my stoma is the size of the Grand Canyon.  It’s cause I’m special, damnit.  I’m a lemon, and don’t you forget about it.

BTW — hello Medscape?  You have many typos on your dates today.  You should correct that, given, you know, that you are an important resource to us peeps out here in the interwebz.

From Medscape:

Gastric Bypass Relieves GERD Syndromes in Most Obese Patients

By Michelle Rizzo

NEW YORK (Reuters Health) Jan 08 – Gastric bypass alleviates gastroesophageal reflux disease (GERD) in most obese patients and provides “substantial” improvement in heartburn by 6 months after surgery, report researchers from Brazil in the December 10th online issue of the Annals of Surgery.

Obese GERD patients also have an improved quality of life after gastric bypass, and they use fewer proton pump inhibitors, senior author Dr. Fernando Fornari, from the University of Passo Fundo, told Reuters Health.

“GERD is highly prevalent in patients with morbid obesity, contributing to compromise the quality of life of these patients,” Dr. Fornari noted. “In the last 50 years, the conventional surgical treatment for GERD has been a gastric fundoplication.”

However, he added, GERD symptoms often recur after gastric fundoplication in obese patients.

In their study, he and his colleagues followed 86 morbidly obese patients who were evaluated for GERD symptoms before and 6 months after their gastric bypass operations.

Overall, the mean age was 38 years, the mean preoperative body mass index was 45.3, 25 patients were male, and most (n=84) were white Brazilians.

The overall prevalence of GERD was 64% before gastric bypass and 33% at 6 months after the surgery (p < 0.0001).

Forty-seven patients had typical reflux syndrome before surgery, which resolved in 39. Of the 39 patients without preoperative reflux syndrome, 4 developed symptoms postoperatively.

The chief complaint before surgery was heartburn (in 96%); after surgery, it was regurgitation (in 64%).

After gastric bypass, the esophageal mucosa was improved in 27 patients, unchanged in 51 patients, and worse in 8 patients. Postoperatively, the number of patients with extra-esophageal injury was reduced from 16 to 1.

There was also a significant decrease in acid exposure in the overall population, from a median of 5.1% before surgery to 1.1% afterward.

After surgery, 74 patients had a pH below 4 in their gastric pouch. Although there was no difference in typical reflux syndrome symptoms in patients with or without an acid gastric pouch (18% versus 8%), reflux esophagitis was more frequent with an acid gastric pouch (26% versus 0%; p = 0.041).

“Based on our study, we believe that gastric bypass may replace the conventional surgical technique for patients with morbid obesity who suffer from GERD,” Dr. Fornari noted. “In addition, it is well established that gastric bypass increases both quantity and quality of life by treating obesity and its related comorbidities.”

He and his colleagues conclude, “Whether regurgitation post-gastric bypass corresponds to reflux disease or bad eating behavior deserves further studies.”

Ann Surg 2009.

Thiamin deficiency post RNY

On January 9, 2010, in Vitamins, Water Solubles, by Andrea

Two CMEs off Medscape cause I was working on the Thiamin post and I found them.  Only referenced one cause I had only read it when I wrote up the stuff.  Maybe should have read the other, too, eh?

Thiamine Deficiency May Complicate Gastric Bypass

News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP

Dec. 30, 2005 — Thiamine deficiency with a nonclassic presentation may follow gastric bypass for obesity, according to a case report in the December 27 issue of Neurology.

“The neurological complications following gastric bypass surgery are diverse,” coauthor Raul N. Mandler, MD, from George Washington University in Washington, DC, said in a news release. “Vitamin B1 deficiency and Wernicke encephalopathy should be carefully considered in surgically treated obese patients.”

The authors describe a 35-year-old woman who developed many symptoms following bariatric gastric bypass, including nausea, anorexia, fatigue, apathy, hearing loss, psychomotor slowing, forgetfulness, ataxia, and bilateral hand paresthesias. By the twelfth postoperative week, she had lost 40 lb and had lethargy, confusion, and difficulty walking, which necessitated hospitalization.

Examination showed inattention, fluent speech with decreased comprehension, decreased hearing, strength 3/5 in the lower extremities, vibratory sense decreased in the feet, deep tendon reflexes absent, and wide-based gait. Laboratory abnormalities were a slight elevation in liver enzymes, high serum glucose level (163 mg/dL), and low serum potassium level (2.6 MEq/L). Her mental status continued to decline despite treatment for dehydration.

When hospitalized, her heart rate was 125 beats per minute; she opened her eyes to nail bed pressure but followed no commands and was nonverbal. Pupils were round and fixed at 3 mm; oculocephalic and deep tendon reflexes were absent; and general muscle tone was flaccid without spontaneous movements or withdrawal to painful stimuli. Cerebral spine fluid protein level was 90 mg/dL, and there was diffuse slowing on electroencephalogram.

Brain magnetic resonance imaging (MRI) revealed bilateral symmetric hyperintense signal on T2-weighted and fluid attenuated inversion recovery images at the floor of the fourth ventricle, periaqueductal gray matter, the medial portions of both thalami, and the premotor and motor cortices, with contrast enhancement in all T2 hyperintense regions.

When she was given intravenous (IV) vitamin B 1, 100 mg every 8 hours, her oculocephalic reflexes gradually returned to normal, and she eventually became responsive. Follow-up brain MRI 11 days after thiamine repletion showed interval improvement, with less contrast enhancement, but with increased signal on precontrast T1-weighted images in the premotor and motor cortices, likely representing petechial hemorrhages.

“Wernicke encephalopathy is a well-defined syndrome, but difficult to identify in the absence of the classic triad of oculomotor abnormalities, ataxia, and confusion,” the authors write. “When a patient presents with unusual symptoms (in our case with progressive hearing loss, most likely secondary to thalamic involvement), then blood work (red blood cell transketolase levels) and MRI become helpful tools in making the diagnosis.”

The authors have disclosed no relevant financial relationships.

“This case highlights the variability of Wernicke encephalopathy where the classic trio of eye movement abnormalities, confusion, and ataxia are seen in less than 20% of patients,” says Heidi Schwarz, MD, who wrote a related commentary. “It is unusual because the patient also had hearing loss.”

Dr. Schwarz notes that bariatric surgery may have other complications, including anemia, vitamin D deficiency and bone resorption, rhabdomyolysis, vitamin A deficiency, and hypocalcemia. Neurologic complications are common, especially when there is intractable vomiting causing myelopathy and ataxia due to deficiencies in vitamin B 12, copper, or vitamin E; or peripheral neuropathy, plexopathies, and mononeuropathies due to vitamin or micronutrient deficiencies or as yet unknown causes.

“Although thiamine deficiency was not documented serologically [in this case report], the course, MRI findings, and response to thiamine establish the diagnosis,” Dr. Schwarz writes. “Patients who have had bariatric surgery require a high index of suspicion for Wernicke encephalopathy so that prompt treatment can be given to prevent devastating and often permanent disability.”

Neurology. 2005;65:1847, 1987

Wernicke Encephalopathy After Bariatric Surgery: A Systematic Review

Erlend Tuseth Aasheim, MD


Objective: To review the clinical essentials of Wernicke encephalopathy (WE) after bariatric surgery.
Summary Background Data: An estimated 205,000 bariatric surgical procedures were performed in the United States in 2007. Such procedures may potentially lead to severe nutritional complications.
Methods: Literature searches were performed in Medline, Embase, and abstract collections. Inclusion criteria were WE after bariatric surgery, diagnosed by the presence of two or more of the following signs: mental status changes, eye movement abnormalities, cerebellar dysfunction, and dietary deficiency.
Results: Of 104 reported cases of WE after bariatric surgery, 84 cases were included. Gastric bypass or a restrictive procedure had been performed in 80 cases (95%). Admission to hospital for WE occurred within 6 months of surgery in 79 cases (94%). Frequent vomiting was a risk factor in 76 cases (90%) and had lasted for a median of 21 days at admission. Intravenous glucose administration without thiamine was a risk factor in 15 cases (18%). Brain magnetic resonance imaging identified lesions characteristic of WE in 14 of 30 cases (47%). Incomplete recovery was observed in 41 cases (49%); memory deficits and gait difficulties were frequent sequela. The recent increase in the use of bariatric surgery in the United States was associated with an increase in reported WE cases.
Conclusions: The number of WE cases after bariatric surgery is substantially higher than previously reported. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and symptoms to prevent and optimize the management of this condition.


Nearly 7% of adult U.S. women presently have a body mass index above 40 kg/m2.[1] Bariatric surgery is presently the only treatment likely to yield substantial and durable weight loss, and has beneficial effects on medical conditions associated with severe obesity.[2] As a result, more than 100,000 weight-loss procedures are performed annually in the United States alone, and numbers are rising.[3] The sheer volume suggests that any physician involved in clinical medicine will meet patients who have been treated with obesity surgery. Practitioners will therefore need to familiarize themselves with the potential adverse effects linked with this therapy.

Anastomotic leakage and pulmonary embolism are feared complications of bariatric surgery procedures. However, acute nutritional disturbances may also occur in the early postoperative period. The numerous reports of severe thiamine (vitamin B1) deficiency after obesity surgery have led to the expression bariatric beriberi.[4] Beriberi is derived from the Singhalese word beri meaning weakness and refers to the clinical spectrum of deficiency in thiamine, including affection of the peripheral and central nervous system.[5] The most frequent central neurologic complication of thiamine deficiency is Wernicke encephalopathy (WE), a condition which needs immediate treatment to prevent death or permanent neurologic sequela. The classic presentation is that of mental confusion, eye movement abnormalities, and gait instability. Autopsy series indicate that WE is underdiagnosed.[6] The general epidemiology, pathophysiology, and treatment of this condition was recently reviewed.[6]

Patients have a limited capacity for food intake during the initial weeks after a bariatric procedure. The body’s reserves of thiamine can be depleted after only 20 days of inadequate supply.[6] Patients treated with bariatric surgery may thus still be frankly obese when presenting with symptoms caused by nutritional derangement. Such patients are a diagnostic challenge to physicians not familiar with WE as a potential complication of weight-loss operations. The aim of this paper is to review the clinical essentials of WE after bariatric surgery, with emphasis on presentation, findings on supplementary tests, and patient outcomes.


Search Strategy

Systematic literature searches were performed by one investigator in Medline and Embase (from their inceptions to May 2008), with no language restrictions, for reports of Wernicke encephalopathy after bariatric surgery. The core search consisted of the MeSH terms Wernicke encephalopathy, bariatric surgery, morbid obesity, malnutrition, and polyneuropathies. These terms were also substituted with related terms (eg, bariatric surgery was substituted with obesity surgery, gastric bypass, gastroplasty, gastric banding, and biliopancreatic diversion). Further searches were done in abstract collections published in Obesity Surgery (1991-May 2008) and Surgery for Obesity and Related Diseases (2005-May 2008). Daily e-mails enlisting new articles identifiable in PubMed by using the term obesity were perused throughout February 2005 to May 2008. Nonsystematic literature searches were done using PubMed’s related articles feature, Google Scholar’s cited by feature, Wikipedia (the English version at http://www.wikipedia.org), and UpToDate (http://www.uptodate.com). Bibliographies of original reports and reviews were scanned for additional references. A citing author kindly provided 2 otherwise unattainable abstracts.[7,8] Additional information was sought from the authors of 3 reports.[9-11]

Selection Criteria

Identified publications dealing with bariatric surgery were scrutinized for WE cases. WE was diagnosed in the presence of 2 or more of the following signs[12]: mental status changes (confusion, memory deficits, or impaired consciousness), eye movement abnormalities (nystagmus or palsy of ocular muscles), cerebellar dysfunction (gait incoordination or ataxia), and dietary deficiency (assumed in all cases).

Eleven cases were likely to appear in multiple reports and were only counted once.[8,9,13-22] Patients with encephalopathy after jejunoileal bypass were not included as their presentations were atypical and investigators noted that WE was unlikely.[23-28] Cases were excluded if too limited information was available to confirm a diagnosis of WE.

Data Extraction

One physician extracted data from the included reports. Data were recorded on designated forms. All data were cross-checked and entered in a database including more than 100 items on demographics, clinical symptoms, results of diagnostic tests, and patient outcome. Outcome was recorded at the latest reported follow-up and categorized as complete recovery (including improved when no information of residual deficits was given) or incomplete recovery (any sequela observed clinically).

Data Management

Reported data are number of cases (percentage) or median (range), as appropriate. Software packages used for the management of references, statistics, and graphics included Reference Manager 11 (Thomson ResearchSoft, Carlsbad, CA), SPSS 14 (SPSS Inc., Chicago, IL), and SigmaPlot 10 (Systat Software Inc., San Jose, CA).

Included Studies

Literature searches identified a total of 104 cases of WE reported after bariatric surgery. 20 cases were excluded: 19 described in too limited detail to confirm the WE diagnosis[10,19,29-31] and 1 diagnosed 13 years after bariatric surgery in a setting of excessive alcohol intake.[32] Thus, 84 cases were included in the systematic review. These cases were described in 58 reports published 1977-2008 (Figure 1).[11,13-15,17,21,33-84]

Figure 1. (click image to zoom) Case selection.

Patient Characteristics

The type of bariatric surgical operation performed in the 84 WE cases was gastric bypass in 43 (51%), diverse restrictive procedures in 37 (44%), and the malabsorptive procedure biliopancreatic diversion in 4 (5%). Median patient age was 32 years (range 14-55) and 69 were women (82%).

Duration from surgery until admission to hospital for WE was less than 6 months in 79 cases (94%), and ranged from 3 weeks to 18 months (Figure 2). Median weight loss from surgery to admission was 35 kg (12-129) and weight loss rate was 0.44 kg/d (0.11-1.6) (data on weight loss were reported in 54 patients).

Figure 2. (click image to zoom) Onset of Wernicke encephalopathy (n = 81). Three additional cases were admitted within 6 to 20 weeks (precise week not reported).[39,40] One patient was diagnosed 5 weeks after a reoperation (14 months after the primary procedure)[35] and was considered to be admitted at 5 weeks. One patient diagnosed at 78 weeks used a self-controlled device to infuse a morphine and 5% dextrose solution in water, after a panniculectomy.[54]

Symptoms and Signs

The clinical features are summarized in Figure 3. Recurrent vomiting was reported in 76 cases (90%), and had lasted for a median duration of 21 days (4-90) when patients were admitted to hospital (duration of vomiting was reported in 26 cases). When vomiting was not reported, patients had rapid weight loss, loss of appetite or eating avoidance, or did not take vitamin supplements.[11,15,34,35,46,52,55] Intravenous glucose had been administered without thiamine in 15 patients (18%).[11,17,21,47,54,59-61,63,67,74,75,80,83]

Figure 3. (click image to zoom) Clinical features reported in Wernicke encephalopathy cases (n = 84). Eye movement signs include nystagmus and gaze palsy; mental status changes include confusion, memory deficits, and impaired consciousness; gait ataxia includes incoordination of gait and posture.

The classic WE triad of eye movement abnormalities, mental status changes, and ataxia was present in 32 patients (38%); 2 signs were present in 36 patients (43%); and 1 sign was present in 16 patients (19%). Less common features included visual hallucinations,[17,37,51,67,71] behavioral disturbances,[51,62,76,85] and depression.[52,53,64,76] Also reported were dysarthria,[38,42,52,60,66,76,80] hearing loss,[15,37,38,40,45,52] and dysphagia.[46,49,80] Blurred vision or impaired visual acuity was noted in 17 patients.[14,37,38,40,48,54,56,60,64,70,76,81] Fundoscopy confirmed papilledema in 4 patients and 3 of these had peripapillary or retinal hemorrhages.[14,34,48] A few patients had myoclonus[36,44] or chorea,[41,76] and some eventually became comatose.[34,70,74,86]

Peripheral polyneuropathy occurred in 64 patients (76%). Motor and sensory neuropathy was reported with similar rates (56 versus 55 patients). Neuropathy was more frequent in the lower limbs than in the upper limbs (61 versus 30 patients).


Upper endoscopy or gastrointestinal series demonstrated stomal obstruction in 18 of 41 cases. Specific findings included anastomotic and bandelet stenoses (after gastric bypass),[35,36,51,54,57,58] pouch inlet, and outlet stenoses (vertical banded gastroplasty),[64,71] partition obstruction (gastric partitioning),[73,75] pouch outlet obstruction (adjustable gastric banding),[81] and gastric wall edema (sleeve gastrectomy).[83] Anastomotic leaks and jejunal erosions were also observed (gastric bypass).[46,54]

Results of thiamine assays, lumbar puncture, neuroimaging, and electrodiagnostic studies are shown in Table 1. Notably, brain computed tomography (CT) imaging did not reveal pathology in any of 39 examined cases, whereas brain magnetic resonance (MR) imaging identified lesions characteristic of WE in 14 of 30 cases (47%).[40,43-45,47,48,57,58,66-70] Brainstem evoked potential was delayed in 2 of 4 cases.[60,61,76,79] Autopsy in 2 patients revealed brain changes in the periaqueductal gray matter,[86] mammillary bodies, and about the third ventricle, with capillary proliferations and relative sparing of neurons; consistent with WE.[34,86]

Clinical Outcomes

The clinical outcome was reported in 83 of 84 patients, after a median follow-up of 5 months (0-20). Outcomes ranged from complete recovery to death. Complete recovery was observed in 42 cases (51%), whereas 41 cases (49%) were considered to have had an incomplete recovery. Frequent sequelae were cognitive impairments (n = 16), gait difficulties (n = 13), and nystagmus (n = 7). Brain MR imaging repeated 3 to 28 days after thiamine treatment was initiated showed improvement in 5 of 5 cases.[44,45,47,69,70]

Incidence Trends

Of 84 WE cases undergoing systematic review, 45 (54%) were reported from the United States. The number of WE cases reported from this country increased during the years 2001 to 2007, when the annual number of bariatric surgical procedures increased steeply (Figure 4).

Figure 4. (click image to zoom) Reported cases of Wernicke encephalopathy after bariatric surgery (shown as dots, n = 45) and the number of bariatric procedures (solid line) in the United States. Procedure number estimates data were not available prior to 1992. Courtesy of American Society for Metabolic and Bariatric Surgery, Gainesville, FL.

Among the large bariatric surgery series identified, none reported the incidence of WE after gastric bypass or restrictive bariatric operations. However, 2 series from Southern Europe reported a combined total of 6 WE cases among 3241 patients undergoing biliopancreatic diversion,[18,30] corresponding to an estimated incidence of 19 WE cases per 10,000 procedures (95% confidence interval, 7-40). In one of these series, 3 WE cases were observed after 791 operations, but after starting administration of large doses of thiamine to patients reporting small food intakes during the early postoperative weeks, no WE cases were observed after the next 1450 operations[18] (P = 0.044, Fisher exact test).


This systematic review identified more than 100 reported patients with WE after elective bariatric surgical procedures. Most cases were complications of gastric bypass, the procedure most widely performed at present. The increasing use of bariatric surgery to induce weight loss is linked with an increasing number of patients at risk for WE and its associated potentially lasting neurologic impairments. WE is a medical emergency, yet it is readily preventable.

Predisposing Factors

Severe deficiency in thiamine is the cause of WE, which is most commonly associated with alcoholism.[87] Persistent vomiting leads to inadequate dietary intake of thiamine and is the dominating risk factor after obesity surgery. Pregnant women with hyperemesis may also develop WE.[6] Vomiting after any gastrointestinal surgical procedure might be caused by intestinal obstruction. In spite of this, results of upper endoscopy or gastrointestinal series were reported in less than half of patients in the present review. Glucose loading in patients with thiamine deficiency precipitates a focal lactic acidosis in the medial thalamus and thereby contributes to neuronal damage.[88] Parenteral feeding may have aggravated symptoms in as many as 18% of cases. The high proportion of women (82%) among the reported WE cases may simply mirror the proportion of women among patients undergoing bariatric surgery.[89]

Investigations and Treatment

Supplementary testing should never delay thiamine administration in patients with possible WE. Investigations may help to confirm WE and exclude other diseases, but cannot replace the clinical diagnosis. Although brain MR imaging is useful in verifying WE with a specificity of 93%, the low sensitivity of about 50% means that the diagnosis cannot be excluded based on a normal finding.[90] CT imaging is not useful in patients with suspected WE. Transketolase activity assays have some utility, but specific analysis of thiamine esters in blood might prove more useful: complete discrimination of WE patients and controls was reported for thiamine monophosphate, a dephosphorylation product of the coenzyme thiamine pyrophosphate.[91] However, evidence is sparse and thiamine assays have limited availability and usually do not allow for an immediate diagnosis.

WE may emerge with a variety of symptoms (Figure 3) and patients may thus initially present to physicians in a range of medical specialties. The challenge of making the diagnosis is underscored by the diagnostic delays observed in some patients.[39,51,73] A worse outcome may be expected in late-stage WE, which is associated with elevated spinal fluid protein levels and diffuse slowing of postsynaptic potentials on electroencephalography.[6] Only 2[47,54] of 16 patients with such findings had a complete recovery.[14,34,36,47,50,54,62,67,76,79]

There is insufficient evidence from controlled trials to guide clinicians in the dose, frequency, route, or duration of thiamine treatment in patients with suspected WE.[92] Recently suggested regimens include 500 mg thiamine intravenously 3 times daily for 3 days.[6,93] If the patient does not respond, treatment may be discontinued. In responders, parenteral thiamine should be given once daily for at least 5 more days. Oral supplementation may then be indicated, depending on the cause for thiamine deficiency.

Comparison With Previous Studies

Previous reports proposed that most cases of WE occurred between 4 and 12 weeks after bariatric surgery.[39,42,44,46,66,73] This systematic review demonstrates that a substantial proportion of cases occurred after this period (Figure 2). The present findings contrast those of a former review[94] in showing that about half of patients with WE after bariatric surgery may have lasting neurologic impairments. Furthermore, this review includes more than twice the number of cases that have previously been summarized.[94] Still, because only cases that were actually reported are included, the size of the problem is likely to be underestimated.[4] About 19% of patients may not present with the classic WE symptoms[6] and such potential cases[95,96] were not included. Also not included were patients with symptoms only from peripheral nerves,[97] which may be caused by moderate and prolonged nutrient deficiencies.[6] Damage to peripheral nerves may cause an incoordination of gait that clinically is difficult to discriminate from cerebellar ataxia. It is therefore notable that all cases with gait instability also had either eye movement abnormalities or mental status changes, indicating that each included case had encephalopathy.

The included patients’ succinct clinical features were largely consistent with the findings in 245 WE cases reported by Victor et al[87] In their series, horizontal nystagmus and ataxia were permanent in a majority of patients, and recovery from polyneuropathy was a slow process often lasting a year or longer. Deficits in memory and learning that remained after the acute confusion had cleared (Korsakoff syndrome) rarely resolved completely. Patients with such sequelae may need permanent institutional care. Formal neuropsychiatric assessment is sometimes useful in rehabilitation planning.

A system for reporting of cases has been suggested to estimate the incidence of WE in patients undergoing bariatric surgery.[94] The present findings indicate an incidence of about 1 in 500 patients after malabsorptive bariatric operations. This estimate may not be transferable to other bariatric operations and should be interpreted carefully because of the limited data set. The main limitation of this study is the nonsystematic data available from case reports, including a likely preferential reporting of positive findings. Also, WE had been diagnosed retrospectively in a few cases,[55,82] and because of the short follow-up in some of the reports, it is possible that additional patients eventually had a full recovery.


Printen and Mason observed in 1977 that, Even though surgery for obesity is well established we have not yet arrived at a point where we are aware of all the metabolic consequences (…) only meticulous postoperative observation will ensure that we recognize and treat these complications before irreversible damage has been done.[33] This remark holds true 30 years later. WE is caused by severe thiamine deficiency but there are few studies of thiamine status in bariatric surgery patients. One study identified a significant decrease in thiamine concentrations 6 weeks after gastric partitioning,[75] consistent with when WE typically presents (Figure 2). Further research is needed to determine appropriate supplementation and monitoring of thiamine status in patients undergoing current bariatric surgical operations.

The best treatment of WE is prophylaxis.[59] Patients must be instructed in proper eating patterns[33] and warned of nutritional risk factors such as repeated vomiting. Clinicians need to keep in mind that rapid weight loss may lead to nutritional deficiencies also in obese individuals and that behavioral disturbances or uncooperativeness could potentially be features of WE.[76] In particular, bariatric surgery training programs should include education on the possible nutritional complications of weight-loss operations. Thiamine administration is advisable in all patients readmitted or reporting frequent vomiting after a bariatric procedure as a simple, safe, inexpensive, and efficient preventive measure.


Wernicke encephalopathy is a medical emergency that may occur after any weight-loss operation, often leading to lasting disability. Nearly all reported cases presented after a few weeks of recurrent vomiting and within 6 months of surgery. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and the clinical presentation to prevent and optimize the management of this condition.


The author has received lecture fees from Johnson & Johnson, but all honoraria were donated directly to charity so that he received neither income nor a tax deduction.

The author thanks Chantal Tallaksen, MD, PhD, Heidi Eggesbø, MD, PhD, and Thomas Bøhmer, MD, PhD, for their insightful comments on the manuscript; Karianne Hasledalen and Gyri Hval Straumann at Aker University Hospital Library for their excellent assistance in retrieving literature; and colleagues who supplied additional information regarding their reported cases or assisted in the translation of non-English reports.

Funding Information

Supported by a research fellowship grant from Eastern Norway Regional Health Authority.

Reprint Address

Erlend Tuseth Aasheim, Hormone Laboratory, Department of Endocrinology, Aker University Hospital, Trondheimsveien 235, 0514 Oslo, Norway; Email:e.t.aasheim@medisin.uio.no

FDA takes new look at anemia treatments

On January 8, 2010, in Minerals, by Andrea

I can’t tell you how many RNYers suffer from anemia.  It’s one of the potential side effects given the bypass of the duodenum and the lack of Intrinsic Factor from the stomach that limits the absorption of B12 that is needed for proper iron absorption.  Vicious cycle it is.  Given this, many of us get transfusions and take massive iron doses to help combat the anemia that we suffer from, which makes this a bit more alarming to me.

From Medscape:

U.S. FDA to Take New Look at Anemia Drugs

By Lisa Richwine

WASHINGTON (Reuters) Jan 07 – U.S. regulators plan to ask outside experts to re-evaluate the use of Amgen Inc and Johnson & Johnson anemia drugs when given to patients with chronic kidney disease.

Food and Drug Administration officials, in an article published in the New England Journal of Medicine on Wednesday, said the agency “anticipates convening a public advisory committee meeting in 2010 to reevaluate erythropoiesis-stimulating agents (ESAs) in people with chronic kidney disease.

ESAs include Amgen’s Aranesp and Epogen and J&J’s Procrit.

The drugs came under scrutiny after studies showed high doses could lead to cardiovascular complications or death. Strong warnings were added in recent years and sales slumped, but the medicines remain widely used for patients with kidney disease and cancer.

FDA spokeswoman Karen Riley said an “important question” for the advisory panel would be what level of hemoglobin doctors should try to achieve with the drugs.

The FDA officials, in the journal article, said “optimal hemoglobin targets have never been established” for patients with chronic kidney disease.

“Beyond lowering hemoglobin targets and reducing doses of ESAs, it is also possible that more frequent hemoglobin monitoring” and other dosing changes might “improve outcomes” for patients, the FDA officials said.

They said clinical trials had raised “major concerns regarding the use of ESAs to increase hemoglobin concentrations” in chronic kidney disease patients above levels needed to avert blood transfusions.

But the studies “do not rule out the possibility, however, that modest increases in the hemoglobin level could be beneficial,” they added.

Amgen spokeswoman Emma Hurley said the FDA article “highlights areas of incomplete understanding regarding appropriate use” of ESAs in chronic kidney disease.

The advisory panel meeting will “provide an opportunity to discuss the latest evidence on the benefits and risks” of the medicines, she said.

Centocor Ortho Biotech, the J&J unit that sells Procrit, said in a statement the company “will continue to work with the FDA to ensure that Procrit prescribing information accurately reflects the known benefits and risks of the product, and will continue to communicate this information in a timely fashion.”

New Engl J Med, online January 6, 2010.

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