Figure 2. 

Laparoscopic adjustable gastric band (used with permission of the American Society for Bariatric Surgery).

     

Conversely, the use of the LAGB has increased tremendously.^[10,11] It offers the advantages of simplicity of technique, it maintains intestinal continuity, and it is reversible. The data on weight loss are promising.^[12-14] Early weight loss is greater after Roux-en-Y gastric bypass (RYGB), but the difference starts to diminish after 2 yr.^[15,16] Jan et al.^[17] reported similar weight loss compared with RYGB at 5 yr. Because of its lower complication rate, LAGB has become a particularly attractive option for patients with mild to moderate obesity (BMI ≤35).^[18] Disadvantages of LAGB include increased reoperative rate, slower initial weight loss, and lifelong issues of an implanted foreign body in the gastrointestinal tract.

Restrictive With Malabsorption Procedures

The restrictive with malabsorption bariatric procedures encompass techniques that vary gastric restriction and intestinal bypass. Biliopancreatic diversion (BPD) (Fig. 3) produces relatively minor gastric restriction (about 200-300 mL) with considerable intestinal bypass. This leads to an almost purely malabsorptive operation.

Figure 3. 

Biliopancreatic diversion (used with permission of Mayo Foundation for Medical Education and Research).

     

A more recent modification is the duodenal switch (Fig. 4), which preserves the distal stomach and pylorus while maintaining malabsorption. Its advantage is long-term weight loss. Its disadvantage is a resulting increase in the incidence of nutritional deficiencies. It is therefore generally reserved for the super-obese patient (BMI >50).

Figure 4. 

Duodenal switch (used with permission of Mayo Foundation for Medical Education and Research).

     

First described in the 1960s, gastric bypass with a loop gastrojejunostomy was complicated by bile reflux.^[19] This led to the development of the RYGB^[20] (Fig. 5). RYGB consists of creating a small gastric pouch from the cardia of the stomach. The distal stomach and proximal small bowel are bypassed by attaching the distal end of the mid jejunum to the proximal gastric pouch, then reattaching the biliary and pancreatic limb a specific distance along the length of the small intestine that is attached to the proximal stomach. This is the Roux limb. Its length is usually determined by the patient's BMI. Advantages include excellent short- and long-term weight loss with relatively few nutritional complications. Disadvantages include disruption of normal intestinal continuity and anastomotic complications.

Figure 5. 

Roux-en-Y gastric bypass (used with permission of Mayo Foundation for Medical Education and Research).

     

Gastrointestinal and Nutritional Complications

The obese patient is at increased risk for all postoperative complications, and those related to the gastrointestinal tract may be particularly difficult to diagnose and manage. Classic physical findings are often not appreciated during examination of the obese abdomen, and diagnostic tests may be difficult to perform and interpret. The medical team should therefore be vigilant for postoperative complications. Long-term complications may also be missed, particularly in patients prone to functional gastrointestinal tract symptoms that elevate the physician's threshold for ordering investigations. Knowing exactly which bariatric surgery was performed and having a good understanding of the normal postsurgical anatomy facilitate the selection of the appropriate test, procedure, or intervention.

Early Complications

Surgeons usually manage early (≤2 months) postoperative complications. An anastomotic leak or intestinal obstruction may not be easy to diagnose because of the patient's large abdomen.^[21] Thus, there should be a low threshold for ordering a barium radiograph or computed tomogram. Endoscopy is rarely indicated at this time.

Late Complications

The euphoria induced by weight loss in bariatric patients may be replaced by disappointment and regret with the development of new gastrointestinal tract symptoms and complications. Some nutritional, hepatobiliary, luminal, and functional complications are more likely after specific bariatric procedures ( Table 1 ).

Nutritional Complications

Vitamin and Mineral Deficiencies

Iron deficiency is common in RYGB patients, with an incidence as great as 49%.^[22] The pathogenesis of iron deficiency is multifactorial.^[23] Absorption of dietary iron depends on various dietary and physiologic factors.^[24,25] To be absorbed, the ferric iron in foods must first be reduced to the ferrous state. This reduction occurs in the stomach, where it is facilitated by hydrochloric acid. Achlorhydria may develop in RYGB patients, leading to a reduction in iron absorption. Gastric acid secretion from the proximal gastric pouch may be absent after bariatric surgery.^[26] Postsurgical prophylactic use of histamine2 receptor antagonists (H2-blockers) or proton pump inhibitors also reduces acid secretion and subsequent iron absorption. The reduced intake of iron-rich foods declines substantially after RYGB, both because of a decrease in total caloric intake and because of frequent intolerance to iron-rich foods, particularly red meat.^[27,28]

Iron deficiency presents primarily as microcytic anemia. Routine laboratory work (e.g., complete blood cell count, serum iron, transferrin, and ferritin) should be performed and monitored twice a year. Iron supplementation is recommended for all RYGB patients. In many cases, a standard multivitamin with iron is sufficient. However, when iron deficiency is discovered, treatment may include the use of additional oral iron given as ferrous sulfate 300 mg 3 times daily.^[22] Iron supplements should be taken with vitamin C between meals. Some patients will require IV iron infusions because of gastrointestinal intolerance (dyspepsia and constipation) to iron supplements or because of the inability to correct anemia with oral supplements alone. Good food sources of iron include red meat, fish, poultry, shellfish, eggs, soybeans, and legumes.

The absorption of vitamin B₁₂ begins in the stomach, where both pepsin and hydrochloric acid cleave it from foods (primarily meats).B₁₂ deficiency occurs in 26-70% of gastric bypass patients.^[28-30] Mechanisms include achlorhydria, which prevents cleavage of B₁₂ from foods, decreased B₁₂ consumption because of intolerance to meat and milk (2 primary dietary sources), and inadequate secretion of intrinsic factor after surgery.

Clinically significant B₁₂ deficiency may lead to megaloblastic anemia, thrombocytopenia, leukopenia, and glossitis, all reversible with replacement therapy. Despite the low incidence of symptomatic B₁₂ deficiency, the general consensus^[29,30] is that most gastric bypass patients cannot maintain adequate serum levels without supplementation. Intramuscular injections (1,000 μg/month) are recommended, but several studies have shown that a 300- to 500-μg dose of oral vitamin B₁₂ is sufficient.^[29,30] Other forms of supplementation include sublingual (350 μg/d) and nasal spray (500 μg/wk in 1 nostril).

Folic acid deficiency is another potential complication of RYGB, affecting as many as 35% of patients. Folate absorption is facilitated by hydrochloric acid and occurs primarily in the upper one-third of the small intestine.^[30] Additionally, vitamin B₁₂ acts as a coenzyme in converting methyltetrahydrofolate to tetrahydrofolate, so a vitamin B₁₂ deficiency may result in subsequent folate deficiency. Despite these apparent mechanisms for folate deficiency, decreased folate consumption from dietary sources may be the predominant cause.^[28,31] Folate deficiency can present as megaloblastic anemia, thrombocytopenia, leukopenia, or glossitis. Serum deficiencies are quite common (although symptoms are rare), and they are easily corrected with vitamin supplementation. Folate supplementation (1 mg/d) should correct deficiencies. Folate deficiency is a serious threat for women who become pregnant after gastric bypass, with neural tube defects reported in infants. Women of reproductive age should therefore take folate supplementation.

Fat-soluble vitamin deficiency may also occur after RYGB or BPD. Bypassing the duodenum results in delayed mixing of dietary fat with pancreatic enzymes and bile salts, which results in malabsorption of fat and fat-soluble vitamins. This complication occurs more commonly after BPD. Halverson^[22] reported vitamin A deficiency in 10% of gastric bypass patients. The predominant symptom is visual difficulties at night. Oral replacement therapy is occasionally needed.

Vitamin D and calcium deficiencies are less likely because they are absorbed preferentially in the jejunum and ileum. Nonetheless, there have been reports of osteomalacia after RYGB.^[32,33] Daily supplementation of 400 IU of vitamin D and 1,500 mg of elemental calcium is adequate.

Active absorption of thiamine (vitamin B₁) occurs primarily in the proximal small bowel. Humans cannot synthesize thiamine, which is not stored in large quantities, so adequate daily intake is essential. Dietary sources of thiamine include cereals, grains, lean pork, and legumes. Thiamine deficiency may lead to Wernicke-Korsakoff syndrome, which has been described after gastric bypass surgery.^[22,34] Symptom onset is preceded by profuse vomiting along with the rapid weight loss that occurs after bariatric surgery. The restrictive diet after RYGB may lead to a drastic reduction in dietary intake of thiamine. The redirection of the proximal small bowel, where group B vitamins are preferentially absorbed, coupled with persistent nausea and vomiting, increases the risk for thiamine deficiency. A regimen of daily multivitamins should prevent thiamine deficiency. When such deficiency is suspected, a 50-mg intramuscular or IV injection of thiamine should correct it.

Insufficient Weight Loss

The cardiac and metabolic consequences of obesity are improved after just 5-10% weight loss,^[35] but patients undergoing bariatric procedures and the physicians taking care of them generally strive for much greater weight loss. O'Brien et al.^[15] performed a systematic review of bariatric operations in which the pooled data showed that the percentage of excess weight loss (the difference between presurgical and ideal weight) was higher for RYGB compared with LAGB at year 1 (67 vs 42) and year 2 (67 vs 53); however, no differences were noted at 3, 4, 5, 6, and 7 yr (62 vs 55, 58 vs 55, 58 vs 55, 53 vs 50, and 55 vs 51). After RYGB and LAGB, about 15-17% of patients are unable to lose more than 40-50% of their excess weight,^[36-38] which is generally defined as insufficient weight loss.

Inadequate weight loss may be due to the patient's dietary indiscretions or lack of exercise or to the surgical technique. Patients may snack on high-calorie liquids or solids, thereby overcoming the natural restriction caused by the smaller postsurgical gastric pouch. Postoperative support groups are important in helping patients maintain long-term dietary compliance and weight loss.^[39] In the case of RYGB, the surgeon may have made the gastric pouch too large or the Roux limb too short, or there could be dehiscence of the staple line in the undivided stomach. An enlarged gastric pouch may be revised, but revisional procedures carry an increased risk of complications.^[40] After LAGB, the gastric pouch may dilate in about 12% of patients due to proximal herniation of the stomach.^[41] Deflation of the band resolved this problem in 77% of patients. Biertho et al.^[36] reported that after LAGB, 1.2% of patients required repeat operation purely for insufficient weight loss and were converted to RYGB or PBD.

Excessive Weight Loss

The RYGB and the purely restrictive procedures rarely result in protein calorie malnutrition or excessive weight loss. Such complications are more common after the BPD or the duodenal switch, both of which result in a greater degree of malabsorption. Undernutrition may not be obvious, because patients are expected to lose weight and protein levels will often remain normal initially.^[38]

The differential diagnosis includes eating disorders such as anorexia nervosa or bulimia or postsurgical complications .^[42] Stomal stenosis or ulceration may lead to vomiting and inadequate caloric intake. Protracted diarrhea could be due to an excessively long Roux limb or an enteric infection. Shortening the Roux limb after RYGB or lengthening the common channel after BPD or duodenal switch may be necessary in patients with severe fat and protein malabsorption.^[42]

Hepatobiliary Complications

Rapid weight loss predisposes bariatric patients to the formation of cholesterol gallstones, irrespective of the type of procedure performed.^[43-46] Within 6 months after surgery, new gallstones develop in as many as 36% of patients and sludge develops in as many as 13%.^[47,48] Elective cholecystectomy during bariatric surgery appears to be safe,^[49,50] but it increases the length of stay in the hospital and adds considerably to cost.^[51]) Routine intraoperative ultrasound with elective cholecystectomy has been advocated only in patients with existing gallstones, because new symptomatic gallstones occur infrequently (7%) and cholecystectomy is usually well tolerated.^[52] Only 30% of surgeons performing standard RYGB remove normal-appearing gallbladders.^[53] The administration of ursodeoxycholic acid for 6 months after surgery reduces the incidence of postoperatively formed gallstones from 32% to 2%.^[54] Caruana et al.^[55] questioned the necessity of any form of prophylactic treatment when they reported that only 10 of 125 patients who received none after open RYGB ultimately required cholecystectomy for symptomatic gallstones. Laparoscopic bariatric surgery reduces adhesion formation and makes postsurgical cholecystectomy more amenable to the laparoscopic approach.

When cholelithiasis is suspected, alternatives to ultrasound may be necessary because of poor image quality in the obese abdomen.^[56] Computed tomography and magnetic resonance cholangiopancreatography are good alternative diagnostic methods. Exploration of the common bile duct usually must be done intraoperatively or else by a gastrostomy in the excluded stomach because standard endoscopic retrograde cholangiopancreatography is seldom feasible.^[21,57]

Nonalcoholic fatty liver disease is a complication of obesity with no effective medical therapy. In studies with small numbers of patients, weight loss induced by bariatric surgery has been shown to improve the histologic changes caused by this condition.^[58-60]

Luminal Complications

Stomal and Marginal Ulceration

Ulceration occurs in as many as 20% of RYGB patients, usually within 3 months of surgery.^[61,62] The ulcers are usually on the efferent side of the gastrojejunostomy, the marginal ulcer.(^[63] What causes these ulcers is much debatable. Increased rate of ulceration has been reported after undivided gastric bypass.^[64] Local ischemia because of the surgical technique and tension on the pouch may also predispose the RYGB patient to ulceration.^[65] In 1976, Mason et al.^[66] reported that a larger gastric pouch led to an increased incidence of ulceration, possibly because the larger pouch left more parietal cells capable of producing more acid. The modern RYGB, however, leaves a tiny pouch (about 10-20 mL), which may not contain parietal cells and hence would not produce acid. Two recent studies challenge this theory. In one study, parietal cells were found in the gastric pouch after RYGB in all patients tested.^[67] Another study demonstrated lower pH in the gastric pouch in patients with stomal ulcers compared with asymptomatic patients after RYGB.^[68] It would therefore seem logical that acid plays a role in some ulcers after RYGB, particularly in patients with a larger gastric pouch.

Patients with stomal or marginal ulceration may present with abdominal pain, nausea, vomiting, or gastrointestinal tract bleeding. Ulceration may also lead to stenosis, resulting in symptoms similar to dysphagia or excessive weight loss.

In most cases, diagnosis can be made with an upper endoscopy. Biopsy specimens should be taken for Helicobacter pylori, which should be treated when present. The role of Helicobacter pylori in stomal and marginal ulceration, however, has not been determined. Although candidates for bariatric surgery are commonly tested for a treated ulceration before surgery, this is not a routine or standard practice. Patients with uncomplicated ulceration may be treated effectively with a proton pump inhibitor,^[69] which again suggests that acid influences the pathogenesis of these ulcers. In many instances, however, surgical technique varies and the gastric pouch is larger than it should be. Patients with refractory nonhealing ulcers may require surgical revision. Surreptitious ingestion of nonsteroidal anti-inflammatory drugs must always be considered and investigated.

Stomal Stenosis

Stomal stenosis has been reported in as many as 27% of bariatric patients.^[70] Some surgeons modify the RYGB by applying a silastic ring around the proximal pouch or the gastrojejunal anastomosis. This modification may lead to a higher incidence of symptomatic stenosis. A contrast-enhanced radiograph is often performed to investigate suspected stomal stenosis, but an upper gastrointestinal endoscopy is the preferred procedure because it allows therapeutic interventions.^[21] Knowing the diameter of the normal anastomosis (10-12 mm) can help avoid unnecessary dilation. Balloon dilation is the preferred procedure. Although multiple dilation sessions may be needed, patients with a silastic ring may first require surgical removal of the ring or revision of the anastomosis.

Band Erosion and Staple Line Dehiscence

The endoscopic appearance after staple line dehiscence, band erosion, or fistula development may be confusing. Symptoms are nonspecific and include abdominal pain, nausea, and vomiting. A contrast-enhanced radiograph is helpful and always indicated in these patients. Although such complications usually require surgical correction, few fistulas are closed endoscopically. Endoscopic clipping and fibrin glue sealant may be used to close fistula tracts.^[71]

Internal Hernias

Awareness of the possibility of internal hernias is important because they may be difficult to diagnose. Internal hernias do not occur in purely restrictive operations. Laparoscopic surgery leads to fewer adhesions, which may increase small-bowel mobility and the predisposition to internal hernias. Symptoms are nonspecific but may include vomiting and abdominal pain with or without nausea. A computed tomogram or barium radiograph of the upper gastrointestinal tract may not be confirmatory; thus, the decision to operate may be based solely on clinical suspicion. Internal hernias occur at three sites: (a) where the Roux limb passes through the mesocolon, (b) at the jejunojejunostomy, and (c) between the jejunal and colonic mesenteries.^[72]

Bile Reflux

After RYGB, bile reflux into the gastric pouch or proximal Roux limb should not occur unless the Roux limb is inappropriately short. When bile is observed proximally during upper endoscopy, it may indicate obstruction at, or distal to, the jejunojejunostomy. A recent study of cholescintigraphy in RYGB patients also suggests considerable duodenal gastric bile reflux into the excluded stomach compared with controls.^[73] The clinical significance of this complication has not been established.

Gastrointestinal Tract Bleeding

Gastrointestinal tract hemorrhage after gastric bypass is rare and is usually caused by stomal or marginal ulceration.^[74,75] The initial investigation of choice is an esophagogastroduodenoscopy. Knowledge of the surgical anatomy (Figs. 1-5) is a prerequisite to any endoscopic procedure on a bariatric surgery patient. Bleeding may present a management challenge if the bleeding site is not found at esophagogastroduodonoscopy, because of the difficulty in accessing the distal roux limb, the biliary limb, and the excluded stomach.

If the patient had an RYGB or a BPD, a pediatric colonosope may be required when a proximal source of bleeding is not found with a standard upper endoscope. The Roux limb should be inspected as far distally as possible. If no source of bleeding is found, the diagnostic and therapeutic dilemma is how to reach the excluded stomach and the biliary limb. Attempted retrograde passage of a pediatric colonosope up the biliary limb^[76] usually is not successful. A radiologically or laparoscopically placed percutaneous gastrostomy may allow endoscopic access to the excluded stomach.^[77] Rarely, intraoperative endoscopy is required. Double-balloon enteroscopy is a new endoscopic technique that allows direct visualization as well as diagnostic and therapeutic intervention of the entire small bowel,^[78] and it has also been used to access the biliary limb and excluded stomach after RYGB.^[79]

Dumping Syndrome

Dumping syndrome is caused by the rapid emptying of a hypertonic carbohydrate load into the small bowel. Patients may present with abdominal pain, cramping, flushing, palpitations, diaphoresis, tachycardia, or hypotension. Early dumping syndrome occurs within the first hour after ingestion of a meal and may be related to the sudden distension of the jejunum by hypertonic solids or fluids. Late dumping occurs 1-3 h after eating and is most likely caused by the rapid absorption of glucose, with hyperglycemia triggering an exaggerated insulin release that results in rebound hypoglycemia.

Some surgeons look favorably on this complication, because it sensitizes patients to avoid high-calorie meals that may lead to weight gain. In most patients, dumping syndrome can be prevented and treated with dietary changes. To help avoid rapid emptying of the gastric pouch, patients should eat small meals, avoid carbohydrates at the beginning of a meal, and consume food slowly.

Gastroesophageal Reflux Disease

GERD improves or disappears in most patients after RYGB.^[80] The small remaining gastric pouch should not contain parietal cells, which eliminates acid reflux. An added benefit is the distal diversion of bile, which may contribute to reflux symptoms. Conflicting results about the effect of LAGB on GERD have been published. Some have reported a worsening of symptoms,^[81] but a growing body of literature suggests that symptoms and pH may improve after LAGB.^[82-84] Overweight and obesity are risk factors for GERD, and weight loss due to any intervention may reduce GERD.^85-87

Functional Symptoms

Little is known about changes in gastrointestinal tract symptoms after bariatric surgery. Foster et al.^[88] compared symptoms before and 6 months after laparoscopic RYGB and found improvement in functional symptoms, such as abdominal distension, abdominal pain, flatus, and fecal urgency. These patients had no worsening of symptoms.

Vomiting is frequently a long-term problem in as many as 69% of patients after gastric bypass surgery.^[89] Although vomiting is usually caused by overeating, it also may indicate stomal stenosis. If no abnormality is found on endoscopy or a barium imaging study, the patient most likely is eating larger meals than recommended. Binge-eating disorder is common in obese patients,^[90] affecting as many as 49% of bariatric patients before surgery.^[89] Patients who resume binge eating after surgery are more likely to regain weight.^[89] Band slippage must also be considered in the patient with vomiting after LAGB.

The true prevalence of functional symptoms (e.g., diarrhea, constipation, abdominal pain, and bloating) after bariatric surgical procedures has not been well studied.

Conclusion

Gastroenterologists are part of the multidisciplinary team taking care of obese patients. Their familiarity with the range of bariatric procedures, the postsurgical anatomy, and the gastroenterological and nutritional complications common in these patients will facilitate their postsurgical care of bariatric patients.

Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002; 288: 1723-7. Calle EE, Rodriguez C, Walker-Thurmond K, et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U. S. adults. N Engl J Med 2003; 348:1625-38. Calle EE, Thun MJ, Petrelli JM, et al. Body-mass index and mortality in a prospective cohort of U. S. adults. N Engl J Med 1999; 341:1097-1105. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report. National Institutes of Health. Obes Res 1998; 6 :51S-209S. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: A systematic review and meta-analysis. JAMA 2004; 292:1724-37. Erratum in: JAMA. 2005;293:1728. NIH conference. Consensus Development Conference Panel. Gastrointestinal surgery for severe obesity. Ann Intern Med 1991; 115:956-61. National Institutes of Health, National Heart, Lung, and Blood Institute, and the North American Association for the Study of Obesity. The practical guideline: Identification, evaluation, and treatment of overweight and obesity in adults. Available at: http://www.nhlbi.nih.gov/guidelines/obesity/prctgd_c.pdf. Accessed May 30, 2006. Cohn R, Merrell RC, Koslow A. Gastric stapling for morbid obesity. Am J Surg 1981; 142:67-72. Balsiger BM, Poggio JL, Mai J, et al. Ten and more years after vertical banded gastroplasty as primary operation for morbid obesity. J Gastrointest Surg 2000; 4:598-605. Parikh MS, Fielding GA, Ren CJ. U. S. experience with 749 laparoscopic adjustable gastric bands: Intermediate outcomes. Surg Endosc 2005; 19:1631-5. O'Brien PE, Dixon JB, Laurie C, et al. Treatment of mild to moderate obesity with laparoscopic adjustable gastric banding or an intensive medical program: A randomized trial. Ann Intern Med 2006; 144:625-33. Ren CJ, Weiner M, Allen JW. Favorable early results of gastric banding for morbid obesity: The American experience. Surg Endosc 2004; 18:543-6. O'Brien PE, Dixon JB, Laurie C, et al. Treatment of mild to moderate obesity with laparoscopic adjustable gastric banding or an intensive medical program: A randomized trial. Ann Intern Med 2006; 144:625-33. Holloway JA, Forney GA, Gould DE. The Lap-Band is an effective tool for weight loss even in the United States. Am J Surg 2004; 188:659-62. O'Brien PE, McPhail T, Chaston TB, et al. Systematic review of medium-term weight loss after bariatric operations. Obes Surg 2006; 16:1032-40. Biertho L, Steffen R, Ricklin T, et al. Laparoscopic gastric bypass versus laparoscopic adjustable gastric banding: A comparative study of 1,200 cases. J Am Coll Surg 2003; 197:536-44. Jan JC, Hong D, Bardaro SJ, et al. Comparative study between laparoscopic adjustable gastric banding and laparoscopic gastric bypass: Single-institution, 5-year experience in bariatric surgery. Surg Obes Relat Dis 2007; 3:42-50. Angrisani L, Favretti F, Furbetta F, et al. Italian Group for Lap-Band System: Results of multicenter study on patients with BMI < or = 35 kg/m2. Obes Surg 2004; 14:415-8. Mason EE, Ito C. Gastric bypass in obesity. Surg Clin North Am 1967; 47:1345-51. Griffen WO Jr, Young VL, Stevenson CC. A prospective comparison of gastric and jejunoileal bypass procedures for morbid obesity. Ann Surg 1977; 186:500-9. Ukleja A, Stone RL. Medical and gastroenterologic management of the post-bariatric surgery patient. J Clin Gastroenterol 2004; 38:312-21. Halverson JD. Micronutrient deficiencies after gastric bypass for morbid obesity. Am Surg 1986; 52:594-8. Brolin RE. Gastric bypass. Surg Clin North Am 2001; 81:1077-95. Berdainer CD. Advaned nutrition: Micronutrients. Boca Raton: CRC; 1998. Fairweather-Tait SJ. The concept of bioavailability as it relates to iron nutrition. Nutr Res 1987; 7:319-25. Smith CD, Herkes SB, Behrns KE, et al. Gastric acid secretion and vitamin B12 absorption after vertical Roux-en-Y gastric bypass for morbid obesity. Ann Surg 1993; 218:91-6. Balsiger BM, Kennedy FP, Abu-Lebdeh HS, et al. Prospective evaluation of Roux-en-Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc 2000; 75:673-80. Avinoah E, Ovnat A, Charuzi I. Nutritional status seven years after Roux-en-Y gastric bypass surgery. Surgery 1992; 111:137-42. Rhode BM, Arseneau P, Cooper BA, et al. Vitamin B-12 deficiency after gastric surgery for obesity. Am J Clin Nutr 1996; 63:103-9. Brolin RE, Gorman JH, Gorman RC, et al. Are vitamin B12 and folate deficiency clinically important after Roux-en-Y gastric bypass? J Gastrointest Surg 1998; 2:436-42. Updegraff TA, Neufeld NJ. Protein, iron, and folate status of patients prior to and following surgery for morbid obesity. J Am Diet Assoc 1981; 78:135-40. Goldner WS, O'Dorisio TM, Dillon JS, et al. Severe metabolic bone disease as a long-term complication of obesity surgery. Obes Surg 2002; 12:685-92. Amaral JF, Thompson WR, Caldwell MD, et al. Prospective metabolic evaluation of 150 consecutive patients who underwent gastric exclusion. Am J Surg 1984; 147:468-76. Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et al. Wernicke's syndrome after bariatric surgery. Clin Nutr 2000; 19:371-3. Sjostrom CD, Lissner L, Sjostrom L. Relationships between changes in body composition and changes in cardiovascular risk factors: The SOS Intervention Study. Swedish Obese Subjects Obes Res 1997; 5:519-30. Biertho L, Steffen R, Branson R, et al. Management of failed adjustable gastric banding. Surgery 2005; 137:33-41. Sugerman HJ, Kellum JM, Engle KM, et al. Gastric bypass for treating severe obesity. Am J Clin Nutr 1992; 55 :560S-6S. Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg 1995; 222:339-50. Marcus JD, Elkins GR. Development of a model for a structured support group for patients following bariatric surgery. Obes Surg 2004; 14:103-6. Schwartz RW, Strodel WE, Simpson WS, et al. Gastric bypass revision: Lessons learned from 920 cases. Surgery 1988; 104:806-12. Galvani C, Gorodner M, Moser F, et al. Laparoscopic adjustable gastric band versus laparoscopic Roux-en-Y gastric bypass: Ends justify the means? Surg Endosc 2006; 20:934-41. Sugerman HJ, Nguyen NT, eds. Management of morbid obesity. New York: Taylor & Francis; 2006. Kiewiet RM, Durian MF, van Leersum M, et al. Gallstone formation after weight loss following gastric banding in morbidly obese Dutch patients. Obes Surg 2006; 16:592-6. Liddle RA, Goldstein RB, Saxton J. Gallstone formation during weight-reduction dieting. Arch Intern Med 1989; 149:1750-3. Faloon WW. Hepatobiliary effects of obesity and weight-reducing surgery. Semin Liver Dis 1988; 8:229-36. Shiffman ML, Sugerman HJ, Kellum JM, et al. Changes in gallbladder bile composition following gallstone formation and weight reduction. Gastroenterology 1992; 103:214-21. glézias Brandão de Oliveira C, Adami Chaim E, Borges da Silva B. Impact of rapid weight reduction on risk of cholelithasis after bariatric surgery. Obesity Surg 2003; 13:625-8. Shiffman ML, Sugerman HJ, Kellum JM, et al. Gallstone formation after rapid weight loss: A prospective study in patients undergoing gastric bypass surgery for treatment of morbid obesity. Am J Gastroenterol 1991; 86:1000-5. Fobi M, Lee H, Igwe D, et al. Prophylactic cholecystectomy with gastric bypass operation: Incidence of gallbladder disease. Obes Surg 2002; 12:350-3. Liem RK, Niloff PH. Prophylactic cholecystectomy with open gastric bypass operation. Obes Surg 2004; 14:763-5. Hamad GG, Ikramuddin S, Gourash WF, et al. Elective cholecystectomy during laparoscopic Roux-en-Y gastric bypass: Is it worth the wait? Obes Surg 2003; 13:76-81. Villegas L, Schneider B, Provost D, et al. Is routine cholecystectomy required during laparoscopic gastric bypass? Obes Surg 2004; 14:206-11. Mason EE, Renquist KE. Gallbladder management in obesity surgery. Obes Surg 2002; 12:222-9. Sugerman HJ, Brewer WH, Shiffman ML, et al. A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss. Am J Surg 1995; 169:91-6. Caruana JA, McCabe MN, Smith AD, et al. Incidence of symptomatic gallstones after gastric bypass: Is prophylactic treatment really necessary? Surg Obes Relat Dis 2005; 1:564-7. Fiegler W, Felix R, Langer M, et al. Fat as a factor affecting resolution in diagnostic ultrasound: Possibilities for improving picture quality. Eur J Radiol 1985; 5:304-9. Baron TH, Vickers SM. Surgical gastrostomy placement as access for diagnostic and therapeutic ERCP. Gastrointest Endosc 1998; 48:640-1. Klein S, Mittendorfer B, Eagon JC, et al. Gastric bypass surgery improves metabolic and hepatic abnormalities associated with nonalcoholic fatty liver disease. Gastroenterology 2006; 130:1564-72. Mathurin P, Gonzalez F, Kerdraon O, et al. The evolution of severe steatosis after bariatric surgery is related to insulin resistance. Gastroenterology 2006; 130:1617-24. Csendes A, Smok G, Burgos AM. Histological findings in the liver before and after gastric bypass. Obes Surg 2006; 16:607-11. MacLean LD, Rhode BM, Nohr C, et al. Stomal ulcer after gastric bypass. J Am Coll Surg 1997; 185:1-7. Sanyal AJ, Sugerman HJ, Kellum JM, et al. Stomal complications of gastric bypass: Incidence and outcome of therapy. Am J Gastroenterol 1992; 87:1165-9. Dallal RM, Bailey LA. Ulcer disease after gastric bypass surgery. Surg Obes Relat Dis 2006; 2:455-9. Jordan JH, Hocking MP, Rout WR, et al. Marginal ulcer following gastric bypass for morbid obesity. Am Surg 1991; 57:286-8. Sapala JA, Wood MH, Sapala MA, et al. Marginal ulcer after gastric bypass: A prospective 3-year study of 173 patients. Obes Surg 1998; 8:505-16. Mason EE, Munns JR, Kealey GP, et al. Effect of gastric bypass on gastric secretion. Am J Surg 1976; 131:162-8. Siilin H, Wanders A, Gustavsson S, et al. The proximal gastric pouch invariably contains acid-producing parietal cells in Roux-en-Y gastric bypass. Obes Surg 2005; 15:771-7. Hedberg J, Hedenstrom H, Nilsson S, et al. Role of gastric acid in stomal ulcer after gastric bypass. Obes Surg 2005; 15:1375-8. Pope GD, Goodney PP, Burchard KW, et al. Peptic ulcer/stricture after gastric bypass: A comparison of technique and acid suppression variables. Obes Surg 2002; 12:30-3. Matthews BD, Sing RF, DeLegge MH, et al. Initial results with a stapled gastrojejunostomy for the laparoscopic isolated Roux-en-Y gastric bypass. Am J Surg 2000; 179:476-81. Papavramidis ST, Eleftheriadis EE, Papavramidis TS, et al. Endoscopic management of gastrocutaneous fistula after bariatric surgery by using a fibrin sealant. Gastrointest Endosc 2004; 59:296-300. Klein S, Wadden T, Sugerman HJ. AGA technical review on obesity. Gastroenterology 2002; 123:882-932. Sundbom M, Hedenstrom H, Gustavsson S. Duodenogastric bile reflux after gastric bypass: A cholescintigraphic study. Dig Dis Sci 2002; 47:1891-6. Schauer PR, Ikramuddin S, Gourash W, et al. Outcomes after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Ann Surg 2000; 232:515-29. Braley SC, Nguyen NT, Wolfe BM. Late gastrointestinal hemorrhage after gastric bypass. Obes Surg 2002; 12:404-7. Flickinger EG, Sinar DR, Pories WJ, et al. The bypassed stomach. Am J Surg 1985; 149:151-6. Sundbom M, Nyman R, Hedenstrom H, et al. Investigation of the excluded stomach after Roux-en-Y gastric bypass. Obes Surg 2001; 11:25-7. Yamamoto H, Sekine Y, Sato Y, et al. Total enteroscopy with a nonsurgical steerable double-balloon method. Gastrointest Endosc 2001; 53:216-20. Kuno A, Yamamoto H, Kita H, et al. Double-balloon enteroscopy through a Roux-en-Y anastomosis for EMR of an early carcinoma in the afferent duodenal limb. Gastrointest Endosc 2004; 60:1032-4. Frezza EE, Ikramuddin S, Gourash W, et al. Symptomatic improvement in gastroesophageal reflux disease following laparoscopic Roux-en-Y gastric bypass. Surg Endosc 2002; 16:1027-31. Gutschow CA, Collet P, Prenzel K, et al. Long-term results and gastroesophageal reflux in a series of laparoscopic adjustable gastric banding. J Gastrointest Surg 2005; 9:941-8. de Jong JR, van Ramshorst B, Timmer R, et al. The influence of laparoscopic adjustable gastric banding on gastroesophageal reflux. Obes Surg 2004; 14:399-406. Dixon JB, O'Brien PE. Gastroesophageal reflux in obesity: The effect of lap-band placement. Obes Surg 1999; 9:527-31. Tolonen P, Victorzon M, Niemi R, et al. Does gastric banding for morbid obesity reduce or increase gastroesophageal reflux? Obes Surg 2006; 16:1469-74. Corley DA, Kubo A. Body mass index and gastroesophageal reflux disease: A systematic review and meta-analysis. Am J Gastroenterol 2006; 101:2619-28. Jacobson BC, Somers SC, Fuchs CS, et al. Body-mass index and symptoms of gastroesophageal reflux in women. N Engl J Med 2006; 354:2340-8. Hampel H, Abraham NS, El-Serag HB. Meta-analysis: Obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med 2005; 143:199-211. Foster A, Laws HL, Gonzalez QH, et al. Gastrointestinal symptomatic outcome after laparoscopic Roux-en-Y gastric bypass. J Gastrointest Surg 2003; 7:750-3. Mitchell JE, Lancaster KL, Burgard MA, et al. Long-term follow-up of patients' status after gastric bypass. Obes Surg 2001; 11:464-8. Crowell MD, CheskinL J, Musial F. Prevalence of gastrointestinal symptoms in obese and normal weight binge eaters. Am J Gastroenterol 1994; 89:387-91.

Acknowledgements

Editing, proofreading, and reference verification were provided by the Section of Scientific Publications, Mayo Clinic. All authors contributed equally to this manuscript.

Funding Information

There was no financial support.

Reprint Address

G. Anton Decker, M.D., Division of Gastroenterology and Hepatology, Mayo Clinic, 13400 East Shea Boulevard, Scottsdale, AZ 85259.

G. Anton Decker, M.B.B.Ch., M.R.C.P.,¹ James M. Swain, M.D.,² Michael D. Crowell, Ph.D.,James S. Scolapio M.D.,<sup>3

1</sup>Division of Gastroenterology and Hepatology,
²Department of Surgery, Mayo Clinic, Scottsdale, Arizona,
³Division of Gastroenterology and Hepatology, Mayo Clinic, Jacksonville, Florida