RD 911: Nutrition-Related Complications after Bariatric Surgery

| June 1, 2017

by Laura Andromalos, MS, RD, CD, CDE

FUNDING: No funding was provided.

DISCLOSURES: The authors report no conflicts of interest relevant to the content of this manuscript.

AUTHOR AFFILIATION: Ms. Andromalos is a Registered Dietitian and Certified Diabetes Educator practicing in Seattle, Washington. She is a Member-at-Large on the American Society for Metabolic and Bariatric Surgery (ASMBS) Integrated Health Executive Council and a member of the Academy of Nutrition and Dietetics’ Evidence Analysis Library workgroup on bariatric surgery.


This article provides an overview of the pathophysiology of the following nutrition-related side effects of bariatric surgery: nausea/vomiting, diarrhea, constipation, gastroesophageal reflux disease, gout, dumping syndrome, reactive hypoglycemia, and kidney stones. The author discusses causes of these complications and reviews evidence-based strategies for their prevention and management.


nutrition, bariatric surgery, complications, nausea/vomiting, diarrhea, constipation, gastroesophageal reflux disease, gout, dumping syndrome, reactive hypoglycemia, kidney stones

Bariatric Times. 2017;14(6):14–17.


Bariatric surgery is the most effective treatment for obesity.[1] However, as with many chronic disease treatments, it can come with side effects. The most popular bariatric surgeries performed in the United States are Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG), both of which alter the upper gastrointestinal tract anatomy. Less common operations include the adjustable gastric band (AGB) and the biliopancreatic diversion with duodenal switch (BPD-DS), the former being the only surgery that does not permanently alter anatomy.[2]

Any surgery that impacts the gastrointestinal tract anatomy could be expected to have nutrition-related side effects. Many of these can be managed through diet intervention, but sometimes medical and surgical intervention is necessary. Clinicians must be prepared to manage the challenges faced by their patients, and it is important to begin with an understanding of the pathophysiology of the complication. This article provides an overview of the pathophysiology of several nutrition-related side effects of bariatric surgery along with strategies for prevention and management. While micronutrient deficiencies are a significant consideration following bariatric surgery, they will not be addressed in this article.


Causes. Nausea and vomiting are the most common complaints after bariatric surgery.[3] One study with self-reported data indicated that 68.6% of RYGB and 65.1% of AGB patients had an episode of vomiting in the first six postoperative months.[4] Reports of nausea and vomiting should prompt the clinician to inquire about eating behaviors.[3],[5] Sarwer et al reported that additional postoperative counseling by a dietitian resulted in fewer incidences of nausea and vomiting four months after surgery, suggesting that eating behaviors were contributing factors.[6] This could entail not chewing thoroughly or eating too quickly as well as progressing to challenging food textures prematurely. The presence of nausea may also indicate dehydration, which is a common complication in the early postoperative period.[5],[7] Other common causes of nausea include lactose intolerance and displeasure with vitamin and mineral supplements.

Management. Taking smaller bites of food or sips of fluid, chewing food thoroughly, and slowing the pace of eating can often alleviate nausea and vomiting.[3],[8] In some cases, a patient may need to avoid a poorly tolerated food until a later date.[5] In the presence of nausea and vomiting, a clinician should assess the patient’s hydration status. If a dehydrated patient is unable to rehydrate on their own, intravenous fluid would be indicated for repletion. In the case of persistent vomiting, thiamin will need to be repleted.9 If nausea and vomiting cannot be traced to a diet factor, or if the nausea is associated with epigastric pain, a clinician should be alerted to the potential for an acute surgical complication requiring further evaluation.[3]


Causes. Diarrhea is caused by a nutrient moving through the digestive tract without being fully digested. In the context of bariatric surgery, this may be food that was not chewed properly or was hastened through the digestive tract with the use of liquid.[10] Other substances that may not be digested properly are lactose and sugar alcohols. Since lactose is digested in the small intestine, one might expect that patients with RYGB and BPD-DS would be more likely to suffer from lactose intolerance following surgery than patients with SG or AGB; however, lactose intolerance has been reported anecdotally after all types of bariatric surgeries. Sugar alcohols, such as malitol, sorbitol, and xylitol, are not digested in the small intestine but are fermented in the large intestine and can have a laxative effect in some people.[11] They are often found as a sugar substitute in micronutrient supplements and protein bars. Diarrhea is a symptom of dumping syndrome, which will be discussed later in this article. Some medications have been implicated in the cause of diarrhea; one that is occasionally used in bariatric patients is ursodiol (Actigall), which treats and prevents the formation of gallstones. Additionally, small intestine bacterial overgrowth (SIBO), which can cause diarrhea, can occur after RYGB in one of the intestinal limbs.[12]

Management. When troubleshooting reports of diarrhea, a clinician should first help the patient to differentiate between loose stools and diarrhea. Bowel movement inconsistency is common in the early weeks and months following surgery and will likely resolve on its own as the diet normalizes. There are two main types of RYGB: proximal (or short limb), which is considered the standard RYGB today, and distal (or long-limb), which decreases the length of the common channel and causes macronutrient malabsorption. Patients with a distal RYGB, whether as a primary surgery or as a revision, should expect frequent, loose bowel movements throughout the day as a result of the shortened intestinal tract.[13] If the patient is truly having diarrhea, a food log can be helpful to identify offending factors such as lactose or sugar alcohols, or eating behaviors such as poor chewing or liquids combined with solid foods. If SIBO is suspected, it can be diagnosed using a breath test and treated with antibiotics.[12]


Causes. Constipation is a result of lack of intestinal motility and/or hard stools. Constipation may begin developing before surgery if the bariatric team is recommending a preoperative diet low in fiber. Some medications commonly prescribed after surgery, such as opioids and proton pump inhibitors, have been associated with constipation. Iron and calcium are two minerals that must be supplemented postoperatively. Iron, in the form of oral ferrous sulfate and ferrous gluconate, is associated with constipation.[14] While there is no evidence linking calcium supplementation to constipation, it has been seen anecdotally. Compounds in coffee, both caffeinated and decaffeinated, increase colonic motility; program requirements eliminating caffeinated beverages after surgery can increase risk of constipation.[15] Chronic dehydration can lead to constipation by hardening the stool. Lack of physical activity has been connected to constipation although the relationship is not totally understood.[11]

Management. As with diarrhea, it is important for clinicians to help patients differentiate between constipation and the normal effects of surgery. The changes to the digestive tract and limited diet will result in infrequent bowel movements, but not necessarily constipation, for most patients in the early postoperative period. Considering that there are many factors putting patients at risk for constipation postoperatively, it is important for clinicians to be proactive. If a patient has a history of constipation, consider use of fiber supplements during the preoperative diet and continue postoperatively until the patient is achieving adequate fiber intake from their diet.[11] Regular coffee drinkers may consider switching to decaffeinated coffee (as opposed to eliminating coffee) to continue stimulation of colonic motility.[15] Hydration is always a priority following bariatric surgery; however, there is not an exact fluid recommendation to prevent constipation. Clinicians should individualize recommendations based on patient report. While there are no specific guidelines for quantity and intensity of physical activity as it relates to constipation, activity should be encouraged as the patient is able. Stool softeners and laxatives are effective in the short-term to assist with both intestinal motility and texture of stools. Some laxatives, such as lactulose and polyethylene glycol, are indicated for short-term use only as they can become less effective with time.[11]

Gastroesophageal Reflux Disease (GERD)

Causes. GERD is characterized by the flow of stomach acid or content into the esophagus, which irritates the esophageal lining. The esophagus and stomach have built-in mechanisms to prevent this from happening; the esophagus serves as a forward-moving pump, the esophageal sphincter as a one-way valve, and the stomach as a reservoir.[16] The failure of any of these components can result in GERD. Bariatric surgery has varying affects on GERD. RYGB typically improves symptoms and is often considered a treatment for GERD.[17],[18] SG and AGB have less consistent results; some studies have demonstrated an improvement in symptoms while others have demonstrated a worsening of symptoms.[17] In the case of the studies suggesting that SG worsens GERD, it is hypothesized that the surgery reduces lower esophageal sphincter pressure, which means the “valve” relaxes. In addition, the stomach, or “reservoir,” is reduced in size and the resulting shape can increase stomach pressure which propels content upwards.[17],[19] Gastric banding has been suggested to improve GERD in the early post-op period but can cause GERD-like symptoms for some patients in the long-term. It is unclear whether this is true GERD or complications related to the band becoming more restrictive with saline fills.[17]

Management. Weight loss is a primary lifestyle treatment for GERD which is one of the reasons that bariatric surgery can alleviate symptoms. There is limited evidence for most diet interventions for GERD. Specific categories, such as high-fat foods, acidic foods, and caffeine-containing beverages, are not consistently shown to cause symptoms. A clinician should help each patient create their own individualized list of triggers as opposed to recommending that patients avoid entire categories of foods and beverages. Limited evidence suggests the avoidance of eating for 2-3 hours before bed may prevent overnight symptoms.[18] Clinicians should assess eating behaviors of the patient, as fast-paced eating and poor chewing may cause GERD-like symptoms.4 The standard, and most effective, treatment for GERD is proton pump inhibitor (PPI) therapy. In some cases of GERD in patients with AGB or SG, conversion to RYGB may be considered.[18]


Causes. Gout is caused by a build-up of urate crystals in response to high levels of uric acid in the blood. Uric acid is produced by the liver and excreted by the kidney and small intestine. Any situation causing overproduction or under-excretion will lead to excess levels of uric acid in the bloodstream. For reasons that are not totally understood, the urate crystals are frequently deposited in the big toe joint which causes inflammation and severe pain. Normal blood levels of uric acid are 3.5 to 7.2 mg/dL; a uric acid level of 7.0 mg/dL is a risk factor for gout.[20] A purine-rich diet can increase production of uric acid by 1-2 mg/dL. [20],[21] Choi et al. published data demonstrating that higher levels of meat (specifically beef, pork, lamb, and turkey) and seafood consumption increase risk of gout by 35-50%. Their data suggests that an average daily consumption of 2.5 servings of beef, pork, or lamb increases risk of gout by 40% compared to an average daily consumption of 0.5 servings. While many vegetables contain purines, moderate intake of vegetable purines were not associated with increased risk of gout.[22] Fructose is another diet factor which contributes to gout; as fructose is metabolized, it leads to an increase in uric acid production. Substances that are converted into fructose after absorption, such as sorbitol, will also contribute to uric acid production. Factors that reduce excretion of uric acid include ketone bodies, insulin resistance, and leptin production. Many bariatric programs require a very low carbohydrate diet before surgery and in the early weeks following surgery. If this diet is low enough in carbohydrates to cause ketone bodies, it can inhibit excretion of uric acid.[20] Some diet factors are protective against gout, such as dairy foods and vitamin C, which facilitate excretion of uric acid and prevent uric acid build-up.[20],[22]

Management. With an understanding of factors that impact uric acid balance, it becomes clear that successful diet interventions will reduce uric acid levels in the blood by limiting production or increasing excretion. Patients can be encouraged to limit consumption of meats and seafood that are high in purines. High-purine vegetables do not need to be limited. Consumption of fructose-rich processed foods and beverages should be avoided. Natural fructose found in fruits can contribute to gout as well; results from one study suggest limiting fructose-rich fruits and juices, such as apple and orange.[23] Increasing carbohydrate intake above 30 grams per day during the preoperative and postoperative diets is encouraged to prevent ketosis.[24] Insulin sensitivity is typically improved with bariatric surgery; additional lifestyle and medication treatments could be considered if a patient continues to struggle with insulin resistance. Supplementing with 500 mg vitamin C daily and encouraging dairy products can assist the body with excreting uric acid.[20],[21]

Dumping Syndrome

Causes. Dumping syndrome is caused by the rapid passage of nutrients to the small intestine and an osmotic fluid shift. This is typically in response to consumption of foods and beverages high in sugar, such as candies, sweet baked goods, ice cream, juices, and soda. When the poorly digested particles of food reach the small intestine, there is a fluid shift from the intravascularcomponent to the intestinal lumen. This triggers gastrointestinal (abdominal pain, nausea, bloating, diarrhea) and vasomotor (perspiration, tachycardia, hypotension) symptoms which begin during or immediately after consumption of the offending food or beverage.[25],[26] Since these symptoms occur quickly after the offending food is consumed, it is sometimes called “early dumping syndrome.” Reactive hypoglycemia, sometimes termed “late dumping syndrome,” is discussed in the next section. While dumping syndrome is most commonly seen in patients with RYGB, there is limited evidence suggesting that dumping syndrome can occur in SG patients as well.[25]

Management. Diet modification is the primary treatment for dumping syndrome. The goal is to prevent nutrients from passing into the intestine too quickly. Patients should avoid foods that contain rapidly absorbable carbohydrates, such as simple sugars, and should wait to drink beverages until at least 30 minutes after meals.[25],[26] Dumping syndrome that cannot be managed by diet modification warrants referral to a surgeon for further work-up.

Reactive Hypoglycemia

Causes. Reactive hypoglycemia is severe postprandial hypoglycemia that can develop months to years after RYGB.[27]. As mentioned previously, it is sometimes called late dumping syndrome as the symptoms tend to occur 1-3 hours after consumption of a carbohydrate-based food. With reactive hypoglycemia, the offending food, often a simple carbohydrate, moves to the small intestine too quickly and triggers the release of incretin hormones GLP-1 and GIP. These hormones stimulate an exaggerated insulin response which leads to hypoglycemia. Hypoglycemic symptoms include sweating, dizziness, rapid heartbeat, blurry vision, and loss of consciousness.[25]

Management. The initial treatment intervention for reactive hypoglycemia is diet modification that delays the passage of nutrients into the intestine to prevent an exaggerated insulin response.[25],[26] Strategies include eating small, frequent meals that contain protein and/or fat, limiting carbohydrates to 15-30 grams per meal while avoiding simple carbohydrates, and avoidance of beverages during and immediately following a meal.[25],[26],[28] There is some evidence supporting the use of pectin, glucomannan and guar gum to prolong transit time through the gastrointestinal tract.[25] If diet modification is unsuccessful, medications such as acarbose may be added to the treatment plan. [25],[29] In extreme cases, revisional surgery may be required.[25]

Kidney Stones

Causes. Kidney stones occur when urine contains more crystal-forming substances than can be diluted and/or urine is lacking the substances required to prevent formation of crystals. While there are several types of kidney stones, calcium oxalate stones are the most common in the general population. Research suggests that patients are at greater risk of calcium kidney stones following bariatric surgery.[30],[31] The majority of the research has been conducted in RYGB patients, but there appears to be an increased risk for patients having had malabsorptive surgeries such as long-limb RYGB and BPD-DS as well.[31] After surgery, the urinary chemistry profile changes significantly with an increase in urinary oxalate and a decrease in urinary citrate. This increases risk for kidney stones because oxalate is a crystal-forming substance and citrate is a stone-inhibitor. There are several theories as to why the urinary chemistry profile is altered following surgery, such as change in gut flora, gastrointestinal tract’s increased permeability to oxalate, metabolic acidosis, and after some surgeries, fat malabsorption. An additional risk factor observed in postoperative bariatric surgery patients is a decrease in urinary volume due to decreased fluid intake; this facilitates crystal-saturated urine.[30]

Management. Several diet interventions can minimize the risk of calcium kidney stones. Increased hydration can help to dilute urine to prevent supersaturation. Supplementation with calcium citrate versus calcium carbonate promotes increased urinary citrate, which can inhibit stone formation. Limiting oxalate-rich foods, such as soy products, nuts, dark green vegetables, chocolate, and coffee, can minimize the amount of oxalate that is entering the body. Supplementation with citric salts, such as potassium citrate, can treat metabolic acidosis.30 This can also be achieved with increased intake of fruits and vegetables and decreased intake of sodium.[32]


While bariatric surgery has the potential for many nutrition-related side effects, most can be effectively managed with diet intervention. This article provides guidance for a clinician managing these challenges, but interventions should always be individualized based on the patient’s unique presentation. Educating the patient on the impact of surgery on the many functions of the body and the pathophysiology of complications can empower the patient to become a troubleshooting partner when challenges arise.


1. Maciejewski ML, Arterburn DE, Van Scoyoc L, et al. Bariatric Surgery and Long-term Durability of Weight Loss. JAMA Surg. 2016;151(11):1046-1055.

2. Estimate of Bariatric Surgery Numbers, 2011-2015. https://asmbs.org/resources/ estimate-of-bariatric-surgery-numbers. Published 2016. Accessed October 10, 2016.

3. Pandolfino JE, Krishnamoorthy B, Lee TJ. Gastrointestinal complications of obesity surgery. Medscape Gen Med. 2004;6(2).

4. Kalarchian MA, Marcus MD, Courcoulas AP, et al. Self-report of gastrointestinal side effects after bariatric surgery. Surg Obes Relat Dis. 2014;10(6):1202–1207.

5. Shikora SA, Kim JJ, Tarnoff ME. Nutrition and gastrointestinal complications of bariatric surgery. Nutr Clin Pract. 2007; 22(1):29–40.

6. Sarwer DB, Moore RH, Spitzer JC, et al. A pilot study investigating the efficacy of postoperative dietary counseling to improve outcomes after bariatric surgery. Surg Obes Relat Dis. 2012; 8(5):561–568.

7. Kellogg TA, Swan T, Leslie DA, et al. Patterns of readmission and reoperation within 90 days after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2009; 5(4):416–423.

8. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient-2013 update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery. Obesity. 2013;21(S1):S1–S27.

9. Isom KA, Andromalos L, Ariagno M, et al. Nutrition and metabolic support recommendations for the bariatric patient. Nutr Clin Pract. 2014;29(6): 718–739.

10. Lee CW, Kelly JJ, Wassef WY. Complications of bariatric surgery. Curr Opin Gastroen. 2007;23(6):1–10.

11. Foxx-Orenstein AE, McNally MA, Odunsi ST. Update on constipation: One treatment does not fit all. Clev Clin J Med. 2008;75(11):813–824.

12. Greenstein AJ, O’Rourke RW. Abdominal pain following gastric bypass: suspects & solutions. Am J Surg. 2012;201(6): 819–827.

13. Potoczna N, Harfmann S, Steffen R, et al. Bowel habits after bariatric surgery. Obes Surg. 2008;18(10):1287–1296.

14. Malinowski SS. Nutritional and metabolic complications of bariatric surgery. Am J Med Sci. 2006;331(4): 219–225.

15. Rao S, Welcher K, Zimmerman B, Stumbo P. Is coffee a colonic stimulant? Eur J Gastroen Hepat. 1999;10(2).

16. Stein H, DeMeester T. Outpatient physiologic testing and surgical management of foregut motility disorders. Curr Prob Surg. 1992; 29(7):413–555.

17. Tack J, Deloose E. Complications of bariatric surgery: Dumping syndrome, reflux and vitamin deficiencies. Best Pract Res Cl Ga. 2014;28(4):741–749.

18. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. 2013;108(3):308–328.

19. Laffin M, Chau J, Gill RS, et al. Sleeve gastrectomy and gastroesophageal reflux disease. J Obes. 2013.

20. de Oliveira EP, Burini RC. High plasma uric acid concentration: causes and consequences. Diabetol Metab Syndr. 2012;4(1):12.

21. Shulten P, Thomas J, Miller M, et al. The role of diet in the management of gout: a comparison of knowledge and attitudes to current evidence. J Hum Nutr Diet. 2009;22:3–12.

22. Choi H, Atkinson K, Karlson E, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093–1103.

23. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. Brit Med J. 2008;336(7639):309–312.

24. Hite AH, Berkowitz VG, Berkowitz K. Low-carbohydrate diet review: shifting the paradigm in clinical practice. Nutr Clin Pract. 2011;26:300–308.

25. Tack J, Arts J, Caenepeel P, et al. Pathophysiology, diagnosis and management of postoperative dumping syndrome. Nat Rev Gastro Hepat. 2009; 6:583–590.

26. Hammer HF. Medical complications of bariatric surgery: Focus on malabsorption and dumping syndrome. Digest Dis. 2012;30:182–186.

27. Singh E, Vella A. Hypoglycemia after gastric bypass surgery. Diabetes Spectr. 2012;25(4):217–221.

28. Botros N, Rijnaarts I, Brandts H, et al. Effect of carbohydrate restriction in patients with hyperinsulinemic hypoglycemia after Roux-en-Y Gastric bypass. Obes Surg. 2014.

29. Ritz P, Vaurs C, Bertrand M, et al. Usefulness of acarbose and dietary modifications to limit glycemic variability following Roux-en-Y Gastric bypass as assessed by continuous glucose monitoring. Diabetes Technol The. 2012;14(8):736–740.

30. Canales B, Gonzalez RD. Kidney stone risk following Roux-en-Y gastric bypass surgery. Transl Androl Urol. 2014; 3(3):243–249.

31. Lieske JC, Mehta RA, Milline DS, et al. Kidney stones are common after bariatric surgery. Kidney Int. 2015; 87(4):839–845.

32. Schwalfenberg GK. The alkaline diet: Is there evidence that an alkaline pH diet benefits health? J Environ Public Health. 2012;2012:727630.

Acknowledgment: This article was originally published by the Weight Management Dietetic Practice Group. Copyright 2017, Weight Management, a dietetic practice group of the Academy of Nutrition and Dietetics. Used with permission.

Category: Current Issue, Nutritional Considerations in the Bariatric Patient

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