Dumping Syndrome 

Updated: Jun 11, 2019
Author: Rajan Kanth, MD; Chief Editor: BS Anand, MD 



Anatomic structures of the stomach are divided into the cardia, fundus, body, and pylorus. The fundus serves as the reservoir for ingested meals, while the distal stomach churns and mixes food with digestive enzymes and initiates the digestive process. Once the foods are processed, the pylorus releases the food in a controlled fashion downstream into the duodenum.

The capacity of the stomach in adults is approximately 1.5-2 liters, and its location in the abdomen allows for considerable distensibility. Gastric motility is controlled by myogenic (intrinsic), circulating hormonal, and neural activity (gastric plexus, myenteric plexus, sympathetic and parasympathetic nerves). Alterations in the gastric anatomy after surgery or interference in its extrinsic innervation (vagotomy) may have profound effects on the gastric reservoir and pyloric sphincter mechanism and, in turn, alter gastric emptying. These effects, for convenience, have been termed postgastrectomy syndromes.

Postgastrectomy syndromes include small capacity, dumping syndrome, bile gastritis, afferent loop syndrome, efferent loop syndrome, anemia, and metabolic bone disease. Postgastrectomy syndromes are iatrogenic conditions that may arise from partial gastrectomies, independent of whether the gastric surgery was initially performed for peptic ulcer disease, cancer, or weight loss (bariatric). The surgical procedures include Billroth-I, Billroth-II, and Roux-en-Y gastric bypass.[1]

Hertz made the association between postprandial symptoms and gastroenterostomy in 1913.[2] Hertz stated that the condition was due to "too rapid drainage of the stomach." Wyllys et al first used the term "dumping" in 1922 after observing radiographically the presence of rapid gastric emptying in patients with vasomotor and GI symptoms.[3]


Dumping syndrome is the effect of altered gastric reservoir function, abnormal postoperative gastric motor function, and/or pyloric emptying mechanism.[4, 5] See the image below.

Pathophysiology of dumping syndrome. Pathophysiology of dumping syndrome.

Clinically significant dumping syndrome occurs in approximately 10% of patients after any type of gastric surgery and in up to 50% of patients after laparoscopic Roux-en-Y gastric bypass. Dumping syndrome has characteristic alimentary and systemic manifestations. It is a frequent complication observed after a variety of gastric surgical procedures, such as vagotomy, pyloroplasty, gastrojejunostomy, and laparoscopic Nissan fundoplication. Dumping syndrome can be separated into early and late forms, depending on the occurrence of symptoms in relation to the time elapsed after a meal.

Postprandially, the function of the body of the stomach is to store food and to allow the initial chemical digestion by acid and proteases before transferring food to the gastric antrum. In the antrum, high-amplitude contractions triturate the solids, reducing the particle size to 1-2 mm. Once solids have been reduced to this desired size, they are able to pass through the pylorus. An intact pylorus prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by the fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters each of these mechanisms in several ways.

Gastric resection reduces the fundic reservoir, thereby reducing the stomach's receptiveness (accommodation) to a meal. Vagotomy increases the gastric tone, similarly limiting accommodation. An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric emptying. Duodenal feedback inhibition of gastric emptying is lost after a bypass procedure, such as gastrojejunostomy. Accelerated gastric emptying of liquids is a characteristic feature and a critical step in the pathogenesis of dumping syndrome. Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of digestion are affected adversely. All these factors interplay in the pathophysiology of dumping syndrome.

The accommodation response and the phasic contractility of the stomach in response to distention are abolished after vagotomy or partial gastric resection.[6] This probably accounts for the immediate transfer of ingested contents into the duodenum.

Early dumping syndrome and reflux gastritis are less frequent when segmented gastrectomy rather than distal gastrectomy is performed for early gastric cancer.[7] In persons with long segment Barrett esophagus treated with a truncal vagotomy, partial gastrectomy, and Roux-en-Y gastrojejunostomy, 41% developed dumping within the first 6 months after surgery, but severe dumping is rare (5% of cases).[8] The dumping syndrome occurs in 45% of persons who are malnourished and who have had a partial or complete gastrectomy.[9]

The late dumping syndrome is suspected in the person who has symptoms of hypoglycemia in the setting of previous gastric surgery, and this late dumping can be proven with an oral glucose tolerance test (hyperinsulinemic hypoglycemia), as well as gastric emptying scintigraphy, which shows the abnormal pattern of initially delayed and then accelerated gastric emptying.[10]

Early dumping

Rapid emptying of gastric contents into the small intestine or colon may result in high amplitude propagated contractions and increased propulsive motility, thereby contributing to the diarrhea seen in persons with the dumping syndrome.[11] The emptying of liquids is fast relative to persons without distal gastrectomy with Billroth-I reconstruction.[12]

Symptoms of early dumping syndrome occur 30-60 minutes after a meal. Symptoms are believed to result from accelerated gastric emptying of hyperosmolar contents into the small bowel. This leads to fluid shifts from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and an increase in the frequency of bowel contractions. Rapid instillation of liquid meals into the small bowel has been shown to induce dumping symptoms in healthy individuals who have not had gastric surgery. Bowel distention may be responsible for GI symptoms, such as crampy abdominal pain, bloating, and diarrhea. Intravascular volume contraction due to osmotic fluid shifts is perhaps responsible for the vasomotor symptoms, such as tachycardia and lightheadedness.

This hypothesis has been questioned for several reasons. First, the severity of dumping is not reliably related to the volume of hypertonic solution ingested. Second, intravenous infusion sufficient to prevent the postprandial fall in plasma volume may not abolish the dumping symptoms. Furthermore, Kalser and Cohen measured intrajejunal osmolarity and glucose content using a continuous perfusion method.[13] They found that the degree of dilution of the hyperosmolar glucose in patients who are postgastrectomy was similar in symptomatic and asymptomatic subjects.

Provocation with oral glucose in patients with early dumping generally provokes an increase in the heart rate. Although vasoconstriction is expected in a volume-contracted state, patients with dumping syndrome have vasodilation.[14] An increase in blood flow to the superior mesenteric artery has been described in patients with dumping syndrome. This peripheral and splanchnic vasodilatory response seems to be pivotal in the pathogenesis of dumping.

In experimentally induced dumping in dogs, symptoms can be induced in a healthy animal by the transfusion of portal vein blood. This led to the hypothesis that humoral factors may have an important role in the pathogenesis of dumping. Some evidence suggests that hyperosmolar small intestine content leads to serotonin release which, in turn, leads to mesenteric and peripheral vasodilation. It results in fluid shifts and hypotension in the early phase of dumping syndrome.

The postprandial release of gut hormones, such as enteroglucagon, peptide YY, pancreatic polypeptide, vasoactive intestinal polypeptide, glucagonlike peptide-1 (GLP-1), and neurotensin, is higher in patients with dumping syndrome compared with asymptomatic patients after gastric surgery. Some or all of these peptides are likely to participate in the pathogenesis of dumping syndrome. Glucagon, GLP-1 and glucose-dependent insulinotropic peptide (GIP) levels were higher in those with Roux-en-Y gastric bypass, as compared with those nonsurgical patients who were overweight or morbidly obese.[15] The exaggerated postprandial GLP-1 release contributes to the symptoms of early dumping by activating sympathetic outflow.[16]

One of the effects of these hormones is the retardation of proximal GI motility and the inhibition of secretion. This function is called the ileal brake. Some authors have suggested that the accelerated release of these hormones is an attempt to activate the ileal brake, thereby delaying proximal transit time in response to the rapid delivery of food to the distal small bowel.

Late dumping

Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early development of hyperinsulinemic (reactive) hypoglycemia.[17, 18] Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose. This is countered by a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia. Intrajejunal glucose induces a higher insulin release than does the intravenous infusion of glucose.[19] The serum glucose levels were the same in both experiments. This effect of enhanced insulin release after an enteral glucose load as compared to intravenous glucose administration is called the incretin effect.

Two hormones are thought to play a pivotal role in the incretin effect. These are glucose-dependent insulinotropic peptide and GLP-1. In human studies, an increase in GLP-1 response has been noted after an oral glucose challenge. An increased GLP-1 response has been noted in patients after total gastrectomy, esophageal resection, and partial gastrectomy. Furthermore, a positive correlation was found between the rise in plasma GLP-1 and insulin release.

An exaggerated GLP-1 response likely plays an important role in the hyperinsulinemia and hypoglycemia in patients with late dumping. The reason why some patients remain asymptomatic after gastric surgery whereas others develop severe symptoms remains elusive.


Dumping can be separated into early and late forms depending on the occurrence of symptoms in relation to the time elapsed after a meal. Both forms occur because of the rapid delivery of large amounts of osmotically active solids and liquids to the duodenum. This is a direct result of alterations in the storage function of the stomach and/or pyloric emptying mechanism.

The severity of dumping syndrome is proportional to the rate of gastric emptying. Postprandially, the stomach assumes its reservoir function to allow initial chemical digestion by acid and proteases before transferring food to the antrum. In the antrum, high-amplitude contractions triturate solids. Once solids have been reduced to 1-2 mm, they are able to empty through the pylorus. An intact pylorus has a separating function that prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters these mechanisms in several ways.

Gastric resection can reduce the fundic reservoir, thereby reducing the receptiveness of the stomach to a meal. Similarly, vagotomy increases gastric tone, limiting accommodation.

Any operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric emptying. Duodenal feedback inhibition of gastric emptying is also lost after bypass of the duodenum with gastrojejunostomy. Accelerated early gastric emptying of liquids is a characteristic feature and a critical step in the pathogenesis of dumping syndrome.

Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of digestion are adversely affected.


The global incidence and severity of symptoms in dumping syndrome are related directly to the extent of gastric surgery.[5, 20] ​[21]

United States data

An estimated 20-50% of all patients who have undergone gastric surgery have some symptoms of dumping.[21] However, only 1-5% are reported to have severe disabling symptoms.[21] The incidence of significant dumping has been reported to be 6-14% in patients after truncal vagotomy and drainage and from 14-20% after partial gastrectomy. The incidence of dumping syndrome after proximal gastric vagotomy without any drainage procedure is less than 2%. Newer gastric operations, such as proximal gastric vagotomy (which produces minimal disturbance of gastric emptying mechanisms), are associated with a much lower incidence of postgastrectomy syndromes. In the pediatric population, dumping syndrome is described almost exclusively in children who have undergone Nissen fundoplication.[22]

Reductions in the need for elective gastric surgery have led to a decline in the frequency of postgastrectomy syndromes. A 10-fold reduction has occurred in elective operations for peptic ulcer disease in the last 20-30 years. Although this trend preceded the advent of histamine-2 receptor antagonists, these drugs and proton pump inhibitors have accelerated the decline. Helicobacter pylori treatment and eradication in patients with peptic ulcer disease have further decreased the need for surgery.

Although the need for elective surgery for peptic ulcer disease has declined, the need for emergency surgery has remained the same over the last 20 years. Emergency surgery tends to be more mutilating to the stomach. This increases the incidence of more severe symptoms.

Gastric surgery is also performed as part of the care of persons with a gastric malignancy, or as an approach to weight loss (bariatric surgery). Bariatric surgery is the only satisfactory long-term treatment for severe obesity (body mass index [BMI] 40 kg/m² or greater, or 35 kg/m² or greater with severe obesity-associated comorbidities, such as diabetes, obstructive sleep apnea, or debilitating degenerative arthritis). Even in specialized units, the mortality rate of bariatric surgery may be 1%, and serious complications may occur in about 10% of cases.[23]

Some 80% of the deaths that occur within a month of bariatric surgery arise from anastomotic leaks, pulmonary emboli, and respiratory failure. Other authors report that long-acting octreotide is as effective in the long term as subcutaneous octreotide, with superior symptom control as assessed by the Gastrointestinal Specific Quality of Life Index, better maintenance of body weight, and higher quality of life.[24] Pancreatic nesidioblastosis or pancreatic islet cell hyperplasia has been speculated to contribute to the sometimes disabling neurologic immune restoration inflammatory syndrome (NIRIS). Resection of this hyperplasia -- and therefore removing the exaggerated insulin response -- has been proposed.

Sex-related demographics

A female preponderance exists in the incidence of postgastrectomy syndromes.




The clinical presentation of dumping syndrome can be divided into GI symptoms and vasomotor symptoms.[20] GI symptoms include early satiety, crampy abdominal pain, nausea, vomiting, and explosive diarrhea. Vasomotor symptoms include diaphoresis, flushing, dizziness, palpitations, and an intense desire to lie down.

The expression of these symptoms varies in different individuals. Most patients with early dumping have both GI and vasomotor symptoms, while patients with late dumping have mostly vasomotor symptoms. Patients with severe dumping often limit their food intake to avoid symptoms. This leads to weight loss and, over time, malnutrition.

Early dumping syndrome generally occurs within 15 minutes of ingesting a meal and is attributable to the rapid transit of food into the small intestine, whereas late dumping syndrome occurs later and may be attributed to hypoglycemia with tremors, cold sweats, difficulty in concentrating, and loss of consciousness.[21]

Early dumping systemic symptoms are as follows:

  • Desire to lie down

  • Palpitations

  • Fatigue

  • Faintness

  • Syncope

  • Diaphoresis

  • Headache

  • Flushing

Early dumping abdominal symptoms are as follows:

  • Epigastric fullness

  • Diarrhea

  • Nausea

  • Abdominal cramps

  • Borborygmi

Late dumping symptoms are as follows:

  • Perspiration

  • Shakiness

  • Difficulty to concentrate

  • Decreased consciousness

  • Hunger

Physical Examination

Dumping syndrome is diagnosed based on typical symptoms in patients who have undergone gastric surgery. Typical signs and symptoms can be elicited with an oral glucose challenge of 50 g. Sigstad developed a diagnostic scoring system on weighing factors allocated to the symptoms of dumping. A diagnostic index greater than 7 is suggestive of dumping syndrome.

Sigstad's diagnostic index, indicating symptoms and the points assigned for those symptoms, is as follows:

  • Shock: +5

  • Almost fainting, syncope, unconsciousness: +4

  • Desire to lie or sit down: +4

  • Breathlessness, dyspnea: +3

  • Weakness, exhaustion: +3

  • Sleepiness, drowsiness, yawning, apathy, falling asleep: +3

  • Palpitation: +3

  • Restlessness: +2

  • Dizziness: +2

  • Headaches: +1

  • Feeling of warmth, sweating, pallor, clammy skin: +1

  • Nausea: +1

  • Fullness in the abdomen, meteorism (distention because of gas): +1

  • Borborygmus: +1

  • Eructation: -1

  • Vomiting: -4

The Visick classification is also used to characterize the severity of symptoms after gastric surgery. A rise in the heart rate by 10 beats per minute or more in the first hour after an oral glucose challenge of 50 g was found to be 100% sensitive and 92% specific for early dumping.

A self-assessment questionnaire, the Dumping Symptom Rating Scale (DSRS) has also been used to identify patients with pronounced dumping symptoms after 6 months to 1 year after surgery.[25]



Approach Considerations

Note the following:

  • Signs and symptoms can be elicited with the glucose challenge test (50 g oral glucose).

  • A positive result from a hydrogen breath test after ingestion of glucose is also 100% sensitive.

  • A gastric emptying study may be helpful to document rapid gastric emptying.

  • An endoscopy or a barium study can be helpful in discerning the anatomy.



Medical Care


The use of acarbose, an alpha-glycoside hydrolase inhibitor, interferes with carbohydrate absorption and thus may decrease the time delay between hyperglycemia and insulin response. This may lead to coinciding the peak of glucose and insulin levels and thus prevent hypoglycemic symptoms in patients with late dumping. Imhof et al showed that acarbose produced a 5-fold decrease in postprandial glucagon-like peptide 1 levels which, in turn, may lead to a decrease in insulin release.[26]

Acarbose use may be limited by the occurrence of diarrhea secondary to fermentation of unabsorbed carbohydrates as manifested by increased breath hydrogen excretion and symptoms such as flatulence.

Acarbose delays production of monosaccharides by inhibiting alpha-glucosidases associated with the brush border of the intestine. These enzymes are responsible for the digestion of complex polysaccharides and sucrose.

In healthy individuals, acarbose in doses of 100-200 mg significantly blunts the postprandial rise in glucose, insulin, and triglycerides. Acarbose has been shown to significantly lower postprandial blood glucose levels.


Somatostatin and its synthetic analogue octreotide (Sandostatin, SMS 201-995) have been used with short-term success in patients with dumping syndrome, but the long-term efficacy of octreotide is much less favorable. They exert a strong inhibitory effect on the release of insulin and several gut-derived hormones.

In patients with dumping syndrome, octreotide likely decreases gastric emptying by resetting the migrating motor complex to the fasting level.

The effectiveness of octreotide in controlling the symptoms of both early and late dumping has been demonstrated in several randomized control trials.

The mechanisms of action of octreotide in dumping syndrome are as follows:

  • Delay in the accelerated initial gastric emptying

  • Delay in small intestinal transit time

  • Inhibition of enteral hormone release

  • Induction of a fasting intestinal pattern

  • Inhibition of insulin release

  • Splanchnic vasoconstriction

  • Inhibition of postprandial vasodilation

The usual initial dose of octreotide is 50 mcg administered subcutaneously bid/tid 30 minutes prior to each meal. The dose may be increased if smaller doses are not effective; however, higher doses are seldom effective if the smaller doses do not work.

Octreotide improves the symptoms in about 90% of patients with severe dumping refractory to other forms of medical interventions.

In all studies, octreotide in the short term decreased the symptom score, pulse rate, and plasma insulin levels when compared with placebo. However, whether long-term octreotide use is as beneficial as short-term use is unclear. Reports on the long-term use of octreotide are scarce, and the number of patients in these reports is small.

During octreotide treatment, fecal fat excretion increases significantly. Despite this increase in steatorrhea, an increase in mean body weight is reported. This probably occurs because of increased energy intake as patients are able to tolerate more food.

Octreotide appears to be safe in the long-term management of refractory dumping syndrome; however, the occurrence of diarrhea in patients who already have malabsorption and maldigestion may be a major limiting factor.

Depot long-acting release octreotide (Sandostatin-LAR), as compared with octreotide, resulted in a significantly greater improvement in GI-specific quality-of-life index and body weight gain.[24, 27] However, the effect of octreotide on late dumping symptoms was superior to the effect of long-acting octreotide.[28]

Although the results of long-term use of octreotide injections are less dramatic than short-term use, nonetheless, symptoms are reduced by about 50%.[29] Other authors report that long-acting octreotide is as effective long term as subcutaneous octreotide, with superior symptom control as assessed by the Gastrointestinal Specific Quality of Life Index, better maintenance of body weight, and higher quality of life.[24]

The addition of verapamil may also be considered.[30] Although there is enthusiasm for the use of electrical stimulation of the small intestine to achieve gastrointestinal pacing as a treatment of dumping syndrome,[31] there are no placebo-controlled trials, thus, possible placebo effects cannot be excluded.

Surgical Care

Preventing dumping syndrome is preferable to treating its symptoms. Consider anatomic factors that relate to the syndrome, and, if possible, determine the exact type of surgical procedure needed. Numerous alimentary reconstruction methods have been proposed to treat the dumping syndrome.[32] Proximal gastric vagotomy is now the procedure of choice for the surgical management of intractable ulcer disease. Although the long-term ulcer recurrence rate is higher after this procedure compared with antrectomy and truncal vagotomy, it has the lowest incidence of postoperative dumping and diarrhea. If more extensive surgery is necessary, resection is preferable to a Roux-en-Y gastrojejunostomy, because it decreases the rate of dumping syndrome compared with pyloroplasty or loop gastrojejunostomy.

Remedial surgery can be considered in patients whose condition is refractory to medical treatment or in patients unwilling to continue medical therapy. Patients should be approached conservatively, because most patients improve with time and remedial surgery is not always effective.

Several surgical procedures have been designed to rectify the symptoms of dumping. These include surgical narrowing of the gastrojejunal stoma, conversion of Billroth II anastomosis to Billroth I gastroduodenostomy, jejunal interposition, conversion to Roux-en-Y gastrojejunostomy, and pyloric reconstruction. No long-term studies have assessed the effectiveness of these procedures. Furthermore, no controlled trials have examined the efficacy of one procedure compared to the other.

For early gastric cancer, the postoperative outcome is better in those having a pylorus-preserving gastrectomy.[33] Unfortunately, about one quarter of patients undergoing a pylorus-preserving gastrectomy may have sufficiently symptomatic delayed gastric emptying that the quality of their life may be adversely affected.[34]

Stomal revision

One strategy for surgical correction of the pathophysiology of dumping is to slow gastric emptying.

Porter and Claman reported good results by narrowing the gastrojejunal stoma.[35]

Determining the exact size of the stomal reconstruction is difficult.

Stomal strictures with gastric outlet obstruction are common adverse effects of the operation.

This technique has been abandoned in favor of other procedures.

Conversion of Billroth II to Billroth I anastomoses

Conversion of a Billroth II to a Billroth I gastroduodenostomy improves dumping syndrome in 75% of patients.[36]

This procedure restores the physiologic delivery of the meal to the duodenum, without the risk of gastric outlet obstruction.

Overall, the procedure is useful because of its simplicity and low rate of complications.

Pyloric reconstruction

In this procedure, the pyloroplasty scar is identified and is cut along its length. The sphincter muscle is identified and approximated. The incision is then closed longitudinally.

In a series of 14 patients reported by Koruth et al, 9 showed excellent results, whereas another 3 had good resolution of their dumping symptoms.[37]

Cheadle and coworkers reported a series of 9 patients, 8 of whom had excellent results.[38]

Taki et al reported significantly improved gastric emptying in 24 patients with pylorus-reconstruction gastrectomy compared to 26 patients with conventional Billroth-I reconstruction.[39]

This procedure is low-risk and seems to be fairly effective in patients who have severe dumping after pyloroplasty.

Jejunal interposition

Schoemaker is credited with the first attempt at interposing an isoperistaltic jejunal loop after gastric surgery.

Henley has reported extensive use of an interposed jejunal segment between the gastric pouch and the duodenum for correction of postgastrectomy dumping in more than 300 patients.[40] In his series, all patients improved, including those with early postprandial dumping. However, other smaller series have failed to show such excellent results with the use of isoperistaltic interposition.

Sawyers and Herrington had only a 20% satisfactory result in 10 patients with isoperistaltic jejunal segments.[41]  However, in an 11-year experience using antiperistaltic jejunal loops in 28 patients, they reported excellent results in 20 patients and good results in another 6 patients. In their experience, a 10-cm reversed jejunal segment effectively prolongs the gastric emptying time without obstruction.

Unsuccessful results with interposition of 6 cm of reversed jejunal segments have been reported, whereas good results have been reported with 10-cm segments.

Using longer lengths of jejunum has resulted in ulcerations and stenosis in the interposed segment. Care should be taken to rotate the interposed segment no greater than 180° to avoid undue torsion on the mesentery. Mesenteric defects should be carefully repaired to avoid internal herniation.

Reversed segments have been shown to be effective for as long as 10 years after interposition.

Double iso-antiperistaltic jejunal limb pouches have also been used, but their efficacy is inferior to the antiperistaltic loop interposition.

Roux-en-Y conversion

Conversion to a Roux-en-Y gastrojejunostomy as a remedial operation has gained favor relatively recently. With this operation, favorable outcomes have been reported in 85-90% of patients. Of patients with dumping symptoms after Billroth I and II gastrectomy, 85-90% have favorable outcomes with Roux-en-Y conversion.

Vogel et al reported 19 of 22 patients with favorable outcomes with this operation.[42] Of the 3 failures, 1 had persistent dumping syndrome, whereas the other 2 patients had Roux stasis syndrome.

The mechanism by which this conversion works in providing relief from dumping is unknown, but it may be due to interruption of the migration motor complex, diminished jejunal contractions, and retrograde jejunal contractions.

This procedure is easier to perform and has fewer long-term adverse effects.

Bariatric surgery[43]

Hyperinsulinemic hypoglycemia with neuroglycopenia (shortage of glucose in the brain) is an increasingly recognized complication of Roux-en-Y gastric bypass due to the changes in gut hormonal milieu.[44] Management includes strict low carbohydrate diet, followed by pharmacotherapy.

The dumping syndrome that occurs after gastric bypass surgery is not due to an increase in pancreatic beta cell formation or mass; instead, it is due to the hypersensitivity of the postprandial insulin response.[41] This inappropriately increased insulin secretion may be due to excessively high incretin levels, or to "…a failure to adequately decrease insulin secretion…."[41]

Within 30 minutes after a high-carbohydrate meal, 12 of 14 patients were shown-to develop hyperglycemia and hyperinsulinemia (noninsulinoma, pancreatogenous hypoglycemic syndrome [NIPHS]) some 30 minutes after a test meal, whereas this and the associated symptoms did not occur with a low-carbohydrate diet.[45]

Dietary considerations are important after bariatric surgery, and the patient’s diet may need to be specifically formulated to deal with symptoms such as dumping, altered bowel habit, nausea and vomiting, dehydration, food intolerance, and overeating.[46]

Diffuse islet cell hyperplasia and expansion of the beta cell mass have been described in 3 patients with severe postprandial hyperglycemia and hyperinsulinemia unresponsive to diet, octreotide, and diazoxide.

Laparoscopic conversion

Laparoscopic conversion of laparoscopic Roux-en-Y gastric bypass to laparoscopic sleeve gastrectomy, biliopancreatic diversion with duodenal switch, or original anatomy has been tried recently as a feasible and safe option for cases refractory to medical treatment.[47, 48, 49] However, 33-40% of patients after laparoscopic sleeve gastrectomy may still have symptoms of dumping syndrome 6-12 months after surgery. In these cases, symptoms include both early and late dumping symptoms, but there is progressive increase in late symptoms.[50]

Experimental procedures

Because no operation for intractable dumping is uniformly successful, new approaches have been considered

In dogs prepared with truncal vagotomy, distal gastrectomy, and Roux-en-Y reconstruction, retrograde electrical pacing of the Roux-en-Y reconstruction significantly delayed gastric emptying and absorption of a glucose meal and decreased postcibal hemoconcentration.

Summary of remedial operations

For patients with prior pyloroplasty, pyloric reconstruction should be the initial remedial operation.

For patients with Billroth I and Billroth II gastrectomies, Roux-en-Y reconstruction is the simplest and most effective therapy.

For patients who already have a Roux-en-Y reconstruction, a 10-cm antiperistaltic jejunal loop should be interposed.


Dumping syndrome is a common postsurgical complication after gastric surgery. The symptoms of dumping produce considerable morbidity. Fortunately, the indications for gastric surgery are declining, although the need for gastric surgery in emergency cases has not changed.

Initially, patients with this condition should be treated medically with dietary modifications and octreotide. Close attention should be given to the patient's nutritional status. If medical management fails to provide adequate symptom relief, remedial surgery should be offered with the understanding that even surgical intervention may not be successful.


Dietary prohibitions and instructions are very important in the management of dumping syndrome. Note the following:

  • Daily energy intake is divided into 6 meals.

  • Fluid intake during and with meals is restricted. Avoiding liquids for at least half an hour after a meal is helpful.

  • Simple sugars are best avoided.

  • Milk and milk products are generally not tolerated and should be avoided.

  • Because carbohydrate intake is restricted, protein and fat intake should be increased to fulfill the energy needs.

  • Most patients have relatively mild symptoms and respond well to dietary manipulations. In some patients with postprandial hypotension, lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return, thereby minimizing the chances of syncope.

  • Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of the bowel transit time.

  • This dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping.[51, 52] This is preferential to a subtotal or total pancreatectomy in those persons with severe symptoms.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Hypoglycemic agents

Class Summary

Shown to be helpful for late dumping.

Acarbose (Precose, Prandase)

Lowers blood sugar by delaying GI absorption of carbohydrates. Decreases postprandial hyperglycemia.

Antisecretory agents

Class Summary

These agents may improve morbidity.

Octreotide (Somatostatin)

Acts primarily on somatostatin receptor subtypes II and V. Inhibits growth hormone secretion and has a multitude of other endocrine and nonendocrine effects, including inhibition of insulin, glucagon, VIP, and GI peptides.


Questions & Answers


What is dumping syndrome?

What is the pathophysiology of dumping syndrome?

What is the pathophysiology of early dumping syndrome?

What is the pathophysiology of late dumping syndrome?

What causes dumping syndrome?

What is the global incidence of dumping syndrome?

What is the prevalence of dumping syndrome in the US?

What are sexual predilections of dumping syndrome?


Which clinical history findings are characteristic of dumping syndrome?

What are early symptoms of dumping syndrome?

What are late symptoms of dumping syndrome?

What is Sigstad's diagnostic index for dumping syndrome?

How is dumping syndrome diagnosed?

What is the Visick classification and how is it used in the evaluation of dumping syndrome?


Which tests are performed in the workup of dumping syndrome?


What is the role of acarbose in the treatment of dumping syndrome?

What is the role of octreotide in the treatment of dumping syndrome?

What are the mechanisms of action of octreotide in the treatment of dumping syndrome?

How is octreotide administered in the treatment of dumping syndrome?

What is the role of surgery in the treatment of dumping syndrome?

What is the role of stomal revision in the treatment of dumping syndrome?

What is the role of conversion of Billroth II to Billroth I gastroduodenostomy in the treatment of dumping syndrome?

What is the role of pyloric reconstruction in the treatment of dumping syndrome?

What is the role of jejunal interposition in the treatment of dumping syndrome?

What is the role of Roux-en-Y conversion in the treatment of dumping syndrome?

What is the role of bariatric surgery in the treatment of dumping syndrome?

What is the role of conversion of Roux-en-Y gastric bypass to sleeve gastrectomy in the treatment of dumping syndrome?

Which experimental procedures have been investigated for the treatment for dumping syndrome?

When are remedial operations indicated in the treatment of dumping syndrome?

Which dietary modifications are used in the treatment of dumping syndrome?


What is the goal of drug treatment for dumping syndrome?

Which medications in the drug class Antisecretory agents are used in the treatment of Dumping Syndrome?

Which medications in the drug class Hypoglycemic agents are used in the treatment of Dumping Syndrome?