Review

Continuing Medical EducationNature Reviews Gastroenterology and Hepatology 6, 583-590 (October 2009) | doi:10.1038/nrgastro.2009.148

Subject Categories: Motility | Surgery

Pathophysiology, diagnosis and management of postoperative dumping syndrome

Jan Tack1, Joris Arts1, Philip Caenepeel1, Dominiek De Wulf1 & Raf Bisschops1  About the authors

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Learning objectives

Upon completion of this activity, participants should be able to:

  1. Describe the main causes of postoperative dumping syndrome.
  2. Describe differences between early and late dumping in postoperative dumping syndrome.
  3. Describe Sigstad's diagnostic scoring system for dumping syndrome.
  4. Describe dietary approaches to managing postoperative dumping syndrome.
  5. Describe treatment approaches to postoperative dumping syndrome.

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Dumping syndrome is a frequent complication of esophageal, gastric or bariatric surgery. Rapid gastric emptying, with the delivery to the small intestine of a significant proportion of solid food as large particles that are difficult to digest, is a key event in the pathogenesis of this syndrome. This occurrence causes a shift of fluid from the intravascular component to the intestinal lumen, which results in cardiovascular symptoms, release of several gastrointestinal and pancreatic hormones and late postprandial hypoglycemia. Early dumping symptoms comprise both gastrointestinal and vasomotor symptoms. Late dumping symptoms are the result of reactive hypoglycemia. Besides the assessment of clinical alertness and endoscopic or radiological imaging, a modified oral glucose tolerance test might help to establish a diagnosis. The first step in treating dumping syndrome is the introduction of dietary measures. Acarbose can be added to these measures for patients with hypoglycemia, whereas several studies advocate guar gum or pectin to slow gastric emptying. Somatostatin analogs are the most effective medical therapy for dumping syndrome, and a slow-release preparation is the treatment of choice. In patients with treatment-refractory dumping syndrome, surgical reintervention or continuous enteral feeding can be considered, but the outcomes of such approaches are variable.

Key points

  • Dumping syndrome is a common complication of esophageal and gastric (including bariatric) surgery
  • Symptoms include early (gastrointestinal and vasomotor) and late (hypoglycemia) symptoms
  • Diagnosis is based on a suggestive symptom pattern in patients with the appropriate surgical history; a modified oral glucose tolerance test might help to establish the diagnosis
  • Initial therapy should focus on dietary measures; acarbose can be added to these measures in patients with hypoglycemia
  • In patients who have not responded to initial therapy, (slow-release) somatostatin analogs are the treatment of choice
  • In patients with treatment-refractory dumping syndrome, surgical reinterventions or continuous enteral feeding can be considered, but the outcomes of such approaches are variable

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Introduction

The stomach carries out an important role in digestion, not only through the secretion of hormones and digestive enzymes and its mechanical action on ingested food, but also by its role in the timed release of ingested nutrients into the duodenum. The 'accommodation reflex' involves a reduction in gastric tone and an increase in gastric compliance in response to food intake, which enables an increase in fundic volume without an accompanying rise in intragastric pressure.1 This reflex provides a means of temporarily storing ingested food before its controlled release into the intestine. Gastric accommodation is controlled by a vago–vagal reflex pathway that induces activation of inhibitory motor neurons in the proximal stomach.2 However, smooth muscle contractions in the antrum gradually break down large food particles to 1–2 mm fragments, the size at which they can pass through the pylorus into the duodenum. Abnormalcies in the coordination of gastric storage and emptying processes lead to impaired food processing and symptoms that are worsened by further food intake.2, 3

Dumping syndrome refers to symptoms and signs that occur when food reaches the small bowel too rapidly; the condition commonly occurs after partial or total gastrectomy, for reasons that are outlined below. Dumping syndrome can also occur after esophageal surgery and, exceptionally, in the absence of previous surgery. Dumping syndrome was first described by Hertz in 1913, who reported the occurrence of 'dumping-like' symptoms after gastroenterostomy.4 He reported that patients felt excessively full after meals, had diarrhea and needed to lie down because they felt unwell. Radiographic examination revealed very rapid emptying of contrast dye from the stomach. Rapid emptying of liquids from the stomach is an important contributor to the pathogenesis of dumping syndrome.5 Studies conducted in the 1980s demonstrated that a defect in grinding or sieving within the stomach, which resulted in the delivery of a considerable proportion of solid food as large, less easily digested particles to the small intestine (rather than rapid emptying itself), was a key event in the pathogenesis of dumping syndrome.5, 6

Dumping syndrome is now a well-established complication of gastric and esophageal surgery. The condition has been estimated to occur in up to 20% of patients who undergo vagotomy with pyloroplasty and in up to 50% of patients who undergo esophagectomy.7, 8 Dumping syndrome has also been reported after Nissen fundoplication in children and adults.9, 10 In recent years, bariatric surgery has become the principal cause of postoperative dumping syndrome.11

With an increasing number of patients undergoing bariatric surgery, the incidence of dumping syndrome is likely to increase, and clinicians should recognize the syndrome and be familiar with its management. In this Review, we summarize the diagnosis, pathophysiological basis and management options for postoperative dumping syndrome.

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Symptoms

The symptom profile of patients with dumping syndrome is summarized in Box 1. Symptoms of dumping syndrome can be classed as early or late, depending on how soon after ingestion they occur. Early symptoms comprise both gastrointestinal and vasomotor symptoms. Gastrointestinal symptoms include abdominal pain, diarrhea, borborygmi, nausea and bloating. Vasomotor symptoms include fatigue, a desire to lie down after meals, facial flushing, palpitations, perspiration tachycardia, hypotension and syncope. Late dumping symptoms include hypoglycemia, perspiration, palpitations, hunger, fatigue, confusion, aggression, tremor and syncope. Both early and late dumping symptoms are socially and professionally incapacitating, especially when syncope occurs.

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Diagnosis

A suggestive symptom pattern in a patient who has undergone upper abdominal surgery should give cause to investigate the possibility of dumping syndrome. In 1970, Sigstad proposed a scoring system, based on the occurrence of different symptoms of dumping syndrome, to calculate a diagnostic index (Box 2).12 The presence of hypoglycemia concurrently with several other symptoms is a strong indicator of dumping syndrome (although the occurrence of insulinoma needs to be excluded).

A provocative test for assessing dumping syndrome can be used to confirm clinical suspicion. This test is a modification of the oral glucose tolerance test and involves the ingestion of 50 g or 75 g glucose in solution after an overnight fast. Immediately before and up to 180 min after ingestion of this solution, the blood glucose concentration, hematocrit, pulse rate and blood pressure are measured at 30 min intervals. The provocative test is considered positive if late (120–180 min) hypoglycemia occurs, or if an early (30 min) increase in hematocrit of more than 3% occurs. The best predictor of dumping syndrome seems to be a rise in the pulse rate of more than 10 bpm after 30 min.13

Assessments of the speed of gastric emptying might show that this process occurs rapidly in patients with dumping syndrome—especially for liquid nutrients—but this test does not seem to have good diagnostic sensitivity or specificity, probably because rapid emptying occurs early after meal ingestion, a phase that is not analyzed closely or separately in most protocols of gastric emptying testing.7, 13, 14

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Pathophysiological mechanisms

The mechanisms that underlie dumping syndrome are not completely understood. The symptoms of early and late dumping syndrome are believed to have distinct underlying pathophysiologies (Figure 1).2, 5, 6, 7, 15

Figure 1 | Pathophysiology of dumping syndrome and mode of action of different therapeutic agents.
Figure 1 : Pathophysiology of dumping syndrome and mode of action of different therapeutic agents. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.comThe key event in the pathophysiology of dumping syndrome is the rapid delivery of nutrients into the duodenum. The presence of hyperosmolar contents in the duodenum induces the release of a number of vasoactive agents, incretins and glucose modulators, which cause early dumping symptoms. The rapid absorption of glucose induces a hyperinsulinemic response, which leads to the late dumping symptoms of hypoglycemia. The mode of action of octreotide, diazoxide, viscosity-increasing agents and acarbose is shown. Abbreviations: GIP, glucose-dependent insulinotropic polypeptide (also known as gastic inhibitory polypeptide); GLP-1, glucagon-like peptide 1; VIP, vasoactive intestinal peptide.

Early dumping

After partial gastrectomy, vagotomy and related surgeries, gastric volume is reduced. This decreased capacity causes the rapid passage of nutrients to the small intestine, which induces a cascade of pathophysiological events. The arrival of hyperosmolar contents to the duodenum causes fluid to move from the intravascular component to the intestinal lumen.16 This movement might lead to a decrease in the volume of circulating fluid, tachycardia and, rarely, syncope. The fluid shift into the duodenum might also cause duodenal distention, followed by cramp-like contractions. However, whether this fluid shift has any role in dumping syndrome or is a consequence of it is a matter of controversy, as intravenous fluid substitution is unable to prevent early dumping symptoms.16

Another important mechanism that contributes to the pathogenesis of early dumping might be the increased release of several gastrointestinal peptide hormones, such as enteroglucagon, peptide YY, pancreatic polypeptide, vasoactive intestinal polypeptide, glucagon-like peptide 1 and neurotensin, in postoperative dumping syndrome.2, 6, 15 These hormones' mode of action might include changes in gastrointestinal motility and secretion, as well as hemodynamic effects—for example, systemic hemoconcentration and hypotension occur as a result of splanchnic vasodilation induced by neurotensin or vasoactive intestinal polypeptide.17

Late dumping

Late dumping symptoms occur 1–3 h after ingestion of a meal and are attributed to reactive hypoglycemia. Under 'normal' conditions, the presence of glucose in the jejunum is a strong stimulus for insulin secretion; the rapid delivery of carbohydrates to the small intestine in dumping syndrome, therefore, causes excessive insulin secretion that subsequently results in hypoglycemia.18 One of the mediators implicated in this late hypoglycemic effect is glucagon-like peptide 1.19

However, not all cases of postprandial hypoglycemia are attributable to dumping syndrome. Several patients were reported to suffer from hyperinsulinemic hypoglycemia with nesidioblastosis after gastric bypass surgery; these patients were characterized by severely symptomatic postprandial hypoglycemias and hyperinsulinemias that did not respond to treatment for dumping syndrome. These patients were subsequently found to have pancreatic islet cell hyperplasia or nesidioblastosis on analysis of resected pancreatic specimens.20, 21 Diagnosis of this syndrome, which is cumbersome, might involve selective stimulation of the celiac artery by use of calcium as an insulin secretagogue with subsequent sampling of insulin levels from hepatic venous serum (after insulinoma has been ruled out) as well as pancreatic debulking and confirmation of islet cell hyperplasia on a resected specimen.20, 21 Hormonal changes after Roux-en-Y gastric bypass surgery, including increased release of glucagon-like peptide 1 (which increases the mass of beta cells in rodents), might cause hyperplasia of islet cells. A study has, however, challenged this theory: the findings showed that the beta-cell mass in patients with hyperinsulinemic hypoglycemia after gastric bypass surgery was comparable to that in BMI-matched control individuals.22

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Treatment of dumping syndrome

The first step in treating dumping syndrome is the introduction of dietary measures. If this approach is insufficient, medical therapy and (in some cases) surgery, might be considered (Figure 2). Evidence of the efficacy of several of these therapies is limited, as most studies involve only a few patients and are not controlled.

Figure 2 | Proposed treatment algorithm for dumping syndrome.
Figure 2 : Proposed treatment algorithm for dumping syndrome. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.comThis algorithm for the management of patients with dumping syndrome is used at the Neurogastroenterology and Motility Clinic of the University Hospitals in Leuven, Belgium. In case of clinical suspicion, we use a modified oral glucose tolerance test to help establish the diagnosis. Our initial therapy is based on dietary measures for 3–4 weeks, plus acarbose treatment in patients who have hypoglycemia. In patients who fail to respond to this initial therapy, slow-release octreotide is used. In patients with treatment-refractory dumping syndrome, surgical reintervention or continuous enteral feeding can be considered, but the outcomes of such approaches are variable. Abbreviations: i.m., intramuscular; LAR, long-acting repeatable.

Dietary measures

Dietary measures are the first approach to manage dumping syndrome and are probably helpful for the majority of patients.7, 11, 23, 24, 25 Dietary measures include advising patients to consume smaller amounts in one go by dividing the recommended daily energy intake between six meals. Patients are also advised to delay any liquid intake until at least 30 min after a meal. All rapidly absorbable carbohydrates (for example, all sweet or sweetened foods) should be eliminated from the diet to prevent late dumping symptoms. Lying down for 30 min after meals can prolong gastric emptying and help to reduce the symptoms of hypovolemia.

Pectin and guar gum

Increasing the viscosity of food, which slows down gastric emptying, is another approach to improve dumping symptoms (Table 1) and is achieved by ingesting up to 15 g of guar gum or pectin with each meal. Short-term studies have shown a potential efficacy of this approach.26, 27, 28, 29, 30, 31, 32 However, the palatability and tolerability of these supplements is poor. Moreover, these substances are usually not readily available as pharmaceutical products at sufficiently high doses.


Acarbose

Acarbose is an alpha-glycosidase hydrolase inhibitor that interferes with carbohydrate absorption in the small intestine. Acarbose inhibits the alpha-glycosidase-mediated production of monosaccharides from carbohydrates in the epithelial brush border cells of the small intestine. In healthy individuals, a 100–200 mg dose of acarbose inhibits the postprandial rise in glycemia, triglycerides and insulin. The results from a number of small studies, in which acarbose was given three times daily at 50–100 mg doses to patients with dumping syndrome, showed an improvement in glucose tolerance, a decreased release of gastrointestinal hormones and a reduction in the incidence of hypoglycemia (Table 2).33, 34, 35, 36, 37, 38 These results were associated with an improvement in dumping symptoms in these patients.


This treatment approach, however, affects only the symptoms of late dumping owing to the mode of action of acarbose (as mentioned above, the production of monosaccharides in the small intestine is the target of acarbose). In addition, acarbose treatment often results in bloating, flatulence or diarrhea, as the unabsorbed carbohydrates undergo bacterial fermentation in the small intestine; these adverse effects might hamper treatment compliance.

Somatostatin analogs

Somatostatin and its synthetic analogs have been used successfully in the treatment of dumping syndrome and have displayed a number of pathophysiologically attractive effects. Somatostatin analogs can retard the gastric emptying rate, retard transit through the small bowel, inhibit the release of gastrointestinal hormones, inhibit insulin secretion and inhibit postprandial vasodilation.14, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50 As such, these analogs show a broad range of activity against the full spectrum of symptoms of dumping syndrome. Both short-acting and delayed-release somatostatin analogs have been used in the treatment of dumping syndrome. Short-acting or long-acting repeatable (LAR) formulations of octreotide are the agents that have been most commonly studied.14, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63

Studies of short-acting somatostatin analog octreotide

The results of several short-term studies of subcutaneously administered octreotide have shown efficacy at improving symptoms, improving glycemia and slowing gastric emptying (Table 3).55, 56, 57, 58, 59, 60 However, the need for 3–4 daily injections is potentially a major limitation for the long-term application of short-acting somatostatin analogs. Three studies have evaluated the long-term use of subcutaneously administered octreotide in the treatment of dumping syndrome. Geer et al. found that long-term octreotide therapy (15 months on average) provided sustained symptom control.57 Of 10 patients, eight received three daily injections of 100 microg octreotide, which resulted in good symptom control; seven individuals were able to resume work. Similarly, Vecht et al. evaluated the long-term effect of three daily doses of 25–200 microg octreotide in 20 patients with a mean follow-up of 37 months.61 All patients had an initial positive response; at 3 months, 80% continued this positive response. After 10 years, however, 11 of the 20 patients had stopped therapy for a variety of reasons, including lack of effect at 3 months (n = 4), diarrhea (n = 4), painful injections (n = 1), reversible alopecia (n = 1) and weight loss (n = 1). Similar data were obtained in a larger group of patients, in whom long-term effects seemed less favorable than short-term effects, although 41% of the cohort continued octreotide therapy after the follow-up period of 93 plusminus 15 months.62


Studies of long-acting octreotide LAR

Slow-release preparations of somatostatin analogs, which require only monthly intramuscular injections, are an attractive alternative to multiple daily injections of the short-acting formulations. Two studies have investigated the efficacy of a slow-release preparation of octreotide in dumping syndrome. Penning et al. compared the efficacy of monthly octreotide LAR (10 mg) to subcutaneous octreotide and found both formulations to be effective at improving symptoms.63 The long-acting form seemed superior at increasing body weight and improving quality of life. The 10 mg dose is only available in a limited number of countries; the 20 mg dose is the usual standard dose for octreotide LAR.

A multicenter study in Belgium confirmed the efficacy of monthly octreotide LAR (20 mg) in the treatment of dumping syndrome that was refractory to dietary measures and acarbose treatment.14 The study compared the control of symptoms and underlying pathophysiological mechanisms after 3 days of subcutaneous treatment with octreotide (50 microg, 3 times daily) with 3 months of treatment with octreotide LAR at 20 mg. Both the short-acting and the long-acting formulations had a favorable effect on dumping symptoms, glycemia and pulse rate during provocative testing for dumping. The short-acting form showed greater efficacy than the long-acting form at improving hypoglycemia. However, treatment with the long-acting formulation was associated with a significant improvement in patients' quality of life and was markedly preferred by recipients over the short-acting preparation.14

Adverse effects of somatostatin analogs

The main adverse events related to the use of somatostatin analogs are pain at the site of injection, gallstone formation and the occurrence of steatorrhea. The latter symptom is usually mild, and the long-term use of somatostatin analogs is usually associated with a weight gain of approximately 1% in spite of the occurrence of steatorrhea. Gallstone formation is not an uncommon complication of the long-term use of somatostatin analogs and should be taken into account when considering treatment options for dumping syndrome.64, 65 Another disadvantage of somatostatin analogs is their considerable cost. For this and the aforementioned reasons, treatment with somatostatin analogs is not the first-line treatment option for patients with dumping syndrome. However, dumping syndrome is associated with major impairment of quality of life, and the improvement in this parameter with somatostatin analogs is impressive.14, 57

Diazoxide

Diazoxide is a potassium channel activator that hyperpolarizes cells, including beta cells, and, therefore, inhibits voltage-sensitive calcium channels. The drug has been used clinically in the treatment of hypertension and insulinoma, as it inhibits calcium-induced insulin release. The use of diazoxide administered three times daily at 100–150 mg for late dumping symptoms has been anecdotally reported,21 but no effect on the early symptoms of dumping syndrome is expected with diazoxide treatment owing to its mode of action.

Rescue therapies

In spite of some successful therapeutic options, a number of patients continue to have treatment-refractory dumping symptoms. In these difficult cases, surgical interventions or continuous enteral feeding can be considered.

Surgery

Depending on the previous type of gastric surgery, several types of reintervention have been proposed, including narrowing of the anastomosis, conversion of Bilroth type II to Bilroth type I gastroenterostomy, conversion to a Roux-en-Y construction, reconstruction of the pylorus or interposition of a 10 cm antiperistaltic jejunal loop.66, 67, 68, 69, 70, 71 The results from case series support the conversion of Bilroth type II to Bilroth type I gastroenterostomy in the treatment of dumping syndrome.66

In patients who develop the syndrome after vagotomy with pyloroplasty, surgical reconstruction of the pylorus improves symptoms and decreases the gastric emptying rate.66, 68, 69 The reversal of rapid initial gastric emptying has been implicated in the therapeutic effect of pyloric reconstruction.69 In addition, Roux-en-Y reconstruction has a favorable effect on dumping symptoms after partial gastrectomy and results in retardation of gastric emptying.70 Concomitant vagotomy improves the therapeutic outcome of Roux-en-Y reconstruction.71 Jejunal interposition of an antiperistaltic loop is superior to an isoperistaltic (Henley) loop in the management of refractory dumping.66, 67, 72 However, our own experience suggests that the outcomes of these interventions are often unpredictable in clinical practice.

Continuous enteral feeding

A final approach to treatment of patients with refractory dumping syndrome is the creation of a feeding jejunostomy, through which a continuous background flow of nutrients can be provided. This is a rather invasive intervention, with a major effect on daily life, but it seems to be effective at avoiding the symptoms of the syndrome that are triggered by meal ingestion (on the basis of one published case report and on our own, unpublished, experience).73

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Conclusions

Dumping syndrome is a well-established complication of upper gastrointestinal surgery and is likely to become more prevalent with increasing rates of bariatric surgery. A diagnosis is made on the basis of clinical suspicion in case of suggestive symptoms, aided by a modified oral glucose tolerance test. Initial therapy should focus on dietary measures for 3–4 weeks. If insufficient improvement occurs, acarbose can also be administered to patients with predominant late dumping symptoms. Somatostatin analogs are the next approach to consider in patients with well-established dumping syndrome who have failed to respond to initial therapy and whose quality of life is substantially affected by their symptoms; the approach of choice is treatment with slow-release formulations because of their ease of administration and superior effect on quality of life. After an initial 3-month treatment with somatostatin analogs, long-term therapy should be continued only if a substantial improvement in symptoms is seen. Whether increasing the dose (for example, of octreotide LAR from 20 mg to 30 mg) improves symptom control in dumping syndrome is currently unclear, but our personal experience would argue against dose increments in patients who fail to respond. In these patients, surgery or continuous enteral feeding might be necessary, but the outcome of these approaches is variable.

Review criteria

To identify relevant studies, the MEDLINE database was searched. Medical subject headings and free-text terms for (postoperative) dumping were combined with the terms "pathophysiology", "symptoms", "management", "diet", "pectin", "guar gum", "acarbose", "diazoxide", "somatostatin analog", "octreotide", "somatulin" and "surgery". The reference lists from retrieved articles were also examined for relevant papers.

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Acknowledgments

Désirée Lie, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the MedscapeCME-accredited continuing medical education activity associated with this article.

Competing interests statement

The authors declare no competing interests.

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Author affiliations

  1. Department of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium.

Correspondence to: J. Tack, Department of Gastroenterology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium
Email: jan.tack@med.kuleuven.ac.be

Published online 1 September 2009

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