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Dumping Syndrome

Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Sukhdeep Padda, MD, Assistant Professor, Department of Internal Medicine, Section of Gastroenterology, University of Arizona Health Sciences Center; Francisco Ramirez, MD, FACG, Chief, Section of Gastroenterology, Carl T Hayden VA Medical Center; Associate Professor, Department of Medicine, University of Arizona; Thomas Aguirre, MD, Gastroenterology Fellow, Department of Internal Medicine, University of Arizona

Updated: Jun 10, 2008

Introduction

Background

The stomach serves as the receptive and storage site of ingested food. The primary functions of the stomach are to act as a reservoir, to initiate the digestive process, and to release its contents downstream into the duodenum in a controlled fashion. 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 regulated by the enteric nervous system, which is influenced by extrinsic innervation and by circulating hormones. Alterations in gastric anatomy after surgery or interference in its extrinsic innervation (vagotomy) may have profound effects on gastric emptying. These effects, for convenience, have been termed postgastrectomy syndromes.

Postgastrectomy syndromes include small capacity, dumping, bile gastritis, afferent loop syndrome, efferent loop syndrome, anemia, and metabolic bone disease.

Pathophysiology

Clinically significant dumping syndrome occurs in approximately 10% of patients after gastric surgery.  Dumping syndrome has characteristic alimentary and systemic manifestations. It is the most common and often disabling postprandial syndrome 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. Both forms occur because of rapid delivery of large amounts of osmotically active solids and liquids into the duodenum. Dumping syndrome is the direct result of alterations in the storage function of the stomach and/or the pyloric emptying mechanism.

Azpiroz and Malagelada have shown that the accommodation response and the phasic contractility of the stomach in response to distention are abolished after vagotomy or partial gastric resection.1 This probably accounts for the immediate transfer of ingested contents into the duodenum. 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."2 Mix first used the term dumping in 1922.3 Mix observed radiographically the presence of rapid gastric emptying in patients with vasomotor and GI symptoms.3

The severity of dumping syndrome is proportional to the rate of gastric emptying. Postprandially, the function 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 the 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 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 stomach's receptiveness to a meal. Similarly, vagotomy increases gastric tone, 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.

Early dumping

Symptoms of early dumping syndrome (30-60 min postprandial) 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. 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 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.4 They found that the degree of dilution of the hyperosmolar glucose in patients postgastrectomy was similar in symptomatic and asymptomatic subjects.

Provocation with oral glucose in patients with early dumping generally provokes an increase in heart rate. Although vasoconstriction is expected in a volume-contracted state, patients with dumping syndrome have vasodilation, first reported by Hinshaw et al.5 Vasodilatation has been demonstrated by some investigators, but not by others. 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 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 indicates that serotonin and the kallikrein-kinin system may be involved, but this evidence is not impressive.

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 to asymptomatic patients after gastric surgery. Some or all of these peptides are likely to participate in the pathogenesis of dumping syndrome. 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 rapid delivery of food to the distal small bowel.

Late dumping

Late dumping occurs 1-3 hours after a meal. 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 are responsible for the subsequent hypoglycemia. Holdsworth et al showed that intrajejunal glucose induces a higher insulin release than intravenous infusion of glucose.6 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. 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. 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, while others develop severe symptoms, remains elusive.

Frequency

United States

Incidence and severity of symptoms in dumping syndrome are related directly to the extent of gastric surgery. An estimated 25-50% of all patients who have undergone gastric surgery have some symptoms of dumping. However, only 1-5% are reported to have severe disabling symptoms. Incidence of significant dumping has been reported to be 6-14% in patients after truncal vagotomy and drainage and from 14-20% in patients after partial gastrectomy. Incidence of dumping syndrome after proximal gastric vagotomy without any drainage procedure is less than 2%. In the pediatric population, dumping syndrome is described almost exclusively in children who have undergone Nissen fundoplication.

Changes 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. 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.

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.

Sex

A female preponderance exists for the incidence of postgastrectomy syndromes.

Clinical

History

The clinical presentation of dumping syndrome can be divided into GI symptoms and vasomotor symptoms. 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 systemic symptoms
    • Desire to lie down
    • Palpitations
    • Fatigue
    • Faintness
    • Syncope
    • Diaphoresis
    • Headache
    • Flushing
  • Early dumping abdominal symptoms
    • Epigastric fullness
    • Diarrhea
    • Nausea
    • Abdominal cramps
    • Borborygmi
  • Late dumping
    • Perspiration
    • Shakiness
    • Difficulty to concentrate
    • Decreased consciousness
    • Hunger

Physical

  • Dumping syndrome is diagnosed based on typical symptoms in patients who have undergone gastric surgery. Signs and symptoms can be elicited with the glucose challenge test.
  • 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 - +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.

Causes

  • 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.

Workup

Laboratory Studies

  • Signs and symptoms can be elicited with the glucose challenge test.

Other Tests

  • 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.

Procedures

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

Treatment

Medical Care

  • Acarbose
    • The use of acarbose, an alpha-glycoside hydrolase inhibitor, interferes with carbohydrate absorption and has been shown to help in patients with late dumping.
    • 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 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.
  • Octreotide
    • 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 (see Table below).
    • 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 to placebo (see Table below). However, whether long-term octreotide use is as beneficial as short-term use is unclear. Reports on long-term use of octreotide are scarce, and the number of patients in these reports is small. In one study, Geer et al reported 8 of 10 patients with continued diminution of symptoms after 15 months of follow-up.7 They reported 11% weight gain. No major adverse effects were noted, and liver enzyme levels remained normal.
    • 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 a 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 GI specific quality of life index and body weight gain.
  • Table. Randomized, Double-Blinded, Placebo-Controlled Crossover Trials of Octreotide Treatment for Severe Dumping
Author, Year
n
Treatment
Symptom Score
Pulse Rate
Hematocrit, %
Hopman et al, 1988
1
Control
11.7 ±2.1
85 ±7
41 ±2
2
Octreotide
4.6 ±1.6
67 ±7
41 ±2
Tulassay et al, 1989
8
Control
 
102 ±3
43 ±3.5
 
Octreotide
 
70 ±2
38 ±1
Geer et al, 1990
1
Control
8.5 ±0.5
87 ±5
 
0
Octreotide
1.7 ±0.5
66 ±4
 
Gray et al, 1991
9
Control
15.7 ±1.6
105 ±6
41 ±2
 
Octreotide
4.6 ±1.7
80 ±3
39 ±1

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. 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 to 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 to pyloroplasty or loop gastrojejunostomy.

Consider remedial surgery in patients 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.

  • Stomal revision
    • One strategy for surgical correction of the pathophysiology of dumping is to slow down gastric emptying.
    • Porter and Claman reported good results by narrowing the gastrojejunal stoma.8
    • 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
    • Woodward et al and Perman have shown that conversion of a Billroth II to a Billroth I gastroduodenostomy improves dumping syndrome in 75% of patients.9
    • This procedure restores the physiologic delivery of the meal to the duodenum, without 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, while another 3 had good resolution of their dumping symptoms.10
    • Cheadle and coworkers reported a series of 9 patients, 8 of whom had excellent results.11
    • 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.12 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.13 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 a good response has 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
    • Recently, conversion to a Roux-en-Y gastrojejunostomy as a remedial operation has gained favor.
    • 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.14 Of the 3 failures, 1 was due to persistent dumping syndrome, while 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.
  • 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.
  • Conclusion
    • 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.

Diet

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

  • 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 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 of dietary fibers 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 bowel transit time.

Medication

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

Hypoglycemic agents

Shown to be helpful for late dumping.


Acarbose (Precose, Prandase)

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

Dosing

Adult

100-200 mg PO tid

Pediatric

Not established

Interactions

Serum digoxin concentrations may be reduced with coadministration; digestive enzymes or charcoal may reduce effect

Contraindications

Documented hypersensitivity, active liver disease, ketoacidosis, GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adverse effects include flatulence, diarrhea, and abdominal discomfort, which generally diminish in frequency and intensity

Antisecretory agents

These agents may improve morbidity.


Octreotide (Somatostatin)

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

Dosing

Adult

Initially: 50 mcg SC bid/tid 30 min ac

Pediatric

Not established

Interactions

May reduce effects of cyclosporine; patients on insulin, PO hypoglycemics, beta-blockers, and calcium channel blockers may need dosage adjustments

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adverse effects are primarily related to altered GI motility and include nausea, abdominal pain, diarrhea, and increased incidence of gallstones and biliary sludge; hypoglycemia or hyperglycemia may occur because of alteration in counter-regulatory hormones (eg, insulin, glucagon, GH); bradycardia, cardiac conduction abnormalities, and arrhythmias have been reported; hypothyroidism may occur because of inhibition of TSH secretion; use caution in patients with renal impairment

Multimedia

Pathophysiology of dumping syndrome.

Media file 1: Pathophysiology of dumping syndrome.

References

  1. Azpiroz F, Malagelada JR. Gastric tone measured by an electronic barostat in health and postsurgical gastroparesis. Gastroenterology. Apr 1987;92(4):934-43. [Medline].

  2. Hertz AF. IV. The Cause and Treatment of Certain Unfavorable After-effects of Gastro-enterostomy. Ann Surg. Oct 1913;58(4):466-72. [Medline].

  3. Mix CL. Dumping following gastrojejunostomy. Surg Clin North Am. 1922;2:617.

  4. Kalser MH, Cohen R. Correlation of jejunal transfer of water and electrolytes with blood volume in postgastrectomy patients: response to hypertonic glucose meal. Ann Surg. Nov 1966;164(5):821-9. [Medline].

  5. Hinshaw DB, Joergerson EJ, Davis HA. Peripheral blood flow and blood volume studies in the dumping syndrome. Arch Surg. 1957;74:686.

  6. Holdsworth CD, Turner D, McIntyre N. Pathophysiology of post-gastrectomy hypoglycaemia. Br Med J. Nov 1 1969;4(5678):257-9. [Medline].

  7. Geer RJ, Richards WO, O'Dorisio TM, Woltering EO, Williams S, Rice D, et al. Efficacy of octreotide acetate in treatment of severe postgastrectomy dumping syndrome. Ann Surg. Dec 1990;212(6):678-87. [Medline].

  8. Porter HW, Claman ZB. A preliminary report on the advantage of small stoma in partial gastrectomy for ulcer. Ann Surg. 1954;129:417.

  9. Woodward ER, Desser PL, Gasster M. Surgical treatment of postgastrectomy dumping syndrome. West J Surg. 1955;63:567.

  10. Koruth NM, Krukowski ZH, Matheson NA. Pyloric reconstruction. Br J Surg. Oct 1985;72(10):808-10. [Medline].

  11. Cheadle WG, Baker PR, Cuschieri A. Pyloric reconstruction for severe vasomotor dumping after vagotomy and pyloroplasty. Ann Surg. Nov 1985;202(5):568-72. [Medline].

  12. Henley FA. Experiences with jejunal interposition for correction of postgastrectomy syndromes. In: Harkins HN, Nyhus LM, eds. Surgery of the stomach and duodenum. Boston, Mass: Little Brown and Company; 1969:777.

  13. Sawyers JL, Herrington JL Jr. Superiority of antiperistaltic jejunal segments in management of severe dumping syndrome. Ann Surg. Sep 1973;178(3):311-21. [Medline].

  14. Vogel SB, Hocking MP, Woodward ER. Clinical and radionuclide evaluation of Roux-Y diversion for postgastrectomy dumping. Am J Surg. Jan 1988;155(1):57-62. [Medline].

  15. Abbott WE, Krieger H, Levey S. Technical surgical factors which enhance or minimize postgastrectomy abnormalities. Ann Surg. 1958;148:567.

  16. Andreasen JJ, Orskov C, Holst JJ. Secretion of glucagon-like peptide-1 and reactive hypoglycemia after partial gastrectomy. Digestion. 1994;55(4):221-8. [Medline].

  17. Blackburn AM, Christofides ND, Ghatei MA, Sarson DL, Ebeid FH, Ralphs DN, et al. Elevation of plasma neurotensin in the dumping syndrome. Clin Sci (Lond). Oct 1980;59(4):237-43. [Medline].

  18. Bloom SR, Royston CM, Thomson JP. Enteroglucagon release in the dumping syndrome. Lancet. Oct 14 1972;2(7781):789-91. [Medline].

  19. Burkhalter E. Incidence of gastrectomy in United States army hospitals worldwide from 1975 to 1985. Am J Gastroenterol. Nov 1988;83(11):1231-4. [Medline].

  20. Carvajal SH, Mulvihill SJ. Postgastrectomy syndromes: dumping and diarrhea. Gastroenterol Clin North Am. Jun 1994;23(2):261-79. [Medline].

  21. Cranley B, Kelly KA, Go VL, McNichols LA. Enhancing the anti-dumping effect of Roux gastrojejunostomy with intestinal pacing. Ann Surg. Oct 1983;198(4):516-24. [Medline].

  22. Didden P, Penning C, Masclee AA. Octreotide therapy in dumping syndrome: Analysis of long-term results. Aliment Pharmacol Ther. Nov 1 2006;24(9):1367-75. [Medline].

  23. Duthie HL, Irvine WT, Kerr JW. Cardiovascular changes in post-gastrectomy syndrome. Br J Surg. 1959;46:350.

  24. Eisenberg MM, Woodward ER, Carson TJ, Dragstedt LR. Vagotomy and drainage procedure for duodenal ulcer: the results of ten years' experience. Ann Surg. Sep 1969;170(3):317-28. [Medline].

  25. Gray JL, Debas HT, Mulvihill SJ. Control of dumping symptoms by somatostatin analogue in patients after gastric surgery. Arch Surg. Oct 1991;126(10):1231-5; discussion 1235-6. [Medline].

  26. Gustavsson S, Kelly KA, Melton LJ 3rd, Zinsmeister AR. Trends in peptic ulcer surgery. A population-based study in Rochester, Minnesota, 1956-1985. Gastroenterology. Mar 1988;94(3):688-94. [Medline].

  27. Hasler WL, Soudah HC, Owyang C. Mechanisms by which octreotide ameliorates symptoms in the dumping syndrome. J Pharmacol Exp Ther. Jun 1996;277(3):1359-65. [Medline].

  28. Hockings MP, Vogel SB. Woodward's postgastrectomy syndromes. Philadelphia, Pa: WB Saunders; 1991:195.

  29. Hoffmann J, Jensen HE, Christiansen J, Olesen A, Loud FB, Hauch O. Prospective controlled vagotomy trial for duodenal ulcer. Results after 11-15 years. Ann Surg. Jan 1989;209(1):40-5. [Medline].

  30. Holst JJ. Glucagonlike peptide 1: a newly discovered gastrointestinal hormone. Gastroenterology. Dec 1994;107(6):1848-55. [Medline].

  31. Hopman WP, Wolberink RG, Lamers CB, Van Tongeren JH. Treatment of the dumping syndrome with the somatostatin analogue SMS 201-995. Ann Surg. Feb 1988;207(2):155-9. [Medline].

  32. Johnson LP, Jesseph JE. Evidence of a humoral etiology of the dumping syndrome. Surg Forum. 1961;12:316.

  33. Johnston D, Blackett RL. A new look at selective vagotomies. Am J Surg. Nov 1988;156(5):416-27. [Medline].

  34. Karamanolis G, Tack J. Nutrition and motility disorders. Best Pract Res Clin Gastroenterol. 2006;20(3):485-505. [Medline].

  35. Khoshoo V, Reifen RM, Gold BD, Sherman PM, Pencharz PB. Nutritional manipulation in the management of dumping syndrome. Arch Dis Child. Dec 1991;66(12):1447-8. [Medline].

  36. Krieger H, Levey S. Technical surgical factors which enhance or minimize postgastrectomy abnormalities. Ann Surg. 1958;148:567.

  37. Lamers CB, Bijlstra AM, Harris AG. Octreotide, a long-acting somatostatin analog, in the management of postoperative dumping syndrome. An update. Dig Dis Sci. Feb 1993;38(2):359-64. [Medline].

  38. Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN. Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis. Scand J Gastroenterol. Jan 1983;18(1):73-80. [Medline].

  39. Layer P, Holst JJ, Grandt D, Goebell H. Ileal release of glucagon-like peptide-1 (GLP-1). Association with inhibition of gastric acid secretion in humans. Dig Dis Sci. May 1995;40(5):1074-82. [Medline].

  40. LeQuesne LP, Hobsley M, Hand BH. The dumping syndrome I. Factors responsible for the symptoms. Br Med J. 1960;1:141.

  41. Lygidakis NJ. A new method for the surgical treatment of the dumping syndrome. Ann R Coll Surg Engl. Nov 1981;63(6):411-4. [Medline].

  42. Machella TE. The mechanism of postgastrectomy dumping. Surg. 1949;130:145.

  43. Mackie CR, Jenkins SA, Hartley MN. Treatment of severe postvagotomy/postgastrectomy symptoms with the somatostatin analogue octreotide. Br J Surg. Nov 1991;78(11):1338-43. [Medline].

  44. Meyer JH, Thompson JB, Cohen MB. Motility of the stomach and the gastroduodenal junction. In: Johnson LR, ed. The Physiology of the Gastrointestinal Tract. 2nd ed. New York, NY: Raven Press; 1987:625-9.

  45. Meyer JH, Thomson JB, Cohen MB, Shadchehr A, Mandiola SA. Sieving of solid food by the canine stomach and sieving after gastric surgery. Gastroenterology. Apr 1979;76(4):804-13. [Medline].

  46. Miholic J, Reilmann L, Meyer HJ, Körber H, Kotzerke J, Hecker H. Extracellular space, blood volume, and the early dumping syndrome after total gastrectomy. Gastroenterology. Oct 1990;99(4):923-9. [Medline].

  47. Norryd C, Dencker H, Lunderquist A, Olin T, Tylén U. Superior mesenteric blood flow during experimentally induced dumping in man. Acta Chir Scand. 1975;141(3):187-96. [Medline].

  48. Overton RC, Jordon GLJ, DeBakey ME. The postgastrectomy syndrome: studies of pathogenesis. Ann Surg. 1957;145:471.

  49. Paimela H, Tuompo PK, Perakyl T, Saario I, Hockerstedt K, Kivilaakso E. Peptic ulcer surgery during the H2-receptor antagonist era: a population-based epidemiological study of ulcer surgery in Helsinki from 1972 to 1987. Br J Surg. Jan 1991;78(1):28-31. [Medline].

  50. Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A. Effect of neurotensin in the dumping syndrome. Scand J Gastroenterol. May 1986;21(4):478-82. [Medline].

  51. Penning C, Vecht J, Masclee AA. Efficacy of depot long-acting release octreotide therapy in severe dumping syndrome. Aliment Pharmacol Ther. Nov 15 2005;22(10):963-9. [Medline].

  52. Perman E. The so-called dumping syndrome after gastrectomy. Acta Med Scan. 1947;128 (suppl 196):361.

  53. Ralphs DN, Thomson JP, Haynes S, Lawson-Smith C, Hobsley M, Le Quesne LP. The relationship between the rate of gastric emptying and the dumping syndrome. Br J Surg. Sep 1978;65(9):637-41. [Medline].

  54. Roberts KE, Randall HT, Farr HW. Cardiovascular and blood volume alterations resulting from intrajejunal administration of hypertonic solutions to gastrectomized patients: The relationship of these changes to the dumping syndrome. Ann Surg. 1954;140:631.

  55. Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR. Release of vasoactive intestinal peptide in the dumping syndrome. Br Med J (Clin Res Ed). Feb 14 1981;282(6263):507-10. [Medline].

  56. Sawyers JL. Management of postgastrectomy syndromes. Am J Surg. Jan 1990;159(1):8-14. [Medline].

  57. Sigstad H. A clinical diagnostic index in the diagnosis of the dumping syndrome. Changes in plasma volume and blood sugar after a test meal. Acta Med Scand. Dec 1970;188(6):479-86. [Medline].

  58. Snook JA, Wells AD, Prytherch DR, Evans DH, Bloom SR, Colin-Jones DG. Studies on the pathogenesis of the early dumping syndrome induced by intraduodenal instillation of hypertonic glucose. Gut. Dec 1989;30(12):1716-20. [Medline].

  59. Tack J. Gastric motor disorders. Best Pract Res Clin Gastroenterol. 2007;21(4):633-44. [Medline].

  60. Tulassay Z, Tulassay T, Gupta R, Cierny G. Long acting somatostatin analogue in dumping syndrome. Br J Surg. Dec 1989;76(12):1294-5. [Medline].

  61. Ukleja A. Dumping syndrome: pathophysiology and treatment. Nutr Clin Pract. Oct 2005;20(5):517-25. [Medline].

  62. van der Kleij FG, Vecht J, Lamers CB, Masclee AA. Diagnostic value of dumping provocation in patients after gastric surgery. Scand J Gastroenterol. Dec 1996;31(12):1162-6. [Medline].

  63. Vetch J, Lambers RJ. Octreotide influences small intestinal motility and transit time in fasting and fed states. Gastro. 1994;106:A583.

  64. Visick AH. A study of the failures after gastrectomy. Ann R Coll Surg Engl. 1948;3:266.

  65. Wong PY, Talamo RC, Babior BM, Raymond GG, Colman RW. Kallikrein-kinin system in postgastrectomy dumping syndrome. Ann Intern Med. May 1974;80(5):577-81. [Medline].

  66. Zeitlin IJ, Smith AN. 5-hydroxyindoles and kinins in the carcinoid and dumping syndromes. Lancet. Nov 5 1966;2(7471):986-91. [Medline].

Keywords

postgastrectomy syndromes, small stomach capacity, dumping, bile gastritis, afferent loop syndrome, efferent loop syndrome, anemia, metabolic bone disease, postprandial syndrome, peptic ulcer disease, vagotomy, partial gastric resection, stomach surgery, Nissen fundoplication, rapid gastric emptying, gastrojejunostomy, bloating, explosive diarrhea, early satiety, epigastric fullness, crampy abdominal pain, syncope, borborygmi, Sigstad's diagnostic index, Visick classification

Contributor Information and Disclosures

Author

Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Alan BR Thomson, MD, MSc, PhD is a member of the following medical societies: American Federation for Aging Research, American Federation for Clinical Research, American Gastroenterological Association, American Geriatrics Society, American Physiological Society, Canadian Association of Gastroenterology, Gastroenterology Research Group, New York Academy of Sciences, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Sukhdeep Padda, MD, Assistant Professor, Department of Internal Medicine, Section of Gastroenterology, University of Arizona Health Sciences Center
Sukhdeep Padda, MD is a member of the following medical societies: American College of Gastroenterology
Disclosure: Nothing to disclose.

Francisco Ramirez, MD, FACG, Chief, Section of Gastroenterology, Carl T Hayden VA Medical Center; Associate Professor, Department of Medicine, University of Arizona
Francisco Ramirez, MD, FACG is a member of the following medical societies: American College of Gastroenterology
Disclosure: Nothing to disclose.

Thomas Aguirre, MD, Gastroenterology Fellow, Department of Internal Medicine, University of Arizona
Thomas Aguirre, MD is a member of the following medical societies: American College of Gastroenterology and American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Vivek Gumaste, MD, Chief, Clinical Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Elmhurst Hospital Center, Mount Sinai School of Medicine
Vivek Gumaste, MD is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

BS Anand, MD, Department of Internal Medicine, Division of Gastroenterology, Professor, Baylor University College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

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