Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Dumping Syndrome

  • Author: Rajan Kanth, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 03, 2016
 

Background

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 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 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.[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]

Next

Pathophysiology

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 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 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.[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 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 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 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.

Previous
Next

Etiology

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.

Previous
Next

Epidemiology

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 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.

Previous
 
 
Contributor Information and Disclosures
Author

Rajan Kanth, MD Hospitalist, Ministry Saint Joseph’s Hospital

Rajan Kanth, MD is a member of the following medical societies: American College of Physicians, Society of Hospital Medicine, Nepal Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Praveen K Roy, MD, AGAF Chief of Gastroenterology, Presbyterian Hospital; Medical Director of Endoscopy, Presbyterian Medical Group; Adjunct Associate Research Scientist, Lovelace Respiratory Research Institute

Praveen K Roy, MD, AGAF is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor 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, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Vivek V Gumaste, MD Associate Professor of Medicine, Mount Sinai School of Medicine of New York University; Adjunct Clinical Assistant, Mount Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center at Elmhurst; Program Director of GI Fellowship (Independent Program); Regional Director of Gastroenterology, Queens Health Network

Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association

Disclosure: Nothing to disclose.

Acknowledgements

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.

Sukhdeep Padda, MBBS Staff Physician, Arrowhead Gastroenterology

Sukhdeep Padda is a member of the following medical societies: American College of Gastroenterology

Disclosure: Nothing to disclose.

Francisco Ramirez, MD, FACG Consultant, Gastroenterology Director, Esophageal Clinic Quality; Professor of Medicine, Mayo School of Medicine

Francisco Ramirez, MD is a member of the following medical societies: American College of Gastroenterology

Disclosure: Nothing to disclose.

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. Borrelli D, Borrelli A, Presenti L, Bergamini C, Basili G. [Surgical approach of the functional post-partial gastrectomy syndromes] [Italian]. Ann Ital Chir. 2007 Jan-Feb. 78(1):3-10. [Medline].

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

  3. Wyllys E, Andrews E, Mix CL. "Dumping stomach" and other results of gastrojejunostomy: Operative cure by disconnecting old stoma. Surg Clin Chicago. 1920. 4:879-92.

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

  5. Berg P, McCallum R. Dumping syndrome: a review of the current concepts of pathophysiology, diagnosis, and treatment. Dig Dis Sci. 2016 Jan. 61 (1):11-8. [Medline].

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

  7. Ishikawa K, Arita T, Ninomiya S, et al. Outcome of segmental gastrectomy versus distal gastrectomy for early gastric cancer. World J Surg. 2007 Nov. 31(11):2204-7. [Medline].

  8. Braghetto I, Papapietro K, Csendes A, et al. Nonesophageal side-effects after antireflux surgery plus acid-suppression duodenal diversion surgery in patients with long-segment Barrett's esophagus*. Dis Esophagus. 2005. 18(3):140-5. [Medline].

  9. Rivera I, Ochoa-Martinez CI, Hermosillo-Sandoval JM, et al [Spanish]. [Dumping syndrome in patients submitted to gastric resection]. Cir Cir. 2007 Nov-Dec. 75(6):429-34. [Medline].

  10. Thalhammer M, Cuk A, Palitzsch KD. [Postalimentary hypoglycaemia in post-gastrectomy late dumping syndrome] [German]. Dtsch Med Wochenschr. 2005 Feb 25. 130(8):393-6. [Medline].

  11. Spiller R. Role of motility in chronic diarrhoea. Neurogastroenterol Motil. 2006 Dec. 18(12):1045-55. [Medline].

  12. Morioka J, Miyachi M, Niwa M, et al. Gastric emptying for liquids and solids after distal gastrectomy with Billroth-I reconstruction. Hepatogastroenterology. 2008 May-Jun. 55(84):1136-9. [Medline].

  13. 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. 1966 Nov. 164(5):821-9. [Medline].

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

  15. Goldfine AB, Mun EC, Devine E, et al. Patients with neuroglycopenia after gastric bypass surgery have exaggerated incretin and insulin secretory responses to a mixed meal. J Clin Endocrinol Metab. 2007 Dec. 92(12):4678-85. [Medline].

  16. Yamamoto H, Mori T, Tsuchihashi H, et al. A possible role of GLP-1 in the pathophysiology of early dumping syndrome. Dig Dis Sci. 2005 Dec. 50(12):2263-7. [Medline].

  17. Akimov VP, Dvaladze LG, Shengelia TD, Veselov IuE. [A new view on pathogenesis of dumping-syndrome] [Russian]. Vestn Khir Im I I Grek. 2008. 167(6):22-5. [Medline].

  18. Deitel M. The change in the dumping syndrome concept. Obes Surg. 2008 Dec. 18(12):1622-4. [Medline].

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

  20. Seyfried F, Wierlemann A, Bala M, Fassnacht M, Jurowich C. [Dumping syndrome: diagnostics and therapeutic options] [German]. Chirurg. 2015 Sep. 86 (9):847-54. [Medline].

  21. Mala T, Hewitt S, Hogestol IK, Kjellevold K, Kristinsson JA, Risstad H. [Dumping syndrome following gastric surgery] [Norwegian]. Tidsskr Nor Laegeforen. 2015 Jan 27. 135 (2):137-41. [Medline].

  22. Z'graggen K, Guweidhi A, Steffen R, et al. Severe recurrent hypoglycemia after gastric bypass surgery. Obes Surg. 2008 Aug. 18(8):981-8. [Medline].

  23. Schneider A, Gottrand F, Sfeir R, Duhamel A, Bonnevalle M, Guimber D, et al. Postoperative Lower Esophageal Dilation in Children Following the Performance of Nissen Fundoplication. Eur J Pediatr Surg. 2012 Jul 7. [Medline].

  24. Virji A, Murr MM. Caring for patients after bariatric surgery. Am Fam Physician. 2006 Apr 15. 73(8):1403-8. [Medline].

  25. Laurenius A, Olbers T, Näslund I, Karlsson J. Dumping Syndrome Following Gastric Bypass: Validation of the Dumping Symptom Rating Scale. Obes Surg. 2013 Jan 14. [Medline].

  26. Imhof A, Schneemann M, Schaffner A, Brändle M. Reactive hypoglycaemia due to late dumping syndrome: successful treatment with acarbose. Swiss Med Wkly. 2001 Feb 10. 131(5-6):81-3. [Medline].

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

  28. Arts J, Caenepeel P, Bisschops R, et al. Efficacy of the long-acting repeatable formulation of the somatostatin analogue octreotide in postoperative dumping. Clin Gastroenterol Hepatol. 2009 Apr. 7(4):432-7. [Medline].

  29. De Cunto A, Barbi E, Minen F, Ventura A. Safety and efficacy of high-dose acarbose treatment for dumping syndrome. J Pediatr Gastroenterol Nutr. 2011 Jul. 53(1):113-4. [Medline].

  30. 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. 1990 Dec. 212(6):678-87. [Medline].

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

  32. Moreira RO, Moreira RB, Machado NA, Gonçalves TB, Coutinho WF. Post-prandial hypoglycemia after bariatric surgery: pharmacological treatment with verapamil and acarbose. Obes Surg. 2008 Dec. 18(12):1618-21. [Medline].

  33. Zhang J, Chen JD. Systematic review: applications and future of gastric electrical stimulation. Aliment Pharmacol Ther. 2006 Oct 1. 24(7):991-1002. [Medline].

  34. Wei HB, Wei B, Zheng ZH, et al. Comparative study on three types of alimentary reconstruction after total gastrectomy. J Gastrointest Surg. 2008 Aug. 12(8):1376-82. [Medline].

  35. Nunobe S, Sasako M, Saka M, et al. Symptom evaluation of long-term postoperative outcomes after pylorus-preserving gastrectomy for early gastric cancer. Gastric Cancer. 2007. 10(3):167-72. [Medline].

  36. Nakane Y, Michiura T, Sakuramoto K, et al. [Evaluation of the preserved function of the remnant stomach in pylorus preserving-gastrectomy by gastric emptying scintigraphy] [Japanese]. Gan To Kagaku Ryoho. 2007 Jan. 34(1):25-8. [Medline].

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

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

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

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

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

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

  43. Malik S, Mitchell JE, Steffen K, et al. Recognition and management of hyperinsulinemic hypoglycemia after bariatric surgery. Obes Res Clin Pract. 2016 Jan-Feb. 10 (1):1-14. [Medline].

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

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

  46. Hammer HF. Medical complications of bariatric surgery: focus on malabsorption and dumping syndrome. Dig Dis. 2012. 30(2):182-6. [Medline].

  47. Zurita Mv LC, Tabari M, Hong D. Laparoscopic conversion of laparoscopic Roux-en-Y gastric bypass to laparoscopic sleeve gastrectomy for intractable dumping syndrome and excessive weight loss. Surg Obes Relat Dis. 2012 Nov 30. [Medline].

  48. Dapri G, Cadière GB, Himpens J. Laparoscopic reconversion of Roux-en-Y gastric bypass to original anatomy: technique and preliminary outcomes. Obes Surg. 2011 Aug. 21(8):1289-95. [Medline].

  49. Parikh M, Pomp A, Gagner M. Laparoscopic conversion of failed gastric bypass to duodenal switch: technical considerations and preliminary outcomes. Surg Obes Relat Dis. 2007 Nov-Dec. 3(6):611-8. [Medline].

  50. Papamargaritis D, Koukoulis G, Sioka E, et al. Dumping symptoms and incidence of hypoglycaemia after provocation test at 6 and 12 months after laparoscopic sleeve gastrectomy. Obes Surg. 2012 Oct. 22(10):1600-6. [Medline].

  51. Meier JJ, Butler AE, Galasso R, Butler PC. Hyperinsulinemic hypoglycemia after gastric bypass surgery is not accompanied by islet hyperplasia or increased beta-cell turnover. Diabetes Care. 2006 Jul. 29(7):1554-9. [Medline]. [Full Text].

  52. Kellogg TA, Bantle JP, Leslie DB, et al. Postgastric bypass hyperinsulinemic hypoglycemia syndrome: characterization and response to a modified diet. Surg Obes Relat Dis. 2008 Jul-Aug. 4(4):492-9. [Medline].

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

  54. Abell TL, Minocha A. Gastrointestinal complications of bariatric surgery: diagnosis and therapy. Am J Med Sci. 2006 Apr. 331(4):214-8. [Medline].

  55. 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].

  56. 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). 1980 Oct. 59(4):237-43. [Medline].

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

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

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

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

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

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

  63. Gonzalez-Sanchez JA, Corujo-Vazquez O, Sahai-Hernandez M. Bariatric surgery patients: reasons to visit emergency department after surgery. Bol Asoc Med P R. 2007 Oct-Dec. 99(4):279-83. [Medline].

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

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

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

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

  68. 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. 1989 Jan. 209(1):40-5. [Medline].

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

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

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

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

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

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

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

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

  77. 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. 1983 Jan. 18(1):73-80. [Medline].

  78. 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. 1995 May. 40(5):1074-82. [Medline].

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

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

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

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

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

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

  85. 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. 1990 Oct. 99(4):923-9. [Medline].

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

  87. 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].

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

  89. 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. 1991 Jan. 78(1):28-31. [Medline].

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

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

  92. 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. 1978 Sep. 65(9):637-41. [Medline].

  93. 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.

  94. Rubio MA, Moreno C. [Nutritional implications of bariatric surgery on the gastrointestinal tract] [Spanish]. Nutr Hosp. 2007 May. 22 Suppl 2:124-34. [Medline].

  95. 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). 1981 Feb 14. 282(6263):507-10. [Medline].

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

  97. 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. 1970 Dec. 188(6):479-86. [Medline].

  98. Smith L, Smithers M, Prins J, O'Moore-Sullivan T. Acute and long-term effect of alpha-glucosidase inhibitor on dumping syndrome in a patient after a vagotomy and pyloric surgery. ANZ J Surg. 2005 Dec. 75(12):1124-6. [Medline].

  99. 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. 1989 Dec. 30(12):1716-20. [Medline].

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

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

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

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

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

  105. Wick JY. Coming to a facility near you: the bariatric surgery patient. Consult Pharm. 2006 Nov. 21(11):874-76, 878-80, 882, 885-6. [Medline].

  106. Yamada M, Ohrui T, Asada M, et al. Acarbose attenuates hypoglycemia from dumping syndrome in an elderly man with gastrectomy. J Am Geriatr Soc. 2005 Feb. 53(2):358-9. [Medline].

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

 
Previous
Next
 
Pathophysiology of dumping syndrome.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.