Dumping Syndrome Treatment & Management

  • Author: Alan BR Thomson, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jan 26, 2010
 

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.
    • The mechanisms of action of octreotide in dumping syndrome are as follows:
      • Delay in the accelerated initial gastric emptying
      • Delay in small intestinal transit time
      • Inhibition of enteral hormone release
      • Induction of a fasting intestinal pattern
      • Inhibition of insulin release
      • Splanchnic vasoconstriction
      • Inhibition of postprandial vasodilation
    • The usual initial dose of octreotide is 50 mcg administered subcutaneously bid/tid 30 minutes prior to each meal. The dose may be increased if smaller doses are not effective; however, higher doses are seldom effective if the smaller doses do not work.
    • Octreotide improves the symptoms in about 90% of patients with severe dumping refractory to other forms of medical interventions.
    • In all studies, octreotide in the short term decreased the symptom score, pulse rate, and plasma insulin levels when compared with placebo. However, whether long-term octreotide use is as beneficial as short-term use is unclear. Reports on long-term use of octreotide are scarce, and the number of patients in these reports is small. One study reported 8 of 10 patients with continued diminution of symptoms after 15 months of follow-up, an 11% weight gain, no major adverse effects, and liver enzyme levels remained normal.[20]
    • During octreotide treatment, fecal fat excretion increases significantly. Despite this increase in steatorrhea, an increase in mean body weight is reported. This probably occurs because of increased energy intake as patients are able to tolerate more food.
    • Octreotide appears to be safe in the long-term management of refractory dumping syndrome; however, the occurrence of diarrhea in patients who already have malabsorption and maldigestion may be a major limiting factor.
    • Depot long-acting release octreotide (Sandostatin-LAR), as compared with octreotide, resulted in a significantly greater GI specific quality of life index and body weight gain.[19]
    • Although the results of long-term use of octreotide injections are less dramatic than short-term use, nonetheless, symptoms are reduced by about 50%.[21] Other authors report that long-acting release 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.[19]
    • The addition of verapamil may also be considered.[22] Although there is enthusiasm for the use of electrical stimulation of the small intestine to achieve gastrointestinal pacing as a treatment of dumping syndrome,[23] there are no placebo-controlled trials, thus, possible placebo effects cannot be excluded.
Next

Surgical Care

Preventing dumping syndrome is preferable to treating its symptoms. Consider anatomic factors that relate to the syndrome, and, if possible, determine the exact type of surgical procedure needed. Numerous alimentary reconstruction methods have been proposed to treat the dumping syndrome.[24] Proximal gastric vagotomy is now the procedure of choice for the surgical management of intractable ulcer disease. Although the long-term ulcer recurrence rate is higher after this procedure compared with antrectomy and truncal vagotomy, it has the lowest incidence of postoperative dumping and diarrhea. If more extensive surgery is necessary, resection is preferable to a Roux-en-Y gastrojejunostomy, because it decreases the rate of dumping syndrome compared with pyloroplasty or loop gastrojejunostomy.

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

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

For early gastric cancer, the postoperative outcome is better in those having a pylorus-preserving gastrectomy.[25] Unfortunately, about one quarter of patients undergoing a pylorus-preserving gastrectomy may have sufficiently symptomatic delayed gastric emptying that the quality of their life may be adversely affected.[26]

  • Stomal revision
    • One strategy for surgical correction of the pathophysiology of dumping is to slow gastric emptying.
    • Porter and Claman reported good results by narrowing the gastrojejunal stoma.[27]
    • Determining the exact size of the stomal reconstruction is difficult.
    • Stomal strictures with gastric outlet obstruction are common adverse effects of the operation.
    • This technique has been abandoned in favor of other procedures.
  • Conversion of Billroth II to Billroth I anastomoses
    • Conversion of a Billroth II to a Billroth I gastroduodenostomy improves dumping syndrome in 75% of patients.[28]
    • 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, whereas another 3 had good resolution of their dumping symptoms.[29]
    • Cheadle and coworkers reported a series of 9 patients, 8 of whom had excellent results.[30]
    • 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.[31] 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.[32] 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
    • Conversion to a Roux-en-Y gastrojejunostomy as a remedial operation has gained favor recently.
    • With this operation, favorable outcomes have been reported in 85-90% of patients. Of patients with dumping symptoms after Billroth I and II gastrectomy, 85-90% have favorable outcomes with Roux-en-Y conversion.
    • Vogel et al reported 19 of 22 patients with favorable outcomes with this operation.[33] Of the 3 failures, 1 was due to persistent dumping syndrome, whereas the other 2 patients had Roux stasis syndrome.
    • The mechanism by which this conversion works in providing relief from dumping is unknown, but it may be due to interruption of the migration motor complex, diminished jejunal contractions, and retrograde jejunal contractions.
    • This procedure is easier to perform and has fewer long-term adverse effects.
  • Bariatric surgery
    • The dumping syndrome that occurs after gastric bypass surgery is not due to an increase in pancreatic beta cell formation or mass; instead, it is due to hypersensitivity of the postprandial insulin response.[34] This inappropriately increased insulin secretion may be due to excessively high incretin levels, or to "…a failure to adequately decrease insulin secretion…."[34]
    • Within 30 minutes after a high-carbohydrate meal, 12 of 14 patients were shown-to develop hyperglycemia and hyperinsulinemia (noninsulinoma, pancreatogenous hypoglycemic syndrome [NIPHS]) some 30 minutes after a test meal, whereas this and the associated symptoms did not occur with a low-carbohydrate diet.[35]
    • Dietary considerations are important after bariatric surgery, and the patient’s diet may need to be specifically formulated to deal with symptoms such as dumping, altered bowel habit, nausea and vomiting, dehydration, food intolerance, and overeating.[36]
    • Diffuse islet cell hyperplasia and expansion of the beta cell mass have been described in 3 patients with severe postprandial hyperglycemia and hyperinsulinemia unresponsive to diet, octreotide, and diazoxide.
  • 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.
Previous
Next

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 with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time.
  • This dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping.[37, 38] This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms.
Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

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.

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.

Specialty Editor Board

Vivek V Gumaste, MD  Associate Professor of Medicine, Mt Sinai School of Medicine; Adjunct Clinical Assistant, Mt Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center

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

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of 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 & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

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. Jan-Feb 2007;78(1):3-10. [Medline].

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

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

  4. 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].

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

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

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

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

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

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

  11. 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].

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

  13. 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. Dec 2007;92(12):4678-85. [Medline].

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

  15. 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].

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

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

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

  19. 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].

  20. 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].

  21. 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].

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

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

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

  25. 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].

  26. 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. Jan 2007;34(1):25-8. [Medline].

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

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

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

  30. 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].

  31. 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.

  32. 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].

  33. 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].

  34. 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. Jul 2006;29(7):1554-9. [Medline]. [Full Text].

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

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

  37. 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. Dec 2005;75(12):1124-6. [Medline].

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

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

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

  41. 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].

  42. 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].

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

  44. 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].

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

  46. 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].

  47. 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].

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

  49. 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].

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

  51. 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].

  52. 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].

  53. 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].

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

  55. 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].

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

  57. 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].

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

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

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

  61. 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].

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

  63. 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].

  64. 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].

  65. 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].

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

  67. 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].

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

  69. 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].

  70. 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.

  71. 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].

  72. 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].

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

  74. 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].

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

  76. 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].

  77. 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].

  78. 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].

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

  80. 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].

  81. 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.

  82. 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].

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

  84. 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].

  85. 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].

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

  87. 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].

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

  89. 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].

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

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

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

  93. 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].

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

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

 
Previous
Next
 
Pathophysiology of dumping syndrome.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.