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* Removal of a part of the stomach can cause the contents to not digest and flow down undigested in a hyperosmolar manner. This hyperosmolar chyme will cause an osmotic shift from the blood circulation to the intestinal lumen . This my may cause hypotension which will in turn activate the sympathetic nervous system and its associated side effects. | * Removal of a part of the stomach can cause the contents to not digest and flow down undigested in a hyperosmolar manner. This hyperosmolar chyme will cause an osmotic shift from the blood circulation to the intestinal lumen . This my may cause hypotension which will in turn activate the sympathetic nervous system and its associated side effects. | ||
* Pancreatic islet cell hyperplasia, rather than late dumping, is thought to be the underlying mechanism for hyperinsulinemic hypoglycemia with nesidioblastosis after gastric bypass. These patients do not respond to treatment for dumping syndrome, and it is difficult to confirm this rare diagnosis. | * Pancreatic islet cell hyperplasia, rather than late dumping, is thought to be the underlying mechanism for hyperinsulinemic hypoglycemia with nesidioblastosis after gastric bypass. These patients do not respond to treatment for dumping syndrome, and it is difficult to confirm this rare diagnosis. | ||
* | * Glucagonlike peptide-1 (GLP1) plays a key role in the pathogenesis of late hypoglycemia after gastric bypass | ||
==== '''Inappropriate release of hormones''' ==== | ==== '''Inappropriate release of hormones''' ==== | ||
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'''Flowchart''' | '''Flowchart''' | ||
The following flow chart outlines the major events involved in the pathogenesis of dumping syndrome:<ref name="van BeekEmous2017">{{cite journal|last1=van Beek|first1=A. P.|last2=Emous|first2=M.|last3=Laville|first3=M.|last4=Tack|first4=J.|title=Dumping syndrome after esophageal, gastric or bariatric surgery: pathophysiology, diagnosis, and management|journal=Obesity Reviews|volume=18|issue=1|year=2017|pages=68–85|issn=14677881|doi=10.1111/obr.12467}}</ref><ref name="urlwww.practicalgastro.com">{{cite web |url=https://www.practicalgastro.com/pdf/February06/UklejaArticle.pdf |title=www.practicalgastro.com |format= |work= |accessdate=}}</ref>{{Familytree/start}} | The following flow chart outlines the major events involved in the pathogenesis of dumping syndrome (early and late):<ref name="van BeekEmous2017">{{cite journal|last1=van Beek|first1=A. P.|last2=Emous|first2=M.|last3=Laville|first3=M.|last4=Tack|first4=J.|title=Dumping syndrome after esophageal, gastric or bariatric surgery: pathophysiology, diagnosis, and management|journal=Obesity Reviews|volume=18|issue=1|year=2017|pages=68–85|issn=14677881|doi=10.1111/obr.12467}}</ref><ref name="urlwww.practicalgastro.com">{{cite web |url=https://www.practicalgastro.com/pdf/February06/UklejaArticle.pdf |title=www.practicalgastro.com |format= |work= |accessdate=}}</ref>{{Familytree/start}} | ||
{{familytree/start}} | {{familytree/start}} | ||
Revision as of 19:15, 11 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]
Overview
The exact pathogenesis of dumping syndrome is not fully understood. Symptoms of early and late dumping syndrome appear to be caused by distinct pathophysiological mechanisms.
Pathophysiology
Pathogenesis
Dumping syndrome occurs secondary to various conditions such as after gastric surgery (especially on taking meals high in carbohydrates after the procudure), diabetes mellitus, Zolinger-Ellison syndrome, and Ehler-Danlos syndrome. The pathogenesis of dumping syndrome varies according to the etiology but the most essential component is the increased gastric emptying. The exact cause is not yet concluded, although several known phenomena may contribute to the development of early dumping symptoms.[1][2]
The main causes can be subdivided into the following:
- Abnormal motility
- Reduced gastric volume
Accelerated motility
- Reactive hypoglycemia occurs secondary to hyperinsulinemia caused by high concentration of carbohydrates in the proximal small intestine and rapid absorption of glucose (late dumping)
- Alteration of the pyloric muscle that holds the gastric contents till complete digestion, will cause a free fall of gastric contents into the small intestine. This rapid descent will cause an osmotic shift leading to hypotension which will activate the sympathetic nervous system and its associated side effects.
- Removal of a part of the stomach and small intestine will cause bypassing of the gastric contents straight through to the ileum or jejunum which can cause rapid descent and osmotic shifting.
- Dumping syndrome is most common in patients with certain types of stomach surgery, such as a gastrectomy or gastric bypass surgery, that allow the stomach to empty rapidly. Dumping syndrome can also occur as a result of complications after a cholecystectomy (gallbladder removal).[1]
- Dumping is also common for esophageal cancer patients who have had an esophagectomy; surgery to remove the cancerous portion of their esophagus. The stomach is pulled into the chest and attached to what remains of the esophagus, leaving a short digestive tract.
Reduced gastric volume
Surgery is one of the major causes leading to a reduced gastric volume.
- Changes that affect the storage in the stomach or the pyloric muscle cuase delivery of hyperosmolar material into the intestine. Fluid shifts cause rapid small bowel distention and an increased peristalsis (early dumping).
- Supraphysiologic release of GI peptides/vasoactive mediators lead to paradoxical vasodilation in a relatively volume-contracted state.
- Removal of a part of the stomach can cause the contents to not digest and flow down undigested in a hyperosmolar manner. This hyperosmolar chyme will cause an osmotic shift from the blood circulation to the intestinal lumen . This my may cause hypotension which will in turn activate the sympathetic nervous system and its associated side effects.
- Pancreatic islet cell hyperplasia, rather than late dumping, is thought to be the underlying mechanism for hyperinsulinemic hypoglycemia with nesidioblastosis after gastric bypass. These patients do not respond to treatment for dumping syndrome, and it is difficult to confirm this rare diagnosis.
- Glucagonlike peptide-1 (GLP1) plays a key role in the pathogenesis of late hypoglycemia after gastric bypass
Inappropriate release of hormones
Diseased pathogenesis
- Patients with Zollinger-Ellison syndrome, a rare disorder involving extreme peptic ulcer disease and gastrin-secreting tumors in the pancreas, may also have dumping syndrome.
- Patients with connective tissue conditions such as Ehlers-Danlos syndrome can experience "late" dumping as a result of decreased motility.
- In addition, people with this syndrome often suffer from low blood sugar, or hypoglycemia, because the rapid "dumping" of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as "alimentary hypoglycemia".
| Hormone | Role |
|---|---|
| ANP | Vasocontriction |
| GIP | Delays emptying |
| VIP | |
| GLP-1 | Inhibits insulin |
| Peptide YY | |
| Neurotensin |
Early dumping
Early dumping syndrome occurs 15-30 minutes after a meal.[3]
- It starts with the intake of a hyperosmolar content.[4] This leads to a fluid shift from the blood circulation to the gut which in-turn dehydrates and concentrates the intracellular space.
- A decrease in gastric volume [5] via surgery
- Pyloric Dysfunction[5]
- Hormones released;[6][7][8][9]
- Esophageal surgery may also impair gastric retentive capacity because the accompanying vagotomy causes rapid liquid emptying. Hyperosmolar nutrients in the small bowel presumably cause a shift of fluid from the intravascular compartment (i.e. plasma) to the intestinal lumen, resulting in a reduction in plasma volume, tachycardia, and, rarely, syncope. Movement of fluid into the small bowel may also cause distention and contribute to cramp-like contractions, bloating and diarrhoea. Whether this fluid shift contributes to the pathophysiology of dumping syndrome or is mainly a consequence of this process remains unknown. In favour of the latter interpretation, intravenous fluid substitution is not effective in preventing early dumping symptoms[10]
- . Another important mechanism involved in the pathophysiology of early dumping syndrome (and also late dumping syndrome as described below) involves the gi hormones including vasoactive agents (e.g. neurotensin and vasoactive intestinal peptide [VIP]), incretins (e.g. gastric inhibitory polypeptide [GIP] and GLP-1), and glucose modulators (e.g. insulin and glucagon)[11].
- Enhanced release of these GI hormones may induce discoordinated GI motility and inhibit secretion, as well as elicit hemodynamic effects; for example, neurotensin and vasoactive intestinal polypeptide induce splanchnic vasodilation that results in hypotension and systemic hemoconcentration[12]
Late dumping
Late dumping syndrome occurs between
In contrast to the multiple pathophysiologic factors involved in early dumping syndrome, the pathophysiology of late dumping is largely attributable to the development of hyperinsulinemic or reactive hypoglycemia[1]. Rapid delivery of undigested carbohydrates to the small intestine results in high glucose concentrations that induce a hyperinsulinemic response, resulting in subsequent hypoglycemia and related late dumping symptoms[13]. Enteral glucose administration is known to induce enhanced insulin release relative to intravenous administration, a process known as the incretin effect. Two GI hormones are believed to play a pivotal role in the incretin effect: glucose-dependent insulinotropic polypeptide or gastric inhibitory polypeptide and GLP-1. An increased GLP-1 response has been reported in patients after gastric surgery, and a positive correlation has been observed between increasing GLP-1 levels and insulin release[14]. An additional study suggests that GLP-1 analogues may actually stabilize glucose levels in patients with postprandial hypoglycemia after gastric bypass surgery[15]. Therefore, an exaggerated endogenous GLP-1 response appears to be the key mediator of the hyperinsulinemic and hypoglycemic effect that is characteristic of late dumping syndrome[16]. However, the precise mechanism by which GLP-1 contributes to glucose homeostasis and late dumping syndrome is likely to be complex and remains to be fully elucidated.
Flowchart
The following flow chart outlines the major events involved in the pathogenesis of dumping syndrome (early and late):[17][18]
| Meal (Hyperosmolar) | |||||||||||||||||||||||||||||||||||||||||||||||||
| Rapid gastric emptying | Reduced gastric volume | ||||||||||||||||||||||||||||||||||||||||||||||||
| Hyperosmolar chyme jejunum | Release of GI hormones | Rapid glucose absorption into blood | |||||||||||||||||||||||||||||||||||||||||||||||
| •VIP ··Vasodilation ··Relaxation of GIT ··Inhibits Absorption •PYY ··Slows GIT •Neurotensin ··Vasodilation (relaxation) •GIP ··Insulin secretion •GLP-1 ··Slows GIT ··Insulin secretion | |||||||||||||||||||||||||||||||||||||||||||||||||
| Distention of intestine | Increased contractility | Fluid shift from Blood to GI | Postprandial hyperglycemia | ||||||||||||||||||||||||||||||||||||||||||||||
| •Nausea •Abdominal pain (cramps) | •Diarrhea •Bloating | Systemic and GI symptoms | Increased release of GLP-1 | ||||||||||||||||||||||||||||||||||||||||||||||
| Peripheral vasodilation | Hypovolemia | Exaggerated insulin release | |||||||||||||||||||||||||||||||||||||||||||||||
| Hemoconcentration (Dehydrated blood) | Hypotension | Late reactive hypoglycemia | |||||||||||||||||||||||||||||||||||||||||||||||
| Increased heart rate | •Decreased ANP •Increased Aldosterone | •Hunger •Tremor •Perspiration | |||||||||||||||||||||||||||||||||||||||||||||||
| •Flushing •Dizziness •Palpitations | |||||||||||||||||||||||||||||||||||||||||||||||||
References
- ↑ 1.0 1.1 Vecht J, Masclee AA, Lamers CB (1997). "The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment". Scand. J. Gastroenterol. Suppl. 223: 21–7. PMID 9200302.
- ↑ Machella TE (1949). "The Mechanism of the Post-gastrectomy "Dumping" Syndrome". Ann. Surg. 130 (2): 145–59. PMC 1616289. PMID 17859417.
- ↑ Eagon JC, Miedema BW, Kelly KA (1992). "Postgastrectomy syndromes". Surg. Clin. North Am. 72 (2): 445–65. PMID 1549803.
- ↑ Laurenius A, Engström M (2016). "Early dumping syndrome is not a complication but a desirable feature of Roux-en-Y gastric bypass surgery". Clin Obes. 6 (5): 332–40. doi:10.1111/cob.12158. PMID 27487971.
- ↑ 5.0 5.1 Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R (2009). "Pathophysiology, diagnosis and management of postoperative dumping syndrome". Nat Rev Gastroenterol Hepatol. 6 (10): 583–90. doi:10.1038/nrgastro.2009.148. PMID 19724252.
- ↑ Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR (1981). "Release of vasoactive intestinal peptide in the dumping syndrome". Br Med J (Clin Res Ed). 282 (6263): 507–10. PMC 1504318. PMID 6780101.
- ↑ Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A (1986). "Effect of neurotensin in the dumping syndrome". Scand. J. Gastroenterol. 21 (4): 478–82. PMID 3726454.
- ↑ Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN (1983). "Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis". Scand. J. Gastroenterol. 18 (1): 73–80. PMID 6372067.
- ↑ Gebhard B, Holst JJ, Biegelmayer C, Miholic J (2001). "Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome". Dig. Dis. Sci. 46 (9): 1915–23. PMID 11575444.
- ↑ JOHNSON LP, SLOOP RD, JESSEPH JE (1962). "Etiologic significance of the early symptomatic phase in the dumping syndrome". Ann. Surg. 156: 173–9. PMC 1466323. PMID 14452070.
- ↑ Tack J (2007). "Gastric motor disorders". Best Pract Res Clin Gastroenterol. 21 (4): 633–44. doi:10.1016/j.bpg.2007.04.001. PMID 17643905.
- ↑ Sirinek KR, O'Dorisio TM, Howe B, McFee AS (1985). "Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome". Arch Surg. 120 (5): 605–9. PMID 3985800.
- ↑ Eloy R, Garaud JC, Moody A, Jaeck D, Grenier JF (1975). "Jejunal factor stimulating insulin release in the isolated perfused canine pancreas and jejunum". Horm. Metab. Res. 7 (6): 461–7. doi:10.1055/s-0028-1093704. PMID 1213650.
- ↑ Toft-Nielsen M, Madsbad S, Holst JJ (1998). "Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia". Diabetologia. 41 (10): 1180–6. doi:10.1007/s001250051049. PMID 9794105.
- ↑ Abrahamsson N, Engström BE, Sundbom M, Karlsson FA (2013). "GLP1 analogs as treatment of postprandial hypoglycemia following gastric bypass surgery: a potential new indication?". Eur. J. Endocrinol. 169 (6): 885–9. doi:10.1530/EJE-13-0504. PMID 24086087.
- ↑ Salehi M, Gastaldelli A, D'Alessio DA (2014). "Blockade of glucagon-like peptide 1 receptor corrects postprandial hypoglycemia after gastric bypass". Gastroenterology. 146 (3): 669–680.e2. doi:10.1053/j.gastro.2013.11.044. PMC 3943944. PMID 24315990.
- ↑ van Beek, A. P.; Emous, M.; Laville, M.; Tack, J. (2017). "Dumping syndrome after esophageal, gastric or bariatric surgery: pathophysiology, diagnosis, and management". Obesity Reviews. 18 (1): 68–85. doi:10.1111/obr.12467. ISSN 1467-7881.
- ↑ "www.practicalgastro.com" (PDF).