Gastric dumping syndrome pathophysiology: Difference between revisions
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Revision as of 19:23, 3 November 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
The exact pathogenesis of dumping syndrome is not fully understood. Relatively few recent studies have been devoted to elucidating the mechanisms involved in early and late dumping syndromes, and much of our current knowledge is based on older literature[1]. Symptoms of early and late dumping syndrome appear to be caused by distinct pathophysiological mechanisms.
Pathophysiology
Pathogenesis
Dumping syndrome isn't due to one single cause but rather a combination of many causes. The exact reason isn't yet concluded, although several known phenomena may contribute to the development of early dumping symptoms[2].
| Hyperosmolar meal | |||||||||||||||||||||||||||||||||
| Rapid glucose absorption into the blood | |||||||||||||||||||||||||||||||||
| Hyperglycemia | |||||||||||||||||||||||||||||||||
| Release of hormones | |||||||||||||||||||||||||||||||||
| VIP | PYY | Neurotensin | GIP | GLP-1 | |||||||||||||||||||||||||||||
| Environmental factors | |||||||||||||||||||||||||||||||||
Early dumping
Early dumping syndrome occurs between 30-60 minutes.
- Hyperosmolar contents[3]
- Decreased gastric volume [4]
- Pyloric Dysfunction[4]
- Hormone release[5][6][7][8]
- Vasoactive agents (VIP, Neurotensin)
- Incretins (GIP, GLP-1)
- Glucose-modulating hormones (Glucagon, Insulin)
- 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[9]
- . Another important mechanism involved in the pathophysiology of early dumping syndrome (and also late dumping syndrome as described below) involves the increased release of multiple 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)[10].
- 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[11]
Late dumping
Late dumping syndrome occurs between 60-180 minutes.
- Rapid glucose absorption
- Incretin release (GLP-1)
- Amplified insulin secretion
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[2]. 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[12]. 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[13]. An additional study suggests that GLP-1 analogues may actually stabilize glucose levels in patients with postprandial hypoglycemia after gastric bypass surgery[14]. 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[15]. 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.
Role of splanchnic vasodilation
Rapid emptying of stomach contents
Role of autonomic nervous system
Changes in serum glucose levels and plasma volume
- 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]
- 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.
- 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. Both early and late dumping syndrome can occur.
- Finally, 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".
Genetics
Gross Pathology
Microscopic Pathology
References
- ↑ Machella TE (1949). "The Mechanism of the Post-gastrectomy "Dumping" Syndrome". Ann. Surg. 130 (2): 145–59. PMC 1616289. PMID 17859417.
- ↑ 2.0 2.1 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.
- ↑ 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.
- ↑ 4.0 4.1 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.