Gastric dumping syndrome pathophysiology
|
Gastric dumping syndrome Microchapters |
|
Differentiating Gastric dumping syndrome from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Gastric dumping syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Gastric dumping syndrome pathophysiology |
|
Risk calculators and risk factors for Gastric dumping syndrome pathophysiology |
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 completely understood. Symptoms of early and late dumping syndrome appear to be caused by distinct pathological mechanisms. The pathogenesis can be divided into accelerated gastric emptying and reduced gastric volume.
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, Zollinger-Ellison syndrome, and Ehlers-Danlos syndrome. The pathogenesis of dumping syndrome varies according to the etiology but the most essential component is the rapid 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 pathogenesis can be subdivided into the following:
Accelerated gastric emptying
- Alteration of the pyloric muscle that holds the gastric contents till complete digestion, leads to a rapid transit of gastric contents into the small intestine. This rapid descent of partially digested food into the intestines causes an osmotic shift of fluids from the extracellular compartment leading to hypotension which leads to the activation of the sympathetic nervous system
- Reactive hypoglycemia occurs secondary to hyperinsulinemia caused by high concentration of carbohydrates in the proximal small intestine and rapid absorption of glucose (late dumping)[3][4]
- Removal of a part of the stomach and small intestine causes the food to bypass the stomach and rapidly descent through to the ileum or jejunum which may lead to osmotic shifting[5]
- 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)[6]
- Patients with esophageal cancer who undergo esophagectomy to remove the cancerous portion of their esophagus are also at an increased risk of developing dumping syndrome. The stomach is pulled into the chest and attached to what remains of the esophagus, leaving a short digestive tract[1]
Reduced gastric volume
Surgery is one of the major causes leading to a reduced gastric volume. The following mechanisms lead to the development of dumping syndrome post surgery:[5]
- Changes that affect the storage of food in the stomach or the alteration and manipulation of 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 gastrointestinal 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. This leads to a large hyperosmolar load entering into the intestines. This hyperosmolar chyme leads to an osmotic shift of fluids from the vascular compartment to the intestinal lumen. The major sequelae of this is hypotension and activation of the sympathetic nervous system
- 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.
- Glucagon-like peptide-1 (GLP1) plays a key role in the pathogenesis of late hypoglycemia after gastric bypass
Hormones of dumping syndrome
The following are hormonal changes occur in dumping syndrome:[7][8][9][10][11][12]
| Hormone | Role |
|---|---|
| ANP | Vasoconstriction |
| Gastric inhibitory polypeptide (GIP) | Delays emptying, insulin secretion |
| Vasoactive intestinal peptide (VIP) | Relaxation of gastrointestinal tract, vascular relaxation |
| Glucagon-like peptide-1 (GLP-1) | Insulin secretion, slows gastrointestinal transit time |
| Peptide YY | Inhibits gastric acid secretion, delays emptying |
| Neurotensin | Relaxation, splanchnic vasodilation |
| Serotonin | - |
The following are effects caused by specific hormones:
| Effect | Hormone |
|---|---|
| Insulin secretion | GIP, GLP-1 |
| Vasodilation | Neurotensin, VIP |
| Slows GIT | Peptide YY, VIP, neurotensin |
| Inhibits absorption | VIP |
| - | Serotonin |
Approach to pathophysiology of dumping syndrome
The following illustraion outlines the major events involved in the pathogenesis of dumping syndrome (early and late):[13][14]
| 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 | |||||||||||||||||||||||||||||||||||||||||||||||||
Exceptional diseases
There are a few diseases that have a different mechanism compared to conventional risk factors such as surgery leading to dumping syndrome. The following are the diseases:
- Zollinger-Ellison syndrome:
- A rare disorder involving extreme peptic ulcer disease and gastrin-secreting tumors in the pancreas, may also have dumping syndrome
- Connective tissue disorders such as Ehlers-Danlos syndrome
- Can experience "late" dumping as a result of decreased motility.
- 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".
- Diabetes:
- Neuropathy can cause damage to the nerves supplying the GIT
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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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).