Gastric dumping syndrome classification: Difference between revisions
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* Pyloric Dysfunction<ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref> | * Pyloric Dysfunction<ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref> | ||
* Hormones released;<ref name="pmid6780101">{{cite journal |vauthors=Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR |title=Release of vasoactive intestinal peptide in the dumping syndrome |journal=Br Med J (Clin Res Ed) |volume=282 |issue=6263 |pages=507–10 |year=1981 |pmid=6780101 |pmc=1504318 |doi= |url=}}</ref><ref name="pmid3726454">{{cite journal |vauthors=Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A |title=Effect of neurotensin in the dumping syndrome |journal=Scand. J. Gastroenterol. |volume=21 |issue=4 |pages=478–82 |year=1986 |pmid=3726454 |doi= |url=}}</ref><ref name="pmid6372067">{{cite journal |vauthors=Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN |title=Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis |journal=Scand. J. Gastroenterol. |volume=18 |issue=1 |pages=73–80 |year=1983 |pmid=6372067 |doi= |url=}}</ref><ref name="pmid11575444">{{cite journal |vauthors=Gebhard B, Holst JJ, Biegelmayer C, Miholic J |title=Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome |journal=Dig. Dis. Sci. |volume=46 |issue=9 |pages=1915–23 |year=2001 |pmid=11575444 |doi= |url=}}</ref> | * Hormones released;<ref name="pmid6780101">{{cite journal |vauthors=Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR |title=Release of vasoactive intestinal peptide in the dumping syndrome |journal=Br Med J (Clin Res Ed) |volume=282 |issue=6263 |pages=507–10 |year=1981 |pmid=6780101 |pmc=1504318 |doi= |url=}}</ref><ref name="pmid3726454">{{cite journal |vauthors=Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A |title=Effect of neurotensin in the dumping syndrome |journal=Scand. J. Gastroenterol. |volume=21 |issue=4 |pages=478–82 |year=1986 |pmid=3726454 |doi= |url=}}</ref><ref name="pmid6372067">{{cite journal |vauthors=Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN |title=Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis |journal=Scand. J. Gastroenterol. |volume=18 |issue=1 |pages=73–80 |year=1983 |pmid=6372067 |doi= |url=}}</ref><ref name="pmid11575444">{{cite journal |vauthors=Gebhard B, Holst JJ, Biegelmayer C, Miholic J |title=Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome |journal=Dig. Dis. Sci. |volume=46 |issue=9 |pages=1915–23 |year=2001 |pmid=11575444 |doi= |url=}}</ref> | ||
* 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<ref name="pmid14452070">{{cite journal |vauthors=JOHNSON LP, SLOOP RD, JESSEPH JE |title=Etiologic significance of the early symptomatic phase in the dumping syndrome |journal=Ann. Surg. |volume=156 |issue= |pages=173–9 |year=1962 |pmid=14452070 |pmc=1466323 |doi= |url=}}</ref> | * 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<ref name="pmid14452070">{{cite journal |vauthors=JOHNSON LP, SLOOP RD, JESSEPH JE |title=Etiologic significance of the early symptomatic phase in the dumping syndrome |journal=Ann. Surg. |volume=156 |issue= |pages=173–9 |year=1962 |pmid=14452070 |pmc=1466323 |doi= |url=}}</ref> | ||
* . Another important mechanism involved in the pathophysiology of early dumping syndrome (and also late dumping syndrome as described below) involves the | * . 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)<ref name="pmid17643905">{{cite journal |vauthors=Tack J |title=Gastric motor disorders |journal=Best Pract Res Clin Gastroenterol |volume=21 |issue=4 |pages=633–44 |year=2007 |pmid=17643905 |doi=10.1016/j.bpg.2007.04.001 |url=}}</ref>. | ||
* 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<ref name="pmid3985800">{{cite journal |vauthors=Sirinek KR, O'Dorisio TM, Howe B, McFee AS |title=Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome |journal=Arch Surg |volume=120 |issue=5 |pages=605–9 |year=1985 |pmid=3985800 |doi= |url=}}</ref> | * 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<ref name="pmid3985800">{{cite journal |vauthors=Sirinek KR, O'Dorisio TM, Howe B, McFee AS |title=Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome |journal=Arch Surg |volume=120 |issue=5 |pages=605–9 |year=1985 |pmid=3985800 |doi= |url=}}</ref> | ||
===Late dumping=== | ===Late dumping=== | ||
Late dumping syndrome occurs between | 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<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref>. 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<ref name="pmid1213650">{{cite journal |vauthors=Eloy R, Garaud JC, Moody A, Jaeck D, Grenier JF |title=Jejunal factor stimulating insulin release in the isolated perfused canine pancreas and jejunum |journal=Horm. Metab. Res. |volume=7 |issue=6 |pages=461–7 |year=1975 |pmid=1213650 |doi=10.1055/s-0028-1093704 |url=}}</ref>. 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<ref name="pmid9794105">{{cite journal |vauthors=Toft-Nielsen M, Madsbad S, Holst JJ |title=Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia |journal=Diabetologia |volume=41 |issue=10 |pages=1180–6 |year=1998 |pmid=9794105 |doi=10.1007/s001250051049 |url=}}</ref>. An additional study suggests that GLP-1 analogues may actually stabilize glucose levels in patients with postprandial hypoglycemia after gastric bypass surgery<ref name="pmid24086087">{{cite journal |vauthors=Abrahamsson N, Engström BE, Sundbom M, Karlsson FA |title=GLP1 analogs as treatment of postprandial hypoglycemia following gastric bypass surgery: a potential new indication? |journal=Eur. J. Endocrinol. |volume=169 |issue=6 |pages=885–9 |year=2013 |pmid=24086087 |doi=10.1530/EJE-13-0504 |url=}}</ref>. 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<ref name="pmid24315990">{{cite journal |vauthors=Salehi M, Gastaldelli A, D'Alessio DA |title=Blockade of glucagon-like peptide 1 receptor corrects postprandial hypoglycemia after gastric bypass |journal=Gastroenterology |volume=146 |issue=3 |pages=669–680.e2 |year=2014 |pmid=24315990 |pmc=3943944 |doi=10.1053/j.gastro.2013.11.044 |url=}}</ref>. 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. | 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<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref>. 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<ref name="pmid1213650">{{cite journal |vauthors=Eloy R, Garaud JC, Moody A, Jaeck D, Grenier JF |title=Jejunal factor stimulating insulin release in the isolated perfused canine pancreas and jejunum |journal=Horm. Metab. Res. |volume=7 |issue=6 |pages=461–7 |year=1975 |pmid=1213650 |doi=10.1055/s-0028-1093704 |url=}}</ref>. 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<ref name="pmid9794105">{{cite journal |vauthors=Toft-Nielsen M, Madsbad S, Holst JJ |title=Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia |journal=Diabetologia |volume=41 |issue=10 |pages=1180–6 |year=1998 |pmid=9794105 |doi=10.1007/s001250051049 |url=}}</ref>. An additional study suggests that GLP-1 analogues may actually stabilize glucose levels in patients with postprandial hypoglycemia after gastric bypass surgery<ref name="pmid24086087">{{cite journal |vauthors=Abrahamsson N, Engström BE, Sundbom M, Karlsson FA |title=GLP1 analogs as treatment of postprandial hypoglycemia following gastric bypass surgery: a potential new indication? |journal=Eur. J. Endocrinol. |volume=169 |issue=6 |pages=885–9 |year=2013 |pmid=24086087 |doi=10.1530/EJE-13-0504 |url=}}</ref>. 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<ref name="pmid24315990">{{cite journal |vauthors=Salehi M, Gastaldelli A, D'Alessio DA |title=Blockade of glucagon-like peptide 1 receptor corrects postprandial hypoglycemia after gastric bypass |journal=Gastroenterology |volume=146 |issue=3 |pages=669–680.e2 |year=2014 |pmid=24315990 |pmc=3943944 |doi=10.1053/j.gastro.2013.11.044 |url=}}</ref>. 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. | ||
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|- | |- | ||
|'''Onset''' | |'''Onset''' | ||
| | |15-30 minutes after a meal | ||
| | |60-180 minutes after a meal | ||
|- | |- | ||
|''' | |'''Risk Factor''' | ||
| | |Bariatric Surgery | ||
| | |Hyperosmolar chyme | ||
|- | |- | ||
|'''Mechanism''' | |'''Mechanism''' | ||
| | | | ||
* Increased release of multiple GI hormones | |||
* Decrease in gastric volume | |||
* Impaired retention | |||
* Possible Pyloric dysfunction | |||
| | | | ||
* Rapid glucose absorption | |||
* Incretin release (GLP-1) | |||
* Amplified insulin secretion | |||
|- | |- | ||
|'''Symptoms''' | |'''Symptoms''' | ||
| | | | ||
* Nausea | |||
* Bloating | |||
* Vomiting | |||
* Diarrhea | |||
* Borborygmus | |||
* Epigastric fullness | |||
* Abdominal cramps | |||
* Diaphoresis | |||
* Desire to lie down | |||
* Headache | |||
* Flushing | |||
* Fatigue | |||
* Lightheadedness | |||
* Pallor | |||
* Palpitations | |||
* Syncope | |||
| | | | ||
* Tremor | |||
* Hunger | |||
* Perspiration | |||
* Difficulty with concentration | |||
* Decreased consciousness | |||
|- | |- | ||
|'''Hormones''' | |'''Hormones''' | ||
| | | | ||
* Vasoactive agents (VIP, Neurotensin) | |||
* Incretins (GIP, GLP-1) | |||
* Glucose-modulating hormones (Glucagon, Insulin) | |||
| | | | ||
* Incretin | |||
|} | |} | ||
Revision as of 19:43, 7 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Dumping syndrome can be divided into two classifications. These classifications are based on the onset of symptoms after the first meal.
Classification
Early dumping
Early dumping syndrome occurs 15-30 minutes after a meal.[1]
- It starts with the intake of a hyperosmolar content.[2] 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 [3] via surgery
- Pyloric Dysfunction[3]
- Hormones released;[4][5][6][7]
- 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[8]
- . 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)[9].
- 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[10]
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[11]. 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.
| Early Dumping | Late Dumping | |
|---|---|---|
| Onset | 15-30 minutes after a meal | 60-180 minutes after a meal |
| Risk Factor | Bariatric Surgery | Hyperosmolar chyme |
| Mechanism |
|
|
| Symptoms |
|
|
| Hormones |
|
|
References
- ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ 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.
- ↑ 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.