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Dumping syndrome (DS) occurs when largely undigested foods, especially sugar, transits relatively fast from the stomach to the first part of the small intestine, the duodenum. This presents with many complications such as nausea, bloating, abdominal pain, hypoglycemia, tachycardia and changes in consciousness. These arise as a result of the osmotically active food particles causing a fluid shift from the intravascular compartment to the intestinal lumen.
DS may be classified as early dumping syndrome (EDS), which is characterized by symptoms within 30 minutes to 1 hour after a meal, or late dumping syndrome (LDS), which arises 1 to 3 hours later. DS may be treated in many ways including changes to eating habits, nutrition and diet. Likewise, pharmacotherapy and surgery may be used to alleviate the problems caused by DS. Most people tend to have mild symptoms and show improvement over time. Furthermore, they respond well to simple changes in their dietary regimen.
DS is largely manageable by diet - this entails the avoidance of certain foods and quantities that may trigger it. Patients are advised to have 5 or 6 small meals per day as opposed to eating 3 larger meals and to delay their fluid intake for at least half of an hour after eating. An increased intake of protein, complex carbohydrates and fiber is recommended. If food is thin (i.e. watery) patients may increase its thickness by adding plant-based extracts. The avoidance of simple sugars (e.g. table sugar in candy and beverages) is advised. Some patients note that lying down after meals helps to reduce their associated symptoms.
Several agents may be used to treat DS symptoms - acarbose is one such drug. It is an alpha-glycosidase inhibitor that interferes with the absorption of carbohydrates. This may effectively reduce the time delay between the insulin response to hyperglycemia and prevent hypoglycemia symptoms in patients with LDS. Its use, however, is limited by the undesirable side effect of diarrhea due to bacterial fermentation in the gut of unabsorbed carbohydrates. This is demonstrated by increased flatulence and increased breath hydrogen excretion.
Octreotide, a somatostatin analogue, may also be used to treat DS symptoms. It shows great short-term success but poor long-term efficacy. Octreotide, like somatostatin, inhibits insulin secretion as well as several other intestinal hormones. In DS, octreotide decreases gastric emptying by its effect on the migrating motor complex to baseline levels. In addition to these effects, octreotide also causes splanchnic vasoconstriction and inhibits vasodilation that occurs after eating. Side effects include steatorrhea (i.e. fatty stools) and weight gain.
If all the usually preferred conservative means of management prove ineffective then surgery may be an option for treatment. However, this is done with caution since most patients do get better over time and surgery itself often presents with unsuccessful results.