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Dumping syndrome is a known problem for persons who have undergone gastric, esophageal or bariatric surgeries. It is believed to as a direct consequence of the rapid transit of large osmotically active food particles into the lumen of the small intestine. It is estimated that up to 1 in 5 people who have had parts of their stomach surgically removed develop the condition.
Depending on the timing of the occurrence of symptoms after a meal, dumping syndrome may be classified as early dumping syndrome (EDS) or late dumping syndrome (LDS), which both are due to the rapid transit of food in the body, but are proposed to have slightly different underlying pathophysiological mechanisms. Despite some overlap, they each have different symptoms. The majority of people will tend to present with EDS symptoms while approximately 25% will present with LDS clinical manifestations.
EDS tends to occur 30 to 60 minutes after a meal and is due to the hyperosmolarity produced by the largely undigested particles in the small bowel lumen. This leads to fluid shifting from the intravascular compartment to the lumen and this is the main cause of the symptoms associated with EDS. These symptoms include, but are not limited to:
The signs and symptoms of EDS have been tested by several studies which demonstrate that the depletion of intravascular volume and fluid shifts leads to the cardiovascular and gastrointestinal manifestations observed. Dumping experimentally induced in dogs by transfusing them with portal vein blood, has led some to propose that humoral factors may be significant players in the pathogenesis of EDS. There is evidence that suggest a hyperosmolar small intestinal lumen causes the release of serotonin which mediates the vasodilation of the mesenteric and peripheral vessels thereby causing fluid shifts and hypotension.
Other studies have demonstrated that postprandial release of gut hormones such as glucagon-like peptide-1 (GLP-1) may also be implicated in the symptoms of EDS by its activation of sympathetic outflow. GLP-1 tries to slow proximal gut motility and reduce acid secretion. It thereby attempts to delay the proximal transit time as a response to the rapid delivery of large food particles to the distal parts of the small intestines.
LDS is believed to be due to an overwhelming increase in insulin that leads to reactive hypoglycemia (i.e. low blood sugar level). It occurs anywhere between 1 to 3 hours after eating. The hypoglycemia associated with LDS causes symptoms such as:
LDS-reactive hypoglycemia occurs due to a rapid absorption of glucose from the small intestine and a responsive hyper-secretion of insulin that stays elevated for a period longer than usual. GLP-1 is thought to play a crucial role in LDS as it is a potent anti-hyperglycemic hormone. It is often found to have an elevated response in patients who have had operations that speed up gastric emptying and causes increased insulin secretion, further compounding hypoglycemia.