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Dumping Syndrome NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #35 Carol Rees Parrish, R.D., M.S., Series Editor Dumping Syndrome Andrew Ukleja Dumping syndrome is a constellation of gastrointestinal and vasomotor symptoms resulting from changes in the anatomy and physiology of the stomach created by gas- tric surgery. Dumping syndrome is frequently attributed to the rapid emptying of gastric content into the small bowel. However, the etiology of dumping syndrome is multifactorial. Severe dumping can be complicated by malnutrition and it can be asso- ciated with poor quality of life. Most patients with dumping syndrome can be treated conservatively with dietary modifications. Octreotide is the most effective drug therapy for patients with incapacitating symptoms. Those patients who failed medical therapy may be considered as surgical candidates. The aim of this article is to review the clini- cal features and pathophysiology of dumping syndrome in addition to providing guide- lines for its management. INTRODUCTION The incidence and severity of the symptoms asso- perations on the stomach can lead to a variety of ciated with dumping correlate with the type of gastric undesirable and chronic sequelea. The dumping surgery. Dumping occurs in approximately 15%–20% Osyndrome refers to gastrointestinal (GI) and of patients after partial gastrectomy (3). Significant vasomotor symptoms that occur following ingestion dumping has been reported in 6%–14% of patients of a meal in individuals after gastric surgery. The asso- who have undergone truncal vagotomy with drainage. ciation between postprandial symptoms and rapid A lower incidence of dumping has been observed after drainage of the stomach after gastroenterostomy was proximal gastric vagotomy without drainage proce- first described by Hertz in 1913 (1). The term “dump- dure. After Roux-en-Y gastric bypass, 50% to 70% of ing” was introduced by Andrews and Mix in 1920, patients experience dumping syndrome in the early who reported a radiographic observation of rapid gas- post-operative period (4). However, symptoms of tric emptying of contrast in patients with typical dumping subside after 15–18 months from gastric dumping symptoms after gastrectomy (2). bypass. In children, dumping syndrome has been reported almost exclusively after fundoplication (5). Andrew Ukleja, M.D., Assistant Professor of Medicine, Only a minority (1%–5%) of patients with dumping Department of Gastroenterology, Cleveland Clinic, syndrome suffer from severe, disabling symptoms. Weston, Florida. (continued on page 34) 32 PRACTICAL GASTROENTEROLOGY • FEBRUARY 2006 Dumping Syndrome NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #35 (continued from page 32) CLINICAL FEATURES OF DUMPING SYNDROME to under- and malnutrition. Weight loss of up to 30% The clinical manifestations of dumping include GI and from preoperative weight has been reported in patients vasomotor symptoms. Dumping syndrome can be with severe dumping (8). divided into early and late dumping depending on the relation of symptoms to the time elapsed after a meal PATHOPHYSIOLOGY OF DUMPING SYNDROME (Table 1). The severity of symptoms varies between The pathogenesis of a dumping syndrome is poorly individuals. Symptoms of early dumping occur within understood and it is likely to be multifactorial (Table 10–30 minutes after meals. They result from acceler- 2). The alterations of gastric anatomy by surgery, ated gastric emptying of hyperosmolar content into the including resection or bypass of the pylorus, and inter- duodenum or small bowel, followed by fluid shifts ference with gastric innervation, have a profound from the intravascular compartment into the intestinal effect on the rate of gastric emptying. The accommo- lumen. This leads to small bowel distention and dation and the cyclic contractility of the stomach in increased intestine contractility, both, believed to be response to distention are abolished after partial gas- responsible for GI symptoms such as nausea, bloating, trectomy, allowing immediate dumping of gastric con- abdominal cramps, and explosive diarrhea (6). The tents into the jejunum (9). This accelerated gastric majority of patients have early dumping and they suf- emptying of liquids is a critical step in the pathogene- fer from both GI and vasomotor symptoms. sis of dumping syndrome. Rapid delivery of large Late dumping occurs 1–3 hours after a meal, and it amounts of hyperosmolar chyme into the upper small is characterized predominantly by systemic vascular intestine leads to bowel distention and intestinal hyper- symptoms including flushing, dizziness, palpitations, motility. However, no difference in rate of gastric emp- and an intense desire to lie down. Physical exam of tying was found between patients with and without these patients may reveal profound orthostatic changes dumping symptoms after surgery in a few studies sug- including drop in blood pressure and increased heart gesting other mechanisms may be involved in the eti- rate. Late dumping occurs in approximately 25% of ology of dumping (10). patients with dumping syndrome. Those patients with Gastric emptying is under control by fundic tone, late dumping have mostly vasomotor symptoms. Late antropyloric mechanism, and duodenal feedback, regu- dumping is a consequence of reactive hypoglycemia lated by the enteric nervous system and circulating GI from an exaggerated release of insulin (7). hormones. Relative intravascular volume contraction Uncontrolled severe dumping can result in sito- and hemoconcentration occur as a consequence of phobia (fear of food or eating) and weight loss leading osmotic shift of fluids from the intravascular compart- ment into the gut lumen. Rapid Table 1 heart rate, elevated hematocrit and Symptoms of the dumping syndrome drop in plasma volume have been observed in patients in response to Abdominal Vasomotor/Systemic oral hyperosmolar glucose with early dumping (11). This leads to Early dumping Late dumping release of vasoactive GI hormones Epigastric fullness Diaphoresis Difficulty with concentration responsible for peripheral and Nausea Desire to lie down Decreased consciousness splanchnic vasodilatation and vaso- Diarrhea Headache Hunger motor symptoms such as flushing, Vomiting Flushing Perspiration tachycardia and dizziness. Hin- Abdominal cramps Fatigue Tremor shaw, et al first reported peripheral Borborygmi Lightheadedness vasodilatation in patients with Bloating Pallor Palpitations dumping syndrome, despite a vol- Syncope ume-contracted state (12). How- ever, vasodilatation has not been 34 PRACTICAL GASTROENTEROLOGY • FEBRUARY 2006 Dumping Syndrome NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #35 Table 2 Mechanisms responsible for ealy and late dumping confirmed by other investigators (13). Low plasma lev- quent late hypoglycemia (19). However, it is not clear els of atrial natriuretic peptide (ANP) and elevated lev- why only some patients develop dumping symptom els of aldosterone, activation of the rennin-aldosterone while others are asymptomatic after surgery. axis, have been reported in early dumping in response to hypovolemia (14). A role of hormones in the etiology of the syndrome THE DIAGNOSTIC DILEMMA has been confirmed in animal study by induction of Dumping syndrome is diagnosed based on constella- dumping symptoms in a healthy dog after a blood trans- tion of characteristic symptoms after meals in a patient fusion from portal vein of another dog with dumping who has undergone gastric surgery or by a dumping syndrome (15). Higher postprandial levels of gut hor- provocation test. Laboratory studies are rarely helpful mones such as pancreatic polypeptide, enteroglucagon, in establishing the diagnosis. In severely malnourished peptide YY (PYY), vasoactive intestinal polypeptide patients, anemia and hypoalbuminemia may be found. (VIP), neurotensin and glucagon-like peptide (GLP) A diagnostic scoring system has been developed by have been documented in patients with a dumping syn- Sigstad (20) (Table 3). The score index is very helpful in drome (16,17). Neurotensin, VIP, and PYY delay assessing a response to therapy. It is based on weighing motility of the upper GI tract and reduce gastric and factors assigned to symptoms of dumping. A score index intestinal secretions. In response to rapid delivery of a higher than 7 points is suggestive of dumping syndrome. meal to the small intestine, high concentration of car- Oral glucose provocation and hydrogen breath bohydrates is seen in the proximal small bowel fol- tests are useful when the diagnosis is in doubt. Symp- lowed by rapid absorption of glucose into the circula- toms of early dumping can be elicited by an oral glu- tion. Hyperglycemia stimulates rapid insulin secretion cose challenge. A rise in heart rate by 10 beats per followed by reactive hypoglycemia. Glucose-depen- minute or more in the first hour after an oral glucose dent insulinotropic peptide and GLP-1 produced in the challenge (with 50 g of glucose), following 10-hour small bowel and colon, respectively, are believed to be fasting is diagnostic. This test was found to be highly mediators of late dumping (18). Exaggerated release of sensitive and specific, 100% and 92%, respectively GLP-1 induces hyperinsulinemic response and subse- (continued on page 39) PRACTICAL GASTROENTEROLOGY • FEBRUARY 2006 35 Dumping Syndrome NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #35 (continued from page 35) be restricted. Patients should be instructed to avoid liq- Table 3 Dumping symptoms according to the uids for at least 30 minutes after
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