Hi Crystal,
Here is an article on it.
Source:
Dumping Syndrome=
Dumping Syndrome
William L. Hasler, MD Current Treatment Options in Gastroenterology 2002,
5:139-145
Current Science, Inc. ISSN 1092-8472
Copyright © 2006 by
Current Science, Inc.Opinion StatementThe dumping syndrome consists of early postprandial abdominal and vasomotor symptoms, resulting from osmotic fluid shifts and release of vasoactive neurotransmitters, and late symptoms secondary to reactive hypoglycemia. Effective relief of symptoms of dumping syndrome can be achieved with dietary modifications to minimize ingestion of simple carbohydrates and to exclude fluid intake during ingestion of the solid portion of the meal. More severely affected individuals may respond to agents such as pectin and guar, which increase the viscosity of intraluminal contents, or to drugs such as the alpha-glucosidase inhibitor acarbose, which blunts the rapid absorption of glucose, and the somatostatin analog octreotide, which alters gut transit and impairs release of vasoactive mediators into the bloodstream.
Introduction
The dumping syndrome complicates the course of 10% to 20% of patients who have undergone gastric surgery for ulcer disease or neoplasm. The most consistent functional defect in dumping syndrome is the rapid emptying of liquids from the stomach into the intestine. As a consequence, a constellation of symptoms develops in response to hydrodynamic and neurohumoral responses to this fluid and nutrient load. Early dumping symptoms, including diarrhea, abdominal discomfort, and vasomotor symptoms, occur in the initial 10 to 60 minutes after eating, whereas late dumping symptoms secondary to reactive hypoglycemia are manifest 90 to 240 minutes postprandially. Adaptation to these dumping symptoms may occur over time; however, a subset of patients experiences persistent, intractable symptoms.
Pathogenesis
Any surgery that involves section of the abdominal vagus may lead to development of dumping syndrome. The syndrome also may develop after operations that involve no nerve transection but that enhance the drainage of the distal stomach, including pyloroplasty, pylorectomy, or antrectomy. Recent investigations of pylorus-preserving gastrectomies for early gastric cancer report fewer problems with dumping syndrome, indicating the importance of the barrier function of the gastroduodenal junction [
1]. Finally, surgeries such as fundoplications that impair accommodation of ingested food or that reduce proximal gastric compliance can lead to dumping syndrome [
2,
3]. In general, all such procedures lead to the acceleration of emptying of liquids from the gastric remnant with variable effects on transit of solid meal residue [
4]. Several pathophysiologic mechanisms underlie the development of rapid emptying in patients with dumping syndrome [
5]. The loss of vagal input leads to impairment of receptive relaxation prior to meal bolus entry into the stomach and blunted intragastric accommodation. The volume of the gastric remnant may be too small to physically hold the ingested meal. Resection of the pylorus and antrum may eliminate the normal physiologic retarding function of the distal stomach. Finally, the construction of a gastrojejunostomy may bypass the duodenal mucosal receptors that normally participate in nutrient-mediated feedback inhibition of gastric emptying. Factors other than rapid liquid emptying most likely participate in the development of dumping syndrome, because most patients who exhibit rapid liquid emptying after vagotomy have no symptoms [
6]. Furthermore, slowing the rate of nutrient entry into the intestine does not ameliorate all symptoms in patients who have dumping syndrome [
7].
The symptoms of dumping syndrome are consequences of the exuberant postprandial delivery of nutrient liquids (and to a lesser degree solids) into the small intestine. The abdominal discomfort of dumping syndrome is reproducible by inflation of a small intestinal balloon, indicating that mechanical factors may contribute to generation of this symptom [
8]. The rapid emptying of liquids evokes an osmotically driven movement of fluid from the intravascular space into the intestinal lumen. This augmented liquid volume in concert with the rapid transit observed after vagotomy promotes the development of urgent watery diarrhea in the early postprandial period [
9]. Vasomotor symptoms result from both the contraction of the intravascular space as well as exaggerated postprandial release of vasoactive gut hormones including serotonin, bradykinin, substance P, gastric inhibitory peptide, neurotensin, and vasoactive intestinal polypeptide [
10,
11]. In healthy individuals who have had no gastric surgery, nutrients are digested and absorbed in the proximal intestine. After vagotomy or gastric drainage surgery, liquid meal residue overwhelms the normal absorptive capabilities of the proximal gut and exposes the distal small intestine to a considerable nutrient load. Mucosal tissues of the ileum and colon are the source many of the peptides released in excess. Furthermore, early dumping syndrome is associated with activation of the renin-aldosterone axis with increases in plasma renin activity and aldosterone and decreases in atrial natriuretic peptide [
12]. In the late postprandial period, reactive hypoglycemia may develop as a consequence of exaggerated release of insulin and glucagon-like peptide 1 [
13*]. The norepinephrine level also increases during the late postprandial period. In healthy volunteers, intravenous infusion of glucagon-like peptide 1 produces tenfold increases in insulin levels with development of hypoglycemia [
14].
Clinical features
Approximately 75% of patients experience early dumping symptoms, which include alimentary symptoms of pain, diarrhea, gas, borborygmi, bloating, and nausea as well as vasomotor symptoms such as flushing, palpitations, diaphoresis, lightheadedness, tachycardia, and syncope. Symptom severity can range from minor postprandial abdominal symptoms to disabling diarrhea and loss of vascular tone [
15]. Physical examination may be normal or exhibit profound orthostatic or supine tachycardia and hypotension. When severe, the dumping syndrome can be debilitating, producing a 30% weight loss compared with preoperative levels.
Late dumping symptoms such as diaphoresis, palpitations, tremulousness, hunger, weakness, confusion, and syncope occur less commonly than early dumping symptoms and are believed to result from reactive hypoglycemia. Not all patients with late dumping syndrome exhibit low enough glucose levels to produce symptoms, suggesting a role for other undefined factors in the pathogenesis of late symptoms.
Diagnosis
The diagnosis of dumping syndrome relies on recognition of the characteristic symptom profiles in the patient who has undergone prior gastric surgery. Laboratory studies rarely are needed for diagnosis but may define nutritional deficits in patients with disabling illness and can provide evidence of hemoconcentration with early dumping syndrome and hypoglycemia with late dumping syndrome. In severely malnourished patients, anemia or hypoproteinemia may be observed. Responses to oral glucose (50 to 75 g in 300 mL) consistent with dumping syndrome include a rise in postprandial hemoglobin, increase in heart rate by 10 beats per minute or more, elevated plasma glucose 30 to 60 minutes after eating, and low glucose concentrations 120 to 240 minutes after meal ingestion [
16*]. An early rise in breath hydrogen excretion after glucose ingestion indicative of rapid intestinal transit is reported to be a sensitive indicator of the dumping syndrome [
16*]. Scintigraphic quantification of gastric emptying, especially of liquids, usually is abnormal in dumping syndrome but adds little to the clinical management in most cases. Rapid emptying is most impressive in the initial 15 minutes after meal ingestion [
4].
Treatment
•
Dietary manipulations form the mainstay of treatment of dumping syndrome and are reasonably effective in most patients. However, a subset of patients experience refractory symptoms that can lead to weight loss, fear of eating, and disability. These individuals are referred for consideration of medication or surgical therapy of severe dumping syndrome.
Diet and lifestyle
•
Ingestion of a diet high in proteins and fats and low in carbohydrates with minimal intake of fluids during a solid meal is recommended.
•
Nonnutritive fluids should be taken either after or before ingestion of solids.
•
Inclusion of pectin to increase liquid viscosity may delay gastric emptying and reduce dumping symptoms [
17].
•
In patients who have undergone vagotomy, liquid emptying is more rapid when sitting than when supine [[URL="http://javascript<b></b>:void(0)"]7,
18]. Thus, assumption of a supine position after drinking liquids may be beneficial when other dietary measures are inadequate.
•
Patients with late dumping symptoms secondary to postprandial hypoglycemia may respond to the ingestion of simple sugars when symptomatic.
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Pharmacologic treatment
•
Pharmacologic therapies directed at reducing symptoms in dumping syndrome may act via several mechanisms.
•
Agents that increase the viscosity of liquid meals delay emptying of food residue into the small intestine.
•
Drugs that blunt glucose absorption can reduce exaggerated release of insulin and minimize postprandial hypoglycemia.
•
Treatments that slow transit and block release of vasoactive mediators decrease the gastrointestinal, vasomotor, and endocrinologic manifestations of dumping syndrome