Description

GI and vasomotor symptoms resulting from rapid gastric emptying and delivery of large amounts of hyperosmolar content into the small intestine

• Usually occurs following gastric and esophageal surgery (gastrectomy, vagotomy, pyloroplasty, esophagectomy, Nissen fundoplication, or gastric bypass procedures)
• More prevalent with rising numbers of bariatric surgical procedures

Epidemiology

• Overall, ~10% of patients following gastric surgery and up to 50% of patients who undergo esophagectomy develop dumping symptoms.
• Predominant age: middle age to elderly
• Predominant sex: female > male

Incidence

• In the United States, ~1% of patients undergoing proximal gastric vagotomy without any drainage procedure; 10–22% truncal vagotomy and drainage experience dumping syndrome.
  • After partial gastrectomy, 14–20% of patients develop symptoms of dumping.
• Prominent feature after bariatric surgery:
  • >70% of gastric bypass patients experience varying degrees of dumping symptoms.
  • Up to 40% of patients have dumping symptoms 6 to 12 months after sleeve gastrectomy (1)[B].
  • Regarded as a beneficial feature of gastric bypass surgery because patients learn to avoid calorie-rich foods and eat small meals

Etiology and Pathophysiology

The pathogenesis of dumping syndrome is multifactorial.

• Alterations in the storage function of the stomach and/or the pyloric emptying mechanism lead to rapid delivery of hyperosmolar material into the intestine. Fluid shifts from the intravascular compartment into the bowel lumen lead to rapid small bowel distention and an increased peristalsis (early dumping).
• Supraphysiologic release of GI peptides/vasoactive mediators lead to paradoxical vasodilation in a relatively volume-contracted state.
• Reactive hypoglycemia occurs secondary to hyperinsulinemia caused by high concentration of carbohydrates in the proximal small intestine and rapid absorption of glucose (late dumping).
• Pancreatic islet cell hyperplasia, rather than late dumping, is thought to be the underlying mechanism for hyperinsulinemic hypoglycemia with nesidioblastosis after gastric bypass. These patients do not respond to treatment for dumping syndrome, and it is difficult to confirm this rare diagnosis.
• A recent study showed glucagon-like peptide-1 (GLP1) played a key role in the pathogenesis of late hypoglycemia after gastric bypass (2)[B].

Risk Factors

Gastric surgery is the main risk factor. The severity of dumping syndrome is proportional to the rate of gastric emptying following different surgical procedures:

• Bariatric surgery (i.e., Roux-en-Y gastric bypass [RYGB])
  • Laparoscopic sleeve gastrectomy (LSG) is also associated dumping syndrome.
• Gastric drainage procedures (e.g., pyloroplasty)
• Partial gastrectomy
• Total gastrectomy: Pouch formation has less dumping and heartburn.
• Esophagectomy
• Antiulcer surgery (e.g., vagotomy)
• Antireflux surgery (e.g., Nissen fundoplication, especially in pediatric patients)

General Prevention

• Dietary modifications (frequent, small, dry meals that contain limited amount of refined carbohydrates; restrict fluids to between meals; avoid milk products and increase protein/fat intake; increase dietary fiber)
• Postural changes (supine for 30 minutes after meals)
• New bariatric surgical techniques may reduce postoperative dumping syndrome.

Commonly Associated Conditions

• Peptic ulcer disease
• Reactive hypoglycemia
• Gastrectomy/vagotomy/pyloroplasty
• Esophagectomy
• Post-Nissen fundoplication (pediatric reflux)
• After gastric bypass or sleeve gastrectomy procedure for morbid obesity