Dumping Syndrome

Etiology

The severity of dumping syndrome is correlated to the extent of gastric surgery. Surgical etiologies include gastrojejunostomy, antrectomy, pylorectomy, pyloroplasty, esophagectomy, vagotomy, Roux-en-Y bypass, and Nissen fundoplication.[5][6]

Non-surgical etiologies include diabetes mellitus, viral illness, and idiopathic causes.

Epidemiology

In patients who have undergone gastric surgery, an estimated 20% to 50% of patients have symptoms of Dumping syndrome. Patients develop severe symptoms approximately at a rate of 1 to 5%. Early Dumping syndrome appears to have a higher incidence compared to late Dumping syndrome.

Pathophysiology

Dumping syndrome is likely caused by the rapid movement of chyme. In patients without gastric surgery, digestion is initiated in the stomach, and the transition to the duodenum occurs progressively. Acid and proteases initiate the breakdown of food, promoting smaller food particles to be digested in the duodenum. This physiological process is weakened when there is surgical manipulation of this pathway. The pylorus bypass or alteration of the gastric innervation can produce effects of decreased stomach reserve or rapid transit of hyperosmolar food material into the duodenum.

In addition, the enteric nervous system plays a major role in the regulation of gastric emptying, involving several gastrointestinal (GI) hormones and the extrinsic innervation.

There are two types of problems that can arise from gastric surgery- early and late dumping syndromes.

Early Dumping

In early dumping, the symptoms usually occur within 10 to 30 minutes after a meal. The rapid transit of hyperosmolar chyme from the stomach into the duodenum causes fluid to shift from the vasculature to the intestinal lumen, leading to increased volume in the small bowel. This is believed to be the cause of abdominal cramps, tachycardia, nausea, and diarrhea.

GI hormones such as enteroglucagon, pancreatic polypeptide, peptide YY, vasoactive intestinal polypeptide, glucagon-like peptide, and neurotensin have been evident with higher values after meals. Hormonal imbalances may cause delayed motility, decreased gastric and intestinal secretions, which delays the digestion and transit of food that arrives at the small bowel.

Late Dumping

Late dumping, also known as postprandial hyperinsulinemic hypoglycemia, usually occurs 1 to 3 hours after a high-carbohydrate meal. There is an association with hypoglycemia, but the exact mechanism is unknown. It is proposed that the rapid absorption of carbohydrates exaggerates the glucose-mediated insulin response.

History and Physical

Dumping syndrome occurs in patients who have had gastric surgery. Symptoms of early dumping occur within 10 to 30 minutes after a meal. Late dumping can present 1 to 3 hours after a high-carbohydrate meal.

There may be GI or vasomotor symptoms. GI symptoms include nausea, vomiting, diarrhea, or belching. Vasomotor symptoms include shock, syncope, near-syncope, palpitations, dizziness, desire to lie down, or diaphoresis.

Evaluation

Sigstad developed a diagnostic index for Dumping syndrome, which includes multiple signs or symptoms such as nausea, vomiting, and shock. A score of greater than seven may suggest Dumping syndrome.

A rating scale based on a self-assessment questionnaire, the Dumping Symptom Rating Scale, is another way to identify patients with severe symptoms.

An oral glucose challenge test can trigger the signs and symptoms of Dumping syndrome. After a 50-gram oral glucose challenge following a 10-hour fast, if the patient has an elevated heart rate by ten beats or more per minute in the first hour, studies demonstrate 100% sensitivity and 94% specificity for early Dumping syndrome.

Additional methods to elicit more information regarding the anatomy include endoscopy, barium upper GI study, and gastric emptying scan.

Treatment / Management

Diet

Most cases of dumping syndrome are successfully treated with dietary adjustments. The suggested division of meals recommended is at least six times per day. Liquids should be withheld until 30 minutes after the meal. In addition, simple sugars and milk products should be avoided. Protein and fat calories should be increased to compensate for the decreased carbohydrate intake. Fiber-rich food is encouraged and has shown to promote a longer transit time in the bowel.

Medications

In a patient who continues to demonstrate symptoms despite dietary modifications, drug therapy may be considered. Several options include tolbutamide and propranolol.

Octreotide is a somatostatin analog which inhibits several GI hormones. The therapeutic effects occur with delayed gastric emptying, decreased the release of GI hormones, prolonged small intestine transit time, decreased insulin release, and splanchnic vasoconstriction. Multiple studies have shown that octreotide was alleviating symptoms of dumping syndrome both as short and long-term therapy.

Acarbose is a competitive inhibitor of intestinal brush border α-glucosidase that has a higher affinity to the enzyme compared to the normal substrate. However, since it is a reversible interaction, the breakdown of oligosaccharides to monosaccharides is slowed. This delayed conversion helps prevent the adverse effects of late dumping. Studies have demonstrated a reduction in symptoms of postprandial hypoglycemia.

Surgery

Surgical interventions are reserved for patients who fail conservative measures. There are several options, including stomal revision, Billroth II to Billroth I anastomoses, pyloric reconstruction, jejunal interposition, and Roux-en-Y conversion.

Stomal revision encompasses the narrowing of the gastrojejunal stoma, which delays gastric emptying. However, complications such as gastric outlet obstruction and strictures are seen. This intervention no longer has a role in Dumping syndrome.

The Billroth II to Billroth I conversion anastomosis resumes the transit of food to the duodenum. It is a simple intervention with minimal complications. The risk of gastric outlet obstruction is avoided here as well.

Pyloric reconstruction is useful in patients who have dumping syndrome after pyloroplasty. The pyloroplasty scar is cut, and the sphincter muscle is then approximated.

Jejunal interposition involves the interposition of the isoperistaltic jejunal loop. One study demonstrated improvement of the early dumping syndrome, however further studies did not reproduce the same results.

The Roux-en-Y conversion into Roux-en-Y gastrojejunostomy delays gastric emptying and the transit through the Roux limb. Even though the mechanism for improved symptoms of Dumping syndrome is not known, favorable outcomes have been demonstrated.

Differential Diagnosis

Dumping syndrome is mainly characterized by abdominal pain, nausea/vomiting, weight loss, diarrhoea, early satiety, flushing and fatigue. These symptoms are manifestations of a variety of gastrointestinal and endocrine conditions so careful evaluation is warranted.

Prognosis

Most cases of dumping syndrome are successfully treated with dietary adjustments. If dietary adjustments fail, the healthcare provider might recommend medical or surgical management but the success of such interventions is not well established.