Gastric dumping syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

Gastric dumping syndrome is a group of symptoms that occur when food or liquid enters the small intestine too rapidly. These symptoms include cramps, nausea, diarrhea, and dizziness. Dumping syndrome sometimes occurs in people who have had a portion of their stomach removed.

The history of gastric dumping syndrome goes back over a hundred years. Over the years, various methods have been developed to detect it. It was initially described after bariatric surgery but later was found to be present in non-surgical causes as well.

Dumping syndrome can be divided into early dumping and late dumping syndrome based upon the timeline of onset of symptoms and clinical features.

The exact pathogenesis of dumping syndrome is not completely understood. Symptoms of early and late dumping syndrome appear to be caused by distinct pathological mechanisms. The pathogenesis can be divided into accelerated gastric emptying and reduced gastric volume.

Gastric dumping syndrome can be caused mainly by surgeries, diseases, and certain post-surgical diets.

Dumping syndrome may often be confused with other similar diseases that cause upper abdominal pain, nausea, and fatigue.

Incidence and prevalence varies depending on the procedure or disease leading to dumping syndrome.

The most common risk factor in the development of dumping syndrome is bariatric surgery. Dumping syndrome is not limited to surgery but occurs due to other conditions as well. The severity of dumping syndrome is proportional to the rate of gastric emptying following different surgical procedures:

There is insufficient evidence to recommend routine screening for dumping syndrome. Screening is done after exposure to the risk factors for dumping syndrome. The Sigstad score is a table of symptoms used to differentiate dumpers from non-dumpers (healthy). Other methods have been used but were never formally validated.

If left untreated dumping syndrome causes problems with digestion and absorption. This may in turn lead to symptoms such as nausea, vomiting, distention, abdominal pain and diarrhea.

The two most sensitive and specific tests used in confirming the clinical suspicion and in diagnosing Dumping syndrome are the oral glucose tolerance test and the Hydrogen breath test.

The history of dumping syndrome has to do with surgeries or diseases that alter the motility or capacity of the stomach. The most common history of dumping syndrome is a bariatric surgery history. The most common symptoms of dumping syndrome are diarrhea, shock, fainting, syncope, unconsciousness, desire to lay down or sit down, breathlessness, dyspnea, weakness, exhaustion, sleepiness, drowsiness, apathy, falling asleep, palpitation, restlessness, and dizziness.

Common physical examination findings of dumping syndrome include tachycardia, flushing, abdominal pain, abdominal distention, borborygmus, tremor and weight loss in most severe cases.

There are no diagnostic laboratory findings that help in diagnosing dumping syndromebut there are associated laboratory finding that may present if severe.

Other imaging options are useful in determining the anatomy and how well a patient will respond to therapy.

There are no other diagnostic studies associated with Dumping syndrome.

The main therapy for the management of dumping syndrome includes diet and pharmacological intervention.

Surgery is not the first-line treatment option for patients with dumping syndrome. Surgery is usually reserved for patients as a last resort.

Effective measures for the primary prevention of dumping syndrome include preventing or avoiding surgery and preventing risk factor exposure. No vaccines are available for dumping syndrome. Secondary prevention is similar to primary prevention. Investigational therapies of dumping syndrome include continuous enteral feeding, drugs, electrical pacing of the stomach and surgical re-intervention.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

The history of gastric dumping syndrome goes back over a hundred years. Over the years, various methods have been developed to detect it. It was initially described after bariatric surgery but later was found to be present in non-surgical causes as well.

• 1913, the symptoms of rapid emptying of the stomach after surgery was first described by Hertz^[1]
• 1920, the term “dumping” was made known by Andrew and Mix^[2]
• 1948, a British surgeon named Dr. A Hedely Visick developed a classification for dumping syndrome. This classification is based on the severity of the disease^[3]
• 1970, a Norwegian doctor named Dr. Helge Sigstad developed a diagnostic index for dumping syndrome. This index helps distinguish dumping syndrome from non-dumping cases
• 2008, a Belgium doctor named Dr. Joris Arts developed a scoring system using a questionnaire for dumping syndrome. This questionnaire helps distinguish early dumping syndrome from late dumping syndrome^[3][4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

Dumping syndrome can be divided into early dumping and late dumping syndrome based upon the timeline of onset of symptoms and clinical features.

Dumping syndrome may be classified based upon the timeline of the onset of symptoms and clinical features. The following table depicts the major classification systems of dumping syndrome :^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

The exact pathogenesis of dumping syndrome is not completely understood. Symptoms of early and late dumping syndrome appear to be caused by distinct pathological mechanisms. The pathogenesis can be divided into accelerated gastric emptying and reduced gastric volume.

Dumping syndrome occurs secondary to various conditions such as after gastric surgery (especially on taking meals high in carbohydrates after the procudure), diabetes mellitus, Zollinger-Ellison syndrome, and Ehlers-Danlos syndrome. The pathogenesis of dumping syndrome varies according to the etiology but the most essential component is the rapid gastric emptying. The exact cause is not yet concluded, although several known phenomena may contribute to the development of early dumping symptoms.^[1][2]

The main pathogenesis can be subdivided into the following:

• Accelerated gastric emptying
• Reduced gastric volume

• Alteration of the pyloric muscle that holds the gastric contents till complete digestion, leads to a rapid transit of gastric contents into the small intestine. This rapid descent of partially digested food into the intestines causes an osmotic shift of fluids from the extracellular compartment leading to hypotension which leads to the activation of the sympathetic nervous system
• Reactive hypoglycemia occurs secondary to hyperinsulinemia caused by high concentration of carbohydrates in the proximal small intestine and rapid absorption of glucose (late dumping)^[3][4]

• Removal of a part of the stomach and small intestine causes the food to bypass the stomach and rapidly descent through to the ileum or jejunum which may lead to osmotic shifting^[5]

• Dumping syndrome is most common in patients with certain types of stomach surgery, such as a gastrectomy or gastric bypass surgery, that allow the stomach to empty rapidly. Dumping syndrome can also occur as a result of complications after a cholecystectomy (gallbladder removal)^[6]

• Patients with esophageal cancer who undergo esophagectomy to remove the cancerous portion of their esophagus are also at an increased risk of developing dumping syndrome. The stomach is pulled into the chest and attached to what remains of the esophagus, leaving a short digestive tract^[1]

Surgery is one of the major causes leading to a reduced gastric volume. The following mechanisms lead to the development of dumping syndrome post surgery:^[5]

• Changes that affect the storage of food in the stomach or the alteration and manipulation of the pyloric muscle cuase delivery of hyperosmolar material into the intestine. Fluid shifts cause rapid small bowel distention and an increased peristalsis (early dumping)
• Supraphysiologic release of gastrointestinal peptides/vasoactive mediators lead to paradoxical vasodilation in a relatively volume-contracted state
• Removal of a part of the stomach can cause the contents to not digest and flow down undigested. This leads to a large hyperosmolar load entering into the intestines. This hyperosmolar chyme leads to an osmotic shift of fluids from the vascular compartment to the intestinal lumen. The major sequelae of this is hypotension and activation of the sympathetic nervous system
• 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.
• Glucagon-like peptide-1 (GLP1) plays a key role in the pathogenesis of late hypoglycemia after gastric bypass

The following are hormonal changes occur in dumping syndrome:^{[7][8][9][10][11][12]}

The following are effects caused by specific hormones:

The following illustraion outlines the major events involved in the pathogenesis of dumping syndrome (early and late):^[13][14]

There are a few diseases that have a different mechanism compared to conventional risk factors such as surgery leading to dumping syndrome. The following are the diseases:

• Zollinger-Ellison syndrome:
  • A rare disorder involving extreme peptic ulcer disease and gastrin-secreting tumors in the pancreas, may also have dumping syndrome

• Connective tissue disorders such as Ehlers-Danlos syndrome
  • Can experience “late” dumping as a result of decreased motility.

• Low blood sugar, or hypoglycemia:
  • Because the rapid “dumping” of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as “alimentary hypoglycemia“.
• Diabetes:
  • Neuropathy can cause damage to the nerves supplying the GIT

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

Gastric dumping syndrome can be caused mainly by surgeries, diseases, and certain post-surgical diets.

To review the various factors that contribute to the development of dumping syndrome, click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

Dumping syndrome may often be confused with other similar diseases that cause upper abdominal pain, nausea, and fatigue.

• Post-gastrectomy complications:
  • Post-vagotomy diarrhea
  • Small capacity syndrome
  • Short bowel syndrome
  • Afferent loop syndrome
  • Efferent loop syndrome
• Peptic ulcer disease
• Fistula
• Adhesion
• Stenosis
• Ischemia
• Gastritis
• Internal Hernia
• Insulinoma
• Glucose-lowering medication abuse
• Symptomatic gallstone disease
• Postprandial Hypotension
• Irritable bowel syndrome (IBS)

Gastric dumping syndrome should be differentiated from other diseases presenting with nausea, vomiting, diarrhea, fatigue and abdominal pain. The differentials include the following:

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

Gastric dumping syndrome should be differentiated from other diseases presenting with weight loss, vomiting, diarrhea, and abdominal pain. The differentials include the following:^{[1][2][3][4][5]}

Early dumping syndrome should be differentiated from other diseases presenting with abdominal pain, vomiting, nausea and early satiety. The differentials include the following:^[6][7][8]

Late dumping syndrome should be differentiated from other diseases presenting with hypoglycemia and nausea. The differentials include the following:^[9]

To review the differential diagnosis of Abdominal Pain, click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

Incidence and prevalence varies depending on the procedure or disease leading to dumping syndrome.

• The incidence of patients who have undergone gastric surgery ranges from approximately 20,000 to 50,000 per 100,000.^[1]
• Out of these about 1-5% reported severe symptoms.
• After truncal vagotomy with drainage the incidence of dumping syndrome has been reported to be 6,000 to 14,000 per 100,000.
• After proximal vagotomy without drainage the incidence of dumping syndrome has been reported to be is less than 2,000 per 100,000.
• After partial gastrectomy the incidence of dumping syndrome has been reported to be 14,000 to 20,000 per 100,000.
• Proximal vagotomy is a fairly newer procedure that leads to lower incidence rates due to the minimized interference in gastric emptying.^[2]

• Since the advent of proton pump inhibitors, the need for surgery has decreased and so has the incidence of dumping syndrome.
• In gastric surgery 1 out of 10 people develop dumping symptoms.
• In esophagectomy 1 out of 2 people developed symptoms of dumping syndrome.

• Prevalence has not been well studied in gastric dumping syndrome.^[3]

• In 2012, the mortality rate of bariatric surgery leading to dumping syndrome was approximately 1,000 per 100,000 individuals.^[4]

• People aged 45-74 are 2 times more likely to be diagnosed with dumping syndrome
• Children aged less than 1 year are 3 times less likely to be diagnosed with dumping syndrome^[5]
• Toddlers and preschoolers are are 7 times less likely to be diagnosed with dumping syndrome^[5]
• Children aged 5 to 14 years old are 10 times less likely to be diagnosed with dumping syndrome^[5]
• Elderly people whose ages are over 75 years old are 11 times less likely to be diagnosed with dumping syndrome^[5]
• Teenagers and adults aged 15 to 29 years old are 23 times less likely to be diagnosed with dumping syndrome^[5]

• Females have a higher chance of being diagnosed with dumping syndrome in comparison to men.^[5]

• People who are of white ethnicity tend to be more likely diagnosed with dumping syndrome.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

The most common risk factor for the development of dumping syndrome is bariatric surgery. Dumping syndrome is not limited to surgery but occurs due to other conditions as well. The severity of dumping syndrome is proportional to the rate of gastric emptying following different surgical procedures:

Various clinical conditions, procedures and co-morbidities increase the risk of developing dumping syndrome. The risk factors may be divided into those related to surgeries, diet related and those related to comorbid conditions

• Surgical
  • Gastrectomy^[1] (partial and total)
  • Esophagectomy^[2]
  • Billroth I gastroduodenostomy^[3]
  • Billroth II gastrojejunostomy^[3]
  • Roux-en-Y gastric bypass surgery^[3]
  • Antiulcer surgery (vagotomy)^[4]
  • Antireflux surgery (Nissen fundoplication, especially in pediatric patients)^[5]
  • Cholecystectomy^[6]
  • Pyloromyotomy^[7]
  • Esophageal repair of esophageal atresia^[8]
  • Laparoscopic sleeve gastrectomy (LSG)^[9]
• Post-surgical diet
  • High carbohydrate (sugar)
• Diseases^[10][11][12]
  • Diabetes mellitus
  • Zollinger-Ellison syndrome
  • Ehlers-Danlos syndrome^[13]
  • Duodenal ulcer
  • Exocrine Pancreatic insufficiency

• Surgical
  • Gastrectomy
  • Esophagectomy
  • Billroth I gastroduodenostomy
  • Billroth II gastrojejunostomy
  • Roux-en-Y gastric bypass surgery
  • Vagotomy
  • Pyloromyotomy
  • Esophageal repair of esophageal atresia

• Post-surgical diet
  • High carbohydrate (sugar)/hyperosmolar
• In the pediatric population, almost all cases of dumping syndrome occurs in those who have undergone Nissen fundoplication.

• Diabetes mellitus
• Zollinger-Ellison syndrome
• Duodenal ulcer
• Exocrine pancreatic insufficiency
• Ehlers-Danlos syndrome

The following are the risk factors in alphabetical order:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

There is insufficient evidence to recommend routine screening for dumping syndrome. Screening is done after exposure to the risk factors for dumping syndrome. The Sigstad score is a table of symptoms used to differentiate dumpers from non-dumpers (healthy). Other methods have been used but were never formally validated.

There is insufficient evidence to recommend routine screening for dumping syndrome.

• The Sigstad diagnostic score system is used to determine dumping syndrome versus non-dumping syndrome.^[1]
• A score greater than 7 suggests dumping.
• A score less than 4 is suggest other diseases.

The Visick classification is used to determine the severity of dumping syndrome.

The Arts’ questionnaire helps distinguish early dumping syndrome from late dumping syndrome:^[2]

• This questionnaire is scored on a 4-point Likert scale.

• This is a survey used to determine early versus late dumping syndrome.^[3]
• A score greater than 10 mm suggests dumping.

• Helps identify dumping symptoms.^[4]
• The questionnaire consists of 15 total questions.
• This questionnaire is scored on a 6 to 7-point Likert scale.
• It is used 6-12 months after surgery.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Umar Ahmad, M.D.[2]

If left untreated, dumping syndrome causes problems with digestion and absorption. This may in turn lead to symptoms such as nausea, vomiting, abdominal distention, abdominal pain and diarrhea.

• Over time, the symptoms of dumping syndrome tend to resolve.
• The severe symptoms of dumping syndrome usually develop 3-24 months after surgery, and start with symptoms such as nausea, vomiting, abdominal distension, colicky abdominal pain, abdominal fullness and diarrhea.^[1]
• The symptoms of dumping syndrome usually continue in up to 1% to 2% of individuals within the first year after surgery.
• If left untreated, patients with dumping syndrome may progress to develop early satiety, weight loss, malnutrition, hypoglycemia and nesidioblastosis.^[2]

Possible complications of dumping syndrome include:

• Indigestion of food, which results in reduced vitamin, mineral and nutrient absorption into the body.
• Very low blood glucose that can cause mental confusion or incoherence after a meal.
• Weight loss (out of fear of eating meals).

• Prognosis of dumping syndrome is generally good, but it may interfere with the quality of life.

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