5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

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Dumping Syndrome
Updated: Jun 11, 2019
Author: Rajan Kanth, MD; Chief Editor: BS Anand, MD more...

OVERVIEW

Background
Anatomic structures of the stomach are divided into the cardia, fundus, body, and pylorus. The fundus
serves as the reservoir for ingested meals, while the distal stomach churns and mixes food with
digestive enzymes and initiates the digestive process. Once the foods are processed, the pylorus
releases the food in a controlled fashion downstream into the duodenum.

The capacity of the stomach in adults is approximately 1.5-2 liters, and its location in the abdomen
allows for considerable distensibility. Gastric motility is controlled by myogenic (intrinsic), circulating
hormonal, and neural activity (gastric plexus, myenteric plexus, sympathetic and parasympathetic
nerves). Alterations in the gastric anatomy after surgery or interference in its extrinsic innervation
(vagotomy) may have profound effects on the gastric reservoir and pyloric sphincter mechanism and,
in turn, alter gastric emptying. These effects, for convenience, have been termed postgastrectomy
syndromes.

Postgastrectomy syndromes include small capacity, dumping syndrome, bile gastritis, afferent loop
syndrome, efferent loop syndrome, anemia, and metabolic bone disease. Postgastrectomy syndromes
are iatrogenic conditions that may arise from partial gastrectomies, independent of whether the gastric
surgery was initially performed for peptic ulcer disease, cancer, or weight loss (bariatric). The surgical
procedures include Billroth-I, Billroth-II, and Roux-en-Y gastric bypass. [1]

Hertz made the association between postprandial symptoms and gastroenterostomy in 1913. [2] Hertz
stated that the condition was due to "too rapid drainage of the stomach." Wyllys et al first used the
term "dumping" in 1922 after observing radiographically the presence of rapid gastric emptying in
patients with vasomotor and GI symptoms. [3]

Pathophysiology
Dumping syndrome is the effect of altered gastric reservoir function, abnormal postoperative gastric
motor function, and/or pyloric emptying mechanism. [4, 5] See the image below.

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5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

Pathophysiology of dumping syndrome.

Clinically significant dumping syndrome occurs in approximately 10% of patients after any type of
gastric surgery and in up to 50% of patients after laparoscopic Roux-en-Y gastric bypass. Dumping
syndrome has characteristic alimentary and systemic manifestations. It is a frequent complication
observed after a variety of gastric surgical procedures, such as vagotomy, pyloroplasty,
gastrojejunostomy, and laparoscopic Nissan fundoplication. Dumping syndrome can be separated into
early and late forms, depending on the occurrence of symptoms in relation to the time elapsed after a
meal.

Postprandially, the function of the body of the stomach is to store food and to allow the initial chemical
digestion by acid and proteases before transferring food to the gastric antrum. In the antrum, high-
amplitude contractions triturate the solids, reducing the particle size to 1-2 mm. Once solids have
been reduced to this desired size, they are able to pass through the pylorus. An intact pylorus
prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by the
fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters each of these
mechanisms in several ways.

Gastric resection reduces the fundic reservoir, thereby reducing the stomach's receptiveness
(accommodation) to a meal. Vagotomy increases the gastric tone, similarly limiting accommodation.
An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric
emptying. Duodenal feedback inhibition of gastric emptying is lost after a bypass procedure, such as
gastrojejunostomy. Accelerated gastric emptying of liquids is a characteristic feature and a critical step
in the pathogenesis of dumping syndrome. Gastric mucosal function is altered by surgery, and acid
and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of
digestion are affected adversely. All these factors interplay in the pathophysiology of dumping
syndrome.

The accommodation response and the phasic contractility of the stomach in response to distention are
abolished after vagotomy or partial gastric resection. [6] This probably accounts for the immediate
transfer of ingested contents into the duodenum.

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5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

Early dumping syndrome and reflux gastritis are less frequent when segmented gastrectomy rather
than distal gastrectomy is performed for early gastric cancer. [7] In persons with long segment Barrett
esophagus treated with a truncal vagotomy, partial gastrectomy, and Roux-en-Y gastrojejunostomy,
41% developed dumping within the first 6 months after surgery, but severe dumping is rare (5% of
cases). [8] The dumping syndrome occurs in 45% of persons who are malnourished and who have had
a partial or complete gastrectomy. [9]

The late dumping syndrome is suspected in the person who has symptoms of hypoglycemia in the
setting of previous gastric surgery, and this late dumping can be proven with an oral glucose tolerance
test (hyperinsulinemic hypoglycemia), as well as gastric emptying scintigraphy, which shows the
abnormal pattern of initially delayed and then accelerated gastric emptying. [10]

Early dumping
Rapid emptying of gastric contents into the small intestine or colon may result in high amplitude
propagated contractions and increased propulsive motility, thereby contributing to the diarrhea seen in
persons with the dumping syndrome. [11] The emptying of liquids is fast relative to persons without
distal gastrectomy with Billroth-I reconstruction. [12]

Symptoms of early dumping syndrome occur 30-60 minutes after a meal. Symptoms are believed to
result from accelerated gastric emptying of hyperosmolar contents into the small bowel. This leads to
fluid shifts from the intravascular compartment into the bowel lumen, resulting in rapid small bowel
distention and an increase in the frequency of bowel contractions. Rapid instillation of liquid meals into
the small bowel has been shown to induce dumping symptoms in healthy individuals who have not
had gastric surgery. Bowel distention may be responsible for GI symptoms, such as crampy
abdominal pain, bloating, and diarrhea. Intravascular volume contraction due to osmotic fluid shifts is
perhaps responsible for the vasomotor symptoms, such as tachycardia and lightheadedness.

This hypothesis has been questioned for several reasons. First, the severity of dumping is not reliably
related to the volume of hypertonic solution ingested. Second, intravenous infusion sufficient to
prevent the postprandial fall in plasma volume may not abolish the dumping symptoms. Furthermore,
Kalser and Cohen measured intrajejunal osmolarity and glucose content using a continuous perfusion
method. [13] They found that the degree of dilution of the hyperosmolar glucose in patients who are
postgastrectomy was similar in symptomatic and asymptomatic subjects.

Provocation with oral glucose in patients with early dumping generally provokes an increase in the
heart rate. Although vasoconstriction is expected in a volume-contracted state, patients with dumping
syndrome have vasodilation. [14] An increase in blood flow to the superior mesenteric artery has been
described in patients with dumping syndrome. This peripheral and splanchnic vasodilatory response
seems to be pivotal in the pathogenesis of dumping.

In experimentally induced dumping in dogs, symptoms can be induced in a healthy animal by the
transfusion of portal vein blood. This led to the hypothesis that humoral factors may have an important
role in the pathogenesis of dumping. Some evidence suggests that hyperosmolar small intestine
content leads to serotonin release which, in turn, leads to mesenteric and peripheral vasodilation. It
results in fluid shifts and hypotension in the early phase of dumping syndrome.

The postprandial release of gut hormones, such as enteroglucagon, peptide YY, pancreatic
polypeptide, vasoactive intestinal polypeptide, glucagonlike peptide-1 (GLP-1), and neurotensin, is
higher in patients with dumping syndrome compared with asymptomatic patients after gastric surgery.
Some or all of these peptides are likely to participate in the pathogenesis of dumping syndrome.
Glucagon, GLP-1 and glucose-dependent insulinotropic peptide (GIP) levels were higher in those with
Roux-en-Y gastric bypass, as compared with those nonsurgical patients who were overweight or
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5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

morbidly obese. [15] The exaggerated postprandial GLP-1 release contributes to the symptoms of early
dumping by activating sympathetic outflow. [16]

One of the effects of these hormones is the retardation of proximal GI motility and the inhibition of
secretion. This function is called the ileal brake. Some authors have suggested that the accelerated
release of these hormones is an attempt to activate the ileal brake, thereby delaying proximal transit
time in response to the rapid delivery of food to the distal small bowel.

Late dumping
Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early
development of hyperinsulinemic (reactive) hypoglycemia. [17, 18] Rapid delivery of a meal to the small
intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid
absorption of glucose. This is countered by a hyperinsulinemic response. The high insulin levels stay
for longer period and are responsible for the subsequent hypoglycemia. Intrajejunal glucose induces a
higher insulin release than does the intravenous infusion of glucose. [19] The serum glucose levels
were the same in both experiments. This effect of enhanced insulin release after an enteral glucose
load as compared to intravenous glucose administration is called the incretin effect.

Two hormones are thought to play a pivotal role in the incretin effect. These are glucose-dependent
insulinotropic peptide and GLP-1. In human studies, an increase in GLP-1 response has been noted
after an oral glucose challenge. An increased GLP-1 response has been noted in patients after total
gastrectomy, esophageal resection, and partial gastrectomy. Furthermore, a positive correlation was
found between the rise in plasma GLP-1 and insulin release.

An exaggerated GLP-1 response likely plays an important role in the hyperinsulinemia and
hypoglycemia in patients with late dumping. The reason why some patients remain asymptomatic after
gastric surgery whereas others develop severe symptoms remains elusive.

Etiology
Dumping can be separated into early and late forms depending on the occurrence of symptoms in
relation to the time elapsed after a meal. Both forms occur because of the rapid delivery of large
amounts of osmotically active solids and liquids to the duodenum. This is a direct result of alterations
in the storage function of the stomach and/or pyloric emptying mechanism.

The severity of dumping syndrome is proportional to the rate of gastric emptying. Postprandially, the
stomach assumes its reservoir function to allow initial chemical digestion by acid and proteases before
transferring food to the antrum. In the antrum, high-amplitude contractions triturate solids. Once solids
have been reduced to 1-2 mm, they are able to empty through the pylorus. An intact pylorus has a
separating function that prevents the passage of larger particles into the duodenum. Gastric emptying
is controlled by fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters
these mechanisms in several ways.

Gastric resection can reduce the fundic reservoir, thereby reducing the receptiveness of the stomach
to a meal. Similarly, vagotomy increases gastric tone, limiting accommodation.

Any operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric
emptying. Duodenal feedback inhibition of gastric emptying is also lost after bypass of the duodenum
with gastrojejunostomy. Accelerated early gastric emptying of liquids is a characteristic feature and a
critical step in the pathogenesis of dumping syndrome.
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5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased.
Also, hormonal secretions that sustain the gastric phase of digestion are adversely affected.

Epidemiology
The global incidence and severity of symptoms in dumping syndrome are related directly to the extent
of gastric surgery. [5, 20] [21]

United States data

An estimated 20-50% of all patients who have undergone gastric surgery have some symptoms of
dumping. [21] However, only 1-5% are reported to have severe disabling symptoms. [21] The incidence
of significant dumping has been reported to be 6-14% in patients after truncal vagotomy and drainage
and from 14-20% after partial gastrectomy. The incidence of dumping syndrome after proximal gastric
vagotomy without any drainage procedure is less than 2%. Newer gastric operations, such as
proximal gastric vagotomy (which produces minimal disturbance of gastric emptying mechanisms), are
associated with a much lower incidence of postgastrectomy syndromes. In the pediatric population,
dumping syndrome is described almost exclusively in children who have undergone Nissen
fundoplication. [22]

Reductions in the need for elective gastric surgery have led to a decline in the frequency of
postgastrectomy syndromes. A 10-fold reduction has occurred in elective operations for peptic ulcer
disease in the last 20-30 years. Although this trend preceded the advent of histamine-2 receptor
antagonists, these drugs and proton pump inhibitors have accelerated the decline. Helicobacter pylori
treatment and eradication in patients with peptic ulcer disease have further decreased the need for
surgery.

Although the need for elective surgery for peptic ulcer disease has declined, the need for emergency
surgery has remained the same over the last 20 years. Emergency surgery tends to be more
mutilating to the stomach. This increases the incidence of more severe symptoms.

Gastric surgery is also performed as part of the care of persons with a gastric malignancy, or as an
approach to weight loss (bariatric surgery). Bariatric surgery is the only satisfactory long-term
treatment for severe obesity (body mass index [BMI] 40 kg/m² or greater, or 35 kg/m² or greater with
severe obesity-associated comorbidities, such as diabetes, obstructive sleep apnea, or debilitating
degenerative arthritis). Even in specialized units, the mortality rate of bariatric surgery may be 1%, and
serious complications may occur in about 10% of cases. [23]

Some 80% of the deaths that occur within a month of bariatric surgery arise from anastomotic leaks,
pulmonary emboli, and respiratory failure. Other authors report that long-acting octreotide is as
effective in the long term as subcutaneous octreotide, with superior symptom control as assessed by
the Gastrointestinal Specific Quality of Life Index, better maintenance of body weight, and higher
quality of life. [24] Pancreatic nesidioblastosis or pancreatic islet cell hyperplasia has been speculated
to contribute to the sometimes disabling neurologic immune restoration inflammatory syndrome
(NIRIS). Resection of this hyperplasia -- and therefore removing the exaggerated insulin response --
has been proposed.

Sex-related demographics

A female preponderance exists in the incidence of postgastrectomy syndromes.

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5/23/2021 Dumping Syndrome: Background, Pathophysiology, Etiology

Clinical Presentation
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