REvIEWS

pathophysiology, diagnosis and management

of postoperative dumping syndrome
Jan Tack, Joris Arts, Philip Caenepeel, Dominiek De Wulf and Raf Bisschops
abstract | Dumping syndrome is a frequent complication of esophageal, gastric or bariatric surgery.
Rapid gastric emptying, with the delivery to the small intestine of a significant proportion of solid food
as large particles that are difficult to digest, is a key event in the pathogenesis of this syndrome. This
occurrence causes a shift of fluid from the intravascular component to the intestinal lumen, which results in
cardiovascular symptoms, release of several gastrointestinal and pancreatic hormones and late postprandial
hypoglycemia. Early dumping symptoms comprise both gastrointestinal and vasomotor symptoms. Late
dumping symptoms are the result of reactive hypoglycemia. Besides the assessment of clinical alertness and
endoscopic or radiological imaging, a modified oral glucose tolerance test might help to establish a diagnosis.
The first step in treating dumping syndrome is the introduction of dietary measures. Acarbose can be added to
these measures for patients with hypoglycemia, whereas several studies advocate guar gum or pectin to slow
gastric emptying. Somatostatin analogs are the most effective medical therapy for dumping syndrome, and a
slow‑release preparation is the treatment of choice. In patients with treatment‑refractory dumping syndrome,
surgical reintervention or continuous enteral feeding can be considered, but the outcomes of such approaches
are variable.
Tack, J. et al. Nat. Rev. Gastroenterol. Hepatol. 6, 583–590 (2009); published online 1 September 2009; doi:10.1038/nrgastro.2009.148

Continuing Medical Education online
This activity has been planned and implemented in accordance
with the Essential Areas and policies of the Accreditation Council
for Continuing Medical Education through the joint sponsorship of
MedscapeCME and Nature Publishing Group.
MedscapeCME is accredited by the Accreditation Council for
Continuing Medical Education (ACCME) to provide continuing
medical education for physicians.
MedscapeCME designates this educational activity for a maximum
of 0.75 aMa pra Category 1 CreditstM. Physicians should only
claim credit commensurate with the extent of their participation
in the activity. All other clinicians completing this activity will
be issued a certificate of participation. To participate in this
journal CME activity: (1) review the learning objectives and author
disclosures; (2) study the education content; (3) take the post‑test
and/or complete the evaluation at http://cme.medscape.com/
public/naturereviews; and (4) view/print certificate.
learning objectives
Upon completion of this activity, participants should be able to:
1 Describe the main causes of postoperative dumping
syndrome.
2 Describe differences between early and late dumping in
postoperative dumping syndrome.
3 Describe Sigstad’s diagnostic scoring system for dumping
syndrome.
4 Describe dietary approaches to managing postoperative
dumping syndrome.
5 Describe treatment approaches to postoperative dumping
syndrome.
Competing interests
The authors, the Journal Editor N. Wood and the CME questions
author D. Lie declare no competing interests.
Introduction
the stomach carries out an important role in digestion,
not only through the secretion of hormones and diges-
tive enzymes and its mechanical action on ingested food,
but also by its role in the timed release of ingested nutri-
ents into the duodenum. the ‘accommodation reflex’
involves a reduction in gastric tone and an increase in
gastric compliance in response to food intake, which
enables an increase in fundic volume without an
accompanying rise in intragastric pressure.1 this reflex
provides a means of temporarily storing ingested food
before its controlled release into the intestine. Gastric
accommodation is controlled by a vago–vagal reflex
pathway that induces activation of inhibitory motor
neurons in the proximal stomach.2 However, smooth
muscle contractions in the antrum gradually break
down large food particles to 1–2 mm fragments, the size
at which they can pass through the pylorus into the
Department of
duodenum. abnormalcies in the coordination of gastric Gastroenterology,
University Hospital
storage and emptying processes lead to impaired food Gasthuisberg, Leuven,
processing and symptoms that are worsened by further Belgium (J. tack,
food intake.2,3 J. arts, p. Caenepeel,
D. De Wulf,
Dumping syndrome refers to symptoms and signs that r. Bisschops).
occur when food reaches the small bowel too rapidly;
Correspondence:
the condition commonly occurs after partial or total gas- J. Tack, Department of
trectomy, for reasons that are outlined below. Dumping Gastroenterology,
syndrome can also occur after esophageal surgery and, University Hospital
Gasthuisberg,
exceptionally, in the absence of previous surgery. Herestraat 49,
Dumping syndrome was first described by Hertz in B‑3000 Leuven,
Belgium
1913, who reported the occurrence of ‘dumping-like’ jan.tack@
symptoms after gastroenterostomy.4 He reported that med.kuleuven.ac.be

nature reviews | gastroenterology & hepatology volume 6 | oCtoBer 2009 | 583

© 2009 Macmillan Publishers Limited. All rights reserved

 REvIEWS
Key points
■ Dumping syndrome is a common complication of esophageal and gastric
(including bariatric) surgery
■ Symptoms include early (gastrointestinal and vasomotor) and late
(hypoglycemia) symptoms
■ Diagnosis is based on a suggestive symptom pattern in patients with the
appropriate surgical history; a modified oral glucose tolerance test might help
to establish the diagnosis
■ Initial therapy should focus on dietary measures; acarbose can be added to
these measures in patients with hypoglycemia
■ In patients who have not responded to initial therapy, (slow‑release)
somatostatin analogs are the treatment of choice
■ In patients with treatment‑refractory dumping syndrome, surgical
reinterventions or continuous enteral feeding can be considered, but the
outcomes of such approaches are variable
patients felt excessively full after meals, had diar-
rhea and needed to lie down because they felt unwell.
radiographic examination revealed very rapid empty-
ing of contrast dye from the stomach. rapid emptying
of liquids from the stomach is an important contribu-
tor to the pathogenesis of dumping syndrome.5 studies
conducted in the 1980s demonstrated that a defect in
grinding or sieving within the stomach, which resulted
in the delivery of a considerable proportion of solid food
as large, less easily digested particles to the small intes-
tine (rather than rapid emptying itself), was a key event
in the pathogenesis of dumping syndrome.5,6
Dumping syndrome is now a well-established
complication of gastric and esophageal surgery. the
condition has been estimated to occur in up to 20% of
patients who undergo vagotomy with pyloroplasty and
in up to 50% of patients who undergo esophagectomy.7,8
Dumping syndrome has also been reported after nissen
fundoplication in children and adults.9,10 in recent years,
bariatric surgery has become the principal cause of
postoperative dumping syndrome.11
with an increasing number of patients undergoing
bariatric surgery, the incidence of dumping syndrome
is likely to increase, and clinicians should recognize the
syndrome and be familiar with its management. in this
review, we summarize the diagnosis, pathophysiological
basis and management options for postoperative
dumping syndrome.
Symptoms
the symptom profile of patients with dumping syndrome
is summarized in Box 1. symptoms of dumping syn-
drome can be classed as early or late, depending on how
soon after ingestion they occur. early symptoms com-
prise both gastrointestinal and vasomotor symptoms.
Gastrointestinal symptoms include abdominal pain,
diarrhea, borborygmi, nausea and bloating. vasomotor
symptoms include fatigue, a desire to lie down after
meals, facial flushing, palpitations, perspiration tachy-
cardia, hypotension and syncope. late dumping symp-
toms include hypoglycemia, perspiration, palpitations,
584 | OCTOBER 2009 | vOlumE 6
© 2009 Macmillan Publishers Limited. All rights reserved
Box 1 | Symptoms of early and late dumping
early dumping
Gastrointestinal symptoms
■ Abdominal pain, diarrhea, borborygmi, bloating, nausea
vasomotor symptoms
■ Flushing, palpitations, perspiration, tachycardia,
hypotension, syncope
late dumping
Hypoglycemia
Perspiration, palpitations, hunger, weakness, confusion,
tremor, syncope
hunger, fatigue, confusion, aggression, tremor and
syncope. Both early and late dumping symptoms are
socially and professionally incapacitating, especially
when syncope occurs.
Diagnosis
a suggestive symptom pattern in a patient who has
undergone upper abdominal surgery should give cause
to investigate the possibility of dumping syndrome. in
1970, sigstad proposed a scoring system, based on the
occurrence of different symptoms of dumping syn-
drome, to calculate a diagnostic index (Box 2).12 the
presence of hypoglycemia concurrently with several
other symptoms is a strong indicator of dumping syn-
drome (although the occurrence of insulinoma needs
to be excluded).
a provocative test for assessing dumping syndrome
can be used to confirm clinical suspicion. this test is
a modification of the oral glucose tolerance test and
involves the ingestion of 50 g or 75 g glucose in solution
after an overnight fast. immediately before and up to
180 min after ingestion of this solution, the blood glucose
concentration, hematocrit, pulse rate and blood pressure
are measured at 30 min intervals. the provocative test is
considered positive if late (120–180 min) hypoglycemia
occurs, or if an early (30 min) increase in hematocrit of
more than 3% occurs. the best predictor of dumping
syndrome seems to be a rise in the pulse rate of more
than 10 bpm after 30 min.13
assessments of the speed of gastric emptying might
show that this process occurs rapidly in patients with
dumping syndrome—especially for liquid nutrients—but
this test does not seem to have good diagnostic sensi-
tivity or specificity, probably because rapid emptying
occurs early after meal ingestion, a phase that is not ana-
lyzed closely or separately in most protocols of gastric
emptying testing.7,13,14
Pathophysiological mechanisms
the mechanisms that underlie dumping syndrome are
not completely understood. the symptoms of early and
late dumping syndrome are believed to have distinct
underlying pathophysiologies (Figure 1).2,5–7,15
www.nature.com/nrgastro

Box 2 | Sigstad’s scoring system for dumping syndrome20
A total score >7 is suggestive of dumping syndrome,
whereas a score <4 suggests other diagnoses
■ Shock +5
■ Fainting, syncope, unconsciousness +4
■ Desire to lie or sit down +4
■ Breathlessness, dyspnea +3
■ Weakness, exhaustion +3
■ Sleepiness, drowsiness, apathy, falling asleep +3
■ Palpitation +3
■ Restlessness +2
■ Dizziness +2
■ Headaches +1
■ Feeling of warmth, sweating, pallor, clammy skin +1
■ Nausea +1
■ Abdominal fullness, meteorism +1
■ Borborygmus +1
■ Eructation –1
■ vomiting –4
early dumping
after partial gastrectomy, vagotomy and related surger-
ies, gastric volume is reduced. this decreased capacity
causes the rapid passage of nutrients to the small intes-
tine, which induces a cascade of pathophysiological
events. the arrival of hyperosmolar contents to the
duodenum causes fluid to move from the intravascular
component to the intestinal lumen.16 this movement
might lead to a decrease in the volume of circulating
fluid, tachycardia and, rarely, syncope. the fluid shift into
the duodenum might also cause duodenal distention,
followed by cramp-like contractions. However, whether
this fluid shift has any role in dumping syndrome or is
a consequence of it is a matter of controversy, as intra-
venous fluid substitution is unable to prevent early
dumping symptoms.16
another important mechanism that contributes to the
pathogenesis of early dumping might be the increased
release of several gastrointestinal peptide hormones,
such as enteroglucagon, peptide YY, pancreatic poly-
peptide, vasoactive intestinal polypeptide, glucagon-
like peptide 1 and neurotensin, in postoperative dumping
syndrome.2,6,15 these hormones’ mode of action might
include changes in gastrointestinal motility and secre-
tion, as well as hemodynamic effects—for example, sys-
temic hemoconcentration and hypotension occur as a
result of splanchnic vasodilation induced by neurotensin
or vasoactive intestinal polypeptide.17
late dumping
late dumping symptoms occur 1–3 h after ingestion
of a meal and are attributed to reactive hypoglycemia.
under ‘normal’ conditions, the presence of glucose in
the jejunum is a strong stimulus for insulin secretion; the
nature reviews | gastroenterology & hepatology
© 2009 Macmillan Publishers Limited. All rights reserved
REvIEWS
Agents that increase
Impaired gastric volume
capacity or gastroenterostomy meal viscosity
(pectin, guar gum)
Octreotide Rapid delivery of nutrients
into the duodenum
Hyperosmolar contents Rapid absorption
in the duodenum of glucose Acarbose
■ Release of vasoactive agents Hyperinsulinemic response Diazoxide
(neurotensin, VIP)
■ Release of incretins
(GIP, GLP-1)
■ Release of glucose-modulating
hormones (insulin, glucagon) Late dumping
■ Hypoglycemia
Early dumping
■ Vasomotor symptoms
■ Gastrointestinal symptoms
■ Hyperglycemia
Figure 1 | Pathophysiology of dumping syndrome and mode of action of different
therapeutic agents. The key event in the pathophysiology of dumping syndrome is
the rapid delivery of nutrients into the duodenum. The presence of hyperosmolar
contents in the duodenum induces the release of a number of vasoactive agents,
incretins and glucose modulators, which cause early dumping symptoms. The
rapid absorption of glucose induces a hyperinsulinemic response, which leads to
the late dumping symptoms of hypoglycemia. The mode of action of octreotide,
diazoxide, viscosity‑increasing agents and acarbose is shown. Abbreviations: GIP,
glucose‑dependent insulinotropic polypeptide (also known as gastic inhibitory
polypeptide); GLP‑1, glucagon‑like peptide 1; vIP, vasoactive intestinal peptide.
rapid delivery of carbohydrates to the small intestine in
dumping syndrome, therefore, causes excessive insulin
secretion that subsequently results in hypoglycemia.18
one of the mediators implicated in this late hypoglycemic
effect is glucagon-like peptide 1.19
However, not all cases of postprandial hypoglycemia
are attributable to dumping syndrome. several patients
were reported to suffer from hyperinsulinemic hypo-
glycemia with nesidioblastosis after gastric bypass
surgery; these patients were characterized by severely
symptomatic postprandial hypoglycemias and hyper-
insulinemias that did not respond to treatment for
dumping syndrome. these patients were subse-
quently found to have pancreatic islet cell hyperplasia
or nesidioblastosis on analysis of resected pancreatic
specimens.20,21 Diagnosis of this syndrome, which is
cumbersome, might involve selective stimulation of the
celiac artery by use of calcium as an insulin secretagogue
with subsequent sampling of insulin levels from hepatic
venous serum (after insulinoma has been ruled out) as
well as pancreatic debulking and confirmation of islet
cell hyperplasia on a resected specimen.20,21 Hormonal
changes after roux-en-Y gastric bypass surgery,
including increased release of glucagon-like peptide 1
(which increases the mass of β cells in rodents), might
cause hyperplasia of islet cells. a study has, however,
volume 6 | oCtoBer 2009 | 585
 REvIEWS
Suspected dumping
Confirmation by laboratory tests
Dietary measures for 3–4 weeks
Lack of response
Acarbose (in cases of late dumping)
Lack of response
Octreotide LAR 20 mg i.m. for 3 months
Lack of response
Surgical rescue options?
Continuous nutrition?
Figure 2 | Proposed treatment algorithm for dumping
syndrome. This algorithm for the management of patients
with dumping syndrome is used at the
Neurogastroenterology and Motility Clinic of the University
Hospitals in Leuven, Belgium. In case of clinical suspicion,
we use a modified oral glucose tolerance test to help
establish the diagnosis. Our initial therapy is based on
dietary measures for 3–4 weeks, plus acarbose treatment
in patients who have hypoglycemia. In patients who fail to
respond to this initial therapy, slow‑release octreotide is
used. In patients with treatment‑refractory dumping
syndrome, surgical reintervention or continuous enteral
feeding can be considered, but the outcomes of such
approaches are variable. Abbreviations: i.m.,
intramuscular; LAR, long‑acting repeatable.
challenged this theory: the findings showed that the
β-cell mass in patients with hyperinsulinemic hypo-
glycemia after gastric bypass surgery was comparable
to that in Bmi-matched control individuals.22
Treatment of dumping syndrome
the first step in treating dumping syndrome is the intro-
duction of dietary measures. if this approach is insuffi-
cient, medical therapy and (in some cases) surgery,
might be considered (Figure 2). evidence of the efficacy
of several of these therapies is limited, as most studies
involve only a few patients and are not controlled.
Dietary measures
Dietary measures are the first approach to manage
dumping syndrome and are probably helpful for the
majority of patients.7,11,23–25 Dietary measures include
advising patients to consume smaller amounts in one
go by dividing the recommended daily energy intake
between six meals. Patients are also advised to delay any
liquid intake until at least 30 min after a meal. all rapidly
absorbable carbohydrates (for example, all sweet or
sweetened foods) should be eliminated from the diet to
prevent late dumping symptoms. lying down for 30 min
after meals can prolong gastric emptying and help to
reduce the symptoms of hypovolemia.
586 | OCTOBER 2009 | vOlumE 6
© 2009 Macmillan Publishers Limited. All rights reserved
pectin and guar gum
increasing the viscosity of food, which slows down gastric
emptying, is another approach to improve dumping
symptoms (table 1) and is achieved by ingesting up
to 15 g of guar gum or pectin with each meal. short-
term studies have shown a potential efficacy of this
approach.26–32 However, the palatability and tolerability
of these supplements is poor. moreover, these substances
are usually not readily available as pharmaceutical
products at sufficiently high doses.
acarbose
acarbose is an α-glycosidase hydrolase inhibitor that
interferes with carbohydrate absorption in the small intes-
tine. acarbose inhibits the α-glycosidase-mediated pro-
duction of monosaccharides from carbohydrates in the
epithelial brush border cells of the small intestine. in
healthy individuals, a 100–200 mg dose of acarbose inhib-
its the postprandial rise in glycemia, triglycerides and
insulin. the results from a number of small studies, in
which acarbose was given three times daily at 50–100 mg
doses to patients with dumping syndrome, showed an
improvement in glucose tolerance, a decreased release
of gastrointestinal hormones and a reduction in the inci-
dence of hypoglycemia (table 2).33–38 these results were
associated with an improvement in dumping symptoms
in these patients.
this treatment approach, however, affects only the
symptoms of late dumping owing to the mode of action
of acarbose (as mentioned above, the production of
monosaccharides in the small intestine is the target
of acarbose). in addition, acarbose treatment often
results in bloating, flatulence or diarrhea, as the unab-
sorbed carbohydrates undergo bacterial fermentation in
the small intestine; these adverse effects might hamper
treatment compliance.
somatostatin analogs
somatostatin and its synthetic analogs have been used
successfully in the treatment of dumping syndrome
and have displayed a number of pathophysiologically
attractive effects. somatostatin analogs can retard the
gastric emptying rate, retard transit through the small
bowel, inhibit the release of gastrointestinal hormones,
inhibit insulin secretion and inhibit postprandial vaso-
dilation. 14,39–50 as such, these analogs show a broad
range of activity against the full spectrum of symptoms
of dumping syndrome. Both short-acting and delayed-
release somatostatin analogs have been used in the treat-
ment of dumping syndrome. short-acting or long-acting
repeatable (lar) formulations of octreotide are the
agents that have been most commonly studied.14,51–63
Studies of short-acting somatostatin analog octreotide
the results of several short-term studies of subcutane-
ously administered octreotide have shown efficacy at
improving symptoms, improving glycemia and slowing
gastric emptying (table 3).55–60 However, the need for
www.nature.com/nrgastro
 REvIEWS

Table 1 | Summary of studies that evaluated pectin and guar gum in dumping syndrome
study no. of treatment results
patients
Jenkins et al. 5 Pectin 14.5 g, single Improved symptoms and glycemia (normalized in 46%
(1977)30 administration before OGTT of patients) during OGTT
Leeds et al. 11 Pectin 15 g, single Improved vasomotor symptoms and glycemia, lower insulin
(1981)31 administration before OGTT levels and prolonged gastric emptying during OGTT
Lawaetz et al. 4 Pectin 15 g, single Reduced vasomotor symptoms, decreased levels of insulin,
(1983)32 administration before OGTT glucagon, neurotensin and GIP and slower initial gastric
emptying during OGTT
Andersen et al. 5 Pectin 5 g, single administration No effect on symptoms or gastric emptying rate
(1989)29 before muffin meal
Harju et al. (1983)26 11 Guar gum 5 g with meals Improvement of symptoms
Harju et al. (1984) 27
11 Guar gum 5 g with meals Slowing of gastric emptying
Harju et al. (1987)28 11 Guar gum 5 g with a glucose Improvement of symptoms and hyperglycemia after
challenge meal a glucose challenge meal
Abbreviations: GIP, glucose‑dependent insulinotropic polypeptide (also known as gastic inhibitory polypeptide); OGTT, oral glucose tolerance test.

Table 2 | Summary of studies that evaluated acarbose in dumping syndrome

study no. of treatment result
patients
McLoughlin et al. 10 Acarbose 100 mg single Improved symptoms and glycemia during OGTT; reduced rise
(1979)36 administration before OGTT in plasma levels of GIP and insulin; no change in gastric
emptying rate
Gerard et al. 24 Acarbose 100 mg single Improved glycemia during OGTT; reduced rise in plasma levels
(1983)35 administration before OGTT of insulin; inhibition of glucose‑induced glucagon suppression
Lyons et al. 13 Acarbose 50 mg single Significant attenuation of hyperglycemia; reduced rise in
(1985)33 administration before standard plasma levels of GIP, enteroglucagon and insulin; no influence
breakfast on plasma levels of vIP and somatostatin; no significant
effect on symptoms
Hasegawa et al. 6 Acarbose 50–100 mg three Attenuation of glucose fluctuations and improvement
(1998)34 times daily before meals for of dumping symptoms (uncontrolled)
a month
Abbreviations: GIP, glucose‑dependent insulinotropic polypeptide (also known as gastic inhibitory polypeptide); OGTT, oral glucose tolerance test; vIP, vasoactive
intestinal peptide.

3–4 daily injections is potentially a major limitation for
the long-term application of short-acting somatostatin
analogs. three studies have evaluated the long-term use
of subcutaneously administered octreotide in the treat-
ment of dumping syndrome. Geer et al. found that long-
term octreotide therapy (15 months on average) provided
sustained symptom control. 57 of 10 patients, eight
received three daily injections of 100 μg octreotide, which
resulted in good symptom control; seven indivi duals
were able to resume work. similarly, vecht et al. evalu-
ated the long-term effect of three daily doses of 25–200 μg
octreotide in 20 patients with a mean follow-up of
37 months.61 all patients had an initial positive response;
at 3 months, 80% continued this positive response. after
10 years, however, 11 of the 20 patients had stopped
therapy for a variety of reasons, including lack of effect
at 3 months (n = 4), diarrhea (n = 4), painful injec-
tions (n = 1), reversible alopecia (n = 1) and weight loss
(n = 1). similar data were obtained in a larger group of
patients, in whom long-term effects seemed less favor-
able than short-term effects, although 41% of the cohort
continued octreotide therapy after the follow-up period
of 93 ± 15 months.62
Studies of long-acting octreotide LAR
slow-release preparations of somatostatin analogs, which
require only monthly intramuscular injections, are an
attractive alternative to multiple daily injections of the
short-acting formulations. two studies have investigated
the efficacy of a slow-release preparation of octreotide
in dumping syndrome. Penning et al. compared the
efficacy of monthly octreotide lar (10 mg) to sub-
cutaneous octreotide and found both formulations to be
effective at improving symptoms.63 the long-acting form
seemed superior at increasing body weight and improv-
ing quality of life. the 10 mg dose is only available in a
limited number of countries; the 20 mg dose is the usual
standard dose for octreotide lar.
a multicenter study in Belgium confirmed the efficacy
of monthly octreotide lar (20 mg) in the treatment of
dumping syndrome that was refractory to dietary mea-
sures and acarbose treatment.14 the study compared the

nature reviews | gastroenterology & hepatology volume 6 | oCtoBer 2009 | 587

© 2009 Macmillan Publishers Limited. All rights reserved

 REvIEWS

Table 3 | Summary of studies that evaluated octreotide in dumping syndrome

study no. of treatment result
patients
Hopman et al. 12 Octreotide 50 μg vs Improved dumping symptoms and suppression of postprandial
(1988)51 placebo before OGTT rise in pulse rate; reduced peak insulin and increased nadir
glycemia; slowing of gastrointestinal transit
Primrose & Johnston 10 Octreotide 50 μg vs 100 μg Reduced early dumping and abolished late dumping symptoms;
(1989)52 vs placebo before OGTT suppression of early dumping‑associated changes in hematocrit
and pulse rate; inhibition of hypoglycemia
Tulassay et al. 8 Octreotide 50 μg vs Suppression of rise in pulse rate and hematocrit; suppression
(1989)56 placebo before OGTT of rise in plasma levels of vIP; inhibition of postprandial
hypoglycemia; inhibition of rise in plasma levels of insulin and GIP
Geer et al. (1990)57 10 Octreotide 100 μg vs Prevention of development of dumping symptoms and diarrhea;
placebo before a dumping prevention of late hypoglycemia and of the rise in plasma levels
provocative meal of glucose, glucagon, pancreatic polypeptide, neurotensin and
insulin; delayed gastric emptying and intestinal transit
Richards et al. 6 Octreotide 100 μg vs Prevention of dumping symptoms; induction of migrating motor
(1990)58 placebo before a dumping complex phase III in the small intestine; decreased postprandial
provocative meal intestinal motor activity

Gray et al. (1991)59 9 Octreotide 100 μg vs Suppression of rise in pulse rate; inhibition of insulin release;
placebo before a dumping prevention of hypoglycemia; inhibition of dumping symptoms
provocative meal
Hasler et al. 8 Octreotide 50 μg vs Suppression of rise in pulse rate; inhibition of dumping symptoms
(1996)60 placebo before OGTT and diarrhea; no influence on change in hematocrit; inhibition
of insulin release; prevention of hypoglycemia; no influence on
gastric emptying rate
Arts et al. (2009)14 30 Octreotide 50 μg before Suppression of rise in pulse rate and hematocrit; inhibition of
OGTT postprandial hypoglycemia; inhibition of rise in plasma levels
of insulin; improvement of early and late dumping symptoms
Abbreviations: GIP, glucose‑dependent insulinotropic polypeptide (also known as gastic inhibitory polypeptide); OGTT, oral glucose tolerance test; vIP, vasoactive
intestinal peptide.

control of symptoms and underlying pathophysiological
mechanisms after 3 days of subcutaneous treatment with
octreotide (50 μg, 3 times daily) with 3 months of treat-
ment with octreotide lar at 20 mg. Both the short-acting
and the long-acting formulations had a favorable effect on
dumping symptoms, glycemia and pulse rate during provo-
cative testing for dumping. the short-acting form showed
greater efficacy than the long-acting form at improving
hypoglycemia. However, treatment with the long-acting
formulation was associated with a significant improve-
ment in patients’ quality of life and was markedly preferred
by recipients over the short-acting preparation.14
Adverse effects of somatostatin analogs
the main adverse events related to the use of somato-
statin analogs are pain at the site of injection, gallstone
formation and the occurrence of steatorrhea. the latter
symptom is usually mild, and the long-term use of somato-
statin analogs is usually associated with a weight gain of
approximately 1% in spite of the occurrence of steatorrhea.
Gallstone formation is not an uncommon complication of
the long-term use of somatostatin analogs and should be
taken into account when considering treatment options for
dumping syndrome.64,65 another disadvantage of somato-
statin analogs is their considerable cost. For this and the
aforementioned reasons, treatment with somatostatin
analogs is not the first-line treatment option for patients
with dumping syndrome. However, dumping syndrome
is associated with major impairment of quality of life, and
the improvement in this parameter with somatostatin
analogs is impressive.14,57
Diazoxide
Diazoxide is a potassium channel activator that hyper-
polarizes cells, including β cells, and, therefore, inhib-
its voltage-sensitive calcium channels. the drug has
been used clinically in the treatment of hypertension
and insulinoma, as it inhibits calcium-induced insulin
release. the use of diazoxide administered three times
daily at 100–150 mg for late dumping symptoms has been
anecdotally reported,21 but no effect on the early symp-
toms of dumping syndrome is expected with diazoxide
treatment owing to its mode of action.
rescue therapies
in spite of some successful therapeutic options, a number
of patients continue to have treatment-refractory dumping
symptoms. in these difficult cases, surgical interventions
or continuous enteral feeding can be considered.
Surgery
Depending on the previous type of gastric surgery, several
types of reintervention have been proposed, including
narrowing of the anastomosis, conversion of Bilroth

588 | OCTOBER 2009 | vOlumE 6 www.nature.com/nrgastro

© 2009 Macmillan Publishers Limited. All rights reserved

 REvIEWS

type ii to Bilroth type i gastroenterostomy, conversion to
a roux-en-Y construction, reconstruction of the pylorus
or interposition of a 10 cm antiperistaltic jejunal loop.66–71
the results from case series support the conversion of
Bilroth type ii to Bilroth type i gastroenterostomy in the
treatment of dumping syndrome.66
in patients who develop the syndrome after vagotomy
with pyloroplasty, surgical reconstruction of the pylorus
improves symptoms and decreases the gastric emptying
rate.66,68,69 the reversal of rapid initial gastric emptying has
been implicated in the therapeutic effect of pyloric
reconstruction.69 in addition, roux-en-Y reconstruc-
tion has a favorable effect on dumping symptoms after
partial gastrectomy and results in retardation of gastric
emptying.70 Concomitant vagotomy improves the thera-
peutic outcome of roux-en-Y reconstruction.71 Jejunal
interposition of an antiperistaltic loop is superior to an
isoperistaltic (Henley) loop in the management of refrac-
tory dumping.66,67,72 However, our own experience sug-
gests that the outcomes of these interventions are often
unpredictable in clinical practice.
Continuous enteral feeding
a final approach to treatment of patients with refractory
dumping syndrome is the creation of a feeding jejuno-
stomy, through which a continuous background flow of
nutrients can be provided. this is a rather invasive inter-
vention, with a major effect on daily life, but it seems to be
effective at avoiding the symptoms of the syndrome that are
triggered by meal ingestion (on the basis of one published
case report and on our own, unpublished, experience).73
Conclusions
Dumping syndrome is a well-established complication
of upper gastrointestinal surgery and is likely to become
more prevalent with increasing rates of bariatric surgery.
a diagnosis is made on the basis of clinical suspicion in
case of suggestive symptoms, aided by a modified oral
glucose tolerance test. initial therapy should focus on
dietary measures for 3–4 weeks. if insufficient improve-
ment occurs, acarbose can also be administered to
patients with predominant late dumping symptoms.
somatostatin analogs are the next approach to consider
in patients with well-established dumping syndrome
who have failed to respond to initial therapy and whose
quality of life is substantially affected by their symptoms;
the approach of choice is treatment with slow-release
formulations because of their ease of administration and
superior effect on quality of life. after an initial 3-month
treatment with somatostatin analogs, long-term therapy
should be continued only if a substantial improvement
in symptoms is seen. whether increasing the dose
(for example, of octreotide lar from 20 mg to 30 mg)
improves symptom control in dumping syndrome is cur-
rently unclear, but our personal experience would argue
against dose increments in patients who fail to respond.
in these patients, surgery or continuous enteral feeding
might be necessary, but the outcome of these approaches
is variable.
Review criteria
To identify relevant studies, the MEDLINE database was
searched. Medical subject headings and free‑text terms
for (postoperative) dumping were combined with the
terms “pathophysiology”, “symptoms”, “management”,
“diet”, “pectin”, “guar gum”, “acarbose”, “diazoxide”,
“somatostatin analog”, “octreotide”, “somatulin” and
“surgery”. The reference lists from retrieved articles were
also examined for relevant papers.

1. Kindt, S. & Tack, J. Impaired gastric
accommodation and its role in dyspepsia. Gut
55, 1685–1691 (2006).
2. Tack, J. Gastric motor disorders. Best Pract. Res.
Clin. Gastroenterol. 21, 633–644 (2007).
3. Bisschops, R. et al. Relationship between
symptoms and ingestion of a meal in functional
dyspepsia. Gut 57, 1495–1503 (2008).
4. Hertz, A. F. The cause and treatment of certain
unfavorable after‑effects of gastro‑enterostomy.
Proc. R. Soc. Med. 6, 155–163 (1913).
5. MacGregor, I., Parent, J. & Meyer, J. H. Gastric
emptying of liquid meals and pancreatic and
biliary secretion after subtotal gastrectomy or
truncal vagotomy and pyloroplasty in man.
Gastroenterology 72, 195–205 (1977).
6. Mayer, E. A. et al. Gastric emptying and sieving of
solid food and pancreatic and biliary secretion
after solid meals in patients with truncal
vagotomy and antrectomy. Gastroenterology 83,
184–192 (1982).
7. vecht, J., Masclee, A. & Lamers, C. The dumping
syndrome. Current insights into pathophysiology,
diagnosis and treatment. Scand. J. Gastroenterol.
223, 21–27 (1997).
8. McLarty, A. et al. Esophageal resection for cancer
of the esophagus: long‑term function and quality
of life. Ann. Thorac. Surg. 63, 1568–1572 (1997).
9. Pimpalwar, A. & Najmaldin, A. Results of
laparoscopic antireflux procedures in
neurologically impaired children. Semin.
Laparosc. Surg. 9, 190–196 (2002).
10. Zaloga, G. P. & Chernow, B. Postprandial
hypoglycemia after Nissen fundoplication for
reflux esopahgitis. Gastroenterology 84,
840–842 (1983).
11. Abell, T. L. & Minocha, A. Gastrointestinal
complications of bariatric surgery:
diagnosis and therapy. Am. J. Med. Sci. 331,
214–218 (2006).
12. Sigstad, H. A clinical diagnostic index in the
diagnosis of the dumping syndrome. Changes in
plasma volume and blood sugar after a test
meal. Acta Med. Scand. 188, 479–486 (1970).
13. van der Kleij, F. G., vecht, J., Lamers, C. B. &
Masclee, A. A. Diagnostic value of dumping
provocation in patients after gastric surgery.
Scand. J. Gastroenterol. 31, 1162–1166 (1996).
14. Arts, J. et al. Efficacy of the long‑acting
repeatable formulation of the somatostatin
analog octreotide in postoperative dumping.
Clin. Gastroenterol. Hepatol. 7, 432–437 (2009).
15. Lawaetz, O. et al. Gut hormone profile and
gastric emptying in the dumping syndrome.
A hypothesis concerning the pathogenesis.
Scand. J. Gastoenterol. 18, 73–80 (1983).
16. Johnson, L. P., Sloop, R. D. & Jesseph, R. E.
Etiologic significance of the early symptomatic
phase in the dumping syndrome. Ann. Surg.
156, 173–179 (1962).
17. Sirinek, K. R., O’Dorisio, T. M., Howe, B. &
McFee, A. S. Neurotensin, vasoactive
intestinal peptide, and Roux‑en‑Y
gastrojejunostomy: their role in the dumping
syndrome. Arch. Surg. 120, 605–609 (1985).
18. Eloy, R., Garaud, J. C., Moody, A., Jaeck, D. &
Grenier, J. F. Jejunal factor stimulating insulin
release in the isolated perfused canine
pancreas and jejunum. Horm. Metab. Res. 7,
461–467 (1975).
19. Toft‑Nielsen, M., Madsbad, S. & Holst, J. J.
Exaggerated secretion of glucagon‑like
peptide‑1 could cause reactive hypoglycemia.
Diabetologia 41, 1180–1186 (1998).
20. Service, G. J. et al. Hyperinsulinemic
hypoglycemia with nesidioblastosis after
gastric‑bypass surgery. N. Engl. J. Med. 353,
249–254 (2005).
21. Patti, M. E. et al. Severe hypoglycemia post‑
gastric bypass requiring partial
pncreatectomy: evidence for inappropriate
insulin secretion and pancreatic islet
hyperplasia. Diabetologia 48, 2236–2240
(2005).

nature reviews | gastroenterology & hepatology volume 6 | oCtoBer 2009 | 589

© 2009 Macmillan Publishers Limited. All rights reserved

 REvIEWS
22. Meier, J. J., Butler, A. E., Galasso, R. & Butler, P. C.
Hyperinsulinemic hypoglycemia after gastric
bypass surgery is not accompanied by islet
hyperplasia or increased beta‑cell turnover.
Diabetes Care 49, 1554–1559 (2006).
23. Robinson, F. W. & Pittman, A. C. Dietary
management of postgastrectomy dumping
syndrome. Surg. Gynecol. Obstet. 104, 529–534
(1957).
24. Pittman, A. C. & Robinson, F. W. Dietary
management of the “dumping” syndrome:
long‑term follow‑up. J. Am. Diet. Assoc. 40,
108–110 (1962).
25. Khoshoo, v., Reifen, R. M., Gold, B. D.,
Sherman, P. M. & Pencharz, P. B. Nutritional
manipulation in the management of dumping
syndrome. Arch. Dis. Child 66, 1447–1448
(1991).
26. Harju, E. & Larmi, T. K. Efficacy of guar gum in
preventing the dumping syndrome. JPEN 7,
470–472 (1983).
27. Harju, E., Heikkila, J. & Larmi, T. K. Effect of guar
gum on gastric emptying after gastric resection.
JPEN 8, 18–20 (1984).
28. Harju, E. & Makela, J. Reduction in symptoms
after proximal selective vagotomy through
increased dietary viscosity. Am. J. Gastroenterol.
79, 861–863 (1984).
29. Andersen, J. R., Holtug, K. & Uhrenholt, A. Trial of
pectin‑enriched muffins in patients with severe
dumping syndrome after gastric resection:
observations on symptoms and gastric emptying
pattern. Acta Chir. Scand. 155, 39–41 (1989).
30. Jenkins, D. J. et al. Effect of dietary fiber on
complications of gastric surgery: prevention of
postprandial hypoglycemia by pectin.
Gastroenterology 73, 215–217 (1977).
31. Leeds, A. R., Ralphs, D. N., Ebied, F., Metz, G. &
Dilawari, J. B. Pectin in the dumping syndrome:
reduction of symptoms and plasma volume
changes. Lancet 1, 1075–1078 (1981).
32. Lawaetz, O., Blackburn, A. M., Bloom, S. R.,
Aritas, Y. & Raplhs, D. N. Effect of pectin on
gastric emptying and gut hormone release in the
dumping syndrome. Scand. J. Gastroenterol. 18,
327–336 (1983).
33. Lyons, T. J., McLoughlin, J. C., Shaw, C. &
Buchanan, K. D. Effect of acarbose on
biochemical responses and clinical symptoms in
dumping syndrome. Digestion 31, 89–96 (1985).
34. Hasegawa, T. et al. Long‑term effect of
α‑glycosidase inhibitor on late dumping
syndrome. J. Gastroenterol. Hepatol. 13,
1201–1206 (1998).
35. Gerard, J., Luyckx, A. S. & Lefebvre, P. J. Acarbose
in reactive hypoglycemia: a double‑blind study. Int.
J. Clin. Pharmacol. Ther. Toxicol. 22, 25–31 (1983).
36. McLoughlin, J. C., Buchanan, K. D. & Alam, M. J.
α‑Glycoside‑hydrolase inhibitor in treatment of
dumping syndrome. Lancet 2, 603–605 (1979).
37. Ng, D. D. et al. Acarbose treatment of
postprandial hypglycemia in children after Nissen
fundoplication. J. Pediatr. 139, 877–879 (2001).
38. Moreira, R. O., Moreira, R. B., Machado, N. A.,
Goncalves, T. B. & Coutinho, W. F. Postprandial
hypoglycemia after bariatric surgery
pharmacological treatment with verapamil and
acarbose. Obes. Surg. 18, 1618–1621 (2008).
39. Edmunds, M., Chen, J., Soykan, I., Lin, Z. &
McCallum, W. Effect of octreotide on gastric and
small bowel motility in patients with
gastroparesis. Aliment. Pharmacol. Ther. 12,
167–174 (1998).
40. Fuessl, H., Carolan, G., Williams, G. & Bloom, S.
Effect of a long‑acting somatostatin analog
590 | OCTOBER 2009 | vOlumE 6
(SMS 201–995) on postprandial gastric
emptying of 99mTc–tin colloid and
mouth‑to‑caecum transit time in man. Digestion
36, 101–107 (1987).
41. van Berge Henegouwen, M. I., van Gulik, T. M.,
Akkermans, L. M., Jansen, J. B. & Gouma, D. J.
The effect of octreotide on gastric emptying at a
dosage used to prevent complications after
pancreatic surgery: a randomised, placebo
controlled study in volunteers. Gut 41, 758–762
(1997).
42. Foxx‑Orenstein, A., Camilleri, M., Stephens, D. &
Burton, D. Effect of a somatostatin analog on
gastric motor and sensory functions in healthy
humans. Gut 52, 1555–1561 (2003).
43. Di Lorenzo, C., Lucanto, C., Flores, A., Idries, S. &
Hyman, P. Effect of sequential erythromycin and
octreotide on antroduodenal manometry.
J. Pediatr. Gastroenterol. Nutr. 29, 293–296
(1999).
44. Nelson‑Piercy, C. et al. Effect of a new oral
somatostatin analog (SDZCO611) on gastric
emptying, mouth to cecum transit time, and
pancreatic and gut hormone release in normal
male subjects. J. Clin. Endocrinol. Metab. 78,
329–336 (1994).
45. von der Ohe, M., Camilleri, M., Thomforde, G. &
Klee, G. Differential regional effects of octreotide
on human gastrointestinal motor function. Gut
36, 743–748 (1995).
46. Kreanzlin, M. et al. Effect of long‑acting
somatostatin analog SMS 201–995 on gut
hormone secretion in normal subjects. Experintia
41, 738–740 (1985).
47. Williams, G. et al. Postprandial effects of SMS
201–995 on gut hormones and glucose
tolerance. Scand. J. Gastroenterol.
21 (suppl. 119), 73–83 (1986).
48. Parkinson, C. et al. A comparison of the effects of
pegvisomant and octreotide on glucose, insulin,
gastrin, cholecystokinin, and pancreatic
polypeptide responses to oral glucose and a
standard mixed meal. J. Clin. Endocrinol. Metab.
87, 1797–1804 (2002).
49. Kemmer, T. P. et al. Inhibition of human exocrine
pancreatic secretion by the long‑acting
somatostatin analog octreotide (SMS201–995).
Aliment. Pharmacol. Ther. 6, 41–50 (1992).
50. Högenauer, C., Aichbichler, B., Santa Ana, C.,
Porter, J. & Fordtran, J. Effect of octreotide on
fluid absorption and secretion by the normal
human jejunum and ileum in vivo. Aliment.
Pharmacol. Ther. 16, 769–777 (2002).
51. Hopman, W., Wolberink, R., Lamers, C. &
van Tongeren, J. Treatment of the dumping
syndrome with the somatostatin analog
SMS201–995. Ann. Surg. 207, 155–159 (1988).
52. Primrose, J. N. & Johnston, D. Somatostatin
analog SMS 201–995 (octreotide) as a possible
solution to the dumping syndrome after
gastrectomy or vagotomy. Br. J. Surg. 76,
140–144 (1989).
53. Morz, R., Prager, J. & Pointer, H. Influence of
somatostatin (SS‑14) on early dumping reaction
in patients after partial gastrectomy [German].
Z. Gastroenterol. 20, 299–304 (1982).
54. Long, R., Adrian, T. & Bloom, S. Somatostatin
and the dumping syndrome. Br. Med. J. (Clin. Res.)
290, 886–888 (1985).
55. Reasbeck, P. & van Rij, A. The effect of
somatostatin on dumping after gastric surgery: a
preliminary report. Surgery 99, 462–468 (1986).
56. Tulassay, Z., Tulassay, T., Gupta, R. & Cierny, G.
Long acting somatostatin analog in dumping
syndrome. Br. J. Surg. 76, 1294–1295 (1989).
© 2009 Macmillan Publishers Limited. All rights reserved
57. Geer, R. J. et al. Efficacy of octreotide acetate in
treatment of severe postgastrectomy dumping
syndrome. Ann. Surg. 212, 678–687 (1990).
58. Richards, W. O. et al. Octreotide acetate induces
fasting small bowel motility in patients with
dumping syndrome. J. Surg. Res. 49, 483–487
(1990).
59. Gray, J. L., Debas, H. T. & Mulvihill, S. J. Control
of dumping symptoms by somatostatin analog in
patients after gastric surgery. Arch. Surg. 126,
1231–1235 (1991).
60. Hasler, W. L., Soudah, H. C. & Owyang, C.
Mechanisms by which octreotide ameliorates
symptoms in the dumping syndrome.
J. Pharmacol. Exp. Ther. 277, 1359–1365 (1996).
61. vecht, J., Lamers, C. & Masclee, A. Long‑term
results of octreotide‑therapy in severe dumping
syndrome. Clin. Endocrinol. (Oxf.) 51, 619–624
(1999).
62. Didden, P., Penning, C. & Masclee, A. A.
Octreotide therapy in dumping syndrome:
analysis of long‑term results. Aliment. Pharmacol.
Ther. 24, 1367–1375 (2006).
63. Penning, C., vecht, J. & Masclee, A. Efficacy of
depot long‑acting release octreotide therapy in
severe dumping syndrome. Aliment. Pharmacol.
Ther. 22, 963–969 (2005).
64. Ewins, D. L. et al. Assessment of gall bladder
dynamics, cholecystokinin release and the
development of gallstones during octreotide
therapy for acromegaly. Q. J. Med. 83, 295–306
(1992).
65. Moschetta, A. et al. Severe impairment of
postprandial cholecystokinin release and gall‑
bladder emptying and high risk of gallstone
formation in acromegalic patients during
Sandostatin LAR. Aliment. Pharmacol. Ther. 15,
181–185 (2001).
66. Woodward, E. R., Deser, P. L. & Gasster, M.
Surgical treatment of the postgastrectomy
dumping syndrome. West. J. Surg. Obstet.
Gynecol. 63, 567–573 (1955).
67. Sawyers, J. L. & Herrington, J. L. Superiority of
antipersitaltic jejunal segments in management
of severe dumping syndrome. Ann. Surg. 178,
311–321 (1973).
68. Koruth, N. M., Krukowski, Z. H. &
Matheson, N. A. Pyloric reconstruction. Br. J.
Surg. 72, 808–810 (1985).
69. Cheadle, W. G., Baker, P. R. & Cuschieri, A. Pyloric
reconstruction for severe vasomotor dumping
after vagotomy and pylorpoplasty. Ann. Surg. 202,
568–572 (1985).
70. vogel, S., Hocking, M. & Woodward, E. Clinical
and radionuclide evaluation of Roux‑Y diversion
for postgastrectomy dumping. Am. J. Surg. 155,
57–62 (1988).
71. Hocking, M. P., vogel, S. B., Falasca, C. A. &
Woodward, E. R. Delayed gastric emptying of
liquids and solids following Roux‑en‑Y biliary
diversion. Ann. Surg. 194, 494–501 (1981).
72. Ramus, N., Williamson, R. & Jonhston, D. The
use of jejunal interposition for intractable
symptoms complicating peptic ulcer surgery. Br.
J. Surg. 69, 265–268 (1982).
73. veit, F., Heine, R. G. & Catto‑Smith, A. G.
Dumping syndrome after Nissen fundoplication.
J. Pediatr. Child Health 30, 182–185 (1994).
acknowledgments
Désirée Lie, University of California, Irvine, CA, is the
author of and is solely responsible for the content of
the learning objectives, questions and answers of the
MedscapeCME‑accredited continuing medical
education activity associated with this article.
www.nature.com/nrgastro