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Dumping Syndrome: Pathophysiology and Treatment

Andrew Ukleja
Nutr Clin Pract 2005 20: 517
DOI: 10.1177/0115426505020005517

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Invited Review
Dumping Syndrome: Pathophysiology and Treatment
Andrew Ukleja, MD
Department of Gastroenterology, Cleveland Clinic Florida, Weston, Florida
ABSTRACT: Anatomic and physiologic changes intro-
duced by gastric surgery result in clinically significant
dumping syndrome in approximately 10% of patients.
Dumping is the effect of alteration in the motor functions
of the stomach, including disturbances in the gastric
reservoir and transporting function. Gastrointestinal hor-
mones play an important role in dumping by mediating
responses to surgical resection. Treatment options of
dumping syndrome include diet, medications, and surgical
revision. Poor nutrition status can be anticipated in
patients who fail conservative therapy. Management of
refractory dumping syndrome can be a challenge. This
review highlights current knowledge about the mecha-
nisms of dumping syndrome and available therapy.
Approximately 25%–50% of patients after gastric
surgery develop some manifestations of dumping
syndrome, with clinically significant symptoms
observed in 5%–10% of them. However, only 1%–5%
of those patients have severe disabling symptoms.1
Incidence and severity of dumping syndrome are
directly related to the extent and type of gastric
surgery. Significant dumping has been reported in
14%–20% of patients after partial gastrectomy and
in 6%–14% of patients after truncal vagotomy with
drainage.2,3 Lower incidence of dumping syndrome
(⬍2%) is observed after proximal gastric vagotomy
without drainage procedure.4 Dumping is often a
desired side effect after bariatric surgery for morbid
obesity. The incidence of dumping syndrome after
gastric bypass is as high as 75% in the early post-
operative period, with complete resolution in the
majority of patients over 15–18 months from sur-
gery.5 In the pediatric population, dumping syn-
drome is reported almost exclusively in children
after Nissen fundoplication.6,7
Correspondence: Andrew Ukleja, MD, 2950 Cleveland Clinic
Blvd, Cleveland Clinic Florida, Weston, FL 33331. Electronic
mail may be sent to uklejaa@ccf.org.
0884-5336/05/2005-0517$03.00/0
Nutrition in Clinical Practice 20:517–525, October 2005
Copyright © 2005 American Society for Parenteral and Enteral Nutrition
517
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From a historical point, more than 2 decades after
the first partial gastrectomy was performed, dump-
ing-type symptoms were reported by Hertz in 1913.8
He described “rapid drainage of the stomach” and
distention of the jejunum after gastroenterostomy.
Hertz noticed the association between postprandial
symptoms and rapid gastric empting. However, the
term dumping was first used by Andrews and Mix9
in 1920, according to their observation of the rapid
empting of contrast from the stomach in patients
with gastrointestinal (GI) and vasomotor symptoms.
Presentation of Dumping Syndrome
Dumping syndrome can be divided into early and
late forms, depending on the occurrence of symp-
toms in relation to the time elapsed after a meal.
The majority of patients have early dumping,
approximately 25% of them have late dumping, and
only a minority have symptoms of both.10 Clinical
manifestations can be divided into GI and vasomotor
symptoms (see Table 1). GI symptoms include early
satiety, nausea, cramps, and explosive diarrhea.
Vasomotor symptoms comprise sweating, flushing,
palpitations, dizziness, and an intense desire to lie
down. The expression of these symptoms varies
between individuals. Most patients with early
dumping have both GI and vasomotor symptoms,
and those with late dumping have mainly vasomotor
symptoms. Patients with severe dumping often limit
their food intake to avoid undesired symptoms. This
may lead to weight loss and eventually malnutri-
tion.
Pathophysiology of Dumping Syndrome
The mechanisms involved in dumping syndrome
are poorly understood, and they are probably multi-
factorial. The stomach acts as a reservoir, initiates
the digestion, and releases its content downstream
into the duodenum in a controlled fashion. The food
is partially digested by acid and proteases in the
stomach before its transfer to the antrum, where
high-amplitude contractions help to triturate the
solids to smaller particles, 1–2 mm in size. An intact
pylorus prevents the passage of larger particles into
the duodenum. The alteration of gastric anatomy,
removal or bypass of the pylorus, or interference
with its innervation has a profound effect on gastric
518 UKLEJA Vol. 20, No. 5

Table 1 small intestine distention.12 Bowel distention is

Symptoms of dumping syndrome
Early dumping
Vasomotor symptoms
Desire to lie down
Palpitations
Fatigue
Faintness
Syncope
Diaphoresis
Headache
Flushing
Pallor
Abdominal symptoms
Epigastric fullness
Diarrhea
Nausea
Vomiting
Abdominal cramps
Borborygmi
Bloating
Late dumping
Perspiration
Shakiness
Difficulty with concentration
Decreased consciousness
Hunger
emptying. As a result of the reduced reservoir of the
stomach and altered pyloric emptying, rapid deliv-
ery of large amounts of osmotically active solids and
liquids into the duodenum or small intestine is
observed. This accelerated gastric emptying of liq-
uids is a characteristic feature and a critical step in
the pathophysiology of dumping syndrome. Gastric
motility and distensibility are under control of the
enteric nervous system, regulated by extrinsic
innervation and by circulating GI hormones. Gastric
emptying is controlled by fundic tone, antropyloric
mechanisms, and duodenal feedback, which inhibits
gastric emptying. Duodenal feedback is lost after a
bypass procedure such as gastrojejunostomy.
Azpiroz and Malagelada11 have shown that the
accommodation and the cyclic contractility of the
stomach in response to distention are abolished
after partial gastric resection or vagotomy, which
accounts for the immediate dumping of ingested
content into the duodenum. Secretion of GI hor-
mones is also altered after gastric surgery. This is
another important factor in the pathophysiology of a
dumping syndrome.
Early Dumping
Symptoms of an early dumping syndrome occur
10 –30 minutes postprandially. They result from
accelerated gastric emptying of hyperosmolar con-
tent from the stomach into the duodenum or small
bowel, which leads to fluid shifts from the intravas-
cular compartment into the intestinal lumen. This
results in an increased bowel contractility and rapid
believed to be responsible for symptoms such as
bloating and abdominal cramps.
Rapid infusion of glucose into the small bowel has
been shown to provoke dumping symptoms even in
healthy individuals.13,14 Intravascular volume con-
traction due to osmotic fluid shifts is perhaps respon-
sible for vasomotor symptoms such as tachycardia and
dizziness.15 No correlation has been found between the
severity of dumping and the volume of ingested hyper-
tonic solution. Kalser and Cohen16 reported no differ-
ence in the degree of dilution of the hyperosmolar
glucose in the jejunum between symptomatic and
asymptomatic subjects after gastrectomy by measur-
ing intraluminal osmolarity and glucose content.
Interestingly, studies have also revealed no statistical
difference in the rate of gastric emptying after surgery
between patients with and without dumping symp-
toms.17,18
Provocation with oral hyperosmolar glucose in
patients with early dumping induces an increase in
a heart rate and hematocrit, with concomitant drop
in plasma volume.19 The peripheral and splanchnic
vasodilatation seems to be critical in the pathogen-
esis of early dumping and is perhaps responsible for
systemic symptoms.20,21 Hinshaw et al22 reported
that patients with dumping had vasodilatation even
though vasoconstriction was expected in a volume-
contracted state. An increase in the blood flow to the
superior mesenteric artery has been demonstrated
after glucose provocation in patients with dump-
ing.23 However, vasodilatation in patients with
dumping symptoms has not been confirmed by other
investigators.24,25
The hypothesis that humoral factors may have a
pivotal role in the pathogenesis of dumping was
brought to light after dumping symptoms were
induced experimentally in a healthy dog after trans-
fusion of blood from a portal vein obtained from
another dog with dumping.26 The initial studies
indicated that serotonin and the kallikrein-kinin
system may play a role in provoking dumping.27,28
Higher postprandial levels of gut hormones such as
enteroglucagon, pancreatic polypeptide, peptide YY
(PYY), vasoactive intestinal polypeptide (VIP), glu-
cagon-like peptide (GLP), and neurotensin have
been shown in patients with dumping symptoms
when compared with asymptomatic subjects after
gastric surgery.29 –34 Therefore, most of those hor-
mones have been implicated to play a role in the
pathogenesis of dumping. In gastric bypass patients
with dumping, higher levels of neurotensin and VIP
have been detected after surgery when compared
with their preoperative levels.35 Lower levels of
motilin were reported in patients with a dumping
syndrome, but its role in dumping is unclear.36,37
Neurotensin, PYY, and enteroglucagon delay motil-
ity of the proximal GI tract and inhibit gastric and
intestinal secretions. Their release activates “the
ileal brake,” which delays proximal bowel transit
time in response to a rapid delivery of food to the

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October 2005
distal small bowel.38,39 Higher plasma levels of
adrenaline and noradrenaline were found in early
dumping, consistent with pronounced sympathoad-
renal activation, but this response was also seen in
patients without dumping after surgery.40 Lower
plasma levels of atrial natriuretic peptide (ANP) and
elevated levels of aldosterone associated with acti-
vation of the rennin-aldosterone axis have been
observed in early dumping, which reflect hypovole-
mic state.41
Late Dumping
Late dumping occurs 1–3 hours after a meal, and
it is characterized by systemic, vascular symptoms.
It is a consequence of reactive hypoglycemia result-
ing from an exaggerated release of insulin.42 Rapid
delivery of a meal to the small intestine leads to an
initial higher concentration of carbohydrates in the
proximal small bowel, followed by rapid absorption
of glucose into the blood. This is countered by
excessive release of insulin, so-called “hyperinsu-
linemic response,” responsible for the subsequent
reactive hypoglycemia.43,44 A higher insulin release
has been found in response to intrajejunal rather
than IV glucose infusion while allowing mainte-
nance of the same serum glucose levels.45 The
enhanced insulin release after an enteral glucose
delivery is called the incretin effect.46
Two hormones, glucose-dependent insulinotropic
peptide (GIP) and GLP-1 are believed to play a pivotal
role in late dumping.47,48 GIP is produced in a duo-
denum and proximal jejunum, GLP-1 is secreted from
the small bowel and colon. An increased secretion of
GLP-1 has been observed after an oral glucose chal-
lenge in patients after gastric resection and esopha-
gectomy.49 –51 Stimulation of insulin release occurs
in response to GLP-1 secretion.52 This exaggerated
GLP-1 response plays an important role in hyperinsu-
linemia and reactive hypoglycemia in late dumping.
However, it remains elusive why some patients
remain asymptomatic, whereas others develop severe
symptoms after gastric surgery.
Diagnosis
Dumping syndrome is diagnosed according to a
constellation of symptoms in a patient who had
undergone gastric surgery or dumping provocation
test. Sigstad53 developed a diagnostic scoring sys-
tem based on symptoms of dumping (see Table 2). A
diagnostic index ⬎7 is suggestive of a dumping
syndrome. This system is simple to use, but its
disadvantage is difficulty in separating other post-
prandial symptoms from dumping. The score index
is helpful in clinical practice to assess response to
therapy.
Signs and symptoms of dumping can be elicited
with provocation test by the oral glucose challenge.
A rise in the heart rate by 10 beats per minute or
more in the first hour after an oral glucose challenge
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DUMPING SYNDROME 519
Table 2
Sigstad’s diagnostic scoring system
Shock ⫹5
Almost fainting, syncope, unconsciousness ⫹4
Desire to lie or sit down ⫹4
Breathlessness, dyspnea ⫹3
Weakness, exhaustion ⫹3
Sleepiness, drowsiness, yawning, apathy, ⫹3
falling asleep
Palpitation ⫹3
Restlessness ⫹2
Dizziness ⫹2
Headaches ⫹1
Feeling of warmth, sweating, pallor, ⫹1
clammy skin
Nausea ⫹1
Fullness in the abdomen, meteorism ⫹1
Borborygmus ⫹1
Eructation ⫺1
Vomiting ⫺4
of 50 g after 10-hour fasting, was found to be 100%
sensitive and 92% specific for early dumping.54 Use
of higher amount of glucose for provocation test
should be perhaps avoided, because it can induce
symptoms of dumping in nondumpers. A positive
hydrogen breath test after glucose ingestion has
been reported to be 100% sensitive for early dump-
ing by the same authors. Late dumping can be often
confirmed through frequent blood sampling after
provocation with oral glucose. Higher plasma levels
of glucose during the first 60 minutes after provoca-
tion and reduced plasma glucose levels 60 –180 min-
utes later have been used as diagnostic criteria for
dumping. However, late dumpers can be more accu-
rately diagnosed according to symptoms than on
subjective testing after glucose provocation. Mea-
surement of gastric emptying by scintigraphy is
helpful in documenting of rapid gastric empty-
ing.55,56 An endoscopy or a barium upper GI study
can help to determine the anatomy and exclude an
ulcer or stoma obstruction.57
Management of Dumping Syndrome
Diet
The resolution of dumping symptoms is achieved
in most cases by dietary modifications, in particular
by the reduction of carbohydrate intake, and the
adjustment of lifestyle.
Daily food intake should be divided into at least 6
meals. Dietary prohibitions are very important.
Fluid intake during meals should be restricted.
Drinking liquids should be avoided for at least a
half-hour after a meal. Complex carbohydrates (eg,
unsweetened cereals, pasta, potatoes, fresh fruit,
and vegetables) are preferred. Simple sugars (eg,
candies, cookies, sodas, sports drinks, sweets)
should be avoided. Milk and dairy products (eg,
milkshakes, sweetened yogurt, chocolate milk) are
520
generally not well tolerated and should be also
avoided. Protein (meat, fish, chicken, eggs) and fat
intake should be increased to meet daily caloric
needs because of restricted intake of carbohydrates.
Many patients modify their diet according to a
personal experience with food tolerance.
Most individuals with relatively mild symptoms
will respond to dietary changes. For patients with
severe vasomotor symptoms (postprandial hypoten-
sion), lying supine for 30 minutes after meals may
minimize the chance of syncope by delaying gastric
emptying and improving venous return. Supplemen-
tation of dietary fibers (bran, methylcellulose) with
meals has been proven effective in the treatment of
hypoglycemic episodes.58 Pectins (5 g with each
meal), glucomannan, and guar gum have been
tested with good results, especially in the pediatric
population.59 – 61 These dietary additives form gels
with carbohydrates, and they delay glucose absorp-
tion and prolong transit time.
Pharmacologic Therapy
In approximately 3%–5% of patients, severe
dumping will continue despite dietary modifications.
This can result in fear of eating and progressive
weight loss. Drug therapy plays an important role in
patients who failed dietary changes. Tolbutamide
has been shown to cause subjective improvement,
and an adrenergic agent, propranolol, has reduced
vasomotor symptoms.62,63 Serotonin antagonists
such as cyproheptadine (4 – 8 mg, 3 times per day)
and methysergide maleate (4 – 8 mg, 2 times per
day) have been used in prevention of vasomotor
symptoms, with conflicting results.64,65 Prednisolone
and verapamil successfully alleviated symptoms of
dumping in a few reported cases.66,67 Sustained-re-
lease verapamil, at a dose of 120 –240 mg/day, pro-
vided a complete vasomotor symptom relief in 6
patients with dumping.68
Acarbose
Acarbose is a potent, competitive inhibitor of
␣-glycoside hydrolase, which has been found as a
useful adjunct in the management of late dump-
ing.69 Acarbose significantly blunts the postprandial
rise of glucose and insulin by delaying carbohydrate
digestion.70,71 Because of the reversible nature of
the inhibitor-enzyme interaction, conversion of com-
plex carbohydrates (starch and sucrose) to monosac-
charides is delayed rather than completely blocked.
This mechanism is responsible for effectiveness of
acarbose in late dumping. The positive effects of
acarbose have been documented after a test meal in
a few studies. In a double-blind study of 9 patients
after gastric surgery, acarbose given at a dose of 50
mg following a normal carbohydrate rich meal has
been shown to reduce symptoms of postprandial
hypoglycemia, especially in combination with pec-
tin.72 No beneficial effect has been found by using a
higher dose of acarbose (100 mg).
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UKLEJA Vol. 20, No. 5
Lyons et al73 reported negative results with short-
and long-term therapy with acarbose. A significant
attenuation of hyperglycemia and reduced rise in
plasma insulin and enteroglucagon were found in 13
subjects with dumping syndrome after giving 50 mg
of acarbose before a meal, without statistically sig-
nificant improvement in the dumping score. Nine
patients who continued a longer trial of acarbose
(50 mg 3 times per day ⫻ 1 month) had no signifi-
cant reduction in the severity of dumping.
In contrast, a complete disappearance of late
dumping symptoms (palpitation and dizziness) has
been reported after 1 month of therapy with acar-
bose (50 mg or 100 mg 3 times per day) in 6 patients
with dumping and non–insulin dependent diabetes
mellitus.74 These data suggested possible long-term
efficacy of acarbose in late dumping. However, the
use of acarbose may be limited by diarrhea and
flatulence, but severity of those adverse effects usu-
ally decreases over time. Further long-term prospec-
tive studies are needed to confirm the usefulness of
acarbose in dumping syndrome.
Octreotide
Somatostatin and its synthetic analog octreotide
(Sandostatin, Sandoz, East Hanover, NJ) have been
demonstrated to be effective in patients with dump-
ing refractory to standard therapy.75,76 Octreotide
acts at multiple levels in the pathophysiology of dump-
ing77 (see Table 3). It exerts a strong inhibitory effect
on the release of insulin and several gut-derived hor-
mones. In a short-term use, octreotide has been shown
to decrease the symptom index score, pulse rate, and
plasma insulin levels when compared with placebo.78
Octreotide prevents late hypoglycemia by the reduc-
tion in peak insulin concentration and by the prolon-
gation of maximal plasma glucose level.79 It also min-
imizes changes in orthostatic blood pressure, packed
cell volume, and plasma osmolarity. Octreotide has
been shown to decrease the rate of gastric emptying by
resetting the migrating motor complex to the fasting
level.80,81
The usual initial dose of octreotide is 25–50 ␮g
administered subcutaneously, 2–3 times daily, 15–30
minutes before meals. The dose can be increased to
100 ␮g if the smaller dose is ineffective. The effective-
ness of octreotide for ameliorating symptoms of both
early and late dumping has been demonstrated in
Table 3
The mechanisms of action of octreotide in dumping
syndrome
Delay in the accelerated gastric emptying
Delay in small intestine transit time
Inhibition of enteral hormone secretion
Inhibition of insulin release
Inhibition of postprandial vasodilation/splanchnic
vasoconstriction
Increase in intestinal absorption of water and sodium
October 2005 DUMPING SYNDROME 521

small randomized control trials. The evidence of oct-
reotide effectiveness in dumping is summarized in
Table 4.
Hopman et al79 first showed alleviation of symp-
toms in all 12 patients who received short-term
therapy with octreotide 15 minutes before meals in a
placebo-controlled crossover trial. Octreotide stabi-
lized pulse rate and prevented hypoglycemia but
had no effect on packed cell volume. Primrose and
Johnston82 reported 100% symptomatic improve-
ment in patients treated for 3 days in a controlled
crossover trial. Octreotide had a beneficial effect on
pulse rate, blood pressure, packed cell volume, and
blood glucose. However, long-term treatment with
octreotide (50 ␮g 3 times per day up to 4 years) was
effective only in 2 of 5 patients, and 3 of them
developed severe diarrhea.83 In a placebo-controlled
trial, Tulassay et al84 showed that octreotide, given
for 2 days, prevented vasomotor and GI symptoms,
hypoglycemia, hyperinsulinemia, and packed cell
volume changes in 8 patients with early and late
dumping.
Geer et al85 reported that octreotide alleviated
dumping and an increase in pulse or blood pressure,
and prevented late hypoglycemia in 10 patients with
severe dumping. A 15-month therapy with oct-
reotide (3– 4 doses daily) resulted in reduction of
symptoms in 8 of 10 patients. During octreotide
treatment, fecal fat excretion increased signifi-
cantly. Despite steatorrhea, an 11% increase in
mean body weight was found. It was thought to be
related to the increased energy intake as the
patients were able to increase oral intake. No major
adverse effects were noted, except for mild transient
abdominal cramping and diarrhea, relieved with an
extra dose of octreotide. Seven patients were able to
return to work. In another controlled trial, Richards
et al81 confirmed that short-term therapy with oct-
reotide alleviated diarrhea, abdominal pain, and
palpitation in 6 patients with severe early dumping.
Gray et al86 also have shown that octreotide
(100 ␮g) was effective to eliminate clinical dumping
and prevent late hypoglycemia in 4 of 9 patients
with severe dumping. The drug had no effect on
packed cell volume or plasma osmolarity. Similar
results were found by Hasler et al87 in 8 patients
with late dumping. Painful injections were reported
by 4 of them.
In a long-term trial, Mackie et al88 showed sus-
tained symptom improvement with octreotide (50 ␮g
2 times per day) in 6 of 14 patients. The remaining
patients had no benefit or developed unwanted side
effects. In the largest published study up to date,
Vecht et al89 reported outcome of a long-term ther-
apy with octreotide (mean follow-up of 37 months) in
20 patients with severe dumping. Four patients
received a continuous infusion of octreotide via
pump. The initial symptom relief was achieved in all
subjects. However, after 3 months of therapy,
improvement was seen in 80% of patients. Signifi-
cant weight gain (on average 2.4 kg) was found
despite a statistically significant increase in fecal fat
excretion. Eleven patients discontinued treatment
because of lack of improvement or side effects. For
the first time, biliary complications were reported in
3 patients (gallstone formation and hydrops of the
gallbladder).
Octreotide is effective and safe in long-term treat-
ment of severe dumping.90,91 Clinical improvement
was seen in 90% of patients with refractory dump-
ing. Further, improvements in lifestyle have been
reported with long-term therapy.
The use of octreotide is limited by the occurrence
of side effects such as diarrhea and injection aver-
sion. Steatorrhea or early-morning diarrhea associ-
ated with long-term therapy can be managed with
pancreatic enzyme replacement or an extra dose of
octreotide before bedtime.92 However, diarrhea in
patients who already have malabsorption and mal-
digestion can be a major limiting factor in use of
octreotide. Gallstone formation has not been well
documented among trials.
The development of an oral or nasal formulation
should further improve the application of octreotide

Table 4
Randomized controlled trials of octreotide therapy for severe dumping

Author Year Number of Single dose (␮g) Successful Duration (mo) Adverse effects
patients (frequency) therapy (%)

Short-term therapy
Hopman79 1988 12 50 100 Diarrhea
Tulassay84 1989 8 50 100 -
Primrose82 1989 10 50–100 90 Diarrhea
Richards81 1990 6 100 100 -
Geer85 1990 10 100 100 Diarrhea
Gray86 1991 9 50 100 -
Hasler87 1996 8 50 100 Painful injection
Long-term therapy
Geer85 1990 10 100/t.i.d. 90 3–15 Diarrhea
Primrose83 1990 5 50/b.i.d. 50 48 Diarrhea
Mackie88 1991 14 50/b.i.d. 50 3 -
Vecht89 1999 20 25–100/t.i.d. 55 37 Steatorrhea

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522
in the treatment for dumping syndrome. In sum-
mary, octreotide should be offered to patients with
severe dumping when other options have been
exhausted.
Surgical Treatment
Conservative management is always preferred
because most patients will have improvement in
dumping over time, and surgery may not be cura-
tive. Postgastrectomy syndromes often abate with
time. Therefore, medical, dietary, and behavioral
therapy should be given at least a 1-year trial. If
these nonoperative measures fail, corrective surgery
may be considered.
Several surgical procedures have been designed
to correct the symptoms of dumping. Long-term
studies to assess the effectiveness of these proce-
dures are limited. Furthermore, no controlled trials
exist to examine the efficacy of one procedure com-
pared with the others.
Stomal Revision
One of the strategies for surgical correction of
dumping is to slow down gastric emptying. Good
results with narrowing of the gastrojejunal stoma
have been reported.93,94 However, this surgery car-
ries risks of stoma stricture or gastric outlet obstruc-
tion. This technique has been abandoned in favor of
other procedures.
Pyloric Reconstruction
In this procedure, the pyloroplasty scar is modi-
fied by cutting it and creating a longitudinal closure
of the incision. In 2 small series of 14 and 9 patients,
Koruth et al95 and Cheadle et al96 have reported
excellent results in the resolution of dumping symp-
toms. Pyloric reconstruction is a low-risk procedure
and seems to be fairly effective in patients who have
severe dumping after pyloroplasty.
Conversion of Billroth II to Billroth I Anastomosis
This procedure restores the physiologic delivery
of the meal to the duodenum without creating the
risk of gastric outlet obstruction. An improvement in
dumping syndrome in 75% of patients had been
reported by Woodward et al.97 The procedure has a
low rate of complications and it is relatively sim-
ple.98
Jejunal Interposition
Creating a long isoperistaltic limb between stom-
ach and jejunum can provide excellent symptom
relief related to rapid gastric emptying. Henley99
reported excellent results with an interposed jejunal
segment between the gastric pouch and the duode-
num for correction of postgastrectomy dumping in a
study including more then 300 patients.
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UKLEJA Vol. 20, No. 5
In contrast, other smaller series have failed to
show such excellent results with the use of isoperi-
staltic interposition.100 The length of an interposi-
tion segment may influence the surgical outcome as
reported by Ramus et al.101 Suboptimal results were
found with a shorter jejunal segment and a good
outcome with a 10-cm segment. Complications
related to the surgery include ulcerations and ste-
nosis in the interposed segment. Reversed segments
have been shown to be effective for as long as 10
years after interposition.102
Roux-en-Y Conversion
A conversion to a Roux-en-Y gastrojejunostomy
has been preferred as a remedial operation.103 The
Roux-en-Y gastrojejunostomy is useful in patients
with dumping because of slowing down the gastric
emptying and the transit of chyme through the Roux
limb. The mechanisms responsible for the effective-
ness of this surgery in dumping are not well known.
However, the interruption of the migration motor
complex and diminished jejunal contractions may
play a major role. A favorable outcome has been
reported after this operation in 85%–90% of patients
with Billroth I and II gastrectomy.104,105 Vogel et
al106 reported excellent results in 19 of 22 patients
with this operation. This procedure is easier to
perform, and it has fewer long-term complications
(eg, Roux stasis syndrome).107
Experimental Procedures
Because none of the operations for intractable
dumping is uniformly successful, a new approach
has to be considered, including intestinal retrograde
electrical pacing, but no human studies have been
performed yet.108
Overall, surgery has a limited role in the treat-
ment of dumping. Selection of the surgical procedure
is very important. In the summary of remedial
operations for patients after pyloroplasty, pyloric
reconstruction should be the initial corrective oper-
ation. Roux-en-Y reconstruction appears to be the
most effective option for patients with Billroth I and
Billroth II gastrectomies. For those patients who
already have a Roux-en-Y reconstruction, an anti-
peristaltic jejunal loop should be interposed.
Prevention
Prevention of dumping syndrome is preferable to
treatment of its symptoms. The introduction of pro-
ton pump inhibitors and Helicobacter pylori eradica-
tion may further decrease the need for elective surgery
in a peptic ulcer disease. Newer gastric operations,
such as proximal gastric vagotomy, which produces
minimal disturbance of gastric emptying mechanism,
are associated with a lower incidence of dumping
syndrome.
Proximal gastric vagotomy is at present the pro-
cedure of choice for the surgical management of
October 2005 DUMPING SYNDROME
intractable ulcer disease. Although the long-term
ulcer recurrence rate is higher after this procedure
compared with antrectomy and truncal vagotomy, it
has the lowest incidence of postoperative dump-
ing.109 If more extensive surgery is necessary, resec-
tion is preferable to a Roux-en-Y gastrojejunostomy
because of decreased rate of dumping, when com-
pared with pyloroplasty or loop gastrojejunostomy.
Conclusion
Dumping syndrome is a common complication
after gastric surgery. Clinically significant dumping
can produce serious distress and considerable mor-
bidity to the patients. Fortunately, the indications
for gastric surgery are declining, although the need
for emergent gastric surgery has not changed. The
diagnosis of dumping syndrome is based on clinical
presentation, and if needed, it can be confirmed by a
provocation test with oral glucose. The majority of
patients respond to medical therapy, including
dietary modifications. Therapy with octreotide is an
effective alternative before considering a surgical
correction. Close attention must be given to the pa-
tient’s nutrition status. If medical therapy fails to
provide symptom relief, surgical revision should be
offered with the understanding that even this inter-
vention may not be successful.
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