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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1033_Библиотеки_им_академика_М_И_Перельмана
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25 Dumping Syndrome
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3. Hormonal changes: Alterations in gastrointestinal hormone
levels have long been recognized in dumping syndrome.
Hyperosmolar, high volume chyme resulting from rapid gastric emptying increases gastrointestinal hormone secretion to
supraphysiologic levels [5]. Of the many hormonal abnormalities demonstrated, vasoactive intestinal peptide (VIP) and
serotonin appears to have prominent roles in dumping syndrome pathophysiology [6]. VIP increases splanchnic blood
ow, intestinal contractions, and secretion of electrolytes and
water into the intestinal lumen. Similarly, serotonin causes
splanchnic vasodilation. Oversecretion of these hormones may
contribute to rapid transit and uid shifts. Bradykinin has
vasodilatory effects and increases vascular permeability [7].
An exaggerated bradykinin response can increase uid shifts
into peripheral vascular tissues, which may contribute to the
ushing seen in some patients with dumping syndrome.
Norepinephrine levels have also been found to be elevated in
dumping syndrome. This may contribute to early sympathetic
vasomotor symptoms including tachycardia and sweating [8].
Finally, insulinotropic hormones may be major drivers of late
dumping syndrome, which is characterized by delayed hypoglycemia in response to a food bolus. An exaggerated secretion of glucagon-like peptide 1 (GLP-1) and glucose-dependent
insulinotropic polypeptide (GIP) in response to hyperosmolar
chyme is seen in dumping syndrome [9]. This leads to an
increase in insulin secretion and inhibition of glucagon, subsequently causing hypoglycemia.
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Epidemiology andEtiology
Dumping syndrome can be caused by surgical and nonsurgical etiologies. Up to 50% of gastric operations can cause rapid gastric
emptying, albeit with different rates of symptoms severe enough to
warrant work-up and treatment for dumping syndrome [10]. In
adults, Roux-en-Y gastric bypass is the most common cause of sur-
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gical dumping syndrome [11]. In the pediatric population, dumping
syndrome is frequently secondary to Nissen fundoplication [12].
Gastric operations cause dumping syndrome by increasing the
rate of chyme transit from the stomach into the intestines [2]. In
normal gastric physiology, the antrum and pylorus limit gastric
emptying, and the fundus acts as a reservoir for the food bolus.
Roux-en-Y gastric bypass can cause dumping syndrome due to a
small gastric reservoir and bypassing of the pyloric sphincter.
Sleeve gastrectomy, although less frequently, can also cause
dumping syndrome due to decreased gastric volume and increased
emptying times. Nissen fundoplication can disrupt the reservoir
function of the stomach due to decreased fundus volume to
accommodate a food bolus. Vagus transections, on the other hand,
can have mixed effects on gastric emptying. In patients with an
intact pylorus, gastric emptying may be delayed after vagal transection due to a blunted pyloric relaxation. However, vagal
reexes also maintain receptive gastric relaxation following
ingestion of a food bolus and inhibition of gastric emptying in
response to intestinal stretch. Loss of these arcs can promote rapid
gastric emptying.
Nonsurgical causes of dumping syndrome are overall less
common. Although early diabetes typically causes gastroparesis,
patients with long-standing diabetes sometimes experience dumping syndrome [13]. In a subgroup of patients, the onset of dumping syndrome follows an episode of gastroenteritis. This is likely
related to duodenal mucosal damage and the subsequent alteration in duodenal receptors. Finally, there is an idiopathic form of
dumping syndrome. In these patients, vagal function may be
impaired, resulting in decreased gastric accommodation [5].
B. Kahramangil et al.
Clinical Presentation
Dumping syndrome has two distinct forms based on the constellation of symptoms and timing of their onset after a meal [2]
(Table25.1). Early dumping syndrome occurs within 30min of a
meal and is characterized by systemic and abdominal symptoms.
Systemic symptoms include fatigue, lightheadedness, tachycar-
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Table 25.1 Clinical presentations of early and late dumping syndrome
Early dumping syndrome Late dumping syndrome
Onset: Within 30min of a meal Onset: 1–3h after a meal
Driving physiology: Hyperosmolar
chyme and uid shifts
Systemic symptoms Systemic signs
Palpitations Sweating
Lightheadedness Altered level of consciousness
Fatigue Lightheadedness
Headache
Hypotension Biochemical features
Abdominal symptoms Reactive hypoglycemia
Early satiety
Epigastric pain or fullness
Diarrhea
Nausea
Abdominal cramps
Driving physiology: Reactive
hypoglycemia
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dia, ushing or pallor, sweating, and in severe cases, syncope.
Accompanying gastrointestinal symptoms include early satiety,
epigastric pain or fullness sensation, diarrhea, abdominal cramps,
and nausea. Early dumping syndrome is the most common presentation. The second form is late dumping syndrome. The symptoms in this form typically manifest 1–3 h after ingestion of a
meal and include sweating and lightheadedness in the setting of
hypoglycemia, and in severe cases, altered level of consciousness.
It is possible to have concurrent early and late dumping syndrome
[14]. Severe, long-standing dumping syndrome can lead to
protein- energy malnutrition. Other long-term complications
include depression, anxiety, and avoidance of social interactions
involving eating.
Diagnosis
The diagnosis of dumping syndrome is made with the demonstration of rapid gastric emptying in the presence of appropriate
symptoms. Gastric scintigraphy is the gold standard test for gas-
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tric emptying, while oral glucose challenge may help demonstrate
the maladaptive response to a food bolus. Esophagogastroduodenoscopy, colonoscopy, and stool analysis can be used to rule out
other differential diagnoses.
B. Kahramangil et al.
Clinical Evaluation andDiagnostic Modalities
Clinical evaluation for dumping syndrome starts with a thorough
history and physical examination. Suggestive signs and symptoms include abdominal fullness, nausea, pallor, palpitations,
weakness, and lightheadedness. Severe cases can cause altered
mental status and syncope.
– Demonstration of rapid gastric emptying: Radionuclide
gastric scintigraphy is the gold standard test for demonstration
of rapid gastric emptying. Standard meal for the test consists of
a 250-calorie egg-substitute labeled with 99mTc, 120mL of
water, and two slices of whole wheat bread [15]. Images are
taken immediately after ingestion, at 30min, and at 1 h, fol-
lowed by hourly images up to 4h after meal. In each image,
gastric retention is calculated based on the percentage of radio-
isotopes remaining in the stomach. <35% retention at 1h is
diagnostic for rapid gastric emptying. In late dumping syn-
drome, <20% retention at 2h is typical.
– Oral glucose challenge test: Oral glucose challenge test can
be useful to conrm the diagnosis of dumping syndrome.
Patients ingest 50g of glucose after 10h of overnight fasting
[16]. Pulse and blood pressure are monitored at baseline, dur-
ing ingestion and after ingestion. Blood glucose and hemato-
crit can also be measured at these time points and repeated at
30-min intervals. An increase in heart rate of at least 10 beats
per minute is considered positive. A 3% increase in hematocrit
within the rst 30min after ingestion is compatible with early
dumping syndrome. Glucose level<60mg/dL at 2–3h after
ingestion indicates late dumping syndrome.
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Treatment
Treatment of dumping syndrome starts with lifestyle and dietary
modications. If the symptoms persist despite these changes,
pharmacologic treatment is the next step. Surgical procedures are
reserved for most severe cases, where symptoms cannot be controlled by any other means (Table25.2).
• Dietary modications: Dietary modications are the rst line
of treatment for dumping syndrome. Patients should ingest
smaller but more frequent meals, limit carbohydrate intake,
and preferentially eat complex over simple carbohydrates [17].
Lying down after a meal and ingesting solids and liquids separately can also help, as uids are likely to increase gastric emptying. Increasing dietary ber may slow down gastric emptying,
helping avoid hypoglycemia in late dumping syndrome, and
proteins can provide additional calories without worsening
symptoms. Despite low patient compliance due to poor taste,
guar gum and pectin are useful dietary adjuncts [18]. Both
supplements work by increasing the viscosity of food bolus
and subsequently help delay gastric emptying.
Table 25.2 Treatment options for dumping syndrome
Dietary modications
Ingestion of smaller but
more frequent meals
Limited carbohydrate intake Tincture of opium Roux-en-Y gastric
Preferential ingestion of
complex carbohydrates
Separation of liquid and
solid meals
Increased dietary ber GLP-1 agonists
Increased protein intake
Guar gum and pectin
Pharmacologic
modications Surgical treatment
Loperamide Roux-en-Y gastric
bypass reversal
bypass revision
Acarbose Continuous enteral
feeding
Octreotide
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B. Kahramangil et al.
• Pharmacologic treatment: Antimotility drugs can be useful
to treat diarrhea associated with dumping syndrome. Loperamide, a gut opioid receptor agonist, and tincture of opium can
be used to decrease stool liquidity [19]. Anticholinergic agents
can also improve dumping syndrome-related symptoms. They
have antidiarrheal effects, slow gastric emptying, and decreased
gastrointestinal cramps. Acarbose can be used to prevent hypoglycemia in late dumping syndrome. It is an alpha glycosidase
inhibitor, which inhibits the digestion of polysaccharides into
monosaccharides [20]. Decreasing carbohydrate absorption
can help mitigate the maladaptive insulin and glucagon-like
peptide 1 secretion seen in late dumping syndrome. When all
other pharmaceutical options fail, octreotide can be tried.
Octreotide is a somatostatin analog, which slows gastric emptying and decreases splanchnic blood ow [21]. Furthermore,
it inhibits the secretion of intestinal hormones including vasoactive intestinal peptide, insulin, and serotonin. Octreotide
improves the symptoms of both early and late dumping syndrome. More recently, GLP-1 agonists have been successfully
utilized in the management of late dumping syndrome and
hypoglycemia after gastric bypass surgery.
• Surgical treatment: Surgery is the last resort for patients who
continue to be severely symptomatic despite dietary modications and maximal pharmacologic treatment. When undertaken, surgical treatment is usually directed at the underlying
anatomic abnormality causing dumping syndrome.
– Roux-en-Y gastric bypass reversal: In most cases, dump-
ing syndrome following Roux-en-Y gastric bypass can be
adequately controlled with dietary modications and pharmacologic treatment. However, refractory dumping syndrome, especially in the setting of hypoglycemia, may
require surgical revision. Gastric bypass reversal to normal
anatomy has been proposed to help control symptoms of
dumping syndrome. In 2013, Villalonga etal. reported successful laparoscopic gastric bypass reversal in a series of
patients with different pathologies including refractory
dumping syndrome [22]. In the six patients who underwent
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surgery for dumping syndrome, a leak was observed in one
patient, which was managed with laparoscopic drainage.
Despite the possibility of a successful conversion to a normal anatomy, weight regain remains a major concern in
patients with history of obesity. To overcome this issue,
Roux-en-Y gastric bypass reversal with concomitant sleeve
gastrectomy has been proposed. Carter etal. analyzed the
outcomes of 12 patients who underwent conversion of gastric bypass to sleeve gastrectomy due to various complications including refractory dumping syndrome [23]. Seven
major complications were observed in 4 patients including
a portal vein thrombosis, postoperative bleed, pancreatic
leak, pulmonary embolism, seroma, anastomotic leak, and
stricture. Although effective, this is a morbid procedure and
requires very careful patient selection.
– Gastric pouch restriction: In some patients with Roux-
en- Y gastric bypass, refractory hypoglycemia may develop
with concurrent loss of gastric restriction due to gastric
pouch dilation. In this highly selected group of patients,
reconstitution of gastric restriction may help improve hypoglycemia. Different techniques described to restrict gastric
pouch volume include the surgical downsizing of the pouch,
silastic ring placement, and placement of an adjustable band
[17]. Z’graggen etal. analyzed the outcomes of restoration
of gastric restriction in 12 patients with refractory hypoglycemia utilizing silastic ring (n= 8) and adjustable gastric
band (n=4) [24]. In this series, perioperative complication
rate was 8% with resolution of hypoglycemic episodes in 11
out of 12 patients.
– Continuous enteral feeding: Continuous enteral feeding
through a feeding jejunostomy can be used in select patients
with refractory late dumping syndrome. This eliminates the
need for food ingestion and helps prevent hypoglycemia.
Enteral access can be obtained by endoscopic or surgical
procedures.
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B. Kahramangil et al.
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Normal Physiology Findings
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After Hiatal Hernia Repair
26
andFundoplication
RamsesA.Saavedra andEdwardAuyang
Introduction
Hiatal hernia repair and fundoplication are performed in symptomatic patients to help provide relief from the symptoms produced by
the abnormal hiatal anatomy. The goal of surgical repair is restoration of “normal” anatomy. This is achieved by reduction of the hernia and recreation of a functional gastroesophageal junction (GEJ)
below the level of the diaphragm. Various techniques can be used to
achieve this, including Nissen, Toupet, and Dor fundoplications.
Upon recreation of the normal anatomy, restoration of physiologic
function is expected. There are several common studies used to
assess postoperative anatomy and physiology. The studies discussed here include contrasted upper gastrointestinal esophagram
(UGI), computed tomography (CT) scan, esophageal manometry,
pH testing, endoscopy, gastric emptying studies, and endoluminal
functional imaging. Through analysis of these studies, we will clarify what ndings can be considered as normal and address some
common variations seen after different operative techniques.
R. A. Saavedra · E. Auyang (*)
Department of Surgery, University of New Mexico School of Medicine,
Albuquerque, NM, USA
e-mail: rasaavedra@salud.unm.edu; eauyang@salud.unm.edu
© Society of American Gastrointestinal and Endoscopic Surgeons
(SAGES) 2023
A. D. Patel et al. (eds.), The SAGES Manual of Physiologic
Evaluation of Foregut Diseases,
https://doi.org/10.1007/978-3-031-39199-6_26
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