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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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B. Kahramangil et al.
Treatment
Treatment of gastroparesis should be undertaken in a stepwise
fashion starting with dietary modication followed by pharmacologic treatment with prokinetics and antiemetics. Surgical treatment is reserved for severe and refractory cases. Glucose control
is also important in diabetic gastroparesis.
• Dietary modication: Dietary modication is the rst line
treatment for gastroparesis in all patients. Patients should
refrain from fatty, spicy, and acidic foods, and limit the amount
of dietary roughage [18]. In all forms of gastroparesis, oral
nutrition should be maximized as tolerated. For patients who
are unable to meet nutrition goals by oral intake, other enteral
or parenteral routes may become necessary.
• Pharmacologic treatment: Pharmacologic treatment of gastroparesis starts with avoidance of medications that can delay
gastric emptying. Such medications include narcotics, tricyclic
antidepressants, anticholinergics, octreotide, and calcium
blockers (REF: Parkman HP.American Gastroenterological
Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology 2004). For those
patients who continue to experience symptoms despite dietary
modication and avoidance of exacerbating medications, prokinetic agents are the next step in treatment. These medications
are typically administered before every meal and at bedtime.
Metoclopramide, a dopamine 2 receptor antagonist, is usually
the rst line prokinetic drug. A 5mg dose before meals and at
bedtime is appropriate for most patients. In patients who do not
tolerate metoclopramide, domperidone 20mg three times daily
can be an alternative [19]. Other pharmacologic options
include erythromycin, a motilin receptor agonist, and cisapride, a 5-HT4 agonist. Acute hypoglycemia has been shown
to delay gastric emptying [20] and decrease the effect of prokinetic drugs [21]. Good glycemic control is paramount in diabetic patients with gastroparesis. Finally, antiemetic
ab
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medications without prokinetic effects can also be useful for
symptomatic relief.
• Endoscopic and surgical treatment options: Surgical and
endoscopic treatments are the last resort for patients who
remain severely symptomatic despite dietary modication and
pharmacologic treatment. In general, these procedures can be
grouped under gastric electrical stimulator (GES) placement,
botulinum toxin injection, pyloromyotomy, surgical gastric
resection, and enteric access procedures.
– GES placement: Although the precise mechanism of action
remains unknown, GES placement can lead to signicant
symptomatic improvement with good patient selection. The
typical stimulator device consists of two leads which are
placed in the muscularis layer of the greater curvature of the
stomach approximately 10 cm proximal to the pylorus
along with a subcutaneous pulse generator [22] (Fig.24.1).
In some patients, a temporary device may be tried to ensure
symptomatic improvement prior to placement of a permanent stimulator. These stimulators can be effective in diabetic and idiopathic forms of gastroparesis [23].
Gastroparesis-related nausea, vomiting, and abdominal
pain have been reported to decrease after GES placement
Fig. 24.1 Intraoperative pictures demonstrating the laparoscopic placement
of gastric stimulator leads. Leads are placed in the submucosal layer and xed
in place with laparoscopic suturing (a). At completion, both leads are located
along the greater curvature of the stomach (b)
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B. Kahramangil et al.
[24]. GES can also improve quality of life [25] and decrease
prokinetic drug dose [26] in carefully selected patients.
– Botulinum toxin injection: Botulinum toxin injection has
been attempted to treat gastroparesis-related symptoms
based on the observation that pyloric dysfunction could be
seen in a subset of patients with gastroparesis [27]. Patients
with gastroparesis and normal gastric body function have
been reported to experience signicant symptomatic relief
with botulinum toxin injection and pyloric balloon dilation
[28]. On the other hand, two randomized controlled trials
have failed to show efcacy of injections in gastroparesis
treatment [29, 30]. Although there is no evidence to support
widespread use of botulinum injection, certain subsets of
patients with gastroparesis may benet from this procedure.
– Pyloromyotomy: Up to 70% of patients with gastroparesis
have been reported to have loss of interstitial cells of Cajal
and brosis in the pylorus [31]. This nding along with the
improvement of symptoms with botulinum injection in
selected patients led to the use of pyloromyotomy in gastroparesis treatment. Pyloromyotomy can be performed endoscopically in centers with advanced endoscopic skills
(Fig.24.2). Most studies with endoscopic pyloromyotomy
have reported satisfactory short- to medium-term results
[22]. Clinical response rate ranged between 70 and 80% and
an improvement in gastric emptying was observed in 4–64%
of patients [32–34]. Laparoscopic pyloromyotomy can also
be performed when endoscopic procedure is not feasible.
Both laparoscopic and endoscopic pyloromyotomy have
been shown to improve gastroparesis-related symptoms and
decrease prokinetic drug needs [35].
– Surgical gastric resection: For patients who remain symp-
tomatic despite the less invasive treatment options, surgical
gastric resection may be needed. Extensive subtotal or near
total gastrectomy with Roux-en-Y gastrojejunostomy can
improve vomiting in diabetic gastroparesis [36]. In obese
patients with gastroparesis, a Roux-en-Y gastric bypass
cd
ef
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a b
Fig. 24.2 Intraprocedural pictures describing the steps of peroral pyloromyotomy. (a) Endoscopic identication of the pylorus, (b) Injection of the
pyloric mucosa, (c) mucosal dissection using endoscopic electrocautery, (d)
extension of the dissection into the submucosal layers, (e) completion of
pyloromyotomy, (f) closure of the mucosal defect with endoscopic clips
may help decrease nausea in addition to allowing weight
loss [24]. For patients who remain severely symptomatic
despite all other options including a subtotal gastrectomy, a
completion total gastrectomy may be necessary [37].
– Enteric access procedures: When patients are unable to
meet nutritional goals by oral intake, gastrostomy, jejunostomy, and GJ tubes may become necessary to allow venting
and distal enteral access for feeding. These enteral tubes
can be placed endoscopically in most cases. When endoscopic placement fails, laparoscopic or open surgical techniques can be utilized.
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B. Kahramangil et al.
Conclusion
Gastroparesis is a rare disorder which may cause signicant
distress when inadequately treated. Diagnosis requires exclusion of mechanical obstruction and demonstration of delayed
gastric emptying. Dietary modication is the rst line of treatment. Depending on severity of symptoms, pharmacologic
treatment with prokinetic agents and surgical interventions may
be indicated.
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Dumping Syndrome
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BoraKahramangil, EmanueleLo Menzo,
SamuelSzomstein, andRaulRosenthal
Introduction
Dumping syndrome is a gastrointestinal pathology characterized
by vasomotor and gastrointestinal symptoms occurring secondary
to rapid gastric emptying. The changes in gastric emptying are
frequently secondary to postsurgical anatomic alterations following upper gastrointestinal surgery. Although the incidence of
dumping syndrome has historically decreased with the discovery
of the association of Helicobacter pylori with gastric ulcer and the
subsequent decrease in the number of ulcer operations, it is once
again on the rise due to the increasing number of bariatric procedures. A good understanding of this pathology remains important
for clinical practice.
B. Kahramangil · E. Lo Menzo (*) · S. Szomstein · R. Rosenthal
Cleveland Clinic Florida, Department of General Surgery, Bariatric and
Metabolic Institute, Weston, FL, USA
e-mail: lomenze@ccf.org
© 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_25
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Pathophysiology
The main factors in the pathophysiology of dumping syndrome
include rapid transit of chyme, pathologic uid shifts, and the
resulting hormonal changes.
1. Rapid transit of chyme: Rapid transit of chyme is the major
driver of dumping syndrome pathophysiology. The chyme in
dumping syndrome is incompletely digested and hyperosmolar [1]. Large volume, hyperosmolar chyme causes duodenal
distension, which in turn leads to a reexive increase in intestinal contractility [2]. This reex response is mediated by the
intestinal smooth muscles and the myenteric neural plexus. It
causes abdominal symptoms related to dumping syndrome.
Overall, liquid meals are more likely to trigger these symptoms than solids. However, it is worth noting that not every
patient with rapid gastric emptying experiences dumping
syndrome- related symptoms [1]. Neuroplastic changes in the
enteric neural plexus and the resulting adaptation likely underlie the lack of symptoms in some individuals. The patients
with dumping syndrome fail to demonstrate adaptive changes
to handle rapidly transited chyme.
2. Fluid shifts: Distension of the intestine with chyme leads to a
uid shift from the systemic circulation into the intestinal vasculature and lumen. This physiologic response is called
splanchnic blood pooling and is mediated by gastrointestinal
hormones, as well as the parasympathetic response to the distension of the intestine by chyme [3, 4]. In normal individuals,
this is balanced by a compensatory sympathetic discharge. It is
hypothesized that in patients with dumping syndrome, the
splanchnic blood pooling is potent enough to overcome the
compensatory mechanisms [2]. Splanchnic pooling causes
symptoms like fatigue, lightheadedness, and in severe cases
hypotension. Concurrent sympathetic discharge causes palpitations and sweating. All together, these symptoms constitute
the vasomotor symptoms of dumping syndrome.
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