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procedure or to the Heller myotomy with or without a fundoplication may be expected in some of these patients. Treatment decisions ultimately should be tailored to individual patient
characteristics, circumstances, and preferences.
Further Reading
Richter JE.Chicago classication version 4.0 and its impact on current clini-
cal practice. Gastroenterol Hepatol. 2021;17(10):468–75.
Clayton SB, Patel R, Richter JE. Functional and anatomic.esophagogastic
junction outow obstruction: manometry, timed barium esophagram
ndings, and treatment outcomes. Clin Gastroenterol Hepatol.
2016;14(6):907–11.
Khashab MA, etal. Peroral endoscopic myotomy is effective and safe in non-
achalasia esophageal motility disorders: an international multicenter
study. Endosc int open. 2018;6(8):E1031.
Richter JE, Clayton SB.Diagnosis and management of esophagogastric junc-
tion outow obstruction. Am J Gastroenterol. 2019;114(4):544–7.
Ihara E, et al. Diagnosis and treatment strategy of achalasia subtypes and
esophagogastric junction outow obstruction based on high-resolution
manometry. Digestion. 2017;95(1):29–35.
Beveridge C, Lynch K. Diagnosis and Management of Esophagogastric
Junction Outow Obstruction. Gastroenterol Hepatol. 2020;16(3):131.
Porter RF, Gyawali CP.Botulinum toxin injection in dysphagia syndromes
with preserved esophageal peristalsis and incomplete lower esophageal
sphincter relaxation. Neurogastroenterol Motility. 2011;23(2):139–e28.
Garbarino S, etal. Management of functional esophagogastric junction out-
ow obstruction: a systematic review. J Clin Gastroenterol. 2020;54(1):35–
42.
van Hoeij FB, Smout AJPM, Bredenoord AJ.Characterization of idiopathic
esophagogastric junction outow obstruction. Neurogastroenterol Motil.
2015;27(9):1310–6.
Samo S, Qayad E.Esophagogastric junction outow obstruction: Where are
we now in diagnosis and management? World J Gastroenterol.
2019;25:411–7.
Gastric Outlet Obstruction
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23
MichaelT.Fastiggi andMujjahidAbbas
Introduction
Gastric outlet obstruction is a clinical entity that can be dened as
a spectrum of disease processes that contribute to a pathophysiologic disruption in gastric emptying due to mechanical obstruction [1]. This obstruction can be intrinsic or extrinsic and can be
gastric, duodenal, or extraluminal in nature [2]. Common presenting symptoms include early satiety, bloating, epigastric abdominal pain, and postprandial vomiting.
Historically, the most common cause of gastric outlet obstruction was secondary to benign disease, specically peptic ulcer
disease. However, as proton pump inhibitors, H2 receptor blockers, and eradication of Helicobacter pylori became more widespread, malignancy has become the predominant etiology [3, 4].
The most common malignant etiologies include pancreatic adenocarcinoma, distal gastric cancer, duodenal malignancies, and
M. T. Fastiggi · M. Abbas (*)
New Jersey Bariatric Center, Hackettstown, NJ, USA
University Hospitals Cleveland Medical Center, Cleveland, OH, USA
Case Western University School of Medicine, Cleveland, OH, USA
e-mail: Mujjahid.Abbas@UHhospitals.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_23
319
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other less common malignancies such as gastric lymphoma or
cholangiocarcinoma [5, 6]. Other benign causes include gastric
volvulus, inammatory conditions (ex. caustic injury, acute or
chronic pancreatitis, Crohn’s disease, tuberculosis), iatrogenic
(PEG tube migration, postsurgical narrowing), and other less
common causes [2].
In this chapter we will discuss the diagnostic workup and man-
agement of gastric outlet obstruction due to varying etiologies.
M. T. Fastiggi and M. Abbas
Diagnostic Workup
History
Like many disease processes, investigation should begin with a
thorough history. A detailed investigation into the symptoms,
their timing of onset, and chronicity is essential. The most common symptoms include epigastric pain, abdominal bloating, early
satiety, weight loss, and postprandial nausea/vomiting, especially
of undigested food. Timing of symptoms varies with etiology,
from abrupt onset (in rare cases of mechanical obstruction like
gallstone impaction in Bouveret syndrome or gastric volvulus) to
more insidious in onset (peptic ulcer disease, malignancy).
Physical Examination
Often, there are no specic ndings to suggest gastric outlet
obstruction. Historically, the presence of a succussion splash was
thought to be strongly suggestive of gastric outlet obstruction;
however, some reports estimate that a succussion splash is seen in
only 50% of patients with gastric outlet obstruction [7, 8]. The
technique to assess for succussion splash is as follows: the patient
is rocked back and forth at the hips while auscultating in the epigastrium, and if a splashing sound is heard, this is considered
positive [2]. The rest of the physical exam may be nonspecic.
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321
Laboratory Values
With severe gastric outlet obstruction, signicant nausea/vomiting may be present. This can result in a volume contracted state.
Often, metabolic alkalosis is present. This is secondary to both
contraction alkalosis with hypokalemia, but can also be compounded by vomiting with a hypochloremic metabolic alkalosis.
Imaging
Imaging is usually via abdominal radiograph, CT scan, or both.
Abdominal radiographs are likely to show a distended stomach
with retained gastric juices or food particles. Contrast material
will often have delayed transit through the pylorus, and the stomach can be large and atonic [3] (Fig.23.1). CT scan may also
show a large distended stomach with retained food particles and
can also often better diagnose the etiology of gastric outlet
obstruction [9].
Fig. 23.1 Contrast esophagram of gastric outlet obstruction after sleeve gastrectomy
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M. T. Fastiggi and M. Abbas
Endoscopic Evaluation
Endoscopic evaluation of gastric outlet obstruction is an essential
step in conrming the diagnosis, and it can also provide therapeutic options.
Preparation
In order to evacuate the stomach and prevent inadequate viewing,
it is recommended that patients with gastric outlet obstruction fast
for 4h prior to an endoscopy and have the contents of their stomach suctioned via a nasogastric tube [2].
Technique
Endoscopy should be performed with standard technique, with
the patient in the left lateral decubitus position. The entire stomach should be examined to the extent that is possible. If large
amounts of retained food remain present, the endoscopy may have
to be repeated after another attempt at nasogastric suction and
lavage. Care should be taken to examine the pylorus and the site
of obstruction with the aim of revealing the etiology, whether
intrinsic or extrinsic. Biopsies of suspicious areas should be taken.
Depending on the etiology apparent on endoscopy, different endoscopic therapeutic options can be used, and these will be discussed in further detail.
Management
Initial Management
As mentioned previously, patients with gastric outlet obstruction
often have long standing nausea/vomiting which can lead to profound electrolyte disturbances, hypovolemia, and malnourishment. Initial management should focus on resuscitation with
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correction of electrolyte imbalances, as well as nasogastric
decompression with replacement. Depending on the degree of
malnourishment, the possibility of intervention, and the timing
expected to resolution, consideration should be given to the initiation of parenteral or jejunal nutrition [10]. In addition, a proton
pump inhibitor should be started regardless of etiology, as proton
pump inhibitors can decrease gastric secretions leading to an
overall decreased volume of gastric contents [2, 11].
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Medical Management
For acute gastric outlet obstruction secondary to peptic ulcer disease, the etiology is often secondary to edema and inammation
adjacent to the area of ulceration. Conservative techniques of gastric decompression through nasogastric suction, acid suppression,
and eradication of H. pylori can lead to eventual resolution, with
some series reporting up to 90% response rate [11, 12]. In the
minority of cases that do not have symptom resolution and are not
able to tolerate a liquid diet, further therapy is required.
Management by Etiology
Given that gastric outlet obstruction is a spectrum of diseases, the
differences in etiology and thus the variations in treatment are
broad, especially when comparing benign and malignant disease.
Here the treatment strategies are broken into some subgroups.
Benign Disease
As previously discussed, management of benign gastric outlet
obstruction caused by inammatory states such as peptic ulcer
disease begins with medical management. For the minority of
cases that fail medical management, the next step is endoscopic
therapy.
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M. T. Fastiggi and M. Abbas
Endoscopic Dilation
Endoscopic dilation of strictures caused by peptic ulcer disease
has been described since 1981 and has essentially become the rst
line treatment for medically refractory peptic ulcer disease
causing gastric outlet obstruction. Long-term outcomes are very
favorable, with success and long-term remission rates of 75–100%
described for serial dilation [13]. Similarly, endoscopic dilation
has been successful in other benign inammatory conditions,
such as anastomotic and caustic strictures, while having variable
success with conditions like Crohn’s disease and chronic pancreatitis [14–16].
As with the diagnostic upper endoscopy, patients should fast
prior to the procedure, and if signicant retained gastric contents
are present, have these contents suctioned through a nasogastric
tube. The procedure can then be done either under conscious
sedation in the left lateral decubitus position, or if a difcult procedure is anticipated that will cause signicant patient discomfort,
under general anesthesia in the supine position.
After identifying the area of stricture, if possible the scope
should be passed through in order to fully evaluate the length and
diameter of the stricture. If this is not possible with the adult
endoscope, a pediatric endoscope may be used. In addition, biopsies of the strictured segment should also be taken to rule out
malignancy, if not done already.
After performing this, the endoscopist should attempt to pass a
balloon dilator through the stricture. Balloon dilators are available
in inated sizes of 6mm to 20mm. Prior to choosing the balloon
size, the diameter of the stricture should be measured and the
endoscopist should choose the proper diameter balloon [15].
There are two types of balloons - those with a single xed
diameter when inated, and those that can be dilated to sequential
diameters as their pressure increases. The balloon dilators can be
lled with water or with diluted water-soluble contrast to aid in
conrmation of placement via uoroscopy [15, 16]. To place the
dilator, a through the scope (TTS) balloon is passed. The use of a
wire-guided balloon helps aid passage through a narrowed or ste-
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notic pyloric channel compared to non-wire-guided balloon dilators [15]. Fluoroscopy can assist in placement of the wire and
balloon dilator, and the center of the balloon dilator should rest at
the center of the stricture. The TTS method can allow for limited
uoroscopy, using it to conrm placement and dilation success,
rather than performing the entire procedure under uoroscopy.
With a skilled endoscopist and good visualization of the stricture,
safety and outcomes are similar to performing the dilation under
uoroscopy, minimizing the need for ionizing radiation [17].
Once the balloon is in place and ready for dilation, the balloon
is inated to the target pressure as specied by the device parameters. The dilation begins when the balloon is inated and moderate resistance is felt. The general consensus is that for serial
dilations, the dilator should not exceed three sequential dilators
(3mm) of increasing size in a single session, also known as the
“rule of 3,” both for single and multi-diameter balloons [18]. At
the completion of the procedure, the strictured area should be
inspected for any signs of bleeding or perforation, and the patient
should be monitored post-procedure. Any concern for perforation
(ex. pain, tenderness) should be immediately investigated with a
water-soluble contrast study.
The procedure can be repeated every one to 2weeks, with a
goal endpoint of 15–18mm stricture diameter. Dilation beyond
12–15mm increases risk of perforation [15, 19]. After reaching
the goal endpoint, the patients should be monitored for recurrence. There is generally a good response in long-term follow-up
for serial dilations in peptic ulcer disease with continued acid suppression and avoidance of NSAIDs and smoking/nicotine with
long-term remission rates of 80–100% with median follow-up
periods of 28–43months [19, 20].
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Endoscopic Steroid Injection
Inammatory processes can eventually cause brosis and strictures from the subsequent narrowing. Intralesional steroid injection can be performed to reduce this by interfering with collagen
synthesis and scarring [20, 21]. This can be done as an adjunct to
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endoscopic balloon dilation for inammatory strictures related to
peptic ulcer disease refractory to balloon dilatation, caustic strictures, and strictures related to Crohn’s disease.
The preparation is similar to endoscopic balloon dilation.
Triamcinolone acetate (Kenilog) is prepared as a solution of
40mg/mL. At the narrowest area of the stricture, the triamcinolone can be administered in four quadrant injections of 0.5mL
(20mg) aliquots [22]. This can be combined with endoscopic balloon dilation for maximal effectiveness. Compared to placebo,
intralesional steroid injection was associated with signicantly
decreased need for repeat dilation, with 10–13% recurrence rates
within 1year, and similarly good long-term response rates up to
5years [22, 23]. Complications are similar to those in endoscopic
balloon dilation. In addition, there is a risk of intramural infection
or bleeding [23].
M. T. Fastiggi and M. Abbas
Self-Expanding Metal Stents
In benign disease, self-expanding metal stents are generally
reserved for patients with strictures refractory to attempts at dilation who are poor surgical candidates. Most self-expanding metal
stents are made from a woven material of wires of nickel and titanium, offering a superior advantage over the historic stainless
steel bers used previously. In addition, the stents can be coated
or uncoated, with coats of silicone or PTFE [24].
As mentioned previously, in benign disease patient selection is
generally restricted to those with strictures refractory to other
endoscopic therapies who are poor surgical candidates. Patient
preparation is similar to the previous endoscopic procedures
detailed, with most being done under conscious sedation in the
left lateral decubitus position. The stent placement is then usually
performed under uoroscopic guidance. A guidewire is passed
through the area of stenosis, and the positioning is conrmed on
uoroscopy. The stent can then be carefully deployed with endoscopic and uoroscopic guidance, with care taken to include one
to 2cm of overlap proximally and distally to ensure that the stricture is fully covered [24, 25]. Injection of water-soluble contrast
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can then demonstrate that the stent is patent. The stents can then
be removed 3–6months after placement.
Early symptom improvement was demonstrated by Heo etal.,
with all ten patients reporting success. Ninety percent of the
enrolled patients reported being symptom free with long-term
follow-up (median 11 months); however, two patients reported
worsening symptoms after removal, with one requiring replacement stenting. In addition, one patient’s stent was unable to be
removed, but was closely observed and had no symptoms over
17months of follow-up [25]. Thus, major complications include
stent migration, stent obstruction, bleeding, or perforation.
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Surgical Management
While the majority of patients will respond to conservative management or endoscopic therapy, a subset will require surgical
intervention in benign disease. Factors that predict this include
duration of treatment >1year and a need for more than 3 procedures [26].
Surgical management depends on the etiology, but the ultimate
goal is to relieve the gastric outlet obstruction. In the case of peptic ulcer disease, this can be accomplished via antrectomy with
vagotomy to prevent ulcer recurrence, or with vagotomy and a
drainage procedure, either pyloroplasty or gastrojejunostomy. In
Csendes etal., there was no signicant difference in postoperative
course seen between highly selective vagotomy with gastrojejunostomy compared to selective vagotomy with antrectomy, leading the study authors to recommend the highly selective vagotomy
with gastrojejunostomy as the recommended choice [27].
Malignant Disease
Malignant disease represents the most common overall cause of
gastric outlet obstruction. Palliation of this disease and its symptoms can result in improved quality of life for patients with
advanced upper GI malignancies.
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