GASTRIC OUTLET OBSTRUCTION
Gastric outlet obstruction (GOO) is the clinical and pathophysiological consequence of
any disease process that produces a mechanical failure to gastric emptying.
Clinical entities that can result in GOO generally are categorized into benign and
malignant. In the past when peptic ulcer disease (PUD) was more prevalent, benign
causes were the most common; however, a recent review shows that only 37% of
patients with GOO have benign disease and the remaining patients have obstruction
secondary to malignancy. As part of the initial workup, it is important to exclude
functional obstruction such as diabetic gastroparesis. Once a mechanical obstruction is
confirmed, differentiation between benign and malignant disease is important because
definitive treatment is based on recognition of the specific underlying cause.
Aetiology: Benigncauses include PUD, gastric polyps, ingestion of caustics, pyloric
stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome),
pancreatic pseudocysts, and bezoars.
Malignant causes include pancreatic cancer as the most common malignancy causing
GOO. Outlet obstruction may occur in 10-20% of patients with pancreatic carcinoma.
Other tumors that may obstruct the gastric outlet include ampullary cancer, duodenal
cancer, cholangiocarcinomas, and gastric cancer. Metastases to the gastric outlet also
may be caused by other primary tumors
PUD is a cause in approximately 5% of all patients with GOO. Ulcers within the pyloric
channel and first portion of the duodenum usually are responsible for outlet obstruction.
Obstruction may be acute, secondary to acute inflammation and edema or, more
commonly, in a chronic, secondary to scarring and fibrosis. Helicobacter pylori has been
implicated as a frequent associated finding in patients with GOO due to PUD..
In babies, pyloric stenosis constitutes the most important cause of GOO. Pyloric stenosis
occurs in 1 per 750 births. It is more common in boys and first-born children and is the
result of gradual hypertrophy of the circular smooth muscle of the pylorus.
Pathophysiology: Intrinsic or extrinsic obstruction of the pyloric channel or duodenum
causes GOO; as previously noted, the mechanism of obstruction depends upon the
Patients present with intermittent symptoms that progress until obstruction is complete.
Vomiting is the cardinal symptom. Initially, patients may demonstrate better tolerance to
liquids than solid food.
In a later stage, patients develop significant weight loss due to poor intake. Malnutrition
is a late sign, but it may be very profound in patients with concomitant malignancy.
In the acute or chronic phase of obstruction, continuous vomiting may lead to
dehydration and electrolyte abnormalities.
When obstruction persists, patients may develop significant and progressive gastric
dilatation. The stomach eventually loses its contractility. Undigested food accumulates
and may represent a constant risk for aspiration pneumonia.
Clinical: Nausea and vomiting are the cardinal symptoms of GOO. Vomiting usually is
described as nonbilious, and it characteristically contains undigested food particles. In
the early stages of obstruction, vomiting may be intermittent and usually occurs within 1
hour of a meal.
Early satiety and epigastric fullness are common. Weight loss is frequent when the
condition becomes chronic and is most significant in patients with malignant disease.
Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD,
Physical examination often demonstrates the presence of chronic dehydration and
malnutrition. There may be visible peristalsis from left to right and a positive succussion
splash particularly in GOO due to PUD. A dilated stomach may be appreciated as a
tympanitic mass in the epigastric area and/or left upper quadrant.
Dehydration and electrolyte abnormalities can be demonstrated by routine laboratory
examinations. Increases in urea and creatinine are late features of dehydration.
Prolonged vomiting causes loss of hydrochloric (HCl) acid and produces an increase of
bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is
a hypokalemic hypochloremic metabolic alkalosis. Alkalosis shifts the intracellular
potassium to the extracellular compartment, and the serum positive potassium is
increased factitiously. With continued vomiting, the renal excretion of potassium
increases in order to preserve sodium. The adrenocortical response to hypovolemia
intensifies the exchange of potassium for sodium at the distal tubule, with subsequent
aggravation of the hypokalemia.
Obtain a CBC. Check the hemoglobin and hematocrit to rule out the possibility of
Obtain an electrolyte panel. As noted previously, identifying and correcting
electrolyte abnormalities that tend to occur is essential.
Liver function tests may be helpful, particularly when a malignant etiology is
A test for H pylori is helpful when the diagnosis of PUD is suspected.
Plain abdominal x-rays, contrast upper GI studies (Gastrografin or barium), and
CT scans with oral contrast are helpful.
Plain x-rays, the obstruction series (supine abdomen, upright abdomen, and
chest posteroanterior [PA]), can demonstrate the presence of gastric dilatation
and may be helpful with distinguishing the differential diagnosis.
Upper endoscopy can help visualize the gastric outlet and may provide a tissue
diagnosis when the obstruction is intraluminal.
The sodium chloride load test is a traditional clinical nonimaging study that may
o The traditional sodium chloride load test is performed by infusing 750 cc
of sodium chloride solution into the stomach via a nasogastric tube
o A diagnosis of GOO is made if more than 400 cc remain in the stomach
after 30 minutes.
Nuclear gastric emptying studies measure the passage of orally administered
radionuclide over time. Unfortunately, both the nuclear test and saline load test
may produce abnormal results in functional states.
Barium upper GI studies are very helpful because they can delineate the gastric
silhouette and demonstrate the site of obstruction. An enlarged stomach with a
narrowing of the pyloric channel or first portion of the duodenum helps
differentiate GOO from gastroparesis.
The specific cause may be identified as an ulcer mass or intrinsic tumor.
In the presence of PUD, perform endoscopic biopsy to rule out the presence of
In the case of peripancreatic malignancy, CT scan–guided biopsy may be helpful
in establishing a preoperative diagnosis.
Needle-guided biopsy also may be helpful in establishing the presence of
metastatic disease. This knowledge may impact the magnitude of the procedure
planned to alleviate the GOO.
Histologic Findings: Histologic findings relate to the individual underlying cause.
Management: Treatment of patients with GOO due to benign ulcer disease may be
medical if results of imaging studies or endoscopy determine that acute inflammation
and edema are the principle causes of the outlet obstruction (as opposed to scarring and
fibrosis, which may be fixed). If medical therapy conducted for a reasonable period fails
to alleviate the obstruction, then surgical intervention becomes appropriate. The choice
of surgical procedure depends upon the patient's particular circumstances; however,
vagotomy and antrectomy should be considered the gold standard against which the
efficacy of other procedures should be measured.
Weigh the extent of surgical intervention for the relief of GOO against the type and
extent of malignancy and the patient's anticipated long-term prognosis. As a guiding
principle, undertake major tumor resections in the absence of metastatic disease in a
patient who can withstand such a procedure from a nutritional standpoint. In patients
with largely metastatic disease, determine the degree of surgical intervention for
palliation in light of the patient's realistic prognosis and personal wishes
The stomach is located mainly in the left upper quadrant beneath the diaphragm and is
attached superiorly to the esophagus and distally to the duodenum. The stomach is
divided into 4 portions, the cardia, the body, the antrum, and the pylorus. Inflammation,
scarring, or infiltration of the antrum and pylorus are associated with the development of
The duodenum begins immediately beyond the pylorus and mostly is a retroperitoneal
structure, wrapping around the head of the pancreas. The duodenum classically is
divided into 4 portions. It is intimately related to the gallbladder, liver, and pancreas;
therefore, a malignant process of any adjacent structure may cause outlet obstruction
due to extrinsic compression.
Contraindications: Contraindications for surgery relate to the underlying medical
Most patients benefit from an initial period of gastric decompression, hydration, and
correction of electrolyte imbalances. In patients who are severely malnourished,
postponing surgical intervention until the nutritional status has been optimized may be
wise. In selective cases, some patients may benefit from total parenteral nutrition (TPN)
or distal tube feeding (eg, placed via a percutaneous jejunostomy).
One of the relative contraindications for surgery is the presence of advanced
malignancy; in these cases, life expectancy may be limited to a few months.
Overall, every patient with GOO deserves evaluation by a surgeon. Even if the patient
has unresectable disease, other palliative surgical measures may improve the quality of
Medical therapy: Initial management of GOO should be the same regardless of the
primary cause. After a diagnosis is made, admit patients for hydration and correction of
electrolyte abnormalities. Remembering that the metabolic alkalosis of GOO responds to
the administration of chloride is important; therefore, sodium chloride solution should be
the initial IV fluid of choice. Potassium deficits are corrected after repletion of volume
status, and after the chloride has been replaced.
Place a NGT to decompress the stomach. Occasionally, a large tube is required
because the undigested food blocks tubes with small diameters.
Further treatment is tailored to the underlying cause; this is where the distinction
between benign and malignant disease becomes important.
Management of benign disease
When acute PUD has been identified as a primary cause of GOO, focus treatment on
reduction of acid production. Histamine 2 (H2) blockers and proton pump inhibitors
comprise the mainstay of treatment. Treat H pylori infection, when identified, according
to current recommendations. Although most patients improve temporarily with treatment,
scarring and fibrosis may worsen over time. These patients are likely to present with
recurrent GOO. More than 75% of patients presenting with GOO eventually require
surgical intervention (Doberneck, 1987).
Surgical intervention usually provides definitive treatment for GOO, but it may result in its
own comorbid consequences. Operative management should offer both relief of
obstruction and correction of the acid problem.
The most common surgical procedures performed for GOO related to PUD are
vagotomy and antrectomy, vagotomy and pyloroplasty, truncal vagotomy and
gastrojejunostomy, pyloroplasty, and laparoscopic variants of the aforementioned
procedures. Of these, vagotomy and antrectomy with Billroth II reconstruction
(gastrojejunostomy) seems to offer the best results. Vagotomy and pyloroplasty and
pyloroplasty alone, although used with some success, can be technically difficult to
perform due to scarring at the gastric outlet. A combination of balloon dilatation and
highly selective vagotomy has been described, but it is associated with gastroparesis
and a high recurrence rate.
The role of laparoscopic approach in the treatment of GOO is under investigation and
may represent a valid form of therapy with low morbidity.
Pneumatic balloon dilatation of a chronic benign stricture can be performed via
endoscopy. Published series utilizing this technique report success rates over 65% after
multiple dilatations (Gibson, 2000). Patients treated with balloon dilatation, without
treatment for H pylori infection, have a high rate of failure. Patients who are negative for
H pylori do not respond favorably to balloon dilatation and should be considered for
surgical treatment early in the process (Gouma, 1999).
Management of malignant disease
The management of GOO secondary to malignancy is controversial. Of patients with
periampullary cancer, 30-50% present with nausea and vomiting at the time of diagnosis
(Jaffin, 1985; Khullar, 1996). Most of these tumors are unresectable (approximately 40%
of the gastric cancers and 80-90% of the periampullary cancers [Kurtz, 1996; Lillemoe,
1993]). When tumors are found to be unresectable, 13-20% of patients eventually
develop GOO before they succumb to their disease. The 1-year survival rate is poor.
Gastrojejunostomy remains the surgical treatment of choice for GOO secondary to
malignancy. Although surgeons traditionally have preferred an antecolic anastomosis to
prevent further obstruction by advancing tumor growth, a recent publication evaluating
the retrocolic anastomosis in this setting challenges conventional wisdom (Lillemoe,
1999). Results demonstrate that a retrocolic anastomosis may be associated with
decreased incidences of delayed gastric emptying (6% versus 17%) and late GOO (2%
Recently, metallic stents have been used for treatment of GOO in a malignant setting.
Metallic stents previously have been used successfully to treat stenosis of areas such as
blood vessels, bile duct, esophagus, and the trachea. With the development of newer
stents and delivery systems, metallic stents may have a role in the nonsurgical treatment
of gastroduodenal obstruction. Stents may allow the physician to avoid complicated
surgical procedures. A recent literature review reports data from 11 different studies in
which 91 patients with unresectable GOO secondary to malignancy were treated with
metallic stents. Immediate relief was observed in 81 patients (89%); 17 patients had
recurrent obstruction (21%) (Mauro, 2000). The promising results suggest that stents
eventually may replace surgery as palliative intervention for unresectable periampullary
Preoperative details: Perform standard preoperative evaluation in these patients.
Correct fluid and electrolyte abnormalities prior to surgery.
Perform gastric decompression by NGT and suction and alert the anesthesiologist to the
potential risk for aspiration upon induction.
Perform a preoperative nutritional evaluation and initiate appropriate nutritional therapy
(TPN or enteral feedings via a percutaneous jejunostomy placed distal to the
obstruction) as soon as possible.
Intraoperative details: Intraoperative details depend upon the etiology of the underlying
disease and the reason that the specific surgical procedure is undertaken.
Postoperative details: Admit patients to a monitor unit after the procedure. Pay special
attention to fluid and electrolyte status.
Most surgeons agree that perioperative antibiotics are advisable but may be limited to
use during the immediate perioperative period in the absence of intervening infection.
If a gastric reconstruction is performed, an NGT is recommended. The length of time that
the NGT should remain in place is controversial; however, remembering that a
previously dilated stomach, the performance of a vagotomy, and the presence of
metastatic cancer all may contribute to decreased gastric motility is important. An
anatomically patent gastrojejunostomy may fail to empty for days. This syndrome of
delayed gastric emptying is a well-known entity and requires surgical patience.
Aggressive pulmonary toilet, deep venous thrombosis (DVT) prophylaxis, and early
ambulation are advisable.
Follow-up care: Closely monitor patients after surgery and upon discharge. After relief
of GOO, patients may continue to experience gastric dysmotility and may require
medication to stimulate gastric emptying and motility.
In patients with malignancy, the potential for progressive and recurrent disease always
remains. These patients should be monitored by a surgeon or an oncologist.
Closely monitor patients whose treatment consisted of balloon dilatation because most
of these patients require subsequent dilatations in order to achieve satisfactory results
Complications: Although the risk is small, patients undergoing endoscopic treatment
with either balloon dilatation or stenting are at risk for perforation. Several literature
reports exist regarding migration of the stents and reocclusion requiring further
Operative complications in patients undergoing surgery for GOO often are related to the
nutritional status of the patients. Commencing nutritional support upon recognition of the
presence of GOO is important. If surgery is anticipated, delaying the surgery or any
intervention until TPN has been instituted for at least 1 week often is prudent.
Acute intervention may be technically difficult because of significant gastric dilatation and
gastric wall edema. This circumstance may increase the rate of anastomotic leak. On
occasion, delaying surgical intervention for several days while the stomach is
decompressed by nasogastric suction may be prudent.
Alert patients undergoing gastric resection for benign or malignant disease to the
possibility of well-known postgastrectomy syndromes such as dumping, alkaline gastritis,
and afferent loop syndrome. Severe symptoms may be present in 1-2% of patients.
GOO is a clinical condition that may result from a number of underlying causes, both
benign and malignant. Despite medical advances in the acid suppression mechanism,
the incidence of GOO remains a prevalent clinical problem in benign PUD. Also, an
increase in the number of cases of GOO seems to be noted secondary to malignancy;
this possibly is due to improvements in cancer therapy, which allow patients to live long
enough to develop this complication.
Orient initial management to identification of the primary underlying cause and to the
correction of volume and electrolyte abnormalities. Barium swallow studies and upper
endoscopy are the main tests utilized to make the diagnosis. Tailor treatment to the