Gastric outlet obstruction (GOO) is a condition that arises from mechanical impediments to gastric emptying and can be caused by benign or malignant diseases, with symptoms including vomiting and weight loss. The document outlines the anatomy of the stomach, the etiology of GOO, its clinical features, pathophysiology, diagnostic investigations, and various treatment approaches, including medical and surgical interventions. Surgical options depend on the cause and severity of obstruction, with vagotomy and antrectomy among the common procedures performed.

2. Gastric Outlet
Obstruction
BY:
Dr. Muhammad Saad Iqbal
PGT S1 DHQ Sahiwal

3. Definition
• Gastric outlet obstruction (GOO, also known
as pyloric obstruction) is not a single entity; it
is the clinical and pathophysiological
consequence of any disease process that
produces a mechanical impediment to gastric
emptying.

4. Anatomy:
• SAC-LIKE ORGAN LOCATED MOSTLY IN THE LEFT UPPER
PART OF THE ABDOMEN
• It is located beneath the diaphragm and is attached
superiorly to the esophagus and distally to the duodenum.
• The stomach is divided into 4 portions: Cardia, body,
Antrum and Pylorus.
• HAS 2 SURFACES (ANTERIOR & POSTERIOR), 2 CURVATURES
(GREATER & LESSER), & 4 REGIONS (CARDIA, FUNDUS,
PYLORUS,& ANTRUM)
• The gastric wall is made up of 4 layers: Mucosa, Submucosa,
Muscularis Propria, and Serosa
• Inflammation, scarring, or infiltration of the antrum and
pylorus are associated with the development of gastric
outlet obstruction.

6. Relations
• ANTERIOR RELATIONS – DIAPHRAGM, ANTERIOR ABDOMINAL WALL,
LEFT COSTAL MARGIN, & THE
LEFT LOBE OF THE LIVER
• POSTERIOR RELATIONS – LESSER SAC, PANCREAS,
LEFT SUPRARENAL GLAND, LEFT KIDNEY, SPLEEN,
SPLENIC ARTERY, & THE TRANVERSE COLON
• SUPERIOR RELATIONS – LEFT DOME OF THE
DIAPHRAGM

9. Blood Supply
• FROM THE COELIAC Trunk – LEFT GASTRIC, SPLENIC
(SHORT GASTRIC & LEFT GASTROEPIPLOIC), HEPATIC
Artery (GASTRODUODENAL[SUPERIOR
PANCREATICODUODENAL & RIGHT EPIPLOIC],CYSTIC,
& RIGHT GASTRIC)

11. • The veins draining the stomach are generally
parallel to arteries. The left gastric (coronary vein)
and right gastric veins usually drain into the Portal
vein, though occasionally the coronary vein drains
into the Splenic vein. The right gastroepiploic vein
drains into the Superior mesenteric vein near the
inferior border of the pancreatic neck, and the left
gastroepiploic vein drains into the Splenic vein.

12. NERVE SUPPLY
• VAGUS (ANTERIOR & POSTERIOR) The vagus constitutes the
motor and secretory nerve supply for the stomach.
• The extrinsic sympathetic nerve supply to the stomach
originates at spinal levels T5 through T10 and travels in the
splanchnic nerves to the celiac ganglion. Postganglionic
sympathetic nerves then travel from the celiac ganglion to the
stomach along the blood vessels.

14. Background
Clinical entities that can result in GOO generally are
categorized into 2 well-defined groups of causes
 Benign
 Malignant.
This classification facilitates discussion of management
and treatment.

15. Etiology
• Major Benign causes of Gastric outlet
obstruction (GOO) are:
1. PUD
2. Gastric Polyps
3. Ingestion of caustics
4. Pyloric Stenosis
5. Congenital duodenal webs
6. Gall stone obstruction (Bouveret syndrome)
7. Pancreatic pseudocysts
8. Bezoars

16. Malignant causes:
• Pancreatic cancer is 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
a) Duodenal cancer
b) Ampullary cancer.
c) Cholangiocarcinomas.
d) Gastric cancer.
• Metastases to the gastric outlet also may be
caused by other primary tumors.

17. Within the pediatric population, pyloric
stenosis constitutes the most important cause
of GOO.
• Pyloric stenosis occurs in 1 per 750 births. It is
more common in boys than in girls and also is
more common in first-born children.
• Pyloric stenosis is the result of gradual
hypertrophy of the circular smooth muscle of
the pylorus.

19. Epidemiology
• The incidence of gastric outlet obstruction (GOO)
has been reported to be less than 5% in patients
with PUD, which is the leading benign cause of the
problem.
• Five percent to 8% of ulcer-related complications
result in an estimated 2000 operations per year in
the United States.
• The incidence of GOO in patients with peripancreatic
malignancy, the most common malignant etiology, has
been reported as 15-20%.

20. When peptic ulcer disease (PUD) was more prevalent,
benign causes were the most common; however, one
review shows that only 37% of patients with GOO have
benign disease and the remaining patients have
obstruction secondary to malignancy.

21. Pathophysiology
• Intrinsic or extrinsic obstruction of the pyloric
channel or duodenum is the usual pathophysiology of gastric
outlet obstruction; as previously noted, the mechanism of
obstruction depends upon the underlying
etiology.
• 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.

22. • In a later stage, patients may develop significant weight loss
due to poor caloric 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

23. • PUD manifests 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 can occur in an acute setting secondary to
acute inflammation and edema or, more commonly, in a
chronic setting secondary to scarring and fibrosis.
• Helicobacter pylori has been implicated as a frequent
associated finding in patients with GOO, but its exact
incidence has not been defined precisely.

24. Clinical features
Gastric outlet obstruction from a Peptic ulcer or
incomplete obstruction typically present with symptoms
of the following:
1. retention, including early satiety, bloating or
epigastric fullness, indigestion, anorexia, nausea,
vomiting, epigastric pain, and weight loss.
2. More than 90% of patients with PUD complain of
abdominal pain which is typically non-radiating,
burning in quality, and located in the epigastrium.
Two-thirds of patients with duodenal ulcers will
complain of pain that awakens them from sleep.

25. The pain of gastric ulcer more commonly occurs with eating
and is less likely to awaken the patient at night.
3. Nausea and vomiting are the cardinal symptoms.
4. Vomiting – Non-bilious, and it characteristically contains
undigested food particles
5. Loss of periodicity.
6. Early stages of Obstruction: vomiting is intermittent and
usually occurs within 1 hour of a meal.
7. Very often it is possible to recognize foodstuff taken
several days previously.
8. Patient loses weight, appears unwell and dehydrated

26. 9. Frequently malnourished and dehydrated and have a
metabolic insufficiency
10. Weight loss , most significant with malignant
disease

27. Metabolic effects
 Prolonged vomiting causes loss of hydrochloric acid &
produces an increase of bicarbonate in the plasma to compensate
for the lost chloride-------hypokalemic hypochloremic metabolic
alkalosis.
 Alkalosis shifts the intracellular potassium to the extracellular
compartment, and the serum potassium is increased factitiously.
• With continued vomiting, the renal excretion of potassium
increases in order to preserve sodium.
• Dehydration and electrolyte abnormalities-- Increase in BUN and
creatinine are late features of dehydration.

29. Paradoxically acidic urine
 Initially, the urine has a low chloride and high bicarbonate
content, reflecting the primary metabolic abnormality.
 This bicarbonate is excreted along with sodium and so, with
time, the patient becomes progressively hyponatraemic and more
profoundly dehydrated.
 Because of the dehydration, a phase of sodium retention
follows and potassium and hydrogen are excreted in preference.
 This results in the urine becoming paradoxically acidic.
 Alkalosis leads to a lowering of the circulating ionized calcium,
and tetany can occur.

31. • Clinical features of Paradoxical aciduria
1. Irritability, confused status, dehydration
2. Often convulsions can occur.
3. Features of alkalosis like rapid breathing (Cheyne-stokes
breathing and tetany)
• Investigations
1. Serum electrolytes
2. Arterial blood gas analysis
3. Serum calcium level estimation
• Treatment : Double strength normal saline with IV
potassium under ECG monitoring. Plus IV magnesium.

32. Electrolyte changes in pyloric stenosis
1. Hyponatremia
2. Hypokalemia
3. Hypomagnesemia
4. Hypochloraemia
5. Metabolic alkalosis
6. Paradoxical aciduria

33. Physical examination
• Chronic dehydrated and Malnourished patient
On Examination :
1. Distended abdomen and a succussion splash may be
audible on shaking the patient’s abdomen.
Positive succussion splash is done with 4 hours empty
stomach, by placing a stethoscope over the epigastric region
and shaking the patient adequately.

34. 2. A dilated stomach may be appreciated as a tympanic mass
in the epigastric area and/or left upper quadrant
3. Visible gastric peristalsis (VGP) may be elicited by asking
the patient to drink a cup of water.
4. Auscultopercussion test shows dilated stomach.
( This test is done by placing a stethoscope over epigastric region. Skin is
scratched from left side downwards, at several points away from the
epigastrium using finger and these points are joined. Normally the greater
curvature of the stomach lies above the level of umbilicus, while in GOO it lies
below the level of umbilicus.

35. Investigations
1. CBC for Anemia
2. Electrolyte Studies for metabolic Disorder
3. Liver function tests may be helpful, particularly
when a malignant etiology is suspected.
4. A test for H pylori is helpful when the diagnosis
of PUD is suspected
5. Plain abdominal radiographs, contrast upper GI studies
(Gastrografin or barium), and CT scans with oral
contrast are helpful.
6. ECG for Hypokalemia

36. 7. Barium meal study:
• Absence of duodenal cap.
• Dilated stomach where greater curvature is below the
level of iliac crest.
• Mottled stomach
• Barium does not pass into duodenum.

38. Contrast study demonstrating an
enlarged stomach. The point of
obstruction is visualized at the pyloric-
duodenal junction (string sign).

39. Diagnostic Procedures
• Upper GI 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
non-imaging study that may be helpful.
• The traditional sodium chloride load test is performed
by infusing 750 cc of sodium chloride solution into the
stomach via a nasogastric tube (NGT). A diagnosis of
gastric outlet obstruction (GOO) is made if more than 400
cc remain in the stomach after 30 minutes.

40. • Nuclear gastric emptying studies measure the passage of orally
administered radionuclide over time.
• Unfortunately, both the nuclear test and the saline load test may
produce abnormal results in functional states.
• 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 malignancy.
• 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.

41. Conservative Management
1. Correcting the metabolic and electrolyte abnormality by
IV fluids.
2. Rehydrated with intravenous isotonic saline with
potassium supplementation or double strength saline,
calcium, potassium, magnesium.
3. Replacing the sodium chloride and water allows the
kidney to correct the acid–base abnormality
4. Following rehydration it may become obvious that the
patient is also anemic.
5. Blood transfusion if given if there is anemia.

42. 6.Place a NGT to decompress the stomach. Occasionally, a large tube is
required because the undigested food blocks tubes with small
diameters.
7. When acute PUD has been identified as a primary cause of gastric
outlet obstruction (GOO), focus treatment on the reduction of acid
production.(H2) blockers and PPIs are the mainstay of treatment.
8. Treat H pylori infection, when identified, according to current
recommendations.
9.Although most patients improve temporarily with treatment,
scarring and fibrosis may worsen over time.

43. 10. STOMACH WASH: The stomach should be emptied using a
Wide-bore gastric tube/Eswald’s tube. Pass an orogastric tube
and lavage the stomach until it is completely emptied.
11. TPN support.
12.Pneumatic balloon dilatation of a chronic, benign stricture can be
performed via endoscopy.
Patients who are candidates for balloon dilatation are likely to present
with recurrent GOO.

44. • Published series using this technique report success rates of over 76%
after multiple dilatations, although the rate of failure and recurrent
obstruction is higher in patients treated with balloon dilatation who
have not also been treated for H pylori infection.
• 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.

45. Endoscopic Balloon Dilation:
• If the GOO is irreversible, or is caused by fibrotic scarring,
rather than edema and spasm, it requires a definitive treatment.
• Before the advent of endoscopic balloon dilation (EBD), surgery
was the only treatment for these patients.
• Recent data suggest that EBD is an effective alternative to
surgery in a majority of patients with ulcer-related and caustic
induced GOO.
• Patients with a possibility of malignancy would not be candidates
for EBD.
• In inflammatory conditions like Crohn’s disease or infection like
tuberculosis causing GOO, specific treatment for the antecedent
disease is mandatory and may obviate the need for surgery or EBD.

46. GUIDELINES FOR BALLOON DILATION
Patient selection
• Only localized stricture of the stomach should
be chosen.
• The site of gastric cicatrization is not important.
• CT scan to assess antral wall thickness may be
a good modality to identify the “right patients” and to
exclude malignancy.
• Endosonography may also emerge as a useful
adjunct in this regard, especially in helping
direct intralesional steroid injections.

47. When should dilation be started?
• Patients with peptic-GOO can be dilated any time
after gastric decompression is done as most have
chronic cicatrisation.
• In those with active ulceration one can wait for
response to proton pump inhibitors. As stated
previously, it is best to wait for 8 weeks after caustic
ingestion to allow for natural healing.

48. Panel showing barium study in a patient with peptic pyloric
stenosis with trifoliate deformity of duodenal bulb (A), and
endoscopic pictures at the beginning (B), after 2 dilations (C)
and after 4 dilations (D).

49. Indications for Surgery
• Gastric outlet obstruction due to benign ulcer disease maybe
treated medically if results of imaging studies or endoscopy
determine - acute inflammation and edema are the principle causes
(as opposed to scarring and fibrosis, which may be fixed)
• If medical therapy fails, then surgical therapy
• Typically, if resolution or improvement is not seen within
48-72 hours, surgical intervention is necessary

50. Surgical Management
• More than 75% of patients presenting with GOO eventually require
surgical intervention.
• Operative management should offer 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
• Laparoscopic variants of the aforementioned procedures.
• Vagotomy and antrectomy with Billroth II reconstruction
(gastrojejunostomy) seem 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.

51. Pyloroplasty Types:
•Heineke-Mikulicz pyloroplasty involves a longitudinal incision across
the pylorus that is closed transversely; this is the most commonly
performed pyloroplasty
•Jaboulay pyloroplasty involves a side-to-side gastroduodenostomy
without pylorus incision
•Finney pyloroplasty also involves a side-to-side gastro-duodenostomy
but with pylorus incision

55. Truncal Vagatomy with Pyloroplasy

59. • Placement of a jejunostomy tube at the time of
surgery should be considered.
• This provides temporary feeding access in already
malnourished patients. Also, in chronically dilated partial
obstructions, the stomach may be slow to recover a normal
rate of emptying

60. Complications of Vagotomy
• Intraoperative complications can occur with injury
to adjacent structures.
• Early post-operative complications:
– Delayed gastric emptying
– Dysphagia and lesser curve necrosis( lesser
curve necrosis specific to HSV).
• Late complications include postvagotomy
diarrhea, reflux esophagitis,
Gallstones.

61. Complications of gastrectomy
• Early complications
– bleeding
– anastomotic leakage
– obstruction
– hepatobiliary-pancreatic complications
(pancreatitis, bile duct injury)
Late complications are classified as
follows :
– 1) Ulcer recurrence
a) Recurrent ulcer
(anastomotic,stomal,marginal)
b) gastrojejenocolic fistula

62. 2) Mechanical problems
a) Chronic afferent loop obstruction after BII anastomoses –
abdominal pain relieved by vomiting , vomit mainly bile without
food.
b) Chronic efferent loop obstruction
c) Internal herniation, jejenogastric intussusception and late
gastroduodenal obstruction
3) Pathophysiologic problems
a) Alkaline reflux gastritis – reflux of bile into stomach.
Pain not relieved with vomiting. Vomitus contains food and bile.
b) Dumping
(I)Early dumping – symptoms within 20 minutes after meal. Gastro-
intestinal : Abdominal cramps, satiety, nausea, vomiting and
explosive
diarrhea. Cardiovascular : sweating, dizziness,weakness,dyspnea,
palpitations and flushing.

63. – Due to sudden release of high osmolality chyme into duodenum with
fluid shifts and release of gastro-intestinal hormones.
• (II) Late dumping – only vasomotor symptoms. Caused by
enteroglucagon secretion which leads to increased and prolonged insulin
secretion with resultant hypoglycaemia.
4) Malabsorption and Nutritional
problems
a) Malabsorption of protein, carbohydrates and fat
b) Early satiety
c) Anemia : Fe, folate and B12 deficiency. B12 problems mostly after
total or near total gastrectomy.
d) Osteomalacia

64. 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.
• Most of these tumors are unresectable (approximately
40% of gastric cancers and 80-90% of periampullary
cancers.)
• When tumors are found to be unresectable, 13-
20% of patients eventually develop GOO before they
succumb to their disease.

66. • Gastrojejunostomy remains the surgical treatment of choice
for GOO secondary to malignancy.
• Although surgeons traditionally have preferred ante colic
anastomosis to prevent further obstruction by advancing
tumor growth, a publication evaluating the retro colic
anastomosis in this setting challenges conventional wisdom.
• Results demonstrate that a retro colic anastomosis may be
associated with decreased incidences of delayed gastric
emptying (6% vs 17%) and late GOO (2% vs 9%).
Feeding jejunostomy should again be considered to combat
malnutrition and slow recovery of gastric emptying.

68. Postoperative Management
 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, it is important to remember that a previously dilated stomach, the
performance of a vagotomy, and the presence of metastatic cancer may all
contribute to decreased gastric motility.
 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. Again, preoperative planning for feeding access becomes
important during this immediate postoperative period.
 Aggressive pulmonary toilet, prophylaxis for gastritis and deep venous
thrombosis (DVT), and early ambulation are advisable.

69. Follow-up
• Closely monitor patients after surgery and upon
discharge. After relief of gastric outlet obstruction, 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 to achieve satisfactory results.

70. Summary:
Gastric outlet obstruction is most commonly associated with longstanding
peptic ulcer disease and gastric cancer.
• The metabolic abnormality of hypochloraemic alkalosis is usually only
seen with peptic ulcer disease and should be treated with isotonic saline
with potassium supplementation.
• Endoscopic biopsy is essential to determine whether the cause of the
problem is malignancy
• Endoscopic dilatation of the gastric outlet may be effective in the less
severe cases of benign stenosis
• Operation is normally required, with a drainage procedure being
performed for benign disease and appropriate resectional surgery if
malignant.