GASTRIC OUTLET

OBSTRUCTION
 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.

 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

 BLOOD SUPPLY
FROM THE COELIAC Trunk –
• LEFT GASTRIC,
• SPLENIC (SHORT GASTRIC & LEFT GASTROEPIPLOIC),
• HEPATIC Artery
(GASTRODUODENAL[SUPERIOR PANCREATICODUODENAL & RIGHT EPIPLOIC],CYSTIC, &
RIGHT GASTRIC)
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.
 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.
 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.
 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.
 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
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.
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.
 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.
•5% 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%.
 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.
 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.
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
4.Serum electrolytes
5. Arterial blood gas analysis
6. Serum calcium level estimation

Treatment : Double strength normal saline with IV potassium under

ECG monitoring. Plus IV magnesium.
Electrolyte changes in pyloric stenosis

1. Hyponatremia
2. Hypokalemia
3. Hypomagnesemia
4. Hypochloraemia
5. Metabolic alkalosis
6. Paradoxical aciduria
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.
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.
 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
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.

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

To establish the diagnosis

Identify a specific cause

Therapeutic benefit

Endoscopic biopsies to identify H.

pylori and to exclude malignant
conditions causing G O O
• 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.
 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.
• 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.
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.
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.
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.
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).
ENDOSCOPIC STENTING FOR
UNRESECTABLE TUMOR
STENTING
 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
 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.
 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
 VAGOTOMY
Truncal Vagotomy – need a
drainage procedure Finneys
pyloroplasty or Heineke-Mikulicz
pyloroplasty

Selective Vagotomy
Truncal Vagatomy with Pyloroplasy
HIGHLY SELECTIVE VAGOTOMY
•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
 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.
 COMPLICATIONS OF GASTRECTOMY
Early complications
– bleeding
– anastomotic leakage
– obstruction
– hepatobiliary-pancreatic complications (pancreatitis, bile duct injury)
Late complications are classified as follows :
– Ulcer recurrence
a)Recurrent ulcer (anastomotic,stomal,marginal)
b) gastrojejenocolic fistula
1) 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
– 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
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.
•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.
Billroth I Billroth II
Gastrojejunostomy Gastrojejunostomy
ROUXEN- Y GASTROJEJUNOSTOMY
 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.
 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.

 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.