Gastric outlet obstruction

SABNAM BHATTA
INTERN
SURGERY DEPARTMENT
GASTRIC OUTLET
OBSTRUCTION

2/3/2018 CHITWAN MEDICAL COLLEGE 2
Contents
1. Introduction
2. Causes
3. Etiology (Benign and Malignant)
4. Pathophysiology
5. Clinical features
6. Physical examinations
7. Metabolic effects
8. Investigations
9. Management (conservative and surgical along with
indications)
10. Summary

INTRODUCTION
• Gastric outlet obstruction (GOO, pyloric obstruction) is not
a single entity
• Clinical and pathophysiological consequence
of any disease process that produces a mechanical
impediment to gastric emptying

CAUSES
• Two well-defined groups of causes
BENIGN AND MALIGNANT
• Benign causes include pyloric stenosis secondary to
peptic ulceration
• While, Malignant causes include Gastric cancer.
• Previously, peptic ulcer diseases were more common.
• Now, with the decrease in the incidence of peptic
ulceration and the advent of potent medical treatments,
gastric outlet obstruction should be treated as malignant
unless proven otherwise.

• Only 37% have benign disease, with the rest having malignant
cause.
• The term ‘pyloric stenosis’ is a misnomer as the stenosis is
seldom at the pylorus.
• Commonly, when the condition is due to underlying peptic
ulcer disease the stenosis is found in the first part of
duodenum(most common site for peptic ulcer)
• True pyloric stenosis however, can occur as a result of fibrosis
around a pyloric channel ulcer.

Diagnostic and treatment dilemma
• Exclude functional non-mechanical causes of obstruction,
such as diabetic gastroparesis
• Once mechanical obstruction is established, differentiate
between benign and malignant ( definitive treatment
varies)
• Diagnosis and treatment is Urgent, because delay further
compromises patient’s nutritional status
Delay also further compromises edematous tissue and
complicates surgical intervention

Frequency
• The incidence occurs in less than 5% in patients. With peptic
ulcer disease being the leading benign cause
• Peripancreatic malignancy, the most common malignant
etiology- 15-20%.

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. Gallstone obstruction (Bouveret syndrome)
7. Pancreatic pseudocysts
8. Bezoars

Etiology
• PUD : 5% of all patients with GOO
• Ulcers within the pyloric channel & first part of duodenum is
responsible for outlet obstruction
• Obstruction – Acute obstruction is caused secondary to
acute inflammation and edema
• Chronic obstruction is secondary to scarring and fibrosis
• Helicobacter pylori

• Pediatric age group- Congenital Pyloric stenosis
• Occurs in 4 per 1000 births
• Boys˃ Girls (4 : 1)
• More common in first-born children
• It is familial.
• PYLORIC STENOSIS occurs between 3rd and 6th week of age
of an infant, which is the time taken for gradual
hypertrophy of the circular smooth muscle of the pylorus to
cause complete obstruction.
• Visible gastric peristalsis is seen.

Etiology
• Pancreatic cancer is the most common malignancy causing
GOO
• Outlet obstruction may occur in 10-20%
Other tumors include
1. Ampullary cancer
2. Duodenal cancer
3. Cholangiocarcinoma
4. Gastric cancer
5. Metastases to the gastric outlet by other primary tumors

Pathophysiology
• Intrinsic or extrinsic obstruction of the pyloric channel or
duodenum
• Intermittent symptoms that progress until obstruction is
complete. Vomiting is the cardinal symptom. Initially,
better tolerance to liquids than solid food
• In a later stage, significant weight loss due to poor caloric
intake. Malnutrition is a late sign, very profound in patients
with concomitant malignancy

• Continuous vomiting may lead to dehydration and
electrolyte abnormalities
• When obstruction persists, may develop significant and
progressive gastric dilatation
• The stomach eventually loses its contractility. Undigested
food accumulates
• Constant risk for aspiration pneumonia

Clinical features
Gastric outlet obstruction from a duodenal ulcer or
incomplete obstruction typically present with symptoms
of the following:
1. Gastric retention, including early satiety, bloating or
epigastric fullness, indigestion, anorexia, nausea,
vomiting, epigastric pain, and weight loss
2. Pain is severe, persistent, in the epigastric region, and
also with feeling of fullness
3. Nausea and vomiting are the cardinal symptoms

Clinical features
4. Vomiting – Non-bilious, and it characteristically contains
undigested food particles
5. Loss of periodicity.
6. Early stages: vomiting, 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

9. Frequently malnourished and dehydrated and have a
metabolic insufficiency
10. Weight loss , most significant with malignant disease
11. Abdominal pain is not frequent and usually relates to the
underlying cause, such as PUD or Pancreatic Cancer.

Physical examination
• Chronic dehydration and Malnutrition
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
2. Visible gastric peristalsis (VGP) may be elicited by asking
the patient to drink a cup of water.
3. 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.)

5. Goldstein saline load test: half and hour after installation
of 750ml of saline, if volume remained and if more than
250ml is present, suggests obstruction.

Metabolic effects
• Dehydration and electrolyte abnormalities- Increase in BUN
and creatinine are late features of dehydration
• 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
• The adrenocortical response to hypovolemia intensifies the
exchange of potassium for sodium at the distal tubule, with
subsequent aggravation of the hypokalemia

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

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 hyponatremic 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 ionised calcium,
and gastric 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
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.

Investigations
1. 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.
2. Gastroscopy to rule out stomach carcinoma and to visualize the
stenosed area.
3. Electrolyte study for the correction of electrolyte imbalance.
4. ECG to check for hypokalemia.

Management
1. Correcting the metabolic and electrolyte abnormality by
IV fluids.
2. Rehydrated with intravenous isotonic saline with
potassium supplementation or double strength slaine,
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.

6. TPN support.
7. 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.
8. It reduces the edema of the stomach wall and improves
gastric emptying time by increasing the gastric muscle tone.
9. Then endoscopy and contrast radiology
10. Biopsy of the area around the pylorus is essential to exclude
malignancy
11. The patient should also have an anti-secretory agent, initially
given intravenously to ensure absorption

Management
• Early cases : settle with conservative treatment,
presumably as oedema around the ulcer diminishes as the
ulcer is healed
• Endoscopic treatment with balloon dilatation useful in
early cases
(Dilating the duodenal stenosis may result in perforation,
and the dilatation may have to be performed several times
and may not be successful in the long term)

Surgical management
• Highly selective vagotomy(HSV) with gastrojejunostomy is
present recommendation even though it is technically
difficult.
• HSV is better than Truncal vagotomy as it maintains the nerve
supply of the chronically obstructed antrum and so may
eventually reduce the chronic emptying problems.
• Vagotomy, antrectomy (acid secreting area) with Billroth I
anastomosis along with feeding jejunostomy for nutrition is
the other option.

Indications for Surgery
• Gastric outlet obstruction due to benign ulcer disease may
be 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

• The choice of surgical procedure depends upon the
patient's particular circumstances
• In cases of malignant obstruction, weigh the extent of
surgical intervention for the relief of obstruction against
the malignancy's type and extent, as well as the patient's
anticipated long-term prognosis
• As a guiding principle, undertake major tumor resections
in the absence of metastatic disease

• In patients with largely metastatic disease, determine the
degree of surgical intervention for palliation in the light of
patient’s realistic prognosis and personal wishes.

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.

Other causes of Gastric outlet obstruction
• Adult pyloric stenosis
This is a rare condition and its relationship to childhood
condition is unclear, although some patients have a long
history of problems with gastric emptying. It commonly treated
by pyloroplasty that pyloromyotomy.
• Pyloric mucosal diaphragm
The origin of this rare condition is unknown. It usually does not
become apparent until mid life. When found, simple excision of
mucosal diaphragm is all that is required.

References
1. BAILEY AND LOVE
SHORT PRACTICE OF SURGERY ; 25TH EDITION
2. SRB’s Manual of Surgery; Fourth edition
3. CLASS NOTES

THANK YOU

Gastric outlet obstruction

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