1. GASTRIC OUTLET OBSTRUCTION
PROF.MINOCHA

2. Definition
• 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

3. Causes
Two well-defined groups of causes—
Benign & Malignant
• In the past-- peptic ulcer disease more
prevalent, benign causes most common
• Now-- only 37% have benign disease and
the remaining have obstruction secondary to
malignancy

4. Diagnostic and treatment dilemma
Exclude functional nonmechanical causes of
obstruction, such as diabetic gastroparesis
• Once mechanical--- differentiate between
benign and malignant ( definitive Tt varies)
• Diagnosis and treatment Urgent, because delay
further compromise pts. nutritional status
Delay also further compromise edematous
tissue and complicate surgical intervention

5. Frequency
• The incidence less than 5% in pts. with PUD--
leading benign cause
• Peripancreatic malignancy, the most common
malignant etiology--- 15-20%.

6. Etiology
Major benign causes of gastric outlet
obstruction (GOO) are---
 PUD
 gastric polyps
 ingestion of caustics
 pyloric stenosis
 congenital duodenal webs
 gallstone obstruction (Bouveret syndrome)
 pancreatic pseudocysts
 and bezoars

7. Etiology(Contd)
• PUD --- 5% of all patients with GOO
• Ulcers within the pyloric channel & D-1
responsible for outlet obstruction
• Obstruction -- Acute -- secondary to acute
inflammation and edema , Chronic--
secondary to scarring and fibrosis
• Helicobacter pylori

8. Etiology(Contd)
Pediatric age group--- Pyloric stenosis
Pyloric stenosis occurs in 1 per 750 births
Boys˃ Girls
More common in first-born children
Pyloric stenosis ---- gradual hypertrophy of the
circular smooth muscle of the pylorus

9. Etiology(Contd)
• Pancreatic cancer is the most common
malignancy causing GOO
• Outlet obstruction may occur in 10-20%
Other tumors include---
 Ampullary cancer
 Duodenal cancer
 Cholangiocarcinomas
 Gastric cancer
 Metastases to the gastric outlet by other
primary tumors

10. 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

11. Clinical features
• Nausea and vomiting are the cardinal symptoms
• Vomiting -- Nonbilious, and it characteristically
contains undigested food particles
• Early stages --- vomiting intermittent and
usually occurs within 1 hour of a meal
• Very often it is possible to recognise foodstuff
taken several days previously
• Pt. loses weight, appears unwell & dehydrated

12. Clinical features(Contd)
GOO from a duodenal ulcer or incomplete obstruction
typically present with symptoms of-----------
 Gastric retention, including early satiety, bloating or
epigastric
fullness, indigestion, anorexia, nausea, vomiting, epig
astric pain, and weight loss
 Frequently malnourished and dehydrated and have a
metabolic insufficiency
 Weight loss , most significant with malignant disease
Abdominal pain is not frequent and usually relates to
the underlying cause, eg, PUD, pancreatic cancer

13. Physical examination
Chronic dehydration and Malnutrition
On examination :
Distended stomach and a succussion splash
may be audible on shaking the patient’s
abdomen
A dilated stomach may be appreciated as a
tympanitic mass in the epigastric area and/or
left upper quadrant

14. 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

15. 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 ionised
calcium, and tetany can occur.

16. Management
Involves
 Correcting the metabolic abnormality &
 Dealing with the mechanical problem
Rehydrated with i/v isotonic saline with
potassium supplementation. Replacing the
sodium chloride and water allows the kidney
to correct the acid–base abnormality
Following rehydration it may become
obvious that the patient is also anaemic, the
haemoglobin being spuriously high on
presentation

17. Management(contd)
 The stomach should be emptied using a
Wide-bore gastric tube. Pass an orogastric
tube and lavage the stomach until it is
completely emptied
 Then endoscopy and contrast radiology
 Biopsy of the area around the pylorus is
essential to exclude malignancy
 The patient should also have an anti-
secretory agent, initially given intravenously
to ensure absorption

18. Management(contd)
• Early cases -- settle with conservative
treatment, (Oedema around the ulcer
diminishes as the ulcer is healed)
• Severe cases treated surgically, usually with a
gastroenterostomy rather than a pyloroplasty
• 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)

19. Indications(Surgery)
GOO 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
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

20. • In cases of malignant obstruction, weigh the
extent of surgical intervention for the relief of
GOO 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 fit pts)
• 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

21. 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