Gastric Outlet Obstruction

1. GASTRIC OUTLET OBSTRUCTION
DR LALTHLAMUANA
DNB STUDENT GENERAL SURGERY
DEPARTMENT OF SURGERY
CIVIL HOSPITAL AIZAWL.

2. 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.

3. 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.

4. • 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.

5. • 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 oedematous tissue and complicates surgical intervention

6. • 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%.

7. AETIOLOGY
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

8. AETIOLOGY
• 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

9. • 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.

10. AETIOLOGY
• 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

11. 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

12. • 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

13. 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

14. 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

15. 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

16. PHYSICAL EXAMINATION
• Chronic dehydration and Malnutrition
On examination :
Distended abdomen and succussion splash may be audible on shaking the patients
abdomen.
Positive succussion splash is done with 4 hours empty stomach, by placing a
stethoscope over the epigastric region and shaking the patient.

17. 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.)

18. 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.

19. 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

20. • 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

21. ELECTROLYTE CHANGES IN PYLORIC STENOSIS
1. Hyponatremia
2. Hypokalemia
3. Hypomagnesemia
4. Hypochloraemia
5. Metabolic alkalosis
6. Paradoxical aciduria

22. 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 ionized calcium, and gastric tetany can occur.

23. 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.

24. 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.

25. 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.

26. MANAGEMENT
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.

27. 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)

28. 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.

32. 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

33. • 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
long-term prognosis
• As a guiding principle, undertake major tumor resections in the absence of metastatic disease

34. • 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.
• Duodenal stent insertion may be considered in patients with unresectable
malignancy.

38. COMPLICATIONS
• Although the risk is small, patients undergoing endoscopic treatment with either
balloon dilatation or stenting are at risk for perforation.
• Migration of the stents and re occlusion requiring further intervention.
• Operative complications in patients undergoing surgery for gastric outlet
obstruction (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 is often prudent.

39. COMPLICATIONS
• 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 post gastrectomy syndromes, such as dumping, alkaline
gastritis, and afferent loop syndrome.

41. Thank you