Goals of Treatment:
• Resolution of the obstruction
• Maintenance of bowel continuity
• No recurrence
• No complications
BENEFIT RISK COST AVAILABI
Bowel continuity Local recurrence
/// /// MR: 5%
/// /// MR:1%
/// /// MR: 1%
/ /// MR: 1%
*Csendes A. et al. RCT on three techniques for GOO treatment.
*Millat B. Surgical treatment of complicated Duodenal ulcer: RCT
Pre-op preparation: what I will do
• Informed consent secured
• Psychosocial support provided
• Optimized patient’s physical health
– Correction of anemia/electrolytes
– Nutritional build-up
• Patient screened for any health condition
• Operative materials secured
Intra-op Management: How I will do
It (Vagotomy, Gastrojejunostomy)
• Patient supine under GETA
• Asepsis and antisepsis technique
• Sterile drapes place
• Long vertical incision from xyphoid to
Mobilization of left lateral segment
of the liver
Isolation/ligation of nerve trunk,
anterior, posterior and esophageal
• Anterior vagal trunk is encircled with hook
and dissected sharply from esophageal
• Nerve trunk is ligated proximally and
• Postoperative care:
– Intravenous fluids
– nasogastric decompression
• The nasogastric tube is removed upon
return of gastrointestinal transit, and
feeding is slowly begun.
• Resolution of obstruction
• Live patient
• No complications
• Satisfied patient
• No medico-legal suit
SURGERY FOR PEPTIC ULCER
• Ulcer in the GIT is characterized by an
interruption in the mucosa stretching
through the muscularis mucosa into the
submucosa or deeper
• Location - in order of decreasing
Gastric ulcer Duodenal ulcer
Age 40 – 60 20 – 45
Sex M : V = 1.5 : 1 M : V = 3 : 1
Socio-economic Lower Higher
Blood group A O
Classification of Gastric Ulcers(GU)
( Gaintree – Johnson )
• Type 1 = incisura on the lesser curvature.
No increased acid secretion. Mucosal
• Type 2 = Gastric and duodenal ulcer.
Gastric ulcer secondary to gastric stases
caused by duodenal ulcer.
• Type 3 = Prepyloric ulcer within 2-3cm of
the pylorus. Often acid hypersecretors.
Association with blood group O. Treated
like duodenal ulcer.
• Type 4(Csendes) = High on lesser
curvature near gastro-esophageal
junction. As Type 1.
• Type 5 = Secondary to chronic use of
non-steroidal anti-inflammatory drugs
(NSAID). Can occur anywhere in the
• Still debated
• Traditionally duodenal ulcers are seen as
a problem with acid hypersecretion and
gastric ulcers as a mucosal resistance
Gastric acid. Central in pathogenesis – no
benign ulceration occurs without gastric
Gastric stases. Delayed emptying of normal
amounts of acid with increased exposure
Enviromental factors are very important.
a) Helicobacter pylori infection. 90% of
patients with DU and 50% of patients with
b) NSAID use. The mucus gel layer contains
bicarbonate. This layer adheres to the
gastric mucosa. It protects the mucosa
against back diffusion of hydrogen ions.
NSAID’s suppress mucus cell function.
• Surgery is indicated and for the following:
1) Non-healing ulcer ( 8 – 12 weeks for GU, DU
can be managed conservatively for longer since
the risk for malignancy is low)
• a) Perforation
b) Bleeding if massive,
c) Gastric outlet obstruction that does not clear up on
Surgical principle for definitive ulcer
Definitive ulcer operations for
• Type 1 GU partial gastrectomy. Vagotomy
• Type 2 and 3 GU treated as DU. HSV
contra-indicated due to high ulcer
recurrence with prepyloric ulcers.
• Type 4 GU treated with partial
gastrectomy and excision of a long tongue
of lesser curvature including the
Gastric outlet obstruction
• Cycles of inflammation and repair may
cause obstruction at the gastroduodenal
junction as a result of edema, muscular
spasm and fibroses.
• Edema and spasm can resolve with
• Obstruction is mainly caused by DU and
• Malignant tumors is the other important
cause of gastric outlet obstruction.
• normal pylorus is about 20 mm in
diameter and can distend to 25 mm
• gastric outlet obstruction occur when the
diameter of the antroduodenal segment is
below 10 mm
• A saline load test can be utilized in the
objective measurement of outlet
obstruction or gastric atony and the
assessment of response to therapy
• The major benign causes of GOO are
PUD, gastric polyps, ingestion of caustics,
pyloric stenosis, congenital duodenal
webs, gallstone obstruction (Bouveret
syndrome), pancreatic pseudocysts, and
• Longstanding history of PUD
• Progressive worsening of ulcer pain and
• Vomiting after meals of partially digested
food without bile ( food eaten earlier the
day or the previous day).
• Dehydration and severe weight loss.
• Visible peristalses of the dilated stomach
• Succussion splash audible with to and fro
movement of abdomen.
• Tetany in cases of advanced alkaloses.
• Develop hyponatremic, hypokalemic,
hypochloremic metabolic alkaloses
1) Resussitation initially with 0.9% sodium
chloride. Potassium supplementation
only after good urine output is
2) Gastric lavage with thick stomach tube (
32 F) to remove food residue.
3) Diagnostic tests after gastric lavage :
Gastroscopy with biopsies with or
without barium meal to rule out
4) IV H2-blockers or proton pump inhibitors.
5) A nasogastric tube is passed. The patient may
drink water. The amount of oral intake and
drainage is charted. This gives an impression
whether the obstruction is resolving.
6) Balloon dilatation of pyloric channel is
possible but seldom produces a final solution.
7) Surgery is indicated if the obstruction
does not resolve after one week of
conservative treatment. Mostly a truncal
vagotomy and antrectomy is done
although truncal vagotomy with a
drainage procedure is sometimes
Complications due to vagotomy
• Intraoperative complications can occur
with injury to adjacent structures.
• Early post-operative complication
– delayed gastric emptying
– dysphagia and lesser curve necroses( lesser
curve necroses specific to HSV).
• Late complications include postvagotomy
diarrhea, reflux esophagitis and
Complications of gastrectomy
• Early complications
– anastomotic leakage
– hepatobiliary-pancreatic complications
(pancreatitis, bile duct injury)
• Late complications are classified as
– 1) Ulcer recurrence
a) Recurrent ulcer
b) gastrojejenocolic fistula
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
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.
– 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
4) Malabsorption and Nutritional
a) Malabsorption of protein, carbohydrates
b) Early satiety
c) Anemia : Fe, folate and B12 deficiency. B12
problems mostly after total or near total
1. Csendes A. Maluenda F. et al. Prospective randomized controlled trial
comparing three surgical techniques for the treatment of gastric outlet
obstruction secondary to duodenal ulcer. Am J Surg. 1993 Jul 166:45-49
2. Edwards LW, Herrington JL Jr. Vagotomy and
gastroenterostomy—vagotomy and conservative gastrectomy. Ann
Surg, 1953; 137: 873– 83.
3. Emas S, Fernstrom M. Prospective, randomized trial of selective vagotomy
with pyloroplasty and selective proximal vagotomy with and without
pyloroplasty in the treatment of duodenal, pyloric and prepyloric ulcers. Am
J Surg, 1985; 149: 236–43.
4. Fischer AB. Twenty-five years after Billroth II gastrectomy for duodenal
ulcer. World J Surg, 1984; 8: 293–302.
5. Kuwada, S et al. Long-term outcome of endoscopic dilation of nonmalignant
pyloric stenosis. Gastrointestinal Endoscopy 1995; 41(1) 15-17.
6. Gibson JB, Behrman SW, Fabian TC: Gastric outlet obstruction resulting
from peptic ulcer disease requiring surgical intervention is infrequently
associated with Helicobacter pylori infection. J Am Coll Surg 2000 Jul;
7.Millat B, Fingerhut A et al. surgical treatment of
complicated duodenal ulcer. Controlled trial. World J
Surg. 2000 Mar. 24(3) 299-306.
8. Siu WT, Tang CN, Law BK, et al: Vagotomy and
gastrojejunostomy for benign gastric outlet obstruction. J
Laparoendosc Adv Surg Tech A 2004 Oct; 14(5): 266-
9. Haglund UH, Jansson RL, Lindhagen JG, Lundell LR,
Svartholm EG, Olbe LC.Primary Roux-Y
gastrojejunostomy versus gastroduodenostomy after
antrectomy and selective vagotomy.Am J Surg. 1992
1. Gastric Outlet Obstruction secondary to healed pyloric
ulcer may present with which of the following?
d. epigastric pain
e. All of the above
2. What is the most common complication of peptic ulcer
3. The following statements is/are true regarding gastric
1. Cycles of inflammation and repair may cause
obstruction at the gastroduodenal junction as a result
of edema, muscular spasm and fibroses.
2. Edema and spasm can resolve with medical treatment.
3. Obstruction is mainly caused by DU and prepiloric GU.
4. Malignant tumors is the other important cause of
gastric outlet obstruction.
4. Which of the following choices is/are late
complication/s of vagotomy?
1. postvagotomy diarrhea,
2. reflux esophagitis and
4. Delayed gastric emptying
5. Which of the following is/are not early complication of
gastric surgery ?
7. anastomotic leakage
8. hepatobiliary-pancreatic complications (pancreatitis,
bile duct injury)
9. gastrojejenocolic fistula