This document summarizes the surgical management of peptic ulcer disease. It discusses the pathophysiology, clinical presentation, diagnosis, complications and surgical treatments. For surgical management, the key indications are protracted bleeding, perforation, and obstruction. Common procedures include patch closure for perforated duodenal ulcers and distal gastric resection for perforated gastric ulcers. Endoscopic methods are first-line for treating bleeding but surgery is needed for recurrent or severe bleeding. Postoperative care involves NG tube, IV PPIs and H. pylori treatment if present.

1. Surgical manegment of Peptic Ulcer Disease
Presenter Mekuria k. (R IV)
Moderator Dr Jemal R. (assistant professor G.
surgeon)
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2. content
 Introduction
 Pathophysiology and cause
 Clinical feature
 Diagnosis
 Complication
 Surgical management
 Postgastrectomy problems
 References
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3. Introduction
• peptic- relating to or promoting digestion
• Gastroduodenal peptic ulcer disease (PUD)
– are focal defects in the gastric or duodenal mucosa
that extend into the submucosa or deeper.
• epidemiology
• is a common problem with significant geographic variation
• Such variations are likely related to the prevalence of
Helicobacter pylori, smoking, and use of ulcerogenic drugs,
such as nonsteroidal anti-inflammatory drugs (NSAIDs).
• in prevalence.
– In Western-4% with 20% asymptomatic ulcers.
– In developing countries-China, 17.2% -more than
70% of these patients asymptomatic.
• Complications of PUD vary depending on the
geographic location,
– Bleeding- the most common in the United States,
– obstruction may be more common in other
locations in the world.
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4. 4/4/2024 4

5. Pathophysiology and Etiology
• The cause of peptic ulcers is complex and multifactorial,
• caused by an imbalance between mucosal defenses and
acid/peptic injury
• Any entity that either increases acid and pepsin secretion or
weakens the mucosal barrier can result in ulcers
• 90% of serious peptic ulcer complications can be attributed to
– H pylori infection, NSAID use, cigarette smoking.
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6. HELICOBACTER PYLORI
• the most common chronic bacterial infection in humans.
• Once acquired, infection persists and may or may not produce
gastroduodenal disease.
• The incidence of H. pylori is gastric ulcers is 90% and up to 100% in
duodenal ulcers.
• A number of factors determine whether H. pylori infection causes
disease:
– the pattern of histologic gastritis induced;
– changes in homeostasis of gastrin and acid secretion;
– gastric metaplasia in the duodenum;
– interaction of H. pylori with the mucosal barrier; and
– the strain of H. pylori present.
• Vairulent are are vacA and cagA positive.
• genetic predisposition to acquire H. pylori infection.
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7. NONSTEROIDALANTIINFLAMMATORY DRUGS
• More than half of peptic ulcer hemorrhage or perforation
• the risk is drug specific and dose dependent.
• NSAIDs decrease the mucosal defense by suppression of
prostaglandin synthesis
• The presence of gastric acid contributes to NSAID injury
– converting superficial mucosal lesions to deeper ulcers.
– acid interferes with platelet aggregation and impairs
ulcer healing.
• Acid suppression is the mainstay in the therapy of NSAID-
associated ulcer disease.
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8. SEVERE SYSTEMIC DISEASE (STRESS ULCER)
• The pathophysiology of stress ulceration is multifactorial and
undefined.
– A breakdown of the gastroduodenal mucosal barrier,
– splanchnic hypoperfusion,
• Prior to medical therapy i- highly lethal
– total or near-total gastrectomy
• primary goal of therapy- prophylactic measures to patients at risk.
• (EGD) is the first line of intervention. It aids with the diagnosis.
• Smoking,-
– increases gastric acid secretion and duodenogastric reflux.
– Decreases gastroduodenal prostaglandin and bicarbonate
production
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9. Peptic Ulcer pathophysiology by Location
• Duodenal ulcer
• Younger population than GU
• Most occur in the first part of the duodenum
• May be anterior or posterior or both
– Anterior ulcers perforate
– posterior ulcers bleed
• Often produce more gastric acid
• Malignancy is very rare
• Classic symptom of duodenal ulcer is pain
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10. • Gastric ulcer
• Less common than duodenal ulceration
• Older patients, 55-65 yrs
• Sex incidence is equal
• About 10% of gastric ulcers are malignant
– aggressive biopsy and brushings
– careful follow-up to demonstrate healing
• The most frequent complication of GU is perforation
– Most occur on anterior aspect of the lesser
curvature
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11. In gastric ulcer, acid secretion is variable
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. gastric ulcers may have weak mucosal defenses that permit an
abnormal amount of injurious acid back diffusion into the mucosa

12. Clinical Manifestations
abdominal pain
• More than 90% of patients with PUD
– The mechanism of the pain is unclear.
– typically nonradiating, burning in quality, and located in the
epigastrium.
• with duodenal ulcer
• often experience pain 2 to 3 hours after a meal and at night.
• Two-thirds of patients will complain of pain that awakens
them from sleep.
• twice as common in men compared to women,
• gastric ulcer
• The pain is more commonly occurs with eating and is less
likely to awaken the patient at night.
• incidence of gastric ulcer is similar in men and women.
• are older than duodenal ulcer patients,
• suggestive of the diagnosis
– A history of PUD,
– use of NSAIDs, over-the-counter antacids, or
antisecretory drugs.
• Other signs and symptoms include
– nausea, bloating, weight loss,
– stool positive for occult blood, and anemia
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13. Investigation
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14. Barium Upper GI Study.
• Not sensitive in diagnosis of small ulcers (<0.5
cm)
• Unable to obtain biopsy to rule out malignancy
• Plain abdominal X-rays may be helpful in the
diagnosis of
– gastric perforation (pneumoperitoneum) or
– delayed gastric emptying (large air-fluid level).
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15. Esophagogastroduodenoscopy (EGD)
• the most reliable method
• sample tissue for malignancy and H. pylori infection
• is a safe and accurate outpatient procedure performed
under conscious sedation.
• To rule out cancer with a high degree of accuracy,
• The most serious complications of EGD are perforation
(which is rare, but can occur anywhere from the cervical
esophagus to the duodenum), aspiration, and respiratory
depression from excessive sedation.
• Although EGD is a more sensitive test than double-
contrast upper GI series, these modalities should be
considered complementary rather than mutually exclusive.
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16. Medical Treatment of Peptic Ulcer Disease
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17. Current indications for surgical intervention are
• 1. Protracted bleeding despite endoscopic therapy.
– Bleeding is the most common complication in the United States
• 2. Perforation
– is the second most common
– the highest rate of mortality.
– Commonest indication for surgery
• 3. Obstruction
– Due to scarring following healing of prepyloric and/or duodenal
ulcers.
– Second common indication od surgery
• 4. Intractability nonhealing despite maximum medical therapy
– is an uncommon indication for operation.
• 5. Inability to rule out cancer
– when an ulcer remains despite treatment and negative endoscopic
biopsies.
– This is of particular importance with gastric ulcers.
• The goals of surgical procedures are to
 Permit ulcer healing
 revent or treat ulcer complications
 Address the underlying ulcer etiology
 Minimize postoperative digestive consequences
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19. Bleeding peptic ulcers
• the most common cause of upper GI bleeding
• Two-thirds of the emergency operations performed for
PUD
• typically present with melena and/or hematemesis.
• Abdominal pain is quite uncommon.
• Nasogastric aspiration is- confirmatory of upper GI
bleeding.
• 85% of bleeding ulcers stop bleeding spontaneously.
– Of the remaining patients, 85% to 95% can be effectively
treated by endoscopic means.
• Despite endoscopic advances, the mortality rate following
ulcer bleeding has remained stable at 5% to 10%..
• endoscopy
• diagnose the cause and to assess the need for hemostatic therapy.
• The Forrest classification
– to assess the risk of rebleeding based on endoscopic findings
• High-risk patients benefit from endoscopic therapy
• low-risk lesions can discharged and treated as outpatients
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20. • Risk stratification tools
• predicting rebleeding and death
• low risk are
– Blatchford score of 1 or less, or
– a Rockall score of 2 or less,
• Blatchford risk-stratification score
• ranges from 0 to 23
• The shorter modified Blatchford score
– may be just as useful (BUN, Hgb, pulse, BP;
– maximal score 16).
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21. • the Rockall score
• point values assigned for
– clinical variables
– endoscopic variables
• The complete score ranges from 0 to 11
• low risk for rebleeding or death
– Clinical score (Age + Shock + Coexisting
illness) of 0 or
– a complete Rockall score of 2 or less
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22. • endoscopic hemostatic modalities used are
– injection with epinephrine and electrocautery.
– In exposed vessel, mechanical hemostasis using clips
– Biopsy to evaluate for H pylori infection.
• If the bleeding is controlled endoscopically,
– intravenous proton pump inhibitor therapy
– Antibiotics directed against Helicobacter pylori
• if the organism is present-reduce rebleeding rates.
• If bleeding recurs, a second attempt at
endoscopic control should be made.
• 10% to 20% of patients admitted with bleeding
peptic ulcers fail medical therapy and require
urgent surgical intervention.
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23. Current indications for operation
 requiring more than four units in 24 hours or eight units
of blood in 48 hours,
 Failure of endoscopic techniques
 Recurrent hemorrhage after initial stabilization
 those presenting in shock,
 Continued slow bleeding with a transfusion > 3 per day
 GDU
 concurrent indications for surgery- perforation or
obstruction
 Patients with massive bleeding from high-risk lesions
 posterior DU -gastroduodenal artery, or
 lesser curvature GU with -left gastric artery or branch)
 The surgical threshold may have to be lowered in elderly
patients who poorly tolerate prolonged resuscitation,
large-volume transfusion, and periods of hypotension.
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24. Technique When operating to ulcer bleeding,
– Duodenotomy and suture control of hemorrhage,
– pyloroplasty
– truncal vagotomy
• . An initial pyloromyotomy incision
– allows access to the bleeding posterior duodenal ulcer
– duodenal mucosa is inspected for any evidence of active
bleeding, ulceration, or induration
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25. • If active bleeding is encountered-controlled by digital pressure.
– gives time for fluid resuscitation of the patient.
• The bleeding vessel is often the gastroduodenal artery
– at posterior duodenal wall has a T or three-vessel junction.
– Control of bleeding is achieved with three sutures.
– figure-of-eight sutures are placed at the cephalic and caudal
aspects of the ulcer to occlude the gastroduodenal artery.
– An additional U stitch is placed to control small transverse
pancreatic branches from the main vessel.
• Care should be taken to avoid injury to the common bile duct
during suture placement.
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26. • If no bleeding is encountered upon opening the
lumen, the mucosa should be carefully inspected
for an ulcer.
– If identified, the ulcer base should be cleaned to help
to identify a visible vessel
– If no active bleeding is seen careful inspection of the
mucosa, looking for other potential bleeding ulcers
• POSTOPERATIVE MANAGEMENT
• admitted to surgical intensive care unit.
• A NG tube for 2 to 3 days for stomach decompression.
– Prolonged NG tube placement should be avoided
• intravenous proton pump inhibitors and
• treated H. pylori infection if found.
• CO:MPLICATIONS
• Rebleeding can occur in up to 10o/o of patients and
– If it recurs early on. is usually a technical failure due to
inadequate suture placement at the original surgery
– Late rebleeding is usually associated with inadequate
vagotomy or failure to eradicate H. pylori infection
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27. Perforated Peptic Ulcer
• Smoking and NSAIDs are important etiologic factors
• the second most common complication
• but nowadays it is a much more common indication for
operation than bleeding.
• The mortality is around 3% for healthy, younger patients
– can approach 30% in elderly and debilitated
• patient usually presents as an acute abdomen andd shows
peritoneal signs.
– Initially, a chemical peritoniti, but within hours a
bacterial peritonitis supervenes
• Upright chest X-ray shows free air in -80%
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28. • Nonoperative management of perforated ulcers
• its use and patient selection remains a major debate.
• Patients to consider are
– who present with pneumoperitoneum who have a water-
soluble contrast gastroduodenogram showing no
extravasation,
– for individuals who have a perforation of greater than 24
hours’ duration, are stable, and
– often have significant comorbidities that increase the risk
of surgical intervention.
– no signs of septic shock, and
– abdominal examination findings confined to the upper
abdomen
• routinely includes
– nasogastric decompression,
– antibiotics to cover enteric pathogen,
– antibiotics to cover Helicobacter pylori if present
– proton pump inhibitors.
• Such patients should be followed closely with
– regular physical exams and
– laboratory findings for progressive sepsis
• 30o/o of patients -do not improve and require
surgery
• Because perforated gastric ulcers have a higher
rate of reperforation and complications,
– not recommended.
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29. Perforated Duodenal Ulcer
 options are simple patch closure, or with HSV, or V + D.
simple patch closure is appropriate for patients with
• Acute NSAID-related perforation and drugs can be discontinued
• never been treated for PUD but can be treated with PPIs and H. pylori
eradication
• High risk -ongoing shock, delayed presentation, considerable
comorbid disease, or marked peritoneal contamination
definitive antiulcer procedure
Should be considered because the H. pylori status is often unknown
This may be particularly important in those patients with
• Stable patients who are known to be H. pylori-negative,
• patients with a long history ofpeptic ulcer disease, or
• patients with essential medication needs (chronic steroid use
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30. perforated gastric ulcers
• depending on the location and patient stability
 In the stable patient without multiple operative risk factors,
– best treated by distal gastric resection.
– Vagotomy is added for type II and III gastric ulcers.
 the unstable or high-risk patient
 high risk because of advanced age, comorbid disease,
intraoperative instability, or severe peritoneal soilage.,
 perforation in an inopportune location;
– patch repair and biopsy of ulcer or ulcer resection.
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31. technique
• PREOPERATIVE PLANNING
• analgesia
• Antibiotics to cover enteric pathogens
• a nasogastric tube
– to decompress the stomach and limit peritoneal
contamination
• urinary catheter are placed.
• goal-directed crystalloid resuscitation.
• To perform the patch procedure,
• upper midline incision
• intraabdominal organs are inspected.
• bilious fluid in the peritoneal cavity suggests an
upper gastrointestinal perforation.
• pads are placed around the perforation to contain
any further spillage
• Following repair of the perforation, a thorough
irrigation of the abdomen with attention paid at
the right and left subphrenic spaces and pelvis
should be done.
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32. • three to four sutures 3-0 silk or polydioxanone sutures
• take bites of length (0.5 to 1 cm) to prevent the sutures cutting
• Be sure bites that are full thickness, it is recommended that one pass the
needle through the wall of duodenum
• These sutures should not be tied to approximate the ulcer;
• adjacent omentum should be mobilized on an intact vascular pedicle
and brought up.
• The sutures are tied over this omental pedicle to secure this in place.
• These sutures should not be tied too tightly,
• avoid strangulation of the omental patch
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33. falciform ligament patch
 When omentum is not available
• division of the falciform at the anterior
abdominal wall,
• the vascularized falciform graft based on its
attachment to the liver easily reaches the duodenum,
• Three sutures of PDS secure the falciform patch over
the ulcer.
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34. • POSTOPERATIVE MANAGE:MENT
• Inpatient
• duration of nasogastric tube decompression remains
controversial,
– at least a brief period of gastric decompression to allow time
for the patch to fully adhere to the visceral wall.
• • Drains are rarely left anymore
– The peritonitis leads to a significant amount of fibrin
deposition, which makes drains nonfunctional after just a day
or two.
• started on intravenous proton pump inhibitors
postoperatively and converted over to oral once
tolerating a diet.
• Outpatient
• detect H. pylori infection and determine eradicated.
• COMPLICATIONS
• Continued leak -reported in 5o/o to 10o/o
• Patients with suspicion of a continued leak
should be evaluated by a water soluble contrast
study.
• If the leak. is small or contained-percutaneous
techniques:
• If the persistent leak is from a gastric ulcer, a
wedge resection
• if to reoperate on a patient, a definitive antiulcer
procedure in stable pts
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35. Obstructing Peptic Ulcer (GOO
• More than half of gastric outlet obstruction cases are caused by malignant diseasea pancreatic, gastric, or duodenal.
• occurs in no more than 5% of patients with PUD.
• It is usually due to duodenal or prepyloric ulcer disease
• may be acute (from inflammatory swelling and peristaltic dysfunction) or chronic (from cicatrix).
• Patients typically present with nonbilious vomiting,profound hypokalemic hypochloremic metabolic alkalosis and
dehydration.
• Pain or discomfort is common. Weight loss may be prominent, depending on the duration of symptoms.
• A succussion splash may be audible with stethoscope placed in the epigastrium.
• The diagnosis is confirmed by endoscopy.
• Initial treatment is nasogastric suction, IV hydration and electrolyte repletion, and acid suppression.
• Acute ulcers associated with obstruction due to edema and/or motor dysfunction may respond to intensive
antisecretory therapy and nasogastric suction.
• But most patients with significant obstruction from chronic ulceration will require some sort of more substantial
intervention.
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36. • endoscopic balloon dilation
• In a less acute setting in which the
obstruction is incomplete
• 65% of patients experience sustained relief,
but many require more than one dilation
sessionn.
• The most serious complication of dilation is
a perforation.
• it is important to rule out an underlying
malignancy
• Surgical
• Operation in these cases is almost never emergent
• and should be performed only after the patient has been
stabilized and nutritional and electrolyte abnormalities
have been corrected.
• operation is generally indicated if obstruction fails to
resolve despite 48 to 72 hours of adequate intravenous
fluid replenishment, antisecretory therapy, and
nasogastric tube decompression.
• The standard operation for obstructing PUD is vagotomy
and antrectomy.
• vagotomy and gastrojejunostomy should be considered if
a difficult duodenal stump is anticipated with resection.
• HSV and gastrojejunostomy may be comparable
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37. Intractable or Nonhealing Peptic Ulcer
• A refractory peptic ulcer
• def endoscopically proven ulcer greater than 5 mm in
diameter that does not heal after 12 weeks of treatment
with a PPI.
• unusual indication for peptic ulcer operation nowadays.
– Because acid secretion can be blocked and H pylori eradicated
• the question remains:
– “Why does the patient have a persistent ulcer
diathesis?”
• The surgeon should review the differential diagnosis
before any consideration of operative treatment
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38. • when operative intervention is being considered, the strategy continues
to be based on reduction of acid secretion.
• The choices for surgical intervention for intractable duodenal ulcer
disease include either a
– vagotomy with or without a drainage procedure or
– vagotomy with a gastric resection
• Surgical treatment should be considered in patients with nonhealing or
intractable PUD who have
– multiple recurrences,
– large ulcers (>2 cm),
– complications (obstruction, perforation, or hemorrhage), or
– suspected malignancy.
• RECURRENT PEPTIC ULCER DISEASE
• is defined as an endoscopically proven ulcer greater than 5
mm in diameter that develops within 12 months following
complete ulcer healing documented by repeat endoscopy
• The most common cause after an acid-reducing procedure is
an incomplete vagotomy.
• Supradiaphragmatic vagotomy is used.
• involves performing a thoracotomy or thoracoscopy,
identifying the two large nerve trunks, and performing a TV.
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39. • GIANT DUODENAL ULCER
• is benign and measures at least 2 cm in diameter.
• 1% to 2% of all duodenal ulcer.
• NSAID use plays a more prominent role
• It is important to measure the ulcer so as not to
misdiagnose it as a simple peptic ulcer.
– The ulcer usually involves more than 50% of the
duodenal bulb circumference.
• It is essential to rule out cancer,-19%.
• The first line of treatment for an uncomplicated GDU is
– PPI with eradication of H. pylori and
– discontinuation of NSAIDs.
• Operative intervention- is indicated for complication
• A definitive acid-reducing operation should be with
removing the involved duodenum whenever possible.
• The chronic inflammatory changes often make the
operations technically challenging.
– B I reconstruction If the inflammation and edema of the
duodenum is not a factor,
– However, dissection and anastomosis can be hazardous,
and it is best to leave the ulcer bed in situ and perform a
B II.
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40. ELECTIVE OPERATION FOR INTRACTABLE GU
• management
• wedge resection with HSV-considered in thin or frail patients.
• Otherwise, distal gastrectomy (to include the ulcer)
• Prophylactic regimens - reduce the risk of ulcers, include
– the use of PPI and/or prostaglandin analogue
– A definitive antisecretory operation (TV and antrectomy)
• if medical treatment fails or
• if the NSAID treatment cannot be stopped
• TYPE IV GASTRIC ULCER
• difficult to resect as part of a distal gastrectomy,
• alternatives include
• Pauchet procedure -gastrectomy and excision of the ulcer
• Kelling-Madlener procedure nonresective ulcer itself is not excised
• Csendes procedure-near-total gastrectomy wiith Rouxen-Y
esophagogastrojejunostomy
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41. • Zollonger
• Saiston
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42. Thank you
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