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PUD MANAGEMENT
PRESENTOR :- DR. Tesfaye P.(GSR4)
MODERATOR:- DR. Dhabasa M.(Consultant G.SURGEON, GI Onco
Fellow)
4/23/2024 1
• Outline
• Introduction
• Pathogenesis
• Classification
• Complications
• Medical management
• Surgical management
2
INTRODUCTION
• PEPTIC ULCER DISEASE
• Erosions in the gastric or duodenal mucosa that extend through the
muscularis mucosae.
• Epidemiology
• Prevalence of about 2%,
• Lifetime cumulative prevalence of about 10%
• Peak incidence > 70yrs
• Elective operations for PUD has decreased steadily and dramatically over the
past three decades.
• Incidence of emergency surgery and the death rate not decreased nearly so
dramatically.
3
4
• Pathogenesis -Complex and multifactorial
• Helicobacter pylori
• Most common cause (90%DU & 70% of GU)
• 10 -15% develop peptic ulceration
• 1% develop gastric adenocarcinoma.
• Features
• Entry into the surface mucus layer,
• attachment to gastric epithelial cells
• Evasion of immune responses
• persistent colonization despite luminal acidity
5
• NSAIDs (including aspirin)
• Risk of peptic ulcer disease 5-fold
• upper GI bleeding about 4-fold
• Many of these patients (30% – 50 %)
remain asymptomatic
• Until they develop these life-threatening
complications.
• 50% to 75% of bleeding peptic ulcers.
• One third of deaths due to hemorrhage.
• Systemic suppression of prostaglandin
production.
• Heal rapidly when the drug is withdrawn.
6
7
• Diagnosis
• History
• Abdominal pain(90%).
• nonradiating, burning in quality, and located in the
epigastrium.
• DU : pain 2 to 3 hours after a meal and at night pain that
awakens them from sleep.
• GU: pain of gastric ulcer more commonly occurs with eating
• less likely to awaken the patient at night.
• Nausea, bloating, weight loss
• A history of PUD, use of NSAIDs.
• Heartburn
• Chest discomfort
• Hematemesis or melena
• Alarm features
• Bleeding or anemia
• Early satiety
• Unexplained weight loss
• Progressive dysphagia or
odynophagia
• Recurrent vomiting
• Family history of GIT
cancer
• Physical Examination
• Uncomplicated peptic ulcer disease (PUD)
• Few and nonspecific:
• Epigastric tenderness (usually mild)
• Right upper quadrant tenderness
• 20% of patients
• Signs of complications
8
• Investigations
• Endoscopy is the most accurate &
"gold" standard.
• Detect about 90 percent of
gastroduodenal ulcer.
• Multiple biopsies of gastric ulcers
(GUs) are necessary
• The chance of malignancy is
greater in large Gus
• The optimal number of biopsies
has been debated and probably
depends upon the technique
9
• Contrast imaging
• Barium meal X-ray features of
benign gastric ulcer
• Niche on the lesser curve with notch
on the greater curvature
• Ulcer crater projects beyond the
lumen of the ulcer
• Regular/round margin of the ulcer
crater—stomach spoke wheel pattern
• Converging mucosal folds towards the
base of the ulcer
• Symmetrical normal gastric mucosal
folds
10
• Deformed or absence of duodenal
cap (because of spasm).
• ‘Trifoliate’ duodenum
11
12
• Tests for Helicobacter pylori.
13
• Classifications – modified Johnson classification
Modified Johnson classification for
gastric ulcer.
I. Lesser curve, incisura. (60% of
gastric ulcer)
II. Body of stomach, incisura +
duodenal ulcer (active or
healed).
III. Prepyloric.
IV. High on lesser curve, near
gastroesophageal junction.
V. Medication-induced (NSAID/
acetylsalicylic acid), anywhere in
stomach.
• Complications
• Ulcer Hemorrhage
• Perforation
• Gastric outlet obstruction
• Intractability
• Penetration
• Malignant change
14
• Medical management
• Mainstay of modern treatment
• Goals of treatment
• Permit ulcer healing
• Prevent ulcer complications
• Address the underlying ulcer etiology
- H.pylori ( heals > 85% of duodenal ulcers
• NSAIDS
15
• Treating H. pylori
Triple therapy
• Failure of monotherapy and dual therapy
• triple therapy & multidrug regimens.
• Classically a 7 day regimen with twice daily
PPI and two antibiotics
• 10 to 14 day course (particularly in
North America)
• Acid suppression with PPI
• synergistic bactericidal effects and
• stabilizes antibiotics so increasing
their half-life.
• Clarithromycin resistance is a major
determinant of the success of triple therapy
 Quadruple therapy
16
• Surgical management
• Current indications for surgical intervention are:
• Emergency surgery for complicated peptic ulcer disease
• Bleeding
• Perforation
• Obstruction
• Elective surgery for intractable ulcer disease
• Failed medical therapy(intractability)
• Risk of malignancy(gastric ulcer)
17
• Emergency surgery for complicated peptic ulcer disease
• Objectives of surgery in emergency cases:
• Deal with the complication
• Reduce the risk of ulcer recurrence
• Perform a safe, quick, and effective operation
• Minimize long-term effects on the gastrointestinal tract
• Establish the H. pylori status of the patient
18
• Biggest intraoperative dilemma.
• whether to proceed with a definitive antiulcer operation
• Recognition of the role of H. pylori, and improvements in medical therapy have
confused
• trend toward favoring of less complex procedures in the setting of emergencies
• modern trend in peptic ulcer operation could be described as “less is more
• Avoiding vagotomy or gastric resections
• A defnitive procedure is always more appropriate in the setting of NSAIDs
• especially if the patient is unlikely to be able to stop the treatment
• Defnitive operation is generally avoided during emergency procedures
• Major underlying medical illness or
• intraoperative hemodynamic instability.
19
• Bleeding Peptic Ulcer
• Most common cause of ulcer-related
death
• Annual Incidence :19 to 57 cases per
100,000 population
• Mortality : 5% to 10%
• All patients admitted to hospital
• adequately resuscitated and
• started on continuous IV PPI
• 75% will stop bleeding
• 25% will continue to bleed or will
rebleed.
• all the deaths occur in this
group.
• Early identification important
• Clinical/endoscopic
• Clinical
• >60 years of age,
• Presenting in shock
• requiring more than 4 units of blood
in 24 hrs or 8 units in 48 hrs
• Those with rebleeding.
20
• Endoscopic features
• Active bleeding (grade I)
• Non bleeding visible vessel (IIa)
• large ulcers > 2 cm
• especially when localized at the
posterior wall of the duodenal bulb
or lessor curvature
21
22
Risk-stratification tools for upper gastrointestinal hemorrhage
 For Blacthford :- Scores of 6 or more
were associated with a greater than 50%
risk of needing an intervention.
 For Rockall :- clinical Rockall score of 0
& complete Rockall score of <2
• considered to be at low risk of
rebleeding or death
• Good prognosis
• Most widely known risk-
stratification tool
• Total score more than 8 carries
high(>50%) risk of mortality
• Management
• All patients admitted to hospital
• Adequately resuscitated
• started on continuous IV PPI
• Endoscopic examination of the stomach and the first and second part of
duodenum
• Endoscopic hemostatic therapy (cautery, epinephrine injection, clipping)
• 10 - 20% fail medical therapy (25% in 2nd endoscopic attempt)
23
• Current indications for surgery for
bleeding PUD:
• Hemodynamic instability despite
vigorous resuscitation (>4-units or >6-
units)
• Failure of endoscopic techniques
• Recurrent hemorrhage after initial
stabilization
• Shock associated with recurrent
hemorrhage
• Continued slow bleeding with a
transfusion requirement exceeding 3
units per day
• Secondary or relative indications
• rare blood type or difficult
crossmatch, refusal of transfusion,
• Shock on presentation,
• advanced age,
• severe comorbid disease
• bleeding chronic gastric ulcer.
• Lower threshold in elderly patients
• Mortality rate 5-10%
• most patients dying of non–bleeding-
related causes such as MOF
24
25
• Surgery for Bleeding Duodenal Ulcer
• Esophagogastroduodenoscopy- locate
source
• most likely to be bleeding is the
gastroduodenal artery
• Upper midline laparotomy/laparoscopy
• A Kocher maneuver
• Anterior wall of the duodenal bulb is
opened longitudinally
• Manual finger pressure
• Gastroduodenal artery is oversewn
• three-point U stitch
• Heavy suture material on a stout needle
• Not to take excessively deep bites
• Hainake-Mikulicz pyloroplasty.
• Definitive acid-reducing operation TV.
• Even in the era of H. pylori and our ability to eradicate it
• Only 40% to 70% of pts with a bleeding duodenal ulcer are positive for H. pylori.
• H. pylori testing in the setting of an acute hemorrhage is less reliable(18% versus 1%)
• Up to 50% of patients are at risk of recurrent bleeding.
• Conflicting evidence that H. pylori treatment changes the risk of recurrent bleeding.
• less aggressive operation exposes the patient to a high rebleeding risk
postsurgery- ‘less is not more’.
26
• If no bleeding is encountered
• Carefully inspect mucosa for an ulcer to identify a visible vessel
• should be ligated.
• If no active bleeding is seen
• carry out a careful inspection for other potential bleeding ulcers
• can be done by manual palpation of the lumen using a finger.
• On occasion, a second gastrostomy near the esophageal junction
• To inspect the proximal stomach.
27
• Bleeding Gastric Ulcer.
• Distal gastrectomy With
Billroth I or II reconstruction is
preferred.
• Permits excision and histologic
evaluation
• Add TV (2,3)
• Second best is V + D
• with oversewing and biopsy of
the ulcer.
• Oversewing of the bleeder,
biopsy followed by long-term
acid suppression
• Reasonable alternative in high-
risk or unstable patients.
28
• Perforated Peptic Ulcer
• Second most common complication
• More common indication for operation than bleeding.
• NSAID and/or aspirin.
• The outcome depends on:
• Time delay to presentation and treatment
• Site of perforation-gastric perforation poorer prognosis.
• Patient’s age- elderly
• Presence of hypotension at presentation (systolic blood pressure <100)
29
• Stages of Perforation
• Stage of chemical peritonitis
• acid causes chemical peritonitis
• Pain started "as if someone flipped a
switch."
• Stage of reaction (Stage of illusion)
• Peritoneum secretes lot of fluid to
neutralise the escaped content
• temporarily the pain reduces.
• Lasts for about 6 hours
• Stage of diffuse bacterial
peritonitis:
• After about six hours
• Clinical Features
• Presents with severe persistent
pain
• in the epi gastrium initially,
• later in the right side abdomen
• Finally becomes generalised.
• Pain is of sudden in onset
• contact of expelled gastric contents
with the parietal peritoneum.
• Tenderness and rebound
tenderness all over the abdomen
(Blumberg sign)
30
• Plain X-ray abdomen
• gas under diaphragm in 80% of
cases.
• 20% of cases, there is no gas
under diaphragm.
• the gas leak is less than 1 ml
• previous surgery causing adhesions
between liver and diaphragm,
• sealed peptic ulcer.
31
• Perforated Duodenal Ulcer.
• 2% to 10% of DU
• Traditionally performed
• simple patch closure
• TV with pyloroplasty (incorporating the
perforation).
• With the identification of H. pylori
• Ideal surgery again questioned.
• 5% recurrence H. pylori-eradicated
• equivalent to definitive antiulcer procedure.
• Simple patch closure appropriate
for
• Acute NSAID-related perforation
(discontinued postoperatively)
• Who have never been treated for
PUD but who can be treated with PPIs
and H. pylori eradication.
• Perforation in the setting of
• ongoing shock,
• Delayed presentation,
• considerable comorbid disease,
• marked peritoneal contamination
32
• Surgical treatement
• Free omental plug (Graham patch)
• Primary closure with omental
pedicle flap
• Omental pedicle flap (Cellan-Jones
repair)
• Serosal(Thal) patch
33
• Nonoperative management of perforated ulcers
• water-soluble contrast gastroduodenogram showing no
extravasation,
• no signs of septic shock, and
• abdominal examination findings confined to the upper
abdomen
• Perforation > 24 hrs
• Elderly with comorbidities
• Not recommended for gastric perforation
• nasogastric decompression,
• antibiotics to cover enteric pathogens,
• antibiotics to cover Helicobacter pylori if present, and
• proton pump inhibitors
• 30% of patients do not improve and require surgical
intervention.
• extremely high failure rate (70%) in the elderly(>70
34
35
• Perforated Gastric Ulcer.
• overall mortality :10% to 40%,
• Debate in types I and IV gastric
ulcers
• Perform a partial gastrectomy or
• Proceed with a simple patching of the
perforation
• Perforated type I gastric ulcer
• Partial gastrectomy unless the patient is
unstable with significant comorbidities.
• Perforated high type IV ulcer
• Biopsy and patch closure may be an
appropriate
• Antacid procedure is not required
• Adequate four-quadrant biopsy
• Perforated type II ulcers
• Similar to that for perforated duodenal ulcers
• Intraoperative biopsy
• Definitive surgery is not required, unless
• history of recurrent ulcer disease
• previously treated for H. pylori.
• HSV or a TV with drainage
• Perforated type III ulcers
• similar pathogenesis to duodenal ulcers, but d/f Rx
• Patch repair of prepyloric ulcers = high incidence of GOO
• HSV = high recurrence rate for these ulcers.
• Antrectomy with vagotomy may be the best surgical approach.
36
Management of omental pacth leak
March 20, 1999 and March 20,2006 in
Iran
 of 422(375, 88.9% duodenal and
prepyloric [gastric], 47, 11.1%)
perforated
 17(4%) leak
 Age was 60.6 years (range 39 to 80),
Previous history of PUD, 6 (35.3%)
patients and 2 (11.8%) hypotensive on
admission. All reoperated, 5 (patch
gangre), 12 ( unkown cause). Of the 17
patients, 5 died
 Study done from January 2019 to
July 2020, in Egypt
 20 patients reperforation after
initial omental patch
 Triple-tube drainage versus jejunal
serosal patch
 Mortality 1 vs 2, overall (3)
 leak dx (36 hrs – 96hrs)
37
• Obstructing Peptic Ulcer
• 5-8% of ulcer related complications
• Malnourished, dehydrated, and have
a metabolic alkalosis
• Increase the operative risk.
• Operation is generally indicated if
obstruction fails to resolve despite 48
to 72 hours
• Adequate intravenous fluid
replenishment,
• Antisecretory therapy, and
• Nasogastric tube decompression.
• Balloon dilation of the scarred
pylorus
• Acute Incomplete obstruction
• unacceptably high recurrence rate
over the short term
• complication – perforation
• rule out an underlying malignancy
• Era PPI, malignancy in greater than
50% of GOO
• H. pylori’s role in the pathogenesis
of GOO
• Low incidence of H. pylori infection
(33% to 57%).
38
39
• Surgery
• TV with antrectomy is the ideal procedure
• Feeding jejunostomy tube is usually
recommended
• preoperative malnutrition
• GOO predisposes to delayed postoperative
gastric emptying.
• Inflammation and scarring at the
duodenal bulb
• TV and drainage is the preferred approach
• biopsy of the lesion
• Debate persists as to the optimal drainage
procedure.
• Jaboulay side-to side duodenoplasty has
gained popularity
• technical simplicity
• anastomosis is performed in healthy tissue,
distinct from the ulcer bed
40
• Non healing ulcer (Intractability)
• Ulcer fails to heal after 8-12wks of optimal
Rx
• Endoscopy→ diminished ulcer size →2nd
course Rx
• A rare indication for surgery today
• PPIs + H.pylori-eradication…..”why
intractable?”
• Cancer
• Persistent H.pylori infection
• Re-infection
• False –ve tests
• Non-compliant pts.
• Chronic NSAIDs use
• ZES
• Zollinger-Ellison syndrome (ZES).
• Uncontrolled secretion of abnormal amounts of gastrin by gastrinoma.
• 80%) are sporadic, but 20% are inherited(MENI)
• 0.1% of all peptic ulcer disease and in 2%ofpatientswith recurrent ulcer
• 50% to 60% of gastrinomas are malignant
• Five-year survival in metastatic disease is approximately 40%.
• More than 90% of patients with sporadically, completely resected gastrinoma
will be cured.
41
• Epigastric pain, GERD, and diarrhea.
• More than 90% have PUD.
• Most ulcers are in the typical location
(proximal duodenum),
• Atypical ulcer location (distal duodenum,
jejunum, or multiple ulcers) should
prompt an evaluation for gastrinoma.
• Recurrent or refractory peptic ulcer
• symptomatic for several years(6-7yrs
delay)
• diagnosed familial (20s and 30s) while
sporadic ZES (40s and 50s).
•
• Diagnosis
• Fasting serum gastrin concentration (>1000
pg/mL) and an abnormally elevated BAO (>15
mEq/L)
• secretin stimulation test
• 200 pg/mL increase of gastrin concentration
above baseline
• Localization
• preoperative localization difficult
• CT,U/S,EUS,MRI
• somatostatin receptor scintigraphy(SRS) (the
octreotide scan)
• sensitivity and specificity approach 100%.
• Angiographic localization
42
43
• Treatment
• High-dose PPIs
• Two to five limes the usual dose of PPIs to
bep the BAO <10 mEq/h
• PPIs should be continued after surgery
• Titrated 3 to 4months postoperatively
• Surgery For Gastrinoma
• All patients with sporadic gastrinoma
should be considered
• Open rather than Laparoscopic exploration
• Extended Kocher maneuver
• Extensive lymphadenectomy
• No tumor=Generous longitudinal
duodenotomy
• ZES/MEN-1
• Multiple gastrinomas & cure rate is
low
• Surgical resection is controversial.
• Imageable tumor >2 cm
• To prevent metastatic spread
• Prognosis
• postoperative cure rate
• 40% at 5 years.
• 34%at 10years.
44
• Giant duodenal ulcers(GDUs)
• Full-thickness peptic ulcer that is >2 in
diameter and usually involving a large
portion of the duodenal bulb.
• 1 to 2% of all duodenal ulcers
• 5% of peptic ulcers requiring surgery.
• Male to female ratio = 3:1.
• Greater morbidity than usual duodenal
ulcers
• Massive hemorrhage and perforation.
• GDUs associated with H.pylori is less
• when compared to standardized ulcers
• NSAIDS use may play a more prominent role.
45
• Management of GDUs
• H.pyelori eradiation + PPIs and stop NSAID
• Emergent indications for surgery
• Uncontrolled hemorrhage
• Perforation
• obstruction.
• Perforation
• Hazardous because of the extensive duodenal tissue loss and surrounding tissue
inflammation
• Preclude simple closure with omental patch
46
Surgical options for Perforation of GDUs
• Partial gastrectomy with Billroth I
or II reconstructions.
• Gastric disconnection
• vagotomy, antrectomy , gastrostomy
• lateral duodenostomy.
• Feeding jejunostomy
• Conversion of the perforation into
pyloroplasty
• Closure of the perforation using a
serosa patch
47
48
References
 Schwartz, 11th ed.
 MasterTechniques in Surgery/Gastric Surgery
 Sabiston, 21th ed.
 Shackfold, 8th ed.
 Maingot’s abdominal operation 13th ed.
 Journal
 Internet
49
THANK YOU

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PUD MANAGEMENT mekuria.pptxfghjkkkkkkkkkkkkkkkkk

  • 1. PUD MANAGEMENT PRESENTOR :- DR. Tesfaye P.(GSR4) MODERATOR:- DR. Dhabasa M.(Consultant G.SURGEON, GI Onco Fellow) 4/23/2024 1
  • 2. • Outline • Introduction • Pathogenesis • Classification • Complications • Medical management • Surgical management 2
  • 3. INTRODUCTION • PEPTIC ULCER DISEASE • Erosions in the gastric or duodenal mucosa that extend through the muscularis mucosae. • Epidemiology • Prevalence of about 2%, • Lifetime cumulative prevalence of about 10% • Peak incidence > 70yrs • Elective operations for PUD has decreased steadily and dramatically over the past three decades. • Incidence of emergency surgery and the death rate not decreased nearly so dramatically. 3
  • 4. 4 • Pathogenesis -Complex and multifactorial
  • 5. • Helicobacter pylori • Most common cause (90%DU & 70% of GU) • 10 -15% develop peptic ulceration • 1% develop gastric adenocarcinoma. • Features • Entry into the surface mucus layer, • attachment to gastric epithelial cells • Evasion of immune responses • persistent colonization despite luminal acidity 5
  • 6. • NSAIDs (including aspirin) • Risk of peptic ulcer disease 5-fold • upper GI bleeding about 4-fold • Many of these patients (30% – 50 %) remain asymptomatic • Until they develop these life-threatening complications. • 50% to 75% of bleeding peptic ulcers. • One third of deaths due to hemorrhage. • Systemic suppression of prostaglandin production. • Heal rapidly when the drug is withdrawn. 6
  • 7. 7 • Diagnosis • History • Abdominal pain(90%). • nonradiating, burning in quality, and located in the epigastrium. • DU : pain 2 to 3 hours after a meal and at night pain that awakens them from sleep. • GU: pain of gastric ulcer more commonly occurs with eating • less likely to awaken the patient at night. • Nausea, bloating, weight loss • A history of PUD, use of NSAIDs. • Heartburn • Chest discomfort • Hematemesis or melena • Alarm features • Bleeding or anemia • Early satiety • Unexplained weight loss • Progressive dysphagia or odynophagia • Recurrent vomiting • Family history of GIT cancer
  • 8. • Physical Examination • Uncomplicated peptic ulcer disease (PUD) • Few and nonspecific: • Epigastric tenderness (usually mild) • Right upper quadrant tenderness • 20% of patients • Signs of complications 8
  • 9. • Investigations • Endoscopy is the most accurate & "gold" standard. • Detect about 90 percent of gastroduodenal ulcer. • Multiple biopsies of gastric ulcers (GUs) are necessary • The chance of malignancy is greater in large Gus • The optimal number of biopsies has been debated and probably depends upon the technique 9
  • 10. • Contrast imaging • Barium meal X-ray features of benign gastric ulcer • Niche on the lesser curve with notch on the greater curvature • Ulcer crater projects beyond the lumen of the ulcer • Regular/round margin of the ulcer crater—stomach spoke wheel pattern • Converging mucosal folds towards the base of the ulcer • Symmetrical normal gastric mucosal folds 10
  • 11. • Deformed or absence of duodenal cap (because of spasm). • ‘Trifoliate’ duodenum 11
  • 12. 12 • Tests for Helicobacter pylori.
  • 13. 13 • Classifications – modified Johnson classification Modified Johnson classification for gastric ulcer. I. Lesser curve, incisura. (60% of gastric ulcer) II. Body of stomach, incisura + duodenal ulcer (active or healed). III. Prepyloric. IV. High on lesser curve, near gastroesophageal junction. V. Medication-induced (NSAID/ acetylsalicylic acid), anywhere in stomach.
  • 14. • Complications • Ulcer Hemorrhage • Perforation • Gastric outlet obstruction • Intractability • Penetration • Malignant change 14
  • 15. • Medical management • Mainstay of modern treatment • Goals of treatment • Permit ulcer healing • Prevent ulcer complications • Address the underlying ulcer etiology - H.pylori ( heals > 85% of duodenal ulcers • NSAIDS 15
  • 16. • Treating H. pylori Triple therapy • Failure of monotherapy and dual therapy • triple therapy & multidrug regimens. • Classically a 7 day regimen with twice daily PPI and two antibiotics • 10 to 14 day course (particularly in North America) • Acid suppression with PPI • synergistic bactericidal effects and • stabilizes antibiotics so increasing their half-life. • Clarithromycin resistance is a major determinant of the success of triple therapy  Quadruple therapy 16
  • 17. • Surgical management • Current indications for surgical intervention are: • Emergency surgery for complicated peptic ulcer disease • Bleeding • Perforation • Obstruction • Elective surgery for intractable ulcer disease • Failed medical therapy(intractability) • Risk of malignancy(gastric ulcer) 17
  • 18. • Emergency surgery for complicated peptic ulcer disease • Objectives of surgery in emergency cases: • Deal with the complication • Reduce the risk of ulcer recurrence • Perform a safe, quick, and effective operation • Minimize long-term effects on the gastrointestinal tract • Establish the H. pylori status of the patient 18
  • 19. • Biggest intraoperative dilemma. • whether to proceed with a definitive antiulcer operation • Recognition of the role of H. pylori, and improvements in medical therapy have confused • trend toward favoring of less complex procedures in the setting of emergencies • modern trend in peptic ulcer operation could be described as “less is more • Avoiding vagotomy or gastric resections • A defnitive procedure is always more appropriate in the setting of NSAIDs • especially if the patient is unlikely to be able to stop the treatment • Defnitive operation is generally avoided during emergency procedures • Major underlying medical illness or • intraoperative hemodynamic instability. 19
  • 20. • Bleeding Peptic Ulcer • Most common cause of ulcer-related death • Annual Incidence :19 to 57 cases per 100,000 population • Mortality : 5% to 10% • All patients admitted to hospital • adequately resuscitated and • started on continuous IV PPI • 75% will stop bleeding • 25% will continue to bleed or will rebleed. • all the deaths occur in this group. • Early identification important • Clinical/endoscopic • Clinical • >60 years of age, • Presenting in shock • requiring more than 4 units of blood in 24 hrs or 8 units in 48 hrs • Those with rebleeding. 20
  • 21. • Endoscopic features • Active bleeding (grade I) • Non bleeding visible vessel (IIa) • large ulcers > 2 cm • especially when localized at the posterior wall of the duodenal bulb or lessor curvature 21
  • 22. 22 Risk-stratification tools for upper gastrointestinal hemorrhage  For Blacthford :- Scores of 6 or more were associated with a greater than 50% risk of needing an intervention.  For Rockall :- clinical Rockall score of 0 & complete Rockall score of <2 • considered to be at low risk of rebleeding or death • Good prognosis • Most widely known risk- stratification tool • Total score more than 8 carries high(>50%) risk of mortality
  • 23. • Management • All patients admitted to hospital • Adequately resuscitated • started on continuous IV PPI • Endoscopic examination of the stomach and the first and second part of duodenum • Endoscopic hemostatic therapy (cautery, epinephrine injection, clipping) • 10 - 20% fail medical therapy (25% in 2nd endoscopic attempt) 23
  • 24. • Current indications for surgery for bleeding PUD: • Hemodynamic instability despite vigorous resuscitation (>4-units or >6- units) • Failure of endoscopic techniques • Recurrent hemorrhage after initial stabilization • Shock associated with recurrent hemorrhage • Continued slow bleeding with a transfusion requirement exceeding 3 units per day • Secondary or relative indications • rare blood type or difficult crossmatch, refusal of transfusion, • Shock on presentation, • advanced age, • severe comorbid disease • bleeding chronic gastric ulcer. • Lower threshold in elderly patients • Mortality rate 5-10% • most patients dying of non–bleeding- related causes such as MOF 24
  • 25. 25 • Surgery for Bleeding Duodenal Ulcer • Esophagogastroduodenoscopy- locate source • most likely to be bleeding is the gastroduodenal artery • Upper midline laparotomy/laparoscopy • A Kocher maneuver • Anterior wall of the duodenal bulb is opened longitudinally • Manual finger pressure • Gastroduodenal artery is oversewn • three-point U stitch • Heavy suture material on a stout needle • Not to take excessively deep bites • Hainake-Mikulicz pyloroplasty.
  • 26. • Definitive acid-reducing operation TV. • Even in the era of H. pylori and our ability to eradicate it • Only 40% to 70% of pts with a bleeding duodenal ulcer are positive for H. pylori. • H. pylori testing in the setting of an acute hemorrhage is less reliable(18% versus 1%) • Up to 50% of patients are at risk of recurrent bleeding. • Conflicting evidence that H. pylori treatment changes the risk of recurrent bleeding. • less aggressive operation exposes the patient to a high rebleeding risk postsurgery- ‘less is not more’. 26
  • 27. • If no bleeding is encountered • Carefully inspect mucosa for an ulcer to identify a visible vessel • should be ligated. • If no active bleeding is seen • carry out a careful inspection for other potential bleeding ulcers • can be done by manual palpation of the lumen using a finger. • On occasion, a second gastrostomy near the esophageal junction • To inspect the proximal stomach. 27
  • 28. • Bleeding Gastric Ulcer. • Distal gastrectomy With Billroth I or II reconstruction is preferred. • Permits excision and histologic evaluation • Add TV (2,3) • Second best is V + D • with oversewing and biopsy of the ulcer. • Oversewing of the bleeder, biopsy followed by long-term acid suppression • Reasonable alternative in high- risk or unstable patients. 28
  • 29. • Perforated Peptic Ulcer • Second most common complication • More common indication for operation than bleeding. • NSAID and/or aspirin. • The outcome depends on: • Time delay to presentation and treatment • Site of perforation-gastric perforation poorer prognosis. • Patient’s age- elderly • Presence of hypotension at presentation (systolic blood pressure <100) 29
  • 30. • Stages of Perforation • Stage of chemical peritonitis • acid causes chemical peritonitis • Pain started "as if someone flipped a switch." • Stage of reaction (Stage of illusion) • Peritoneum secretes lot of fluid to neutralise the escaped content • temporarily the pain reduces. • Lasts for about 6 hours • Stage of diffuse bacterial peritonitis: • After about six hours • Clinical Features • Presents with severe persistent pain • in the epi gastrium initially, • later in the right side abdomen • Finally becomes generalised. • Pain is of sudden in onset • contact of expelled gastric contents with the parietal peritoneum. • Tenderness and rebound tenderness all over the abdomen (Blumberg sign) 30
  • 31. • Plain X-ray abdomen • gas under diaphragm in 80% of cases. • 20% of cases, there is no gas under diaphragm. • the gas leak is less than 1 ml • previous surgery causing adhesions between liver and diaphragm, • sealed peptic ulcer. 31
  • 32. • Perforated Duodenal Ulcer. • 2% to 10% of DU • Traditionally performed • simple patch closure • TV with pyloroplasty (incorporating the perforation). • With the identification of H. pylori • Ideal surgery again questioned. • 5% recurrence H. pylori-eradicated • equivalent to definitive antiulcer procedure. • Simple patch closure appropriate for • Acute NSAID-related perforation (discontinued postoperatively) • Who have never been treated for PUD but who can be treated with PPIs and H. pylori eradication. • Perforation in the setting of • ongoing shock, • Delayed presentation, • considerable comorbid disease, • marked peritoneal contamination 32
  • 33. • Surgical treatement • Free omental plug (Graham patch) • Primary closure with omental pedicle flap • Omental pedicle flap (Cellan-Jones repair) • Serosal(Thal) patch 33
  • 34. • Nonoperative management of perforated ulcers • water-soluble contrast gastroduodenogram showing no extravasation, • no signs of septic shock, and • abdominal examination findings confined to the upper abdomen • Perforation > 24 hrs • Elderly with comorbidities • Not recommended for gastric perforation • nasogastric decompression, • antibiotics to cover enteric pathogens, • antibiotics to cover Helicobacter pylori if present, and • proton pump inhibitors • 30% of patients do not improve and require surgical intervention. • extremely high failure rate (70%) in the elderly(>70 34
  • 35. 35 • Perforated Gastric Ulcer. • overall mortality :10% to 40%, • Debate in types I and IV gastric ulcers • Perform a partial gastrectomy or • Proceed with a simple patching of the perforation • Perforated type I gastric ulcer • Partial gastrectomy unless the patient is unstable with significant comorbidities. • Perforated high type IV ulcer • Biopsy and patch closure may be an appropriate • Antacid procedure is not required • Adequate four-quadrant biopsy
  • 36. • Perforated type II ulcers • Similar to that for perforated duodenal ulcers • Intraoperative biopsy • Definitive surgery is not required, unless • history of recurrent ulcer disease • previously treated for H. pylori. • HSV or a TV with drainage • Perforated type III ulcers • similar pathogenesis to duodenal ulcers, but d/f Rx • Patch repair of prepyloric ulcers = high incidence of GOO • HSV = high recurrence rate for these ulcers. • Antrectomy with vagotomy may be the best surgical approach. 36
  • 37. Management of omental pacth leak March 20, 1999 and March 20,2006 in Iran  of 422(375, 88.9% duodenal and prepyloric [gastric], 47, 11.1%) perforated  17(4%) leak  Age was 60.6 years (range 39 to 80), Previous history of PUD, 6 (35.3%) patients and 2 (11.8%) hypotensive on admission. All reoperated, 5 (patch gangre), 12 ( unkown cause). Of the 17 patients, 5 died  Study done from January 2019 to July 2020, in Egypt  20 patients reperforation after initial omental patch  Triple-tube drainage versus jejunal serosal patch  Mortality 1 vs 2, overall (3)  leak dx (36 hrs – 96hrs) 37
  • 38. • Obstructing Peptic Ulcer • 5-8% of ulcer related complications • Malnourished, dehydrated, and have a metabolic alkalosis • Increase the operative risk. • Operation is generally indicated if obstruction fails to resolve despite 48 to 72 hours • Adequate intravenous fluid replenishment, • Antisecretory therapy, and • Nasogastric tube decompression. • Balloon dilation of the scarred pylorus • Acute Incomplete obstruction • unacceptably high recurrence rate over the short term • complication – perforation • rule out an underlying malignancy • Era PPI, malignancy in greater than 50% of GOO • H. pylori’s role in the pathogenesis of GOO • Low incidence of H. pylori infection (33% to 57%). 38
  • 39. 39 • Surgery • TV with antrectomy is the ideal procedure • Feeding jejunostomy tube is usually recommended • preoperative malnutrition • GOO predisposes to delayed postoperative gastric emptying. • Inflammation and scarring at the duodenal bulb • TV and drainage is the preferred approach • biopsy of the lesion • Debate persists as to the optimal drainage procedure. • Jaboulay side-to side duodenoplasty has gained popularity • technical simplicity • anastomosis is performed in healthy tissue, distinct from the ulcer bed
  • 40. 40 • Non healing ulcer (Intractability) • Ulcer fails to heal after 8-12wks of optimal Rx • Endoscopy→ diminished ulcer size →2nd course Rx • A rare indication for surgery today • PPIs + H.pylori-eradication…..”why intractable?” • Cancer • Persistent H.pylori infection • Re-infection • False –ve tests • Non-compliant pts. • Chronic NSAIDs use • ZES
  • 41. • Zollinger-Ellison syndrome (ZES). • Uncontrolled secretion of abnormal amounts of gastrin by gastrinoma. • 80%) are sporadic, but 20% are inherited(MENI) • 0.1% of all peptic ulcer disease and in 2%ofpatientswith recurrent ulcer • 50% to 60% of gastrinomas are malignant • Five-year survival in metastatic disease is approximately 40%. • More than 90% of patients with sporadically, completely resected gastrinoma will be cured. 41
  • 42. • Epigastric pain, GERD, and diarrhea. • More than 90% have PUD. • Most ulcers are in the typical location (proximal duodenum), • Atypical ulcer location (distal duodenum, jejunum, or multiple ulcers) should prompt an evaluation for gastrinoma. • Recurrent or refractory peptic ulcer • symptomatic for several years(6-7yrs delay) • diagnosed familial (20s and 30s) while sporadic ZES (40s and 50s). • • Diagnosis • Fasting serum gastrin concentration (>1000 pg/mL) and an abnormally elevated BAO (>15 mEq/L) • secretin stimulation test • 200 pg/mL increase of gastrin concentration above baseline • Localization • preoperative localization difficult • CT,U/S,EUS,MRI • somatostatin receptor scintigraphy(SRS) (the octreotide scan) • sensitivity and specificity approach 100%. • Angiographic localization 42
  • 43. 43
  • 44. • Treatment • High-dose PPIs • Two to five limes the usual dose of PPIs to bep the BAO <10 mEq/h • PPIs should be continued after surgery • Titrated 3 to 4months postoperatively • Surgery For Gastrinoma • All patients with sporadic gastrinoma should be considered • Open rather than Laparoscopic exploration • Extended Kocher maneuver • Extensive lymphadenectomy • No tumor=Generous longitudinal duodenotomy • ZES/MEN-1 • Multiple gastrinomas & cure rate is low • Surgical resection is controversial. • Imageable tumor >2 cm • To prevent metastatic spread • Prognosis • postoperative cure rate • 40% at 5 years. • 34%at 10years. 44
  • 45. • Giant duodenal ulcers(GDUs) • Full-thickness peptic ulcer that is >2 in diameter and usually involving a large portion of the duodenal bulb. • 1 to 2% of all duodenal ulcers • 5% of peptic ulcers requiring surgery. • Male to female ratio = 3:1. • Greater morbidity than usual duodenal ulcers • Massive hemorrhage and perforation. • GDUs associated with H.pylori is less • when compared to standardized ulcers • NSAIDS use may play a more prominent role. 45
  • 46. • Management of GDUs • H.pyelori eradiation + PPIs and stop NSAID • Emergent indications for surgery • Uncontrolled hemorrhage • Perforation • obstruction. • Perforation • Hazardous because of the extensive duodenal tissue loss and surrounding tissue inflammation • Preclude simple closure with omental patch 46
  • 47. Surgical options for Perforation of GDUs • Partial gastrectomy with Billroth I or II reconstructions. • Gastric disconnection • vagotomy, antrectomy , gastrostomy • lateral duodenostomy. • Feeding jejunostomy • Conversion of the perforation into pyloroplasty • Closure of the perforation using a serosa patch 47
  • 48. 48 References  Schwartz, 11th ed.  MasterTechniques in Surgery/Gastric Surgery  Sabiston, 21th ed.  Shackfold, 8th ed.  Maingot’s abdominal operation 13th ed.  Journal  Internet