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Surgical management of

Peptic Ulcer Disease


Presenter : Simon T (R3)
Moderator : Dr. Burqa ( Assistant prof of Surgery )

04/02/2022 mgt of PUD simon


OUTLINE OF PRESENTATION
Introduction
Pathogenesis and etiology
Types of PUD
Clinical manifestation and diagnosis.
Medical treatment
complications.
Surgical management of ulcer disease.

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Peptic ulcer disease
Defined as erosions in the gastric or duodenal mucosa that extend through the
muscularis mucosa.
May be acute or chronic
The incidence is decreasing in developed countereis.
 PUD is one of the most common GI disorders
with a prevalence of about 2%.
a lifetime cumulative prevalence of about 10%,
peaking around age 70 years

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Peptic ulcer disease
H.pylori detection and eradication has led to:-
Decline in incidence of of PUD.
Decrease in elective surgery.
Decrease in complication.
Thus decrease in mortality
M=F in gastric Ulcer
M>F Duodenal Ulcer

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Pathophysiology and etiology
• imbalance between mucosal defenses and acid/peptic injury

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Pathophysiology and etiology
A variety of factors may contribute to the development of PUD.
large majority of duodenal and gastric ulcers are caused by:-
H. pylori infection.
NSAID use.
acid is final common pathway to ulcer (“no acid, no ulcer” remains true).
Smoking

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Helicobacter pylori-Infection

H. pylori is a spiral or helical gram-negative rod


Colonizes the stomachs of ~50% of the world's human population.
80% to 95% duodenal ulcers associated with H. pylori infection.
75% of gastric ulcers are associated with H. pylori infection.

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Mechanisms of H.pylori to induce mucosal injury.

Production of toxic products:-


Cytotoxins(vacA and cagA)
ammonia
Enzymes:-
Mucinase
Phospholipase
Induction of a local mucosal immune response.
Increased gastrin levels with a resultant increase in acid secretion.
Gastric metaplasia occurring in the duodenum.

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Acid Secretion and Peptic Ulcer.

Duodenal ulcer more than gastric ulcer.


There is no correlation between acid secretion and the severity of the
ulcer disease.
Duodenogastric reflux may play a role weakening the gastric mucosal
defenses(bile, lysolecithin, and pancreatic juice)
Increased rates of gastric emptying
Decreased duodenal bicarbonate secretion(decreases the buffering
capacity

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NSAIDS
Inc. risk of peptic ulcer disease about 5-fold.
Inc. upper GI bleeding about 4-fold.
Risk for bleeding and ulceration is proportional to the daily dosage of NSAIDs.
Complications of PUD (hemorrhage and perforation) are much more common.
NSAID-induced ulcers are more often found in the stomach.

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Smoking
Smokers are twice as likely to develop PUD as nonsmokers
Increases gastric acid secretion and duodeno-gastric reflux
Decreases gastro-duodenal prostaglandin production and
Decreases pancreaticoduodenal bicarbonate production

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Stress
Both physiologic and psychologic
Curling ulcer(burn)
Cushing ‘s ulcer(head trauma)
Stressful life events increase the occurrence of PUD complications
 NB….Alcohol is commonly mentioned as a risk factor for PUD but confirmatory
data are lacking

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Types of ulcer

Modify Johnson’s classification

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Clinical Manifestations
90% of patients with PUD complain of abdominal pain.
Referred pain signifies penetration into the pancreases.
Non-radiating, burning in quality, and located in the epigastrium.
Nausea.
Bloating.
Weight loss.
Stool positive for occult blood, and anemia.

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Clinical Manifestations

Duodenal ulcer pain Gastric ulcer pain


Periodical Periodical
Occur 2-3 hour after the meal. Occurs with the meal
Awaken patients from sleep  Pain not felt at night
 Esp. b/12 AM and 3 AM Food aggravates pain.
Food relieves food. Pain not felt empty stomach
Felt empty stomach ‘Hunger-Pain’

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Diagnosis of PUD

History Laboratory
Dyspepsia/epigastric pain. CBC
History of PUD, baseline serum gastrin level is
Use of NSAIDs, appropriate to rule out gastrinoma
OTC antacids, or anti-secretory drugs H.P Test
Upper endoscopy
Double-contrast

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Medical treatment

Treatment Plan: H. Pylori Treatment Plan: Not H. Pylori


Eradication Therapy:- H2 Antagonist:-
Triple therapy for 14 days  Ranitidine 150mg po BID
In the setting of an active ulcer add  Cimetidine 400mg po BID for up to 8
for more 2 weeks of PPI weeks
Goal: complete elimination of H. PPI for 4 weeks
Pylori.
Life style change
Alcohol
smoking
NSAIDs
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Cont..

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Surgical Treatment of PUD
Refractory ulcers
Hemorrhage not responding to endoscopic treatment
Gastric outlet obstruction
Perforation
Suspicious of Malignancy

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Goal of surgical therapy

To reduce gastric acid secretion via:-


Vagotomy
Vagotomy decreases peak acid output by approximately
50%
Antrectomy
Vagotomy plus antrectomy decreases > 85%
To remove risk of malignancy

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Surgical options
VAGOTOMY
 Truncal vagotomy and drainage
 Truncal vagotomy and antrectomy
 Selective vagotomy
 Highly selective
GASTRECTOMY
 Billroth I
 Billroth II
 Subtotal gastrectomy
GRAHAM’S OMENTAL PATCH
SUTURE LIGATION OF GASTRODUODENAL ARTERY
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Surgical options depends on
Type of ulcer(duodenal,gastric,recurrent,marginal)
Condition of the patient
Surgeons experience
Intra-abdominal condition(duodenal scarring/inflammation, adhesions, or difficult
exposure)

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Truncal vagotomy and drainage
The advantage of V + D is that it can be performed safely and quickly
The main disadvantages are the side effect profile
During truncal vagotomy care must be taken not to perforate the esophagus, a
potentially lethal complication.
V + D is widely accepted as a successful definitive operation for complicated
PUD.
Truncal vagotomy denervates the antro-pyloric mechanism

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Drainage

Pyloroplasty
patients who require a
pyloroduodenotomy to deal with the ulcer
complication.
when gastro-jejunostomy is technically
difficult
 types:-
Heineke-Mikulicz:- most commonly
performed
Finney’s and Jaboulay

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Drainage

Gastrojejunostomy
Usually for:-
 GOO
 Severely diseased proximal duodenum.
B/n the proximal jejunum and the most
dependent portion of the greater curvature.
antecolic or retro-colic fashion
Marginal ulceration is a potential complication.

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Selective vagotomy
Vagotomy with sparing the hepatic and • photo
coeliac divisions.
Drainage procedure is also performed
Time consuming and it has being
abandoned
Recurrence rate is 10%

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Highly selective vagotomy
Denervates the proximal 2/3 of the
stomach
preserves inervation to the antrum and
pylorus and the remaining abdominal
viscera
Decreases total gastric acid secretion by
about 75%.
GI side effects are rare.
HSV has largely been supplanted by
long-term PPI treatment

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Vagotomy and antrectomy(V + A)
is associated with a very low ulcer
recurrence rate(<2%)
has a higher operative mortality risk.
Usually for GU
Following antrectomy, GI continuity
may be reestablished with
Billroth I
Billroth II

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CONT..

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Surgical treatment of GU.
• Distal gastrectomy without vagotomy:-
 Usually about a 50% gastrectomy to
include the ulcer
 Has been the procedure of choice for type
I GU.
The addition of vagotomy should be
considered for type II and III GU
Reconstruction done with:-
Billroth I
Billroth II


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Surgical treatment of GU.

Type IV gastric ulcers:- may be


difficult.
procedures used are:-
excision
Sub-total with roux-en-Y reconstructio
Csendes procedure
Pauchet procedure
Kelling-madlener procedure

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Complications of PUD
bleeding
Perforation
Obstruction
Intractability

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Bleeding Peptic Ulcer
Most common complication of PUD.
The most common cause of upper GI bleeding
present with melena and/or hematemesis
NG tube aspirate Is diagnostic
Abdominal pain is quite uncommon
Shock could be the presentation

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Initial approach
Secure airway Early endoscopy
Large IV lines CBC
Crystalloid intravenous fluids PT, PTT, ANR
Transfusion if Hg is <=10g/dl correction of coagulopathy
Keep NPO
NG-tube
 high dose IV PPI
80-mg bolus dose
contineous infusion at 8 mg/hr

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Bleeding Peptic Ulcer
75% of patients will stop bleeding with only supportive measures
 25% will continue to bleed or will re-bleed in hospital
 It is important to identify this high-risk group early by:-
Clinical factors
Endoscopic factors
Two risk scoring systems
Blatchford
rockall

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Surgery indication for bleeding PUD
massive hemorrhage unresponsive to endoscopic control
Transfusion requirement of more than 4-6units of blood, despite attempts at
endoscopic control.
Lack of availability of a therapeutic endoscopist,
Re-bleeding after one or more attempts at endoscopic control,
lack of availability of blood for transfusion
Repeat hospitalization for bleeding ulcer
Concurrent indications for surgery such as perforation or obstruction

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Indications for early elective
Patients with massive bleeding from high-risk lesions.
patients more than 60 years of age,
Shock at presentation.
 Requiring > 4 units of blood in 24hrs or 8 units of blood in 48 hrs.
Those with ulcers >2 cm in diameter.

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Operation for Bleeding duodenal Ulcer
vagotomy and anterectomy
Over sewing without vagotomy.
most commonly used for bleeding Less commonly performed
duodenal ulcer. Low re-bleeding rate
 higher re-bleeding rate Never in unstable patients
lower operative mortality rate
Un-stable patients
• VAGOTOMY AND
Those with high operative risk.
DRAINAGE

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Operation for Bleeding duodenal Ulcer
Initial pyloromyotomy incision allows
access to the bleeding posterior duodenal
ulcer
Heavy suture material
figure-of-eight sutures or U-stitch to secure
the bleeding vessel at the base of the
posterior duodenal ulcer.
Multiple sutures are usually necessary

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Operation for Bleeding duodenal Ulcer

Once the hemostasis is secure,


Pyloroplasty can be performed.
If the patient is stable, vagotomy may be considered(V+D)
If the patient is not a high operative risk and V + A is selected

the duodenum decompression:-


 lateral duodenostomy
 retrograde tube via the proximal jejunum
 NGT secured with tip well into afferent limb.

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Operation for Bleeding gastric Ulcer
Distal gastric resection to include the bleeding ulcer is the procedure of choice
for bleeding gastric ulcer.
Second best is V + D with over sewing and biopsy of the ulcer to rule out cancer.
Over sewing of the bleeder followed by long-term acid

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Perforated PUD

Second most common complication of peptic ulcer


More common indication for operation than bleeding
Sudden onset of the excruciating abdominal pain
Previous Hx of PUD
Phases of peritonitis:-
Chemical peritonitis develops from the gastric and/or duodenal secretions
Bacterial peritonitis supervenes within hour

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Perforated PUD

Clinical examination
Deranged V/S
Marked involuntary guarding
Rebound tenderness
Upright chest X-ray:-
 Free air under diaphram
 80% of patients

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Management approach

Keep NPO
Resuscitation with isotonic fluids
NG-tube
CBC
Antibiotic
Take to OR

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Management approach
• The options for surgical treatment of perforated duodenal ulcer are :-
 simple patch closure
 patch closure and HSV
 patch closure and V + D.

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Management approach
Simple patch closure currently the most commonly performed
 Should be done in patients with
 Hemodynamic instability
 Exudative peritonitis signifying a perforation >24 hours old
 Vagotomy procedures are omitted this days even in stable patients
because of the availability of PPIs

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Surgery
Supra-umblical incision
1st portion of duodenum
Those <1 cm can generally be closed primarily
buttressed with well vascularized omentum.

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Surgery
Larger perforations :-Graham patch repair with a tongue of healthy omentum
is performed.
Stay sutures are placed that incorporate a bite of healthy tissue on the proximal
and the distal side of the ulcer.
The omentum is placed underneath these sutures

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Surgery
Very large perforations (>3 cm)
Primary closure is difficult
The defect should be closed by the application of healthy tissue(omentum)
Bypass the duodenum (Billroth II or Roux-en-Y fashion)
Several weeks, the pyloric exclusion stitches or staples give way

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Post OP care

Keep NG-tube until bowel activity returns


Drains should be kept in place until patients have eaten without a change in
drain output or quality
A routine contrast radiograph
H. pylori–positive patients should undergo eradication with appropriate triple-
therapy
Long term PPI if simple patch only.

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Gastric outlet obstruction
5% of patients with PUD
 due to duodenal or pre-pyloric ulcer disease.
may be acute or chronic
Significant obstruction from chronic ulceration will require some sort of more
substantial intervention
balloon dilatation
surgery

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Clinical features
Non-bilious vomiting
hypokalemic hypo-chloremic metabolic alkalosis
Pain
Weight loss
Suction splash

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Management
Initial treatment is NGT suction,
IV hydration and electrolyte repletion,
acid suppression.
The diagnosis is confirmed by endoscopy.
Either balloon dilation or operation.
Cancer must be ruled out because most patients who present with the symptoms
of GOO will have a pancreatic, gastric, or duodenal malignancy

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Management
The standard operation for obstructing PUD is vagotomy and antrectomy.
Alternatively vagotomy and gastro-jejunostomy
should be considered if a difficult duodenal stump is anticipated with resection.
HSV and gastro-jejunostomy may be comparable to V+A for obstructing ulcer
disease
However, potentially curable gastric or duodenal cancers can be missed with this
approach

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Intractable or Non-healing Peptic Ulcer
Intractability should be an unusual indication for peptic ulcer operation
nowadays.
The patient referred for surgical evaluation because of intractable PUD should
raise red flags for the surgeon:
 Maybe the patient has a missed cancer;
 maybe the patient is noncompliant
 maybe the patient has H.P despite the presence of a negative test or previous
treatment.

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Complications
Gastric stasis
Diarrhea
dumping syndrome
Anemia
Bile Reflux Gastritis and Esophagitis
Weight loss
Bone disease

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Reference

Schwartz principles of surgery 2020


Maingot’s Abdominal operations 13th ed
Sabiston textbook of surgery , 19th ed
Henok T. et al.perforated peptic ulcer disease in a teretiary hospital, A.A ,Ethiopia :
five year retrospective study .Ethiop J health sci. 2020 May : 30(3): 363-370

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• THANK YOU !

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