Surgical management of
peptic ulcer disease (PUD)
Dr Olayinka Lukman Adewunmi
Division of General Surgery
UMTH
6th June, 2022

Outline
• Introduction
• Epidemiology
• Surgical anatomy
• Aetiology/risk factor
• Pathophysiology of PUD
• Classification of PUD
• Surgical complications of PUD
• Clinical features
• Investigations
• Treatments
• Prognosis
• Conclusion/summary
• References
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Introduction
• Peptic ulcer is defined as defects in the mucosa of the stomach or
duodenum that extend into the muscularis mucosa
• Peptic ulcer occur following imbalance between the mucosa defense
and acid/peptic injury
• It may be acute or chronic ulceration
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Introduction
Aggressive factors
• NSAID
• H. pylori infection
• Alcoholism
• Bile salts
• Acid
• pepsin
Defensive factors
• Tight intercellular junction
• Mucus
• Bicarbonate
• Mucosa blood flow
• Cellular restitution
• Epithelial renewal
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Introduction
• PUD is the most common GI disorder in the US with a prevalence of
2% and life time cumulative prevalence of 10%
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Relevant anatomy
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Relevant anatomy
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Relevant anatomy
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Aetiology
• Helicobacter pylori infection
• Drugs e.g. NSAID
• Severe physiological stress- curling's ulcer, Cushing's ulcer
• Lifestyle factors/changes e.g. smoking
• Hyper-secretory states- ZES, G-cell hyperplasia, etc.
• Genetic factors
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Pathophysiology
• H. pylori is a gram negative spirochete, urease producing organism,
flagellated,
• The urease split urea into carbon dioxide and ammonia, creating a
alkaline environment around itself and protecting from acidity of the
stomach
• This further stimulate acid production by the parietal cells and
associated parietal cell hyperplasia.
• With increase acid secretion, more acid is released into the
duodenum and duodenal mucosa undergo metaplastic change to
gastric mucosa
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Pathophysiology
• H. pylori infection of the metaplastic cell leads to acid secretion by
duodenal mucosa, distorting the bicarbonate producing cell of the
duodenum. The bicarbonate secretion reduce significantly
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Pathophysiology
• Other pathophysiological mechanisms
production of toxins- vacA and cagA
local elaboration of cytokines (IL-8) by infected mucosa
recruitments of inflammatory cells and release of inflammatory
mediators
recruitments and activation of local immune factors
increased apoptosis
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Classification of PUD
• Modified Johnson classifications
Type 1- ulcer at angularis incisura
Type 2- ulcer at angularis incisura
+ duodenal ulcer
Type 3- prepyloric ulcer
Type 4- ulcer at the OG junction
Type 5- NSAID-induced ulcer
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Clinical features
Gastric ulcer
• Epigastric pain
• Worse with peppery meal
• Relieved by vomiting or hunger
• Normal weight or slight weight
loss
• Middle age to elderly
Duodenal ulcer
• Epigastric pain relieved by eating
• Patient may gain weight
• Young and middle age
• Periodicity
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Investigations
• Endoscopy
ulcer and location
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Investigations
• Test for Helicobacter pylori
• Non invasive Invasive/Biopsy
Urea breath test Histology
Immunologic/blood test culture
fecal antigen test Urea test
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Treatment
• Medical therapy
PPI + clarithromycin + amoxicillin
PPI + amoxicillin + metronidazole
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Surgical complications and management
• Bleeding
• Perforation
• Obstruction (Gastric Outlet Obstruction)
• Malignancy
• Refractory ulcer (Intractability)
NSAID-induced
Zollinger-Ellison syndrome/Gastrinoma
ulcer at the OG junction
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Bleeding
• Clinical features
hematemesis/upper GI bleeding
malaena in slow/occult bleeding
gastric ulcer- erosion into the left gastric aa
duodenal ulcer- erosion into gastroduodenal artery
medical emergency
lower GI bleeding in massive upper GI bleeding (rare)
rule out differentials- varices, GAVE, esophagitis, etc.
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Bleeding
• Management- Resuscitation
IV access (wide bore cannula)
IV fluid (crystalloids)
Urethral catheter (monitor urine output)
NG tube (controversial)
prophylactic antibiotics
IV proton-pump inhibitors- 80mg stat, then 8mg/hr for 72hrs
urgent PCV, GXM of 3-4pint, clotting profile
• Endoscopy
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Bleeding- endoscopy
FORREST CLASSIFICATION Re-bleeding
Type 1 Signs of active bleeding 80-100%
a spurting 90-100%
b oozing 80-85%
Type 2 Signs of recent bleeding 10-50%
a Non-bleeding visible vessel 40-50%
b Adherent clot on lesion 20-30%
c Hematin/pigmented-covered lesion 5%
Type 3 Lesion without bleeding <3%
Flat spot, clean ulcer base
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Bleeding- endoscopy
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Bleeding
• Scoring systems
Rockall scores- 0-11
Blatchford score- 0-23
AIMS65 score
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Bleeding- Rockall scores
SCORES
Variables 0 1 2 3
Age <60 60-79 >80
Blood pressure Normal Pulse >100
BP > 100
Pulse >100
BP <100
Co-morbidity None CCF, IHD Renal failure, Liver
failure
Diagnosis on
endoscopy
Mallory-Weiss tear,
no lesion, no SRH
All other diagnosis Malignancy of the
upper GI tract
Endoscopy findings None or dark spots Spurting or visible
vessels, adherent
clot
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Bleeding
• Endoscopic management
Thermal method: contact vs non contact
contact- heater probes, bipolar diathermy
non contact- argon plasma coagulation, laser therapy
non-thermal method
mechanical clips
epinephrine: 4-16mls of 1:10,000
sclerotherapy- Na tetradecyl sulphate, polidocanol,
ethanolamine
hemostatic sprays/powder
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Bleeding
• Re-bleeding
Re-endoscopy + any above treatment
• Indications for surgery
re-bleeding
hemorrhagic shock
blood transfusion of >4 pint of blood
failed/absent endoscopic therapy
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Bleeding- Surgical option
• Duodenal ulcer
over sew + vagotomy +
drainage (V + D)
vagotomy + antrectomy
• Gastric ulcer
over sew + biopsy + V + D
distal gastrectomy
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• Surgical resection
partial gastrectomy (giant ulcer >2cm)
Pauchet’s proce
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Perforation
• Clinical features
anterior ulcers (duodenum) and angularis incisura (gastric)
chemical peritonitis (initial)
bacteria peritonitis
mimic appendicitis (right) or diverticulitis (left)
patient usually aware of timing
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Perforation
• Management- Resuscitation
IV access
IV fluid
Urethral catheter
NG tube
antibiotics- broad-spectrum
IV proton-pump inhibitors (PPI)- 20-40mg stat dose
urgent PCV, GXM of 1-2 pint of blood
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Perforation
• Conservative management with
spontaneous closure
antibiotics
IV Fluid
analgesics
PPI
NG tube
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Perforation
• Surgery- Laparotomy
• Gastric
wedge excision + closure +
V+D
distal gastrectomy
• Duodenum
Graham patch, V + D
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Obstruction/GOO
• Clinical features
non-bilious vomiting
stale food, but sometimes recent meal
dehydration
malaise
generalized weakness of the body
epigastric mass
weight loss
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Obstruction/GOO
• Management- Resuscitation
IV access (wide bore cannula)
IV fluid (crystalloids)
Urethral catheter (monitor urine output)
NG tube + lavage of the stomach
prophylactic antibiotics
IV proton-pump inhibitors- 20-40mg
urgent PCV, GXM, EUC
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Obstruction/GOO
• Investigations
PCV/CBC
EUC- ↓Na, ↓K, ↓Cl, ↓HCO3 (paradoxical aciduria)
GXM
• Abdominopelvic USS
dilated stomach
pyloric/antral mass/stenosis
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Obstruction/GOO
• Upper GI Endoscopy + biopsy
antral mass/ulcer
biopsy for Histopathology (tumor vs fibrosis)
• Barium meal
absence of endoscopy
dilated stomach with irregular filling defects
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Obstruction/GOO
• CT abdomen
characterized the gastric mass
peri-gastric & para-aortic LN enlargement
liver lesion/metastasis
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Obstruction/GOO
• Treatment
spontaneous resolution in pyloric spasm/edema
• Surgery for those with cicatrizing ulcer/malignant obstruction
cicatrizing PUD- vagotomy + antrectomy, vagotomy + gastro-
jejunostomy
antral cancer- Gastrectomy
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Refractory/Intractable/non-healing ulcer
• Possible reasons?
• non compliant patient
failure to take prescribed
medications
continuous use of NSAIDs
• missed cancer
Gastric, pancreatic,
duodenal
• persistent H/pylori
false negative test
consider empirical
treatment
• Motility disorders
• Zollinger-Ellison syndrome
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Refractory/Intractable/non-healing ulcer
• Lesser operation is preferable
• HSV ± GJ
• Avoid truncal vagotomy or distal
gastrectomy
• Type IV ulcer
Pauchet procedure
Kelling-Madlener proc
Csendes procedure
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Complications of surgery
• Anastomosis leak
• Anastomosis dehiscence
• Surgical site infection
• Intra-abdominal abscess
• Dumping syndrome
Type 1 and Type 2
• Loop obstruction/syndrome
• Bile duct injury
• Benign biliary stricture
• Anaemia (megaloblastic anaemia)
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Prognosis
• Good in benign aetiology
• Poor in malignant aetiology
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Summary
• PUD can be complicated by bleeding, perforation, obstruction,
malignancy and intractability
• Bleeding is usually due to erosion of the gastroduodenal/left gastric
aa and majority resolve spontaneously or endoscopic intervention
• Perforation may close spontaneously but some will require
laparotomy
• Initial conservative approach is recommended in gastric outlet
obstruction for edema/spasm to resolve and those that fail to resolve
will benefit from surgery
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THANK YOU FOR YOUR
ATTENTION
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References
• Charles F. Brunicardi: Schwartz’s principles of Surgery, 10th edition.
Chapters 25, 26 & 28
• Michael J Zinner and Stanley W Ashley: Maingot’s abdominal
operations, 12th edition. Chapters 21, 22, 29 & 30
• O. James Garden and Simon Peterson-Brown: Oesophagogastric
surgery, a companion to specialist surgical practice, 5th edition
Chapters 3, 8, 16 & 19
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