This document discusses peptic ulcer disease, focusing on duodenal ulcers. It defines peptic ulcers and describes the pathogenesis, including protective and damaging factors. Helicobacter pylori infection plays a major role in ulcer development and the mechanisms by which it causes injury are explained. Diagnosis involves endoscopy, biopsy and testing for H. pylori. Treatment involves eradicating H. pylori with antibiotics and proton pump inhibitors. Complications of duodenal ulcers like bleeding and perforation are discussed. Bleeding ulcers are classified by the Forrest system and managed initially with endoscopic methods or surgery depending on severity. Perforated ulcers require surgical repair.

1. PEPTIC ULCER DISEASE
Dr. Lala Robin. MS Gen. Surgery.
Senior Resident
CMC

2. Definition
 Peptic ulcers are defined as erosions in the gastric or duodenal mucosa that extend
through the muscularis mucosae.
 Benign Gastric Ulcer
 Duodenal Ulcer

3. Pathogenesis
Protective (or defensive) factors
 mucosal bicarbonate secretion,
 mucus production,
 blood flow,
 growth factors,
 cell renewal,
 endogenous prostaglandins

4. Damaging (or aggressive) factors
 hydrochloric acid secretion,
 pepsins,
 ethanol ingestion, smoking,
 duodenal reflux of bile,
 ischemia, hypoxia,
 H. pylori infection.
 NSAIDs.

5. Helicobacter pylori Infection
 H. pylori is a spiral or helical gram-negative rod with four to six flagella that resides
in gastric-type epithelium within or beneath the mucous layer. This location
protects the bacteria from acid and antibiotics. Its shape and flagella aid its
movement through the mucous layer, and it produces enzymes that help it adapt
to this hostile environment.
 Most notably, H. pylori is a potent producer of urease, which is capable of splitting
urea into ammonia and bicarbonate, creating an alkaline microenvironment in the
setting of an acidic gastric milieu.
 H. pylori organisms are microaerophilic and can live only in gastric epithelium.

6. mechanisms responsible for H. pylori–
induced GI injury
 Production of toxic products that cause local tissue injury - Infection with H. pylori
leads to the disruption of the gastric mucous barrier by the enzymes produced by
the organism.
 Induction of a local mucosal immune response.
 Increased gastrin levels with a resultant increase in acid secretion.
 Gastric metaplasia occurring in the duodenum  protective response to decreased
duodenal pH  allows H. pylori to colonize these areas of the duodenum
 Some strains of H. pylori produce cytotoxins, notably the Cag A and Vac A
products, and the production of cytotoxins seems to be associated with the ability
of the organism to cause gastritis, peptic ulceration and cancer.

7.  The causative role of H. pylori infection in the pathogenesis of gastritis and PUD
was first elucidated by Marshall and Warren in Australia in 1984.
 To prove this connection, Marshall himself ingested inocula of H. pylori after first
confirming that he had normal gross and microscopic gastric mucosa. Within days,
he developed abdominal pain, nausea, and halitosis as well as histologically
confirmed presence of gastric H. pylori infection.
 Warren and Marshall, received the Nobel Prize for Medicine and Physiology in
2005.
 H. pylori is now classed by the World Health Organisation as a class 1 carcinogen

8. RUT kit  done in antral biopsy
• 13 C and 14 C breath tests and the CLO test
• Giemsa or the Warthin– Starry stains, and culture

9. H. Pylori Eradication
 PPI + Clarithromycin + Amoxicillin
 PPI + Clarithromycin + Metronidazole
 Duration – 14 days.
 PPI to be continued.
 Ulcer healing to be checked after 8-12 weeks with endoscopy. Then PPI can be
stopped.
 The profound hypochlorhydria produced by proton pump inhibitors combined with
antibiotics is also effective in eradicating the organism.

10. NONSTEROIDAL ANTIINFLAMMATORY
DRUGS AND ULCER DISEASE
 NSAIDs increase the risk of peptic ulcers.
 NSAIDs are the most commonly identified risk factor for peptic ulcer bleeding,
especially in older adults; the risk is drug specific and dose dependent.
 NSAIDs decrease the mucosal defense by suppression of prostaglandin synthesis in
gastric and duodenal mucosa
 Acid suppression is the mainstay in the therapy of NSAID-associated ulcer disease.

11. LOW-DOSE ASPIRIN AND ULCER DISEASE
 Even at very low doses (75 mg daily), aspirin decreases gastric mucosal
prostaglandin levels and can cause significant gastric lesions.
 PPI given with low-dose aspirin, can significantly decrease the risk of developing
peptic ulceration

12. ACID HYPERSECRETORY STATES AND
ULCER DISEASE
 Zollinger-Ellison (ZE) syndrome – gastrinoma
 Anastomotic or Marginal Ulceration

13. SEVERE SYSTEMIC DISEASE (STRESS
ULCER)
 A breakdown of the gastroduodenal
mucosal barrier, often a result of severe
physiologic stress and splanchnic
hypoperfusion, combined with gastric
acid may lead to ulceration and
bleeding.
 It can develop within hours in critically
ill patients, typically starting in the
fundus and spreading distally.
 Head Injury  Cushing ulcer
 Extensive burns  Curling ulcer

14. Duodenal ulceration

15. Incidence
 Incidence has come down drastically due to wide spread use of gastric
antisecretory agents and H. pylori eradication therapy
 peak incidence is now in a much older age group than previously
 more common in men

16. Pathology
 Most occur in the first part of the duodenum
 A chronic ulcer penetrates the mucosa and into the muscle coat, leading to fibrosis
 pyloric stenosis
 kissing ulcers - a posterior and an anterior duodenal ulcer
 Anteriorly placed ulcers tend to perforate
 posterior duodenal ulcers tend to bleed, sometimes by eroding into the
gastroduodenal artery.

17. Histopathology
 destruction of the muscular coat is observed
 base of the ulcer is covered with granulation tissue,
 the arteries in this region showing the typical changes of endarteritis obliterans

18. Clinical Manifestations
 midepigastric abdominal pain
 relieved by food intake
 When the pain becomes constant, this suggests that there is deeper penetration of
the ulcer.
 Referral of pain to the back is usually a sign of penetration into the pancreas.
 Diffuse peritoneal irritation is usually a sign of free perforation

19. Diagnosis
 Routine laboratory studies include complete blood count; liver chemistries; and
serum creatinine, serum amylase, and calcium levels.
 A serum gastrin level should also be obtained in patients with ulcers that are
refractory to medical therapy or require surgery.
 An upright chest radiograph is usually performed when ruling out perforation.

20. Upper gastrointestinal radiography
 demonstration of barium within the ulcer crater,
which is usually round or oval and may or may not
be surrounded by edema
 with double-contrast studies, 80% to 90% of ulcer
craters can be detected

21. Flexible upper endoscopy
 most reliable method for diagnosing gastric and
duodenal ulcers.
 visual diagnosis
 endoscopy provides the ability to sample tissue to
evaluate for malignancy and H. pylori infection
Duodenal Ulcer
Benign Healing Gastric Ulcer

22. Helicobacter pylori testing
 The gold standard for diagnosis of H. pylori is mucosal biopsy performed
during upper endoscopy
 evaluation of biopsy samples with either a urease assay or histologic
examination
 Culturing of gastric mucosa obtained at endoscopy
 can also be performed to diagnose H. pylori. The sensitivity is approximately
80%, and specificity is 100%

23. H. Pylori – Non-invasive testing
 Serology
 used to test for the presence of IgG antibodies to H. pylori
 Antibody titers can remain high for 1 year or longer; consequently, this test cannot
be used to assess eradication after therapy
 Urea breath test
 The carbon-labeled urea breath test is based on the ability of H. pylori to hydrolyze
urea as a result of its production of urease
 Stool antigen
 H. pylori bacteria are present in the stool of infected patients

24. Treatment
 Medical management
 Antiulcer drugs fall into three broad categories—
1. drugs targeted against H. pylori,
2. drugs that reduce acid levels by decreasing secretion or chemical neutralization,
and
3. drugs that increase the mucosal protective barrier.

25. Surgical Treatment Recommendations for
Complications Related to Peptic Duodenal Ulcer
Disease
 Intractable: Parietal cell vagotomy ± antrectomy
 Bleeding: Oversewing of bleeding vessel with treatment of H. pylori
 Perforation: Patch closure with treatment of H. pylori
 Obstruction: Rule out malignancy and gastrojejunostomy with treatment of H. pylori

26. Bleeding Duodenal Ulcer
 Upper GI bleeding
 Most nonvariceal bleeding (70%) is attributable to peptic ulcers
 The initial approach to an upper GI bleed is similar to the approach to a trauma
patient. Large-bore intravenous access, rapid restoration of intravascular volume
with fluid and blood products as the clinical situation dictates, and close
monitoring for signs of rebleeding all are essential to effective management of
these patients.
 NG tube placement
 all patients with a potentially substantial acute upper GI bleed should undergo
endoscopy within 24 hours

27. Bleeding
Duodenal Ulcer
• The most commonly
used system for
classifying the
endoscopic
appearance of
bleeding ulcers is the
Forrest classification

28. Bleeding Duodenal Ulcer
 All patients undergoing endoscopic examination should be tested for H. pylori
status.
 For high-risk patients requiring intervention, the best initial approach is endoscopic
control, which results in primary hemostasis in approximately 90% of patients. The
most common method of control is injection of a vasoconstrictor at the site of
bleeding.
 Thermocoagulation, clipping
 All high-risk patients should be placed in a monitored setting, preferably an
intensive care unit, until all bleeding has stopped for 24 hours.
 all highrisk patients should be placed on a PPI administered intravenously, with an
initial bolus followed by continuous infusion or intermittent dosing for up to 72
hours.
 catheter-directed angiography and endovascular embolization

29. Bleeding Duodenal Ulcer - Surgery
 upper midline laparotomy
 anterior wall of the duodenal bulb is opened
longitudinally, and the incision can be carried
across the pylorus.
 The gastroduodenal artery is oversewn, with a
three-point U stitch technique, which effectively
ligates the main vessel (superior and inferior
stitches) and prevents back-bleeding from any
smaller branches (medial stitch), such as the
transverse pancreatic artery
 duodenotomy is closed transversely to avoid
narrowing

30. Duodenal Ulcer Perforation
 sudden-onset, severe epigastric pain
 free air visible on the chest radiograph
 diffuse peritonitis
 first portion of the duodenum

31. Duodenal Ulcer Perforation - management
 Resuscitation
 NG tube placement
 Laparotomy
 The most important component of
the operation is a thorough
peritoneal toilet to remove all of the
fluid and food debris.
 place an omental patch over the
perforation
 For very large perforations (>3 cm) -
jejunal serosa (Thal patch), pyloric
exclusion procedure

32. Gastric outlet obstruction
 Acute inflammation of the duodenum  functional gastric outlet obstruction 
delayed gastric emptying, anorexia, nausea, and vomiting  patients may become
dehydrated and develop a hypochloremic hypokalemic metabolic alkalosis
secondary to the loss of gastric juice rich in hydrogen and chloride
 Chronic inflammation of the duodenum fibrosis and stenosis of the duodenal
lumen  painless vomiting of large volumes of gastric contents, with metabolic
abnormalities
 Endoscopic dilation and H. pylori eradication are the mainstays of therapy
 Patients with refractory obstruction are best managed with primary antrectomy and
reconstruction along with vagotomy.

33. Intractable peptic ulcer disease
 failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy or if
patients relapse after therapy has been discontinued.
 rule out gastrinoma
 truncal vagotomy, selective vagotomy, or highly selective vagotomy, with or
without an antrectomy.

35. Surgical procedures for peptic ulcers
Truncal Vagotomy

36. Selective Vagotomy

37. Parietal Cell Vagotomy

38. Gastric Ulcers
 Gastric ulcers can occur at any location in the stomach, although they usually
manifest on the lesser curvature, near the incisura.
 Modified Johnson Classification

40.  H. pylori and NSAIDs are the important aetiological factors.
 Gastric ulceration is also associated with smoking
 Chronic gastric ulcers are much more common on the lesser curve (especially at the
incisura angularis)
 Large chronic ulcers may erode posteriorly into the pancreas and, on other
occasions, into major vessels such as the splenic artery. Less commonly, they may
erode into other organs such as the transverse colon

41. Malignancy in gastric ulcers
 any gastric ulcer should be regarded as being malignant, no matter how classical
the features of a benign gastric ulcer. Multiple biopsies should always be taken

45. Thank you