Peptic ulcers form in the stomach or duodenum due to an imbalance between acid secretions and mucosal defenses. Risk factors include H. pylori infection in 90% of cases, NSAID use, and stress. Complications include hemorrhage, perforation, and obstruction. H. pylori survives stomach acid through urease production. Diagnosis involves symptoms and imaging. Treatment depends on complications but usually involves antibiotics to eradicate H. pylori along with acid suppression. Surgery may be needed for perforation or obstruction.

1. PEPTIC ULCER
DISEASE

2. DEFINITION
 The term 'peptic ulcer' generally refers to an
ulcer or erosions in stomach or duodenum.
 It may also occur in the jejunum after surgical
anastomosis to the stomach (Gastrojejunostomy)
or, rarely, in the ileum adjacent to a Meckel's
diverticulum.

3. Peptic Ulcer Disease

4. Risk Factors
 H.pylori infection : 90% of Peptic ulcer patients
are infected with H.pylori.
 NSAIDs
 Stress
 Others :
 Infection : CMV, HSV
 Drugs : Bisphosphonates, Chemotherapy,
Clopidogrel, Crack cocaine, KCl
Glucocorticoids, Mycophenolate Mofetil,
 Misc : Basophilia in Myeloproliferative disease,
Radiation therapy,Infiltrating disease,
Sarcoidosis, Crohn’s disease.
 Life time risk of developing Peptic ulcer is 10%

5. Stomach Defense Systems
 Mucous layer
◦ Coats and lines the stomach
◦ First line of defense
 Bicarbonate
◦ Neutralizes acid
 Prostaglandins
◦ Hormone-like substances that keep blood vessels
dilated for good blood flow
◦ Thought to stimulate mucus and bicarbonate
production

6. H. Pylori
HISTORY
• 1874 : Bircher first described the organism
• 1982 : Warren and Marshall confirmed Koch’s
postulates named it“campylobacter
pyloridis”
• 1985 : Association with peptic ulcer
• 1989 : Named as ‘helicobacter ‘(helico-curved)

7. H. Pylori
• H. pylori inf. is virtually always associated with chronic
active gastritis.
• But only 10–15% develop frank PUD.
• Transmission not yet known. Most likely route is feco-
oral.
• H. pylori is able to fight off the acid with the enzyme
urease.
• Urease converts urea into bicarbonate and ammonia,
which are strong bases.
• These acid neutralizing chemicals around the H. pylori
protect it from the acid in the stomach.

8. General Peptic Ulcer Symptoms
 Epigastric tenderness
◦ Gastric: Epigastrium; left of midline
◦ Duodenal: mid to right of Epigastrium
 Sharp, burning, aching, gnawing pain
 Dyspepsia (indigestion)
 Nausea/vomiting
 Belching

9. Differentiating gastric from peptic
ulcer disease
 Duodenal ulcers - age 25-75 years.
 Gastric ulcer - age 55-65 years
 Pain awakening patient from sleep between
12-3 a.m. present in 2/3 duodenal ulcer
patients and 1/3 gastric ulcer patients

10. Complications of Peptic Ulcers
 Hemorrhage
◦ Blood vessels damaged as ulcer erodes into the muscles of
stomach or duodenal wall
◦ Coffee ground vomitus or occult blood in tarry stools
 Perforation
◦ An ulcer can erode through the entire wall
◦ Bacteria and partially digested food spill into
peritoneum=peritonitis
 Narrowing and obstruction (pyloric)
◦ Swelling and scarring can cause obstruction of food leaving
stomach=repeated vomiting

11. HEMORRHAGE
 Upper GI bleeding is the most common
complication.
 Sudden large bleeding can be life-threatening.
 It occurs when the ulcer erodes one of the blood
vessels, such as the gastro duodenal artery.
 With massive bleeding the patient vomits bright
red or coffee ground blood. Minimal bleeding
from ulcers is manifested by occult blood in a
tarry stool (malena).

12.  Bleeding can occur as slow blood loss that
leads to anemia or as severe blood loss that
may require hospitalization or a blood
transfusion.
 Occurs in about 15% cases.
 More common in Elderly (>60 yrs)

13. OBSTRUCTION
 Gastric outlet obstruction - scarring and
swelling due to ulcers causes pyloric
narrowing. Patient often presents with severe
vomiting.
 Peptic ulcers can also produce scar tissue that
can obstruct passage of food through the
digestive tract, causing pt to become full
easily, to vomit and to lose weight.

14. Clinical feature & management
 Long history of DU
 Persistent vomiting
- Large & projectile
- Contain previous food elements
 Epigastric fullness, visible peristalsis and
succussion splash
 Dehydration & electrolyte disturbances
 Metabolic alkalosis and tetany.
 Wasting & malnutrition.

15. Treatment
 Correct fluid & electrolytes disturbance and
improve nutrition
 Treatment options include balloon dilation and
stenting, but surgery with drainage procedure is
usually required.

16. PERFORATION
 Perforation often leads to catastrophic
consequences.
 Erosion of the gastro-intestinal wall by the ulcer
leads to spillage of stomach or intestinal
content into the abdominal cavity.
 Perforation at the anterior surface of the
stomach leads to acute peritonitis, initially
chemical and later bacterial peritonitis. The first
sign is often sudden intense abdominal pain.
 Posterior wall perforation leads to pancreatitis;
pain in this situation often radiates to the back.
 Perforation in the CBD- aerobilia, cholangitis

17. Perforated peptic ulcer
 The first report of a series of patients
presenting with perforation of a duodenal
ulcer was made in 1817 by Travers.
 The earliest operative description was made by
Mikulicz in 1884 but the first successful
operation for a perforated duodenal ulcer was
not until 1894.

18.  Helicobacter pylori is implicated in 70–92% of all
Perforated Peptic Ulcers.
 The second most common cause of perforated
duodenal ulcer is the ingestion of NSAIDs.
 The least common cause is pathologic
hypersecretory states, such as Zollinger-Ellison
syndrome, although these should be considered
in all cases of recurrent ulcer after adequate
treatment.

19.  Overall incidence for admission with peptic
ulceration is falling.
 The number of perforated ulcers remains
unchanged.
 Sustained incidence possibly due to increased
NSAIDs in elderly.
 80% of perforated duodenal ulcers are H.
pylori positive.
 Men are much more affected than women.
 Ratio is approximately 12 : 1 to 20 : 1.

20. PATHOLOGY
 Acute Perforation
◦ Stage of Peritonism
 Acid peptic juice, bile and pancreatic juice come in
contact with general peritoneal cavity.
 Pt cries out in severe pain during this stage.
◦ Stage of Reaction
 Peritoneum reacts to the chemical insult by secreting
peritoneal fluid copiously(Sterile).
 This gives relief to the pain and lasts for 3-6 hrs.
◦ Stage of Peritonitis
 Acid secretion is abolished once perforation occurs.
 Since there is no acid barrier, bacterial invasion
becomes easy
 There is diffuse bacterial peritonitis.

21. DIAGNOSIS
 The most characteristic symptom is the
sudden onset of Epigastric pain.
 The pain rapidly becomes generalized
although occasionally it moves to the Rt Iliac
Fossa (Through Paracolic gutters).
 The patient stays still.

22.  There may be a history of previous
dyspepsia, previous or current treatment for
a Peptic Ulcer, or ingestion of NSAIDs.
 On examination the patient is in obvious
pain.
 The abdominal findings are characteristically
described as of board-like rigidity.

23.  With time the patient may improve with
dilution of the duodenal contents by exudates
from the peritoneum but this is later replaced
by the signs and symptoms of bacterial
peritonitis.
 Once an ulcer perforates, the subsequent
clinical picture is influenced by whether or
not the ulcer self seals.

25. INVESTIGATIONS
 Plain x-rays of the abdomen with the patient in
the upright position have been used in
diagnosing perforated ulcer. Chest X-ray
standing reveals free air under diaphragm.
 Similarly, use of water-soluble contrast medium
with an upper gastrointestinal tract series or
computed tomography scan may increase the
diagnostic yield.

26. COMPLICATIONS
 In most cases of perforation, gastric and
duodenal content leaks into the peritoneum.
 This content includes gastric and duodenal
secretions, bile, ingested food, and swallowed
bacteria.
 The leakage results in peritonitis, with an
increased risk of infection and abscess formation.
 Subsequent collection of fluid in the peritoneal
cavity due to perforation and peritonitis leads to
inadequate circulatory volume, hypotension, and
decreased urine output.

27.  Abdominal distension as a result of peritonitis
and subsequent ileus may interfere with
diaphragmatic movement, impairing expansion
of the lung bases.
 Eventually, atelectasis develops, which may
compromise oxygenation of the
blood, particularly in patients with coexisting
lung disease.
 In more severe cases, shock may develop.

28. Treatment Options
 Principles of initial conservative treatment
include
nasogastric suction
pain control
antiulcer medication
Antibiotics
 Several surgical techniques have been employed
in the treatment of perforated peptic ulcer.
These include conservative surgery with patching of the
ulcer, peritoneal lavage, and antiulcer medication.
Definitive surgery with truncal vagotomy, highly selective
vagotomy, or partial gastrectomy.

29. Non surgical treatment
 In 1935 Wangensteen noted that ulcers are
able to self seal and reported on seven cases
treated without surgery.
 In 1946 this observation was confirmed by
Taylor and he treated 28 cases without surgery
with good success.
 This was in the context of the high mortality
and morbidity associated with surgical
management at the time.

30.  In 1989 a trial from Hong Kong by Crofts et al.
showed that non-operative treatment for PPU
was accompanied by a low mortality rate and
was not associated with a large number of
complications when the gastroduodenogram
documented a sealed perforation .

31. In a tertiary care GI centre,
 When the diagnosis of a perforated duodenal ulcer is
established the patient is aggressively
resuscitated, nasogastric suction begun, and broad
spectrum antibiotic cover instituted.
 If a tension pneumoperitoneum embarrasses
respiration this can be aspirated to release the
pneumoperitoneum.
 A gastroduodenogram is performed to confirm self-
sealing.
 The peritonitis should resolve in 4 to 6 hours and if
there is continued major fluid loss after this time or if
there are progressive signs of peritonitis or increasing
pneumoperitoneum then surgical intervention is
required

32. Laparoscopic Surgery
 The traditional management of a perforated
duodenal ulcer has been a Graham Omental
Patch and a thorough abdominal lavage.
 More recently this has been shown to be able
to performed using a laparoscope. The only
proven advantage of the laparoscopic
technique appears to be decreased
postoperative pain.
 Operating times are longer compared to open
techniques and hospital time appears to be
similar to conventional treatment.

33. Definitive surgery
 There is good evidence that, in the emergency
situation, highly selective vagotomy (proximal
gastric, or parietal cell vagotomy) combined with
simple omental patch closure of the
perforation, in patients without the risk factors
mentioned above, is just as effective as that
performed in the elective setting .
 This is associated with a less than 1% mortality
rate and a 4–11% ulcer recurrence rate. The
success of this operation is surgeon-dependent.

34.  There has been a return to the use of simple
omental patch closure since the late 1970's
with the introduction of post-operative H2
antagonists and more recently Proton Pump
Blockers.
 Over the last 10 years this trend has only grown
stronger due to the discovery of the role of H.
pylori in the pathogenesis of duodenal ulcer.

35.  Given that H. pylori is able to be implicated in
up to 90% of perforated duodenal ulcers it
would seem logical to utilize patch closure and
subsequent antibiotic treatment of the
infectious agent saving definitive surgical ulcer
management for those who fail this regimen.

36. Anti H. pylori regimen
 Omeprazole (Lanzoprazole) 20 mg BD
 Clarithromycin 250 mg BD
 Metronidazole 500 mg BD / Amoxycillin 1g BD
OR
 Omeprazole 20 mg BD
 Bismuth Subsalicylate 2 tab QID
 Metronidazole 250 mg QID
 Tetracycline 500 mg QID

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