GASTRIC ULCERS

PRESENTED BY: DR. JAWARIA

MEMON & DR. DEEP KUMAR
 OUTLINE
• Introduction
• Pathophysiology
• Etiology/ Risk factors
• Types of PUD
• Clinical Presentation
• Investigation/ Diagnostic test
• Complications of PUD
• Management
• Post-operative complications
 INTRODUCTION
• Peptic Ulcer is a lesion in the lining (mucosa) of the
digestive tract, typically in the stomach or duodenum,
caused by the digestive action of pepsin and stomach acid
and impaired mucosal defenses.
• Common sites are first part of duodenum, lesser curvature
of stomach, gastro-esophageal junction, Meckel's
diverticulum, stoma after gastric surgery, and less
commonly esophagus.
• Gastric ulcers have relatively normal levels of gastric acid
secretion as compared to duodenal ulcers.
PATHOPHYSIOLOGY
 ETIOLOGY/ RISK FACTORS
• H.pylori infection – most important
• Chronic use of NSAIDS and aspirin
• Steriods
• Smoking
DUODENAL ULCERS
1. Duodenal ulcers are more
common in older men.
2. They're rarely malignant.
3. Most common complication is
stenosis, perforation and bleeding.
4. Both anterior and posterior
ulcers together called kissing ulcers.
5. Anteriorly placed ulcers tend to
perforate and posteriorly placed
ulcers tend to bleed.
GASTRIC ULCERS
1. Gastric ulcers occurs in low
socioeconomic groups and are less
common than duodenal ulcers.
2. Can be malignant
3. Fibrosis cause hourglass contraction of
stomach
4. More common on lesser curvature at
the boundary between acid secreting
and non acid secreting part.
5. Very difficult to distinguish benign
ulcer and gastric cancer without biopsy.
Hence, every ulcer should be considered
malignant and biopsy should be sent.
 CLINICAL FEATURES
1. Pain is epigastric, gnawing and radiates to back. Eating
may relieve discomfort. The pain is intermittent.
2. Periodicity is a classical feature. The symptoms may
disappear for months or weeks and then may reappear.
3. Vomiting not noticeable unless stenosis
4. Weight loss (gastric ulcer) or weight gain may occur
5. Bleeding may be chronic and endoscopy must be done.
6. Examination reveals epigastric tenderness.
 DIAGNOSTIC TESTS
• Gastrodeuodenoscopy (GD) – Investigation of choice
– Endoscopic procedure
• Visualizes ulcer crater
• Ability to take tissue biopsy to R/O cancer and diagnose H. pylori
– Upper gastrointestinal series (UGI)
• Barium swallow
• X-ray that visualizes structures of the upper GI tract
– Urea Breath Testing
• Used to detect H.pylori
• Patient drinks a carbon-enriched urea solution
• Exhaled carbon dioxide is then measured

• All mucosal abnormalities at gastroesophageal junction must undergo multiple biopsies

because of increased incidence of cancer.
• In all patients with “Alarming symptoms”
endoscopy is required.
• Dysphagia.
• Weight loss.
• Vomiting.
• Anorexia.
• Hematemesis or Melena
 Complications
• Bleeding (left gastric entry) – gastric ulcers
• Bleeding (gastroduodenal artery) – duodenal
ulcers
• Iron deficiency anemia
• Perforation
• Gastric outlet obstruction
 Medical Treatment
1. Two week treatment with H2 antagonist or proton pump inhibitors causes
healing. Symptoms are relieved within few days. Relapse is almost
universal.
2. Eradication therapy is effective when H.pylori is the cause. OR when
patient doesn't take NSAIDS.
3. Patient taking NSAIDS or having Stomal ulcers or Zollinger Ellison
syndrome should have prolonged treatment with potent antisecretory
agents specially proton pump inhibitor (for ZES).
4. Antacids, Prostaglandin analogues and Mucosal barrier fortifiers also help.
5. Eradication therapy consists of a triple therapy: a proton pump inhibitor +
two antibiotics: Metronidazole + Clarithromycin fpr 14 days OR quadruple
therapy: triple therapy + Bismuth.
 In case of failure
1. Endoscopic re-evaluation should be done if ulcers fail to heal
(differentiates between a refractory ulcer and persistent symptoms
despite ulcer healing)
2. Most common cause is persistent H.pylori infection
3. Biopsies should be done along with endoscopy as false negative
results with breath test are common and serum antibody levels take 6
months or more to fall.
4. Failure of eradication is because of poor compliance or bacterial
resistance so bacterial culture would help.
5.NSAID ingestion needs to be addressed
6. ZES must be suspected in H.pylori negative, non NSAID related
peptic ulcer and serum gastrin should be measured.
 SURGICAL MANAGEMENT
• There is varying degree of morbidity, mortality
and post op side effects so it is important for
clinician to employ surgery if it's absolute
necessity.
 DUODENAL ULCERS
• The aim is to the divert the
acid away from duodenum or
reducing the secretory portion
of stomach or both.
• Billroth 2 Gastrectomy: The
lower portion of the stomach
is removed and the remainder
is anastomosed to the
jejunum.
• Common cause of morbidity is
leakage from duodenal stump.
GASTROENTEROSTOMY:
• Creates a passage between
the body of stomach to small
intestines that allows
regurgitation of alkaline
duodenal contents into the
stomach and keeps acid away
from ulcerated area.
• Alkali reflux is protective
against duodenal ulcer but
stomal ulceration is common.
• PYLOROPLASTY:
Widens the
pylorus to
guarantee
stomach emptying
even without
vagus nerve
stimulation.
Truncal vagotomy and drainage:
Truncal vagotomy involves
denervation of the section of vagus
nerve that is involved in acid
production but this procedure alone
causes gastric stasis hence a
drainage procedure like heineke-
mikulicz pyloroplasty (most popular
drainage procedure) or
gastrojejunostomy (alternative)
should be employed along with it.
This combination is safer than
gastrectomy.
• Highly selective vagotomy: Involves
denervation of only parietal cell mass of the
stomach. This is most satisfactory operation for
duodenal ulcers and is gold standard. Lowest
mortality and morbidity as gastrointestinal
tract isn't opened during procedure. However,
it leads to Epigastric fullness and mild
dumping. Recurrence is common.
Truncal vagotomy and antrectomy: Has
exceedingly low recurrence rate but operative
morality is high.
 GASTRIC ULCERS
Billroth I Gastrectomy:
Distal portion of the
stomach is removed and
the remainder is
anastomosed to the
duodenum.
Same recurrence,
morbidity and mortality
as with any gastric
resection.
 Post-Operative Complications
1. Recurrent ulceration: treated the same as ulcers before
surgery.
• In case of gastrojejunal colic fistula, the anastomotic ulcer
penetrates into transverse colon.
• Patient has severe diarrhea following every meal. They have
foul breath and may vomit formed feaces. Severe weight loss
and vomiting occurs and condition mimics malignancy.
• Best imaging study is CT with IV contrast or barium enema.
• Treatment is to correct dehydration then perform revisional
surgery.
2. Small stomach syndrome: is characterized by early satiety due to
loss of receptive relaxation. This gets better with time on its own.

3. Bile vomiting: Charactetized by vomiting a mixture of food or

sometimes bile after a meal. Abdominal pain and reflux symptoms
are common after eating. Bile chelating agents are ineffective.
Revision surgery depending upon the original operation should be
done.
4. Dumping
Early dumping: the small bowel has food stuff that has high osmotic load
this leads to sequestration of fluid from circulation into GIT. 
Treatment is Dietary manipulation. Small regular meals with protein and fat
and avoid fluids with high carbohydrate content. If itdoesn't improve,
somatostatin analogue octreotide before meals helps. This treatment can
lead to gallstones and also doesn't help with diarrhoea. Revisional surgery
can be performed if everything fails.

Late dumping: reactive hypoglycemia. The carbohydrate in small bowel

causes rise in plasma glucose which increases insulin levels causing
secondary hypoglycemia. The treatment is same as early dumping.
5. Post vagotomy diarrhoea: Is most devastating complication. Looseness
of bowel action is suffered by all patients after surgery but it's rarely
intractable. Precise Aetiology of problem is uncertain. It is related to rapid
gastric emptying. Diarrhea may take several forms from minor episodes
to severe and explosive. The condition is difficult to treat. Antidiarrheal
preparations may help. Octreotide and revisional surgery has no role.

6. Malignant transformation: Risk is increased to approximately 4 times

following gastric surgery. The lag phase between operation and
development of malignancy is at least 10 years.
7. Nutritional consequences: are common like weight loss,
iron deficiency anemia, vitaminb12 deficiency anemia and
bone disease in women.

8. Gallstones: Are strongly associated with truncal

vagotomy. Biliary tree along with stomach is denervated
leading to stasis and hence stone formation. Treatment is
cholecystectomy which may induce or worsen other post-
peptic surgery syndromes.
 Perforated Peptic Ulcer
1. Patient presents with sudden onset severe generalised pain followed by bacterial peritonitis in
few hours accompanied by deterioration in patient's condition. Initially patient is in shock and
tachycardia, pyrexia occurs few hours after the event. Abdomen has board like rigidity and
doesn't move with respiration. Patient needs an operation without which the patient will
detoriate with septic peritonitis. This classic presentation is observed less commonly.
2. Most common site of perforation is anterior aspect of duodenum.
3. Investigation: Erect plain chest radiograph will show gas under diaphragm.
Ct scan is more accurate.
4. Serum amylase to differentiate between peptic ulcer, perforation and pancreatitis. Serum
amylase may be elevated following perforated peptic ulcer but the levels are not as high as in
acute pancreatitis.
5. Treatment involves resuscitation and analgesia.
Analgesia makes clinical signs more obvious.
Laparotomy is treatment of choice. Laparoscopy is alternative treatment.
6. All patients should be given eradication therapy along with anti-secretory agents and stomach
should be kept empty via nasogastric tube.
THANK YOU