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Written by Website Administrator   
Thursday, 25 August 2005
Article Index
Perforated Duodenal Ulceration
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Discussion

Peptic ulceration:
Definition
A peptic ulcer is a break in the epithelial surface of the oesophagus, stomach or duodenum caused by the action of gastric secretions and in the case of duodenal ulcers, H. pylori.

Epidemiology:
0.8% of the population per year develop a duodenal ulcer
0.2% of the population per year develop a gastric ulcer.
Worldwide the incidence is increasing but decreasing in developed countries.
The peak age for duodenal ulceration is increasing (35-45 years)
Gastric ulceration occurs in older age groups.

Aetiology:
Peptic ulcers are caused by the action of gastric acid and pepsin on the mucosa of the gastrointestinal tract.

Predisposing factors:

H. pylori infection:
A gram negative spiral microaerophilic bacillus specific for human gastric mucosa. It produces urease creating an alkaline microenvironment. It is probably causative in duodenal ulcer and may be associated with gastric ulceration.

Image5

Chemicals:
NSAIDs, Alcohol, Cigarettes

Associated diseases:
Alcoholic cirrhosis, chronic renal failure COPD and hyperparathyroidism all act to increase serum calcium which promotes gastrin secretion.

Familial:
There is a familial predisposition. Duodenal ulcers are also more common in HLA B5 and blood group O patients.

Gastrin Hypersecretion:
Zollinger Ellison Syndrome

Pathology:

80% solitary
80% in duodenum
90% in the first part of the duodenum on the anterior surface within a few centimetres of the pyloric ring
19% in Stomach usually in the lesser curvature of the body.

Clinical Features:

Duodenal ulcers and type II gastric ulcers (prepyloric and antral)
• Male: Female 4:1
• Epigstric pain during fasting relieved by food and antacids
• Boring back pain if ulcer is penetrating posteriorly.
• Haematemesis from ulcer penetrating gastro duodenal artery posteriorly
• Peritonitis if perforation
• Vomiting if gastric outlet obstruction occurs.

Type I gastric ulcer (i.e. body of stomach)
• Male :Female 3:1 peak incidence 50+ years
• Epigastric pain induced by eating
• Weight loss
• Nausea and vomiting
• Anaemia from chronic blood loss

Investigations

Endoscopy:
The gold standard. This is essential to exclude malignancy in:
• Patients > 45 at first presentation
• Concomitant anaemia
• Short history of anaemia


At least six biopsies should be taken from any ulcer seen. Clo (campylobacter like organism) test can be performed to test for H pylori.

Image6

Barium Meal
Can be used for patients unable to tolerate OGD

Tests for H pylori
• Blood can be tested for antibodies
• Urea breath test
• Biopsy of mucosa

Treatment of Peptic Ulcers

Medical:
Acid suppression (PPI’s/H2 Blockers)
H. Pylori Treatment (triple therapy- Omeprazole, Metronidazole and Amoxycillin/Clavanulic acid for one week)

Surgical:
Gastric ulcer
• Bilroth I and II
• Vagotomy, pyloroplasty and excision of ulcer
• Vagotomy, antrectomy and Roux en Y
Duodenal ulcer
• Truncal vagotomy
• Selective vagotomy
• Highly selective vagotomy

Perforated Gastric / Duodenal Ulcers

Half a century ago perforated peptic ulceration was mainly seen in young men, yet today, due to awareness of H. pylori infection and increasing NSAIDs useage it is a problem mainly seen in elderly women. Whilst the overall admission with peptic ulceration is falling, the overall number of ulcer perforation remains the same. It should be noted that 80% of perforated ulcers are positive for H pylori. And so eradication therapy is of great importance.

CXR demonstrating air under the diaphragm
CXR demonstrating air under the diaphragm
Clinical features:

  • Most patients have had pre existing dyspepsia
  • However upto a tenth have been asymptomatic
  • The classic presentation is of a sudden onset in upper abdominal pain which rapidly becomes generalised. The patient is found to have a peritonitic abdomen with absent bowel sounds.
  • 10% have an associated episode of malaena
  • 10% have no demonstrable gas on erect CXR (as in seen in this case)
  • Remember that perforated ulceration is a cause of an elevated amylase. It has been previously quoted that the rise is not as high as in pancreatitis, howver, this is not the case and levels diagnostic of pancreatitis are seen in perforated gastric ulcers. (See the pancreatitis tutorial)



Last Updated ( Sunday, 17 February 2008 )
 
 
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