Pathophysiology

Duodenal ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa. Eradication of H pylori has been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer haemorrhage.

NSAIDs are the second major aetiology of ulcer haemorrhage because of their effect on cyclooxygenase-1, which leads to impaired mucosal defense to acid. The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer haemorrhage, although only when not combined with aspirin therapy. Recent concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors.

The combination of H pylori infection and NSAID use may increase the risk of ulcer haemorrhage.

As the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing haemorrhage. The flow through the vessel varies with the radius: small increases in vessel size can mean much larger amounts of blood flow and bleeding. Visible vessels usually range from 0.3–1.8 mm.

Massive haemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb.

The size of the vessel is important in the prognosis in that larger vessels cause faster blood loss, with more severe hypotension and more complications, especially in older patients.

The main disturbances in patients with acute peptic ulcer bleeding are:

1. Acute loss of blood leads to rapid reduction of cardiac output.

2. Activation of simpatico-adrenal system results in peripheric vasoconstriction and centralization of blood supply.

3. Mechanisms of compensation are supplemented with haemodilution (displacement of interstitial liquid into vessels) and increasing of aldosterone production).

4. After loss less 20% of volume of blood circulation the bleeding stops and in absence of haemorrhagic compensation the disturbances of circulation of blood are not observed.

5. After loss more 20% of volume of blood circulation without the proper compensation of haemorrhage such patients can survive, however always there are considerable disturbances of blood circulation with disturbance of functions of liver and kidneys.

6. Inadequate peripheric blood supply leads to hypoxia, stimulates anaerobic glycolysis and results in free radical metabolites (metabolic acidosis).

7. Reological disturbances result in embolism and thrombosis in microcirculation bloodstream.

8. Arteriovenous shunts open, multiple organ failure develops (“sock” lungs, kidneys, liver).

9. Loss of blood cells results in immunodeficiensy.