Mucosal organisms or their breakdown products may permeate the intestinal wall if the mucosal barrier function is breached. This barrier may be compromised by many pathological states and processes. The mucosa at the tip of the villi are particularly prone to ischaemia due to the counter-current exchange mechanism of the vessels. Shunting of blood during low flow states may lead to ischaemia affecting the tips of the villi alone. Subtle mucosal damage, which is only detectable microscopically, may occur following mild ischaemia. In transient hypoperfusion or hypoxia, the mucosal injury is more pronounced during reperfusion when the oxygen supply is re-established. This is due to damage by the putative deleterious oxygen radicals which are generated mainly via the xanthine oxidase pathway. Xanthine oxidase occurs naturally as the dehydrogenase but in ischaemia it is converted by proteolysis to the oxidase form. This latter form then catalyses a reaction which utilizes oxygen to convert hypoxanthine to uric acid with the production of superoxide radicals. These free radicals may damage the mucosa directly due to their cytotoxicity or indirectly via the activation of neutrophils. The accumulation of neutrophils leads to sludging of capillaries, no reflow and worsening of the insult.
At the other extreme is complete disruption of the bowel wall which may occur with perforation or frank infarction. The severity of intestinal barrier function disruption dictates the mode of entry of intraluminal contents and organisms into the systemic circulation. If mild, the initial invasion is via the portal system with systemic bacteraemia delayed because of hepatic filtering. In cases with severe intestinal wall damage, direct peritoneal contamination may occur
Perforation secondary to peptic ulcer, diverticular disease, malignancy, trauma, infarction
Malnutrition Mild ischaemia Hypoxia
allowing bacteria and endotoxin to enter the systemic circulation from the peritoneal cavity (Fig. 5.2).
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