Abstract

Intestinal mucosal injury that results from local ischaemia can be detected by early increases in gut permeability, followed by later morphological, histological, and biochemical abnormalities. Local adaptive mechanisms (for example increased oxygen extraction) can cope with reductions in blood flow of up to 50%, as may occur during episodes of septic shock or cardiac tamponade. Why then does hypoxic injury develop? The peculiar vascular anatomy of the villi allows for oxygen short circuiting to occur at their base, when blood flow is low. Although overall oxygen extraction efficiency may be high, regional hypoxia at the villus tip may, paradoxically occur. The severity of reperfusion injury depends on the duration of preceding hypoxia. Free radical generation through the hypoxanthine xanthine oxidase system is important in mediating cellular damage. In addition, luminal aggressive factors (for example, pancreatic proteases) may cause mucosal damage, as suggested by earlier studies. More recent studies in pigs suggests that pancreatic duct ligation merely delays, but does not prevent development of gut reperfusion injury. Enteral nutrition should benefit patients with the ischaemic intestine because in comparison with total parental nutrition, it stimulates regional blood flow, and attenuates mucosal injury. There are no randomised trials to verify this, but use of tonometry to monitor local ischaemia may help resolve the issue.