Ischemic Bowel Disease

Overview

Ischemic Bowel Disease refers to ischemia of the large or small intestine and can be caused by a number of distinct etiologies which share in common reduced mesenteric blood supply to the bowel. Ischemic injury on an acute timescale can be rapidly fatal whereas ischemia occurring on a chronic timescale displays milder but still significant clinical consequences.

Etiologies

Acute vasoocclusive etiologies of ischemic bowel injury arise from sudden occlusion of mesenteric vasculature which can affect arteries or veins. Sudden arterial occlusions usually arise from emboli, typically thromboemboli from the heart; consequently, atrial fibrillation, valvular heart disease, and recent myocardial infarction are all risk factors. Sudden venous occlusions usually arise from thrombosis of mesenteric veins which can occur in contexts of hypercoagulable states. Finally, bowel volvulus or herniation through the inguinal canal can cut off arterial and venous supply to a defined section of the intestines although it should be pointed out that arteries may remain patent due to their higher intraluminal blood pressures.

Chronic Vasocclusive Etiologies occur due to progressive narrowing of mesenteric arteries as a result of slow expansion and thrombotic complication of atherosclerotic plaques. Although chronic vasocclusive etiologies are uncommon their incidence is rising in parallel with that of atherosclerosis.

Nonocclusive sources of mesenteric ischemia are most frequently encountered in context of severe compensatory mesenteric vasoconstriction in response catastrophic hypotensive states such as shock.

Pathogenesis and Morphology

The mesenteric vascular supply possess extensive collaterals which protect against ischemic injury to the bowel. Furthermore, chronic reductions in perfusion allow for increased compensatory collateralization that further raise the threshold for ischemic injury. Below we connect particular etiologies of ischemic bowel injury to their morphological manifestation.

In general, acute vasoocclusive etiologies lead to "Transmural" infarctions of the entire intestinal wall including the GI mucosa, submucosa, and muscularis propria. Arterioocclusive etiologies produce sharply demarcated infarctions outlining the anatomic arterial vascular supply whereas venoocclusive etiologies typically produce a gradient of pathology reflecting the extensive collateralization of mesenteric vessels. Rapid sloughing of the large or small intestinal mucosa is followed within a day by gangrene of the remaining bowel wall which can be complicated by bowel perforation.

Chronic Vasoocclusive and Nonocclusive Etiologies typically produce "Mucosal" infarctions which manifest as diffuse and multifocal ulcerations of the intestinal mucosa that are ringed with a border of inflammation. Because of the extensive collateralization of the mesenteric vasculature and the fact that these etiologies only reduce and do not eliminate perfusion, more than two of the mesenteric vessels must be affected for ischemia to occur. Catastrophic hypotensive states naturally affect perfusion in all mesenteric vessels and atherosclerotic narrowing, when it does occur, is typically widespread and affects much of the mesenteric vasculature. Even so, mucosal infarctions usually only occur in special "Watershed Areas" which do not receive a direct vascular supply but rather lie in between the areas perfused by two different mesenteric vessels. These locations happen to be at the splenic flexure of the large intestine and the sigmoid colon which are consequently most prone to ischemic injury from chronic or nonocclusive etiologies.

Clinical Consequences

The clinical consequences of ischemic bowel disease largely reflect the extent of infarctive injury to the bowel. Transmural infarctions caused by acute vasoocclusive etiologies typically manifest with a sudden onset of extreme abdominal pain, characteristically out of proportion to the clinical signs, and bloody diarrhea which can be rapidly fatal if left untreated. Mucosal infarctions caused by chronic vasoocclusive and nonocclusive etiologies are fairly well-tolerated and typically present with mild-to-moderate abdominal pain with some evidence of lower GI bleeding. In the context of chronic vaso-occlusion, abdominal pain is usually associated with meals as this context requires greater mesenteric blood flow which cannot be met by the atherosclerotically narrowed arteries.

GoozyGooz