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Etiology:

• Intestinal infarction is caused by caused by ischemic damage secondary to partial or complete obstruction to blood flow usually arterial in origin
• About 50% of Acute Mesenteric infarctions are due to Superior Mesenteric Artery emboli most commonly arising from aortic atheroma
• Arterial thrombosis most commonly due to atherosclerosis, less commonly vasculitis, or hypercoaguable states
• Venous thrombosis represents only 5-10% of cases usually associated with a hypercoagulable state, less commonly inflammation, Portal hypertension or trauma
• Mechanical obstruction most commonly volvulus
• Nonocclusive ischemia may represent up to 25% of acute mesenteric infarction, and is most commonly associated with shock, cardiac arrythmia or acute pulmonary edema

Pathogenesis:

• Whatever the etiology, it appears that intestinal viability can be maintained with reduction of blood flow of up to 25%
• Whether partial or complete obstruction to bloodflow produces ischemic injury is dependant not only on the degree of vascular obstruction, but on other factors such as collateral circulation, presence of contributing diseases such as heart failure, autonomic response to hypoxia and concurrent use of medications

Epidemiology:

General Gross Description:
ischemia and by neutrophil oxidases

General Microscopic Description:

• Usually occurs in people over age 50-55
• Incidence increases with age and is occurring more frequently due to aging of the population
• No sex predilection
• Has a higher frequency in patients with cardiovascular disease and diabetes

Clinical Correlations:

• The appearance of Intestinal infarction secondary to acute mesenteric ischemia is usually arterial in origin and shows sharp demarcation of viable from ischemic tissue. With venous occlusion the margin of viable and affected tissue is less distinct
• Since the Superior Mesenteric Artery is most commonly involved, significant segments of the Small Intestine are affected
• Colonic involvement if present is usually at the splenic flexure which is the watershed of the Superior and Inferior Mesenteric circulation and the least well vascularized segment of the colon
• The early phase of intestinal infarction is never seen grossly, but within several hours reperfusion of the necrotic ischemic tissue occurs leading to intense hemorrhage
• Damage proceeds from the mucosa outward until transmural infarction has occurred
• When first seen, the mucosa is usually hemorrhagic and eventually sloughs into the lumen which is filled with a fresh blood, blood clot and some mucous
• The muscular wall will show varying degrees of hemorrhage and the serosa will initially be congested, turning dusky purple and eventually bright red as transmural necrosis and hemorrhage is complete
• After several days the secondary gross signs of peritonitis may appear either by migration of bacteria through devitalized bowel or frank perforation of the necrotic tissue

References:
•The mucosa is affected first with sloughing of the surface epithelium, initial preservation of villous architecture and hemorrhage in the lamina propria. •Extensive portion of the mucosa may ultimately be sloughed with a variable poly infiltrate •The muscularis will show loss of nuclear detail followed by indistinctness of cellular outline and ultimately with broad areas of hemorrhage •The serosa will show early congestion, with diffuse hemorrhage developing in conjunction with a variable poly infiltrate