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| Infarct | ||
| 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 A •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 blood flow produces ischemic injury is dependent 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 •It is hypothesized that tissue damage is linked to the production of reactive oxygen radicals produced during reperfusion by reduction of oxygen, or by formation of xanthine oxidase from xanthine dehydrogenase during the ischemia and by neutrophil oxidases, | ||
| Epidemiology •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 | ||
| General Gross Description •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 •Examples: | ||
| General Microscopic Description •The mucosa is affected first with sloughing of the surface epithelium, initial preservation of villous architecture and hemorrhage in the lamina propria. •Extensive portions 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 •Examples: | ||
| Clinical Correlation •Acute abdominal pain is the initial symptom in 85% of patients with acute abdominal ischemia, often unaccompanied by other significant abdominal signs •The rate of progression is quite variable but may include sudden evacuation of bowel contents, abdominal distention, and in 75% of cases gross evidence of intestinal bleeding •Progression of the tissue necrosis is accompanied by abdominal tenderness, rebound and guarding •The minority of cases of mesenteric ischemia caused by venous obstruction or non-obstructive ischemia will follow a similar course but at a slower and more variable rate •The mortality in recent series with aggressive attempts at diagnosis and surgical therapy is about 50%. If diagnosis is made before signs of peritonitis appear, survival of up to 90% has been reported | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 787-789 • Sleisenger MH, Fordtran JS. Gastrointestinal disease. 5th ed. Philadelphia: Saunders, 1993, pp. 1927-1948 Please be patient during transfer. Medline will open in a new window. To return, close the Medline Window Infarct
| Synopsis by: Martin Nadel M.D. (T67000M54700)[449]
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