| • Infarcted tissue is diffusely infiltrated by
polys(black arrow)
• Junction of necrotic and viable tissue is sharp
• While the infarcted mucosa is totally necrotic the muscularis mucosa(green arrow) is still viable confirming the greater susceptibility of the mucosa to ischemic insult |
| 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 |
| Clinical |
•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 rate is improved if treatment is initiated before signs of peritonitis occur and is dependent on the underlying associated disease |
| 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 |
| General Micro 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 |
| Reference |
• 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
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