Patients present with very severe abdominal pain that is excessive and out of proportion to the examination. They may have had previous episodes of pain associated with eating; this is known as “intestinal angina”.
Damage to the small intestine is caused both by tissue hypoxia and reperfusion injury. Hypoxic injury causes tissue ischemia and necrosis, while reperfusion injury is caused by neutrophil activation, the release of free radicals, and buildup of toxic byproducts after periods of ischemia. This damage leads to sloughing of cells and blood into the intestinal lumen, causing occult blood in the stool, and bloody diarrhea in severe cases.
Tissue breakdown with subsequent release of lactate, free radicals, and intracellular electrolytes leads to a metabolic acidosis.
Physiologic response to injury leads to a leukocytosis with a predominance of immature white blood cells, which are also known as bands.
Tissue breakdown causes release of lactate into the blood, contributing to the metabolic acidosis. While relatively sensitive, this test has a poor specificity.
Abdominal x-ray is often the initial test ordered, but it is nonspecific and can be normal in up to 25 percent. Plain films may show signs of obstruction (distended loops of bowel with air-fluid levels), bowel wall thickening, or air within the bowel wall. Free intestinal air on upright abdominal x-ray indicates perforation, and need for immediate surgical intervention.
Advanced disease can lead to a finding of air within the bowel wall, which is known as pneumatosis intestinalis.
The gold standard for diagnosis of arterial occlusive disease is mesenteric CT angiography without oral contrast (contrast may obscure the mesenteric vessels). Findings may include atherosclerosis and calcification of mesenteric vessels, vasoconstriction with decreased flow, pneumatosis intestinalis, bowel wall thickening, and bowel wall edema.
Tissue injury leads to bowel wall edema, which is seen on plain radiographs and CT as thickened areas of bowel wall with a characteristic “thumbprinting” appearance.
Treatment for mesenteric ischemia involves rapid volume resuscitation and use of empiric broad spectrum antibiotic therapy. Without proper antibiotic treatment, patients can go into septic shock with risk of multisystem organ failure.
Severe cases with evidence of bowel necrosis or perforation with hemodynamic instability warrant immediate surgical intervention. Patients should be made NPO (nothing by mouth) immediately and taken to the OR for exploratory laparotomy with resection of necrotic areas of bowel, thrombectomy or embolectomy, and abdominal cleanout where necessary. Endovascular thrombolysis with angioplasty and stenting may be indicated in patients who are deemed unfit to undergo surgery.
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