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Acute Mesenteric Ischemia
Acute mesenteric ischemia is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately infarction. Abdominal pain is out of proportion to physical findings. Early diagnosis is difficult, but angiography and exploratory laparotomy have the most sensitivity; other imaging modalities often become positive only late in the disease. Treatment is by embolectomy, revascularization of viable segments, or resection; sometimes vasodilator therapy is successful. Mortality is high.
The intestinal mucosa has a high metabolic rate and, accordingly, a high blood flow requirement (normally receiving 20 to 25% of cardiac output), making it very sensitive to the effects of decreased perfusion. Ischemia disrupts the mucosal barrier, allowing release of bacteria, toxins, and vasoactive mediators, which in turn leads to myocardial depression, systemic inflammatory response syndrome (see Sepsis and Septic Shock), multisystem organ failure, and death. Mediator release may occur even before complete infarction. Necrosis can occur as soon as 10 to 12 h after the onset of symptoms.
Three major vessels serve the abdominal contents:
Celiac trunk: Supplies the esophagus, stomach, proximal duodenum, liver, gallbladder, pancreas, and spleen
Superior mesenteric artery (SMA): Supplies the distal duodenum, jejunum, ileum, and colon to the splenic flexure
Inferior mesenteric artery (IMA): Supplies the descending colon, sigmoid colon, and rectum
Collateral vessels are abundant in the stomach, duodenum, and rectum; these areas rarely develop ischemia. The splenic flexure is a watershed between the SMA and IMA and is at particular risk of ischemia. Note that acute mesenteric ischemia is distinct from ischemic colitis (see Ischemic Colitis), which involves only small vessels and causes mainly mucosal necrosis and bleeding.
Mesenteric blood flow may be disrupted on either the venous or arterial sides. In general, patients > 50 are at greatest risk and have the types of occlusions and risk factors shown in Causes of Acute Mesenteric Ischemia. However, many patients have no identifiable risk factors.
Causes of Acute Mesenteric Ischemia
The early hallmark of mesenteric ischemia is severe pain but minimal physical findings. The abdomen remains soft, with little or no tenderness. Mild tachycardia may be present. Later, as necrosis develops, signs of peritonitis (see Acute Abdominal Pain : Peritonitis) appear, with marked abdominal tenderness, guarding, rigidity, and no bowel sounds. The stool may be heme-positive (increasingly likely as ischemia progresses). The usual signs of shock develop and are frequently followed by death.
Sudden onset of pain suggests but is not diagnostic of an arterial embolism, whereas a more gradual onset is typical of venous thrombosis. Patients with a history of postprandial abdominal discomfort (which suggests intestinal angina) may have arterial thrombosis.
Early diagnosis is particularly important because mortality increases significantly once intestinal infarction has occurred. Mesenteric ischemia must be considered in any patient > 50 with known risk factors or predisposing conditions who develops sudden, severe abdominal pain.
Patients with clear peritoneal signs should proceed directly to the operating room for both diagnosis and treatment. For others, selective mesenteric angiography or CT angiography is the diagnostic procedure of choice. Other imaging studies and serum markers can show abnormalities but lack sensitivity and specificity early in the course of the disease when diagnosis is most critical. Plain abdominal x-rays are useful mainly in ruling out other causes of pain (eg, perforated viscus), although portal venous gas or pneumatosis intestinalis may be seen late in the disease. These findings also appear on CT, which may also directly visualize vascular occlusion—more accurately on the venous side. Doppler ultrasonography can sometimes identify arterial occlusion, but sensitivity is low. MRI is very accurate in proximal vascular occlusion, less so in distal vascular occlusion. Serum markers (eg, creatine kinase, lactate) rise with necrosis but are nonspecific findings that are seen later. Intestinal fatty acid binding protein in the serum may prove valuable in the future as an early marker.
If diagnosis is made during exploratory laparotomy, options are surgical embolectomy, revascularization, and resection. A “second look” laparotomy may be needed to reassess the viability of questionable areas of bowel. If diagnosis is made by angiography, infusion of the vasodilator papaverine through the angiography catheter may improve survival in both occlusive and nonocclusive ischemia. Papaverine is useful even when surgical intervention is planned and is sometimes given during and after surgical intervention as well. In addition, for arterial occlusion, thrombolysis or surgical embolectomy may be done. The development of peritoneal signs at any time during the evaluation suggests the need for immediate surgery. Mesenteric venous thrombosis without signs of peritonitis can be treated with papaverine followed by anticoagulation with heparin and then warfarin.
Patients with arterial embolism or venous thrombosis require long-term anticoagulation with warfarin. Patients with nonocclusive ischemia may be treated with antiplatelet therapy.
Early diagnosis is critical because mortality increases significantly once intestinal infarction has occurred.
Initially, pain is severe but physical findings are minimal.
Surgical exploration is often the best diagnostic measure for patients with clear peritoneal findings.
For other patients, mesenteric angiography or CT angiography is done.
Treatment options include embolectomy, revascularization, and resection.
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