Acute Mesenteric Ischemia

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, multisystem organ failure, and death. Mediator release may occur even before complete infarction.

Necrosis can occur as soon as 6 hours after the onset of symptoms.

Mesenteric Ischemia–Intestinal Blood Supply

3D Model

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, 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 table Causes of Acute Mesenteric Ischemia. However, many patients have no identifiable risk factors.

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 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.

• Clinical diagnosis more important than diagnostic tests

• Mesenteric angiography or CT angiography if diagnosis unclear

Mesenteric Ischemia (CT Angiogram)

Image

Image provided by Parswa Ansari, MD.

Early diagnosis of mesenteric ischemia is particularly important because mortality increases significantly once intestinal infarction has occurred (1). 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. Magnetic resonance angiography can be used if there is a contraindication to standard IV contrast.

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 radiographs 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 ultrasound can sometimes identify arterial occlusion, but sensitivity is low. MRI is very accurate in proximal vascular occlusion but is less accurate in distal vascular occlusion.

Serum markers (eg, creatine kinase, lactate) rise with necrosis but are nonspecific findings that are seen later.

• IV fluids and antibiotics

• Surgical: Embolectomy, revascularization, with or without bowel resection

• Angiographic: Vasodilators or thrombolysis

• Long-term anticoagulation and antiplatelet therapy

Patients should be resuscitated with intravenous fluids to improve visceral perfusion. Broad-spectrum antibiotics should be initiated.

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.

1).

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. Re-establishment of blood flow to the bowel can sometimes be accomplished through endovascular techniques.

Mesenteric venous thrombosis without signs of peritonitis can be treated with anticoagulant medications.

Patients with arterial embolism or venous thrombosis should be considered for long-term anticoagulation and dual antiplatelet therapy and surveillance for graft or stent patency.

If diagnosis and treatment take place before infarction occurs, mortality is low; after intestinal infarction, mortality is high and varies depending on the etiology (1). For this reason, clinical diagnosis of mesenteric ischemia should supersede diagnostic tests, which may delay treatment.