Acute mesenteric ischemia

Acute mesenteric ischemia is a disturbance of blood flow in the intestine caused by embolism, thrombosis, or decreased blood flow. This leads to the release of mediators, inflammation, and ultimately infarction. The pattern of abdominal pain is inconsistent with the physical examination findings.

Early diagnosis is difficult, but the most informative are angiography and diagnostic laparotomy; other methods of investigation allow diagnosis only at a late stage of the disease. Treatment of acute mesenteric ischemia consists of embolectomy, revascularization of viable segments or intestinal resection; sometimes vasodilator therapy is effective. Mortality is high.

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What causes acute mesenteric ischemia?

The intestinal mucosa has a high metabolic rate and, accordingly, a high need for good blood flow (approximately 20-25% of cardiac output), which creates increased sensitivity of the intestine to decreased perfusion. Ischemia destroys the mucous barrier, creating conditions for the penetration of microflora, toxins, and vasoactive mediators, which in turn lead to myocardial weakness, systemic inflammatory response syndrome, multiple organ failure, and death. The release of mediators can occur even before the development of a complete infarction. Necrosis usually develops only 10-12 hours after the onset of initial symptoms.

Three major vessels supply the abdominal organs with blood: the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). The celiac trunk supplies the esophagus, stomach, proximal duodenum, liver, gallbladder, pancreas, and spleen. The superior mesenteric artery supplies the distal duodenum, jejunum, ileum, and colon to the splenic flexure. The inferior mesenteric artery supplies the descending colon, sigmoid colon, and rectum. Collateral vessels are abundant in the stomach, duodenum, and rectum; these areas are rarely subject to ischemia. The splenic flexure represents the boundary of the blood supply between the SMA and IMA and poses a certain risk of ischemia.

Mesenteric blood flow may be impaired by venous or arterial vascular involvement. Typically, the following types of occlusion and risk factors are seen in patients over 50 years of age and at very high risk.

1. Arterial embolism (50%), risk factors: coronary artery disease, heart failure, valvular heart disease, atrial fibrillation and history of arterial embolism.
2. Arterial thrombosis (10%), risk factors: systemic atherosclerosis.
3. Venous thrombosis (10%), risk factors: hypercoagulability, inflammatory diseases (eg, pancreatitis, diverticulitis), trauma, heart failure, renal failure, portal hypertension and decompression sickness.
4. Non-occlusive ischemia (25%), risk factors: decreased blood flow (heart failure, shock, extracorporeal circulation) and spasm of abdominal vessels (vasopressors, cocaine).

However, many patients have no known risk factors.

Symptoms of acute mesenteric ischemia

Early symptoms of mesenteric ischemia are severe abdominal pain but minimal physical findings. The abdomen remains soft with little or no tenderness. Moderate tachycardia may be present. Later, as necrosis develops, signs of peritonitis develop with abdominal tenderness, guarding, rigidity, and absence of peristalsis. Stool may be bloody (more likely as ischemia progresses). Symptoms of shock usually develop, and the disease is often fatal.

Sudden onset of pain is not diagnostic but may suggest arterial embolism, whereas a more gradual onset is typical of venous thrombosis. Patients with a history of postprandial abdominal discomfort (suggesting intestinal angina) may have arterial thrombosis.

Diagnosis of acute mesenteric ischemia

Early diagnosis of acute mesenteric ischemia is particularly important because mortality increases significantly when intestinal infarction occurs. Mesenteric ischemia should be considered in any patient over 50 years of age with sudden severe abdominal pain, known risk factors, or predisposing diseases.

In patients with obvious abdominal symptoms of ischemia, laparotomy is necessary for treatment and diagnosis. In other cases, selective angiography of the mesenteric vessels is the diagnostic method of choice. Other instrumental studies and blood tests may show changes, but they are not specific and informative enough in the early stages of the disease, when timely diagnosis is needed. Routine abdominal radiographs are useful mainly to exclude other causes of pain (eg, perforation of a hollow organ), but gas or pneumatization of the intestine may be visualized if the portal vein is affected. These signs are also detected by CT, which can directly visualize vascular occlusion - more precisely, a venous fragment. Doppler ultrasonography can sometimes identify arterial occlusion, but the sensitivity of the method is insufficient. MRI can accurately diagnose occlusion in the proximal segment of the vessel, but the study is less informative for distal occlusion. Some serum biochemical parameters (eg, creatine phosphokinase and lactate ) increase as necrosis progresses, but they are nonspecific and occur later. Serum intestinal protein-bound fatty acids may prove to be a valuable early marker in the future.

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Treatment of acute mesenteric ischemia

If diagnosis and treatment of acute mesenteric ischemia become possible earlier than infarction develops, mortality is low; later, with the development of intestinal infarction, mortality approaches 70-90%.

If the diagnosis of acute mesenteric ischemia is established during diagnostic laparotomy, treatment options include embolectomy, revascularization, or bowel resection. If the diagnosis is verified by angiography, infusion of the vasodilator papaverine through an angiographic catheter can improve blood flow in both occlusive and nonocclusive etiologies of ischemia. 60 mg of the drug is administered over 2 minutes, followed by an infusion of 30-60 mg/hour. Papaverine is quite effective before surgery, as well as during surgery and in the postoperative period. In addition, thrombolysis or surgical embolectomy are possible in case of arterial occlusion. The development of abdominal symptoms during the diagnostic process suggests surgical intervention. Venous mesenteric thrombosis without signs of peritonitis requires papaverine infusions followed by anticoagulant therapy, including heparin and then warfarin.

Patients with arterial embolism or venous thrombosis require long-term anticoagulant therapy with warfarin. Patients with non-occlusive ischemia can be treated with antiplatelet therapy.