Acute mesenteric ischaemia — is this the time for 24-h angiographic service? The role for endovascular therapy

Abstract

Acute mesenteric ischaemia (AMI) is a clinically heterogenous, relatively seldom occurring disease, which is, however, characterised by poor prognosis. It may be caused by mesenteric artery occlusion (by embolus or thrombus) or spasm (non-occlusive form), or visceral vein thrombosis. Current observations point to an increase in AMI incidence, mainly due to prolonged lifespan in the general population and improved treatment outcomes in severe cardiovascular diseases. Making AMI diagnosis and starting treatment within 24 hours from onset of symptoms is crucial for patient prognosis. This is feasible if disturbances of mesenteric circulation are considered in differential diagnostics of acute abdominal pain, especially in cases with possible impairment of mesenteric perfusion (e.g. atrial fibrillation, dehydration, use of certain substances or drugs). Clinical suspicion should be verified by computer tomography or magnetic resonance angiography. Results of these examinations lead to patient qualification for invasive angiography and an appropriate form of percutaneous intervention. In occlusive AMI, clot or embolus aspiration (percutaneous thrombo-/embolectomy), selective thrombolysis via catheter introduced into superior mesenteric artery, percutaneous angioplasty and/or stenting as well as surgery or hybrid procedures are considered. Percutaneous treatment should be complemented with intraarterial vasodilator, most often papaverine, and intravenous heparin infusions. In non-occlusive AMI, caused by spasm of visceral arteries, e.g. in the course of shock, infusion of papaverine is the only treatment applied. This approach decreases mortality due to AMI by 18–53%. In patients with bowel necrosis and/or signs of peritoneal irritation, bowel sparing surgical resection is the procedure of choice. Each patient surviving an AMI episode requires a detailed diagnostic work-up in order to find out the underlying cause (e.g. cardiogenic embolus, thrombophilia) and set up an appropriate secondary prophylaxis strategy.
Acta Angiol 2011; 17, 4: 237–250