Mesenteric Artery Stenting for Chronic Mesenteric Ischemia
- Volume 4 - Issue 6 - Nov/Dec 2007
- Posted on: 9/5/08
- 1 Comments
- 19434 reads
Hadi Rokni Yazdi, MD, Fadi Youness, MD, Sandeep Laroia, MD, Shiliand Sun, MD, Hicham Abada, MD, Melhem Sharafuddin, MD, Jafar Golzarian, MD
CMI is caused by atherosclerosis in more than 90% of the cases. Nonatheromatous conditions include: median arcuate ligament compression syndrome (compression of celiac artery by diaphragmatic crus), Takayasu arteritis, dysplastic lesions, thromboangiitis obliterans, and radiation-induced vascular injury.1–4 The disease generally presents in patients over 60 years and the incidence is three times higher in women.5 Approximately half of the patients with CMI have significant coronary artery disease and peripheral vascular disease.6,2
The usual cause of the patient symptoms is usually intermittent transient episodes of inadequate intestinal blood supply due to increased metabolic demands at digestion. Symptoms commonly include: “food fear,” postprandial pain, nausea, diarrhea, and weight loss.
CMI involving the celiac arterial distribution may result in disorders such as gasteroparesis, gastric ulceration, and gallbladder dyskinesia.1,3,5
Physical examination is usually unremarkable, except pain that is out of proportion to the physical exam findings. An epigasteric arterial bruit can be heard, but, unfortunately, in less than 50% of patients with arterial stenosis.7,1
Since there is no reliable test available to establish the presence of CMI, the diagnosis must be based on accurate medical history and exclusion of other gastrointestinal causes.3
Duplex ultrasound has proven to be an accurate screening tool for detecting significant stenosis in mesenteric arteries, with 90% accuracy in identifying significant proximal SMA stenosis and 80% accuracy for celiac trunk lesions. Peak systolic velocity of greater than 200 cm/s and end-diastolic velocity exceeding 55 cm/s have been shown to have high correlation with celiac artery stenosis. Lesions of proximal SMA are highly likely when peak systolic velocity is greater than 275 cm/s; however, end-diastolic velocity greater than 45cm/s is more specific.1,5,3
Tonometry of gastrointestinal tract has the unique potential to detect ischemia, irrespective of flow or metabolism. Tonometry is based on association of mucosal ischemia with increased gastrointestinal PCO2, which can be measured using a balloon-tipped catheter, which is attached to a modified carbonogram.1
Magnetic resonance angiography (MRA) is a valuable tool for diagnosing CMI. Coronal three-dimensional MRA images have been shown by several studies to provide high-resolution mesenteric angiograms in greater than 90% of SMA, 75–90% of celiac artery and 25% of IMA vessels. In a study by Sreenarasimhaiah,1 contrast-enhanced MRA had 100% sensitivity for stenosis of celiac artery and SMA, compared to angiography.1
Multislice computed tomography is usually used for pretreatment evaluation of celiac trunk and superior mesenteric artery (SMA) stenosis, if the patient’s renal function is adequate. This confirms the presence of arterial disease and also allows for optimal planning in terms of approach, determination of vessel dimension, and point of reconstitution in cases of total arterial occlusion.2,3
Biplanar selective splanchnic angiography is still the gold standard for evaluation of vascular anatomy and degree of stenosis.7,1
Splanchnic artery anatomy. In order to understand the pathophysiology of CMI, it is necessary to review the anatomy of splanchnic circulation. Three major aortic branches provide the gastrointestinal blood supply: celiac artery (CA), superior mesenteric artery (SMA), and inferior mesenteric arteries (IMA).
The CA divides into three branches: the splenic artery, common hepatic artery, and left gastric artery. The celiac artery supplies the stomach, proximal duodenum, liver, and spleen.
The SMA arises from the aorta very close to the CA at approximately 1 cm caudally. SMA branches include middle, right, and ileocolic arteries, as well as jejunal and ileal arteries. The SMA and its branches supply the distal duodenum, small bowel, and proximal colon up to splenic flexure of colon.
The IMA arises 3–5 cm above the aortic bifurcation. IMA branches include left colic, marginal, and sigmoid arteries, which supply the region from the splenic flexure until the superior portion of the rectum.
In between these vessels, there is a large collateral network that protects against the effects of stenosis in one of the main branches. Therefore, mesenteric ischemia is thought to occur when at least two of the three visceral vessels are affected.2,3,5
Therapeutic Options for Patients with CMI
There are basically two approaches for the treatment of CMI: surgery and endovascular recanalization.
Endovascular recanalization includes percutaneous transluminal angioplasty (PTA) with or without stent placement of one or more mesenteric arteries.3
Treatment of symptomatic CMI is necessary to prevent acute mesenteric ischemia, which may cause bowel infarction and death.5 Asymptomatic disease does not constitute an indication for treatment, although prophylactic treatment may be necessary in cases of planned abdominal surgery because of probable loss of collaterals during surgery.2
Classic surgery includes procedures such as endarterectomy, aortomesenteric and/or celiac bypass grafting. However, the perioperative mortality can be high, reaching 17% and the major complications rate is high, ranging between 15 and 35%.5,3
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