CMI is a rare disease because there are usually abundant collateral vessels among the mesenteric arteries [1–3]. Untreated symptomatic CMI can induce acute exacerbation of intestinal ischemia, which has a poor prognosis [5, 6]. Therefore, it is necessary to accurately diagnose and properly treat CMI before severe intestinal ischemia occurs.
Diagnosis of acute exacerbation of CMI
To diagnose acute exacerbation of CMI correctly, the patient’s symptoms and some imaging modalities are important. The classic symptoms of symptomatic CMI are postprandial pain, food avoidance, and significant weight loss [3]. However, these symptoms are not specific to CMI. It is important to combine analysis of the symptoms and imaging modalities. Imaging modalities include ultrasound (US), endoscopy, CECT, magnetic resonance angiography (MRA), and angiography [7]. In our case, CECT and endoscopy were performed before the mesenteric revascularization. CECT can reveal mesenteric vasculature conditions (calcification, stenosis, and occlusion) and ischemic bowel wall changes (thickening and pneumatosis) [7]. Endoscopy is useful for early detection of intestinal ischemia because intestinal ischemia affects the mucosa first [8]. In our case, the first CECT revealed normal enhancement of the bowel wall, and the endoscopic examination revealed slight erosions of the colon. Because these findings did not indicate severe mesenteric ischemia, it would have been difficult to decide to perform revascularization immediately after admission. However, CECT cannot always reveal definite ischemic changes of the bowel wall in the acute phase [9, 10]. Furthermore, endoscopic findings may not be specific for CMI because other digestive diseases can also induce mucosal changes. These findings of CECT and endoscopy are insufficient to differentiate severe mesenteric ischemia that needs revascularization from other pathologies. To diagnose acute exacerbation of CMI correctly, the combination of analyzing the patient’s symptoms and various imaging modalities is necessary. The prophylactic mesenteric revascularization should have been performed before acute exacerbation to avoid unnecessary broad resection of the intestine because we cannot always predict the acute exacerbation of CMI by standard modalities. In this case, the first intestinal surgical procedure might have expanded the mesenteric ischemia due to injury of the collateral arteries.
Surgical treatment of mesenteric ischemia
In most cases of chronic mesenteric ischemia, diffuse atherosclerotic disease is associated with its pathology [11]. Therefore, vasodilators, antiplatelet, and anticoagulant drugs may be useful medical management for these patients to avoid symptomatic mesenteric ischemia. However, appropriate surgical intervention would be necessary once patients present with abdominal symptoms. Surgical bypass and endovascular procedures are considered useful treatments for severe mesenteric ischemia [12, 13]. An endovascular procedure was difficult because the CA and SMA were totally occluded at their orifices in our case. In surgical bypass, different roots of grafts are selected—antegrade and retrograde are reported to have equal patency rates [5, 14]. Antegrade revascularization accomplishes less angulated, shorter bypass for CA and SMA, but it is unsuitable for high-risk cases because a supraceliac approach is necessary [15]. Retrograde revascularization is less invasive, but we have to take care about kinking of the grafts due to the longer bypass [15]. Although there are no data indicating that an artificial graft has superior patency to an autologous vein graft, artificial grafts have been reported to be desirable to prevent graft kinking in retrograde revascularization [16]. In our case, we selected retrograde revascularization using an autologous vein graft that had a risk of graft kinking because his abdominal cavity had been contaminated. We currently recommend prophylactic mesenteric revascularization using an artificial graft in the case of CMI based on this experience. Single- versus multiple-vessel revascularizations is another controversial issue. While Hollier et al. reported that complete revascularization reduced symptomatic recurrences [17], Park et al. reported that the recurrence rate of symptoms was not different between single- and multiple-vessel revascularizations [4]. In our case, strong peritoneal adhesion made the revascularization to the SMA difficult. Anastomosis only to the gastroduodenal artery, a branch of the CA, improved his symptoms. We presume that the network between the CA and the SMA played an important role for collateral blood supply to the SMA.
