A 54-year-old man who had had postprandial pain for 6 months was admitted to our gastroenterology ward because of vomiting and diarrhea over a few days. While he had been performed an abdominal surgery due to intussusception 21 years ago, the detail was not available. He had no other remarkable past history and atherosclerotic risk factors. He complained of tenderness in the lower abdomen without any signs of peritonitis. Blood examination revealed that the levels of white blood cells (13270/μL) and C-reactive protein level (26.7 mg/dL) were elevated. Contrast-enhanced computed tomography (CECT) showed occlusions of both the celiac artery (CA) and the superior mesenteric artery (SMA) in its proximal region. The inferior mesenteric artery (IMA) was patent and slightly dilated. Contrast enhancement of the bowel wall was good. Endoscopic examination revealed only a healed gastric ulcer and slight mucosal erosions in the cecum, ascending and transverse colon. He was treated by conservative therapy under the diagnosis of common acute enteritis during the first 2 weeks; after that, his acute symptoms once improved. However, he presented with recurrence of digestive symptom after starting meals. Endoscopic examination showed progressive ascending and transverse colon ulcers. He was then diagnosed as inflammatory digestive disease and medical therapy was continued. On hospitalization day 42, he suddenly complained of lower back pain. CT showed abdominal free air, which indicated gastrointestinal perforation. Immediately after the diagnosis, emergency surgery was performed. There was no peritonitis in the abdominal cavity. The perforation point was at 60-cm distal to the origin of the jejunum. There was no particular change in the other intestinal serosa. The perforated jejunum was resected and reconstructed. Pathological examination of the resected specimen indicated a possibility of systemic connective tissue disease. However, the definitive diagnosis was not clear. Two days after the emergency surgery, a second operation was performed because of a leak in the anastomotic site of the jejunum. There was also an obvious necrotic change in the small intestinal serosa; therefore, broad resection (120 cm) of the small intestine was required and a jejunostomy was established. Three days after the second procedure, the jejunostomy necrotized. Endoscopic examination detected extended necrosis in the gastroduodenal mucosa. Abdominal surgeons diagnosed him as having acute exacerbation of CMI, and they consulted us for mesenteric revascularization for the first time. We first tried an endovascular procedure for the occluded CA and SMA without success. Then we performed retrograde surgical bypass using an autologous saphenous vein and established a new jejunostomy as the third operation. We harvested the saphenous vein graft from his lower extremity. The vein was anastomosed to the right external iliac artery. Another side of the vein was anastomosed to the gastroduodenal artery in an end-to-side fashion. Revascularization of the SMA was not possible because of strong peritoneal adhesion. Blood lactate level was 17 mg/dL after the operation. After the revascularization, we confirmed the graft patency by CECT and the recovery of the gastroduodenal mucosa by endoscopic examination. His symptoms subsided, and he was discharged from our hospital 62 days after the revascularization. He is now able to eat some meals orally.