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This case highlights the importance of timely diagnosis and management of acute mesenteric ischaemia and illustrates the compensatory mechanisms of the mesenteric vasculature.A 53-year-old female presented with fever, abdominal pain, and vomiting. The patient had no risk factors for atherosclerosis and was a non-smoker in sinus rhythm with no history of coagulopathy. She was initially treated for viral gastroenteritis. Due to lack of clinical improvement and a rising C-Reactive Protein (416), a CT scan was performed. This demonstrated small bowel ischaemia, chronic occlusion of the coeliac axis, and a long acute-on-chronic occlusion of the superior mesenteric artery (SMA). The length and morphology of the SMA occlusion precluded endovascular treatment. Emergency laparotomy demonstrated 1 m of necrotic small bowel and a pulseless mesentery. An aorto-SMA bypass, using good-quality long saphenous vein was performed, with segmental small bowel resection. Postoperative nutritional support was required with discharge on the 23rd post-operative day. Interval surveillance confirmed graft patency. One year post-discharge, she presented to routine clinic with paroxysmal right iliac fossa pain and decreased appetite. CT angiography showed a long tight 75% stenosis of the graft and she was admitted for mesenteric angioplasty. Angiography confirmed a significantly hypertrophied inferior mesenteric artery, which was now the dominant mesenteric supply.This case demonstrates the importance of emergency mesenteric revascularisation and how it acts as a bridge to anatomical compensation, allowing the collateral circulation to develop and the IMA to hypertrophy, becoming the dominant mesenteric supply.