Clinical analysis and literature review of a complicated superior mesenteric artery stenosis with intestinal necrosis: A case report

**Background:** Superior mesenteric artery (SMA) stenosis is a common arterial disease with prevalence increasing with age, primarily caused by atherosclerosis or thrombosis. While often asymptomatic, SMA stenosis can cause chronic or acute mesenteric ischemia, presenting with the classical triad (post-prandial epigastric pain, weight loss, abdominal vascular murmur) in only 60% of patients. This case report describes a complicated presentation of SMA stenosis with intestinal necrosis, highlighting diagnostic and therapeutic challenges when multiple etiologies for abdominal pain coexist.

**Methods:** A 64-year-old male presented with 12 hours of periumbilical and right lower quadrant pain, persistent with paroxysmal worsening, accompanied by nausea and vomiting. He had a 2-year history of hypertension (highest 160/110 mm Hg) with irregular treatment, and remote abdominal surgery of unknown details. Physical examination revealed periumbilical and right lower abdominal tenderness. Routine blood tests, biochemistry, coagulation, ECG, and cardiac ultrasound were normal. Abdominal CTA showed soft and hard plaques at the SMA origin causing lumen stenosis, small intestinal wall edema, increased mesenteric CT value, and significant pelvic/peritoneal effusion. Admission diagnosis was SMA stenosis, ischemic enteropathy, and hypertension.

After 5 days of fasting and parenteral nutrition with only partial relief, balloon dilatation of SMA with EV3 bare stent (6–30 mm) implantation was performed under local anesthesia. The SMA opening was narrowed with slow blood flow; post-stenting, the stenosis resolved and blood flow improved. Symptoms diminished immediately. On postoperative day 8, the patient began a liquid diet. On day 18, post-prandial abdominal pain and distension recurred. CTA showed the stent was unobstructed but displaced, with proximal SMA narrowing again. A second procedure implanted a balloon-expandable stent (6–40 mm) at the proximal stenosis. Symptoms again improved. On day 16 after the second procedure, right lower quadrant pain and distension recurred post-prandially. After one week of conservative treatment (fasting, acid inhibition, vasodilation, fluid infusion, nutritional support) without improvement, CTA suggested possible ischemic necrosis of the terminal ileum. Ileocecal resection and enterolysis were performed under general anesthesia, revealing ileocecal adhesions, local ischemic necrosis, and an intestinal fistula within the necrotic tissue. The patient received 14 days of perioperative support including anti-infection, fluid infusion, and nutritional support, recovered well, and was discharged.

**Key Results:** The initial SMA stenosis measured approximately 2.51 mm in diameter, 14.3 mm in length, with 64.14% stenosis. After first stent implantation, proximal vascular diameter enlarged to approximately 7.06 mm. Stent displacement occurred (incidence reported as 2–3% in literature, possibly higher), attributed to the ostial lesion location and atherosclerotic plaque affecting stent deployment and adherence. Despite improving inflammatory markers, stable D-dimer, and CTA showing reduced intestinal ischemia/edema after endovascular interventions, the patient continued having post-prandial symptoms. Surgical exploration confirmed intestinal adhesions (reported incidence after abdominal surgery: 63–97%) with localized necrosis and fistula formation. At 9-month follow-up, CTA showed stents well-deployed and unobstructed with no intestinal abnormality.

**Clinical Implications:** This case demonstrates that when undetermined abdominal pain involves possible mesenteric artery ischemia coexisting with other potential causes (e.g., prior abdominal surgery), clinicians must not focus exclusively on vascular pathology. Abdominal symptoms may be multifactorial—related to both local lesions and mesenteric ischemia—and may persist or worsen after the vascular problem is addressed. The treatment algorithm (conservative vs. surgical, simultaneous vs. elective) should be determined through comprehensive preoperative assessment of intestinal ischemia degree, particularly in areas with concomitant lesions. Assessment should include imaging (CTA), laboratory examinations (D-dimer, serum lactic acid, peripheral blood leukocytes), and most importantly, careful monitoring of changes in abdominal symptoms. This integrated approach is essential to prevent serious complications including acute intestinal necrosis and ischemia-reperfusion injury.