Clinical Practice Guideline for Spontaneous Isolated Superior Mesenteric Artery Dissection (2025 Edition)Semantic S...

Published in Annals of Vascular Surgery, 2026, DOI:10.1016/j.avsg.2026.06.010; PMID:42335989; Chinese Spontaneous Isolated Superior Mesenteric Artery Dissection Collaboration Group (ISMAD2022) Disclaimer: This is condensed key‑point summary, not substitute for full‑text original guideline.

Abstract

Spontaneous isolated superior mesenteric artery dissection (SISMAD) is rare but potentially life‑threatening visceral arterial disease. This guideline summarizes evidence covering epidemiology, clinical manifestation, imaging classification, therapeutic strategies and long‑term follow‑up, and provides 19 formal recommendations. Most patients can be managed conservatively. High‑quality prospective evidence remains limited for this entitySemantic S....

1. Definition & Risk Factors

• SISMAD: arterial dissection confined to superior mesenteric artery, without aortic dissection involvement.
• Major risk factors: uncontrolled hypertension, smoking, dyslipidaemia, connective tissue disorder, fibromuscular dysplasia. Male predominance (40‑60 years old).
• Clinical spectrum: severe epigastric/peri‑umbilical abdominal pain (“pain out of proportion to physical examination”), nausea/vomiting; may progress to intestinal ischaemia, infarction, arterial rupture and haemorrhagic shock. Asymptomatic incidental cases are increasingly detected by CT‑A.

2. Diagnostic Work‑up

1. CT angiography (CT‑A of abdomen/pelvis) is first‑line diagnostic modality. It demonstrates intimal flap, true‑/false‑lumen, stenosis‑occlusion, pseudoaneurysm, bowel wall perfusion, retroperitoneal haematoma. Conventional digital subtraction angiography (DSA) is reserved for intra‑procedural use, not routine diagnosis.
2. Yun imaging classification (preferred in this guideline)PubMed
   • Type I: patent false lumen with both entry and re‑entry tear
   • Type IIa: patent false lumen, entry tear only (blind‑pouch false lumen)
   • Type IIb: completely thrombosed false lumen
   • Type III: total occlusion of SMA
3. Laboratory: non‑specific. Lactate, D‑dimer, amylase/lipase are used to screen bowel ischaemia/necrosis.
4. Differential diagnosis: acute mesenteric embolism/thrombosis, pancreatitis, peptic ulcer perforation, aortic dissection, diverticulitis.

3. General Principles of Management

Conservative therapy is first‑line for most uncomplicated SISMAD, irrespective of Yun CT subtype, in absence of bowel necrosis or free ruptureSemantic S.... Three therapeutic pathways: conservative medical management, endovascular intervention, open surgical repair.

3.1 Conservative medical therapy

Indications: no peritoneal sign, no evidence of bowel infarction, no active arterial rupture.

1. Strict blood‑pressure control: target systolic blood pressure 100‑120 mmHg.
2. Bowel rest / gastrointestinal decompression, fluid resuscitation, analgesia.
3. Anti‑platelet versus anticoagulation:
   • For uncomplicated SISMAD: anti‑platelet therapy (aspirin) is preferred.
   • Anticoagulation may be considered when true‑lumen stenosis is severe or extensive thrombus threatens distal flow. Avoid routine anticoagulation for all patients.
4. Serial laboratory monitoring (lactate, D‑dimer) and close clinical abdominal assessment.

3.2 Endovascular intervention (stent‑based therapy)

Indications for urgent/early endovascular repair:

1. Confirmed/progressive intestinal ischaemia without full‑thickness necrosis;
2. Persistent or recurrent severe abdominal pain despite adequate conservative management;
3. False‑lumen pseudoaneurysm ≥ 20 mm or expanding on serial CT‑A;
4. Local contained rupture / retroperitoneal haematoma.

Technical notes:

• Bare‑metal stents are mainstay; aim to cover primary entry tear and restore true‑lumen perfusion.
• Stent‑assisted coiling for large blind‑pouch false‑lumen (Type IIa).
• DSA performed under roadmap guidance.

3.3 Open surgery

Reserved for life‑threatening complicated cases:

1. Bowel transmural necrosis / peritonitis;
2. Free arterial rupture with haemorrhagic shock;
3. Endovascular technical failure or anatomically unsuitable for endovascular approach.

• Procedures: SMA reconstruction, bypass, necrotic bowel resection.

4. Asymptomatic incidental SISMAD

• Initial conservative management with blood‑pressure control and anti‑platelet agents.
• Serial CT‑A surveillance; intervene only when morphological deterioration occurs (pseudoaneurysm enlargement, progressive true‑lumen stenosis).

5. Follow‑up Protocol (strong recommendation)

1. Imaging follow‑up with CT‑A:
   • Acute phase: repeat CT‑A at 7‑14 days after admission to detect early morphological progression.
   • Short‑term: 3 months, 6 months; long‑term: annually for at least 2‑3 years.
2. Persistent risk‑factor modification: strict hypertension control, smoking cessation, lipid management.
3. If dissection stabilises and no pseudoaneurysm, long‑term anti‑platelet is maintained.

6. Major 19‑Recommendation Highlights (selected)

1. CT‑A abdomen/pelvis is recommended as first‑line diagnostic test for suspected SISMAD.
2. Yun classification is recommended for morphological description to support clinical decision‑making.
3. Conservative management is first‑line for uncomplicated SISMAD regardless of CT subtype.
4. Anti‑platelet therapy is preferred for most uncomplicated SISMAD; anticoagulation is not routine.
5. Urgent endovascular repair is indicated for persistent pain, expanding pseudoaneurysm ≥20 mm, contained rupture, mesenteric ischaemia without transmural necrosis.
6. Open surgery is indicated for bowel infarction, free rupture, endovascular failure.
7. Serial CT‑A surveillance is mandatory, even for initially asymptomatic patients.
8. Long‑term risk‑factor control (hypertension, smoking) is essential.

7. Guideline Limitation

Most recommendations are based on retrospective observational cohorts; high‑quality randomized controlled trials are lacking for SISMAD.