Pancreaticoduodenal Artery Aneurysm

The patient had been experiencing abdominal pain prior to presentation — a symptom that was most probably related to the aneurysm itself. The aneurysm was first identified incidentally on CT performed for a separate indication, but the symptom history added clinical weight to what imaging might otherwise have framed as a routine incidental finding. At the initial vascular clinic review, an urgent CT angiogram was requested to characterise the lesion and interrogate the visceral anatomy in full.

Examination Findings

Vascular Interpretation

This is a flow-related inferior pancreaticoduodenal artery aneurysm. Severe proximal coeliac stenosis — consistent with median arcuate ligament compression given the hook morphology and the absence of significant aortic atherosclerosis in a young patient — has redirected perfusion pressure through the SMA–pancreaticoduodenal arcade. The chronic hyperdynamic collateral flow is the engine behind aneurysm formation. The saccular morphology, mural calcification, and partial thrombosis confirm that this is not a benign incidental finding: it is a haemodynamic lesion with meaningful rupture risk.

The diagnosis here is not simply an aneurysm — it is the downstream signature of an upstream problem. Severe coeliac origin stenosis, almost certainly from median arcuate ligament compression, has forced the SMA–pancreaticoduodenal arcade to carry a haemodynamic burden it was not built to sustain. The inferior pancreaticoduodenal artery has compensated — and in doing so, has dilated into a saccular aneurysm that now carries its own independent risk.

The turning point in the clinical reasoning was recognising the hook morphology of the coeliac stenosis. In a 43-year-old with no significant aortoiliac atherosclerosis, this pattern points strongly to extrinsic rather than intrinsic disease — and that distinction is not an incidental anatomical observation. It determines the treatment sequence, the technique, and the risk of getting the order wrong. Treat the aneurysm in isolation and you leave the coeliac problem in place. Stent the coeliac without releasing the ligament and the stent will eventually fracture under ongoing extrinsic compression. The two problems share a single haemodynamic story, and the management plan had to reflect that.

Primary Diagnosis

Inferior pancreaticoduodenal artery saccular aneurysm (19 × 16 × 14 mm), with partial mural calcification and partial luminal thrombosis, in the setting of severe coeliac origin stenosis consistent with median arcuate ligament compression.

Phase 1 — Assessment and MDT Planning

Following urgent CTA, the case was reviewed in the vascular surgery clinic and brought to a formal multidisciplinary team discussion with interventional radiology. Pre-procedural workup was arranged: FBC, renal profile, coagulation profile, ECG, and chest X-ray. Anaesthetic assessment was requested. Vascular risk factor optimisation was initiated alongside — smoking cessation, lipid and glucose control, continuation of antiplatelet therapy. Red flag symptoms were clearly documented and explained to the patient.

Phase 2 — Endovascular Coiling (Completed)

The MDT decision — reached jointly with the interventional radiology team — was to proceed with endovascular coil embolisation of the aneurysm as the first priority. The rationale was clear: the life-threatening risk was the aneurysm. With a narrow 3 mm neck, the anatomy was technically suitable for superselective coiling using the isolation technique, packing proximal and distal to the sac. During the procedure, superselective DSA was performed to confirm that the isolation technique successfully excluded the aneurysm sac while maintaining robust flow through the adjacent pancreaticoduodenal collaterals, thereby ensuring no compromise to hepatic or splenic inflow. The procedure was carried out successfully in collaboration with the IR team, with confirmed aneurysm exclusion.

DSA — Inferior pancreaticoduodenal artery aneurysm prior to embolisation

DSA — Post-embolisation: coil pack in situ, aneurysm excluded

Phase 3 — Staged Laparoscopic MAL Release (Planned)

With the immediate life-threatening risk resolved, the underlying cause — median arcuate ligament compression of the coeliac axis — remains to be addressed. Following a further MDT discussion, the plan is for laparoscopic median arcuate ligament dissection as a staged procedure. Addressing the extrinsic coeliac compression reduces the long-term haemodynamic burden on the SMA–pancreaticoduodenal arcade and mitigates the risk of recurrent aneurysm formation or aneurysm reperfusion. This sequence — fix the life-threatening problem first, address the root cause second — reflects sound surgical prioritisation.

Phase 4 — Surveillance

Post-embolisation surveillance imaging per joint vascular and IR plan, assessing for aneurysm reperfusion and vascular remodelling at 1–2 year intervals in line with SVS recommendations. Following MAL release, reassessment of coeliac patency and haemodynamic normalisation of the pancreaticoduodenal arcade. Ongoing cardiovascular risk factor management in the context of stroke history and right ICA occlusion.

The Disease

Visceral artery aneurysms are rare — reported in 0.01–0.2% of the general population. Pancreaticoduodenal artery aneurysms account for approximately 2% of all visceral aneurysms, making them a rare but clinically consequential entity. Their importance is disproportionate to their incidence: the risk of rupture approaches 50%, and crucially, that rupture risk is independent of aneurysm size.

This is what makes PDAAs different from most other vascular lesions, where size is the dominant trigger for intervention. Here, a 15 mm aneurysm carries the same imperative to treat as a 25 mm one. The reason is aetiology: most PDAAs are not degenerative. They are haemodynamic — built from flow, not from wall failure. A vessel under chronic hyperdynamic stress is unpredictable in a way that a slowly expanding atherosclerotic aneurysm is not.

The mechanism in the majority of cases is coeliac axis obstruction — whether from intrinsic atherosclerosis or extrinsic compression by the median arcuate ligament. The SMA–pancreaticoduodenal arcade becomes the dominant route for hepatic and splenic perfusion. With that comes chronically elevated flow, turbulence, wall stress, and in time, aneurysmal dilatation. A pseudoaneurysm arising in the context of pancreatitis tells a different story: enzymatic digestion of the arterial wall, rupture rates up to 76%, and a patient who is usually already unwell. Distinguishing the two shapes urgency, technique, and the risk calculus of intervention itself.

What the Literature Says

The evidence base for PDAAs is built from case series, systematic reviews, and registry data — there are no randomised trials, and there never will be. The condition is too rare and the rupture stakes too high. What we have is a body of literature that tells a remarkably consistent story about aetiology, intervention thresholds, and the hazards of incomplete anatomical thinking.

Key Lessons