01OverviewDefinition, clinical context and the essential points that orientate the chapter.
A visceral artery aneurysm is a focal dilatation of a mesenteric or renal artery. True aneurysms contain the arterial wall layers and may be degenerative, inflammatory, connective-tissue related or flow-associated. Pseudoaneurysms follow wall disruption from pancreatitis, trauma, infection or intervention and behave differently. Most true aneurysms are incidental, but rupture produces pain, internal bleeding and shock; embolisation or thrombosis can infarct bowel, liver, spleen or kidney. The vessel name, true versus pseudoaneurysm status, symptoms, infection, pregnancy, growth and collateral circulation therefore matter more than memorising one number.
ESVS 2025 replaced broad treatment language with vessel-specific, mostly low-certainty recommendations. A symptomatic true VAA is an urgent repair indication regardless of size and location. For an asymptomatic true splenic, hepatic, coeliac, superior mesenteric or renal artery aneurysm, treatment should be considered at 30 mm; a pancreaticoduodenal aneurysm uses 15 mm. Pregnancy lowers the threshold for splenic and renal lesions to any size, and treatment of any-size splenic aneurysm may be considered in women of childbearing age. These rules do not govern pseudoaneurysms, ruptures or mycotic disease.
Key points
- Resuscitate suspected rupture and involve vascular surgery and interventional radiology immediately; elective size thresholds are irrelevant in shock.
- Symptomatic true visceral artery aneurysms require urgent repair assessment whatever their size or location, after checking that symptoms are plausibly attributable.
- For asymptomatic true aneurysms, use the named vessel: splenic, hepatic, coeliac, superior mesenteric and renal generally use 30 mm, while pancreaticoduodenal uses 15 mm. Pregnancy overrides size for splenic and renal aneurysms, and any-size splenic treatment may be considered in women of childbearing age.
- Pregnancy is an exception: consider treating asymptomatic splenic and renal artery aneurysms regardless of size; in women of childbearing age, splenic treatment at any size may be considered.
- CTA is used for diagnosis, anatomical characterisation and procedure planning; map inflow, outflow, branches, organ perfusion and active bleeding.
- Endovascular repair is recommended when anatomy is suitable, but flow preservation or reconstruction matters when simple occlusion would threaten liver, bowel, spleen or kidney.
- For small asymptomatic true aneurysms, surveillance is active care: ESVS suggests annual imaging for three years then an individual interval; the pancreaticoduodenal observation boundary is below 15 mm.
- Most recommendations are level C because natural-history and comparative-treatment data are observational; explain uncertainty rather than presenting a diameter as biological certainty.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Degenerative and flow related
Atherosclerosis, hypertension and altered collateral flow can weaken mesenteric or renal arterial walls; coeliac obstruction may increase flow through the pancreaticoduodenal arcade.
Inflammatory or inherited
Vasculitis, fibromuscular dysplasia and connective-tissue disorders are uncommon but important, especially with multiple aneurysms, younger age or atypical morphology.
Infection and wall disruption
Mycotic aneurysm follows microbial arterial injury, whereas pancreatitis, trauma and instrumentation more often create pseudoaneurysms that need a separate risk framework.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Wall failure
Progressive loss of medial integrity permits focal dilatation, mural thrombus and increasing wall stress; diameter is an imperfect surrogate for rupture biology.
- 2Rupture
Failure of the aneurysm wall releases blood into peritoneal, retroperitoneal, gastrointestinal or biliary spaces, producing pain, tamponade followed by collapse, and haemorrhagic shock.
- 3Thrombosis and embolisation
Mural thrombus may occlude the parent artery or embolise distally, causing organ infarction even when the aneurysm itself remains intact.
- 4Collateral dependence
Some visceral beds tolerate arterial sacrifice through collaterals, while others depend on the involved branch; repair must balance exclusion against end-organ perfusion.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Pain may be sudden and focal or diffuse, followed by hypotension, syncope, peritonism or gastrointestinal bleeding. A contained retroperitoneal rupture can transiently preserve blood pressure.
Persistent focal abdominal, flank or back pain without another explanation may reflect expansion, compression, embolisation or impending rupture. Symptoms override an elective diameter threshold.
Fever, malaise, positive blood cultures, endocarditis and perivascular inflammation raise concern for infection. The combination of sepsis and arterial wall disruption has high rupture risk.
A well patient often has a lesion found on unrelated cross-sectional imaging. Confirm vessel, maximum orthogonal diameter, morphology, calcification, thrombus and interval growth before labelling risk.
Renal infarction causes flank pain or haematuria; splenic or hepatic infarction causes focal pain; mesenteric embolisation or thrombosis produces acute intestinal ischaemia and peritonitis.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Arterial-phase CT angiographyFirst step - Why
- Confirm the lesion, measure it orthogonally and plan haemorrhage control or elective repair.
- Interpretation and limitations
- Report true versus suspected pseudoaneurysm, parent vessel, neck, branches, inflow and outflow, thrombus, calcification, active bleeding, organ perfusion and collateral routes.
- 02
Full blood count, renal profile, group and crossmatch - Why
- Assess blood loss, organ injury and readiness for contrast or intervention.
- Interpretation and limitations
- Normal haemoglobin does not exclude early rupture. Rising creatinine changes contrast mitigation and renal-preservation planning but must not delay life-saving control.
- 03
Blood cultures and inflammatory markers - Why
- Identify a possible mycotic aneurysm before antibiotics when this does not delay resuscitation.
- Interpretation and limitations
- Positive cultures or surrounding inflammatory change support infection; negative cultures after antibiotics do not exclude it.
- 04
Duplex ultrasound or MRA - Why
- Provide a non-ionising surveillance option when the anatomy and image quality are suitable.
- Interpretation and limitations
- Bowel gas, obesity, deep vessels and coil artefact limit imaging. Use CTA when sonographic quality is inadequate; MRA may better assess flow around coils.
- 05
Catheter angiography - Why
- Define branch anatomy and permit same-session embolisation, stent-grafting or other endovascular treatment.
- Interpretation and limitations
- It is invasive and may miss a thrombosed sac; procedural images must confirm exclusion and preserved essential organ perfusion.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Pseudoaneurysm
Pancreatitis, trauma, surgery or infection causes contained wall disruption rather than a true aneurysm; rupture risk and treatment thresholds differ substantially.
Visceral artery dissection
An intimal flap and false lumen may mimic fusiform aneurysmal change but require dissection-specific assessment of malperfusion, pain and expansion.
Non-vascular abdominal pain
Pancreatic, biliary, peptic, renal and malignant disease can coexist with an incidental aneurysm; symptom attribution must be clinically credible.
Tortuous normal artery
Axial images can exaggerate a curved vessel; multiplanar orthogonal measurement distinguishes tortuosity from genuine focal dilatation.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Emergency pathwayRupture or symptomatic aneurysmFirst stepShock, active bleeding or symptoms plausibly attributable to a visceral aneurysm.+
- 1Resuscitate with major-haemorrhage principles, obtain immediate senior vascular and interventional-radiology involvement, and perform arterial-phase CTA only if it does not delay control.
- 2Treat a symptomatic true aneurysm urgently regardless of diameter; choose endovascular repair when anatomy and physiology permit, with open or hybrid control when necessary.
- 3Plan inflow and outflow control and decide whether embolisation is safe or arterial reconstruction is required to preserve bowel, liver, spleen or kidney perfusion.
- 4After control, monitor haemoglobin, renal function, organ ischaemia, access complications and sac reperfusion, and arrange individualised imaging follow-up.
02Threshold pathwayAsymptomatic true aneurysmA true aneurysm is incidental, non-mycotic and not causing attributable symptoms.+
- 1Name the vessel and measure maximum diameter reproducibly: consider repair at 30 mm for splenic, hepatic, coeliac, superior mesenteric and renal aneurysms, and at 15 mm for pancreaticoduodenal aneurysms.
- 2Apply pregnancy exceptions: consider splenic or renal repair at any size during pregnancy; any-size splenic repair may also be considered in women of childbearing age.
- 3Below threshold, discuss low-certainty natural-history evidence and use individualised surveillance; ESVS suggests annual imaging for three years then tailoring the interval.
03Infection pathwaySuspected mycotic aneurysmA VAA coexists with bacteraemia, endocarditis, fever or perivascular inflammatory change.+
- 1Obtain blood cultures promptly, start severity- and source-appropriate intravenous antibiotics after sampling when possible, and seek microbiology and surgical input.
- 2ESVS advises urgent open surgery plus antibiotics when feasible because infected tissue and source require eradication.
- 3If the patient is unfit for surgery, endovascular exclusion plus antibiotics may be considered as a non-curative bridge or palliative option with explicit relapse risk.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Haemorrhagic shock
Free or contained rupture can progress abruptly to cardiovascular collapse, massive transfusion, abdominal compartment effects and death.
End-organ infarction
Thrombosis, distal emboli or procedural branch sacrifice may injure spleen, liver, bowel or kidney and can lead to abscess or organ failure.
Recanalisation
Coiled aneurysms can refill through incomplete packing or collateral inflow, so technical success at completion angiography does not remove follow-up needs.
Infective persistence
An endovascularly excluded mycotic aneurysm may remain infected, with recurrent bacteraemia, sac expansion, fistulation or late rupture.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- For an observed asymptomatic lesion, record vessel, morphology and the same orthogonal diameter method so apparent growth is not measurement noise.
- ESVS suggests annual ultrasound when adequate, otherwise CTA, for the first three years and an individual interval thereafter for suitable sub-threshold aneurysms.
- After repair, tailor duplex or CTA surveillance to technique and image quality; look for reperfusion, endoleak, recanalisation, migration, stenosis and sac growth.
- Monitor renal function and organ-specific injury after contrast, embolisation or flow sacrifice, including pain, liver enzymes, lactate and haematuria as relevant.
- In mycotic disease, follow cultures, inflammatory response, imaging and source control; endovascular treatment without eradication can relapse.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Vessel before diameter
A 16 mm pancreaticoduodenal aneurysm and a 16 mm splenic aneurysm do not share the same elective recommendation. Say the vessel every time you quote a threshold.
Symptoms need attribution
Urgent repair applies when symptoms plausibly arise from the aneurysm. Common dyspepsia alongside an incidental lesion still needs differential diagnosis, not automatic causation.
Occlusion has a price
Coiling can exclude a sac efficiently but may infarct dependent tissue. Collaterals, branch origins and the consequences of parent-vessel sacrifice belong in planning.
Guidelines legitimately differ
CIRSE 2023 interventional standards retained some 20 mm proposals; ESVS 2025 uses newer vessel-specific 30 mm and 15 mm thresholds. State source, year and scope.
Pseudoaneurysm is separate
A pancreatitis-related pseudoaneurysm lacks the wall biology assumed by true-aneurysm natural-history thresholds. Escalate it for specific urgent assessment rather than applying this table.
11Common pitfallsFrequent interpretation and management errors.
- 01
Applying a universal 20 mm or 30 mm threshold ignores symptoms, vessel, pregnancy, infection and pseudoaneurysm status.
- 02
Calling any abdominal pain aneurysm-related can expose a patient to unnecessary intervention; correlation and alternative diagnoses still matter.
- 03
Sacrifice of a parent artery without mapping collaterals can turn successful exclusion into bowel, hepatic, splenic or renal infarction.
- 04
A stable first scan does not eliminate surveillance because growth, morphology and clinical context can change.
- 05
Treating a mycotic aneurysm as a purely mechanical lesion leaves bacteraemia and infected tissue uncontrolled.