A splenic artery aneurysm is an abnormal dilation of the splenic artery — the tortuous vessel that originates from the celiac axis and carries blood to the spleen. Splenic artery aneurysms are the most common visceral artery aneurysm, accounting for approximately 60% of all visceral artery aneurysms, and are found in approximately 0.8% of the general adult population. Most are incidental imaging findings, but rupture — while uncommon — carries a mortality of 25–40% in non-pregnant patients and up to 70–75% in pregnant women, making identification and appropriate risk stratification essential.
Splenic artery aneurysms share important clinical connections with several other abdominal conditions. Portal hypertension from cirrhosis is one of the most common underlying causes — increased splenic blood flow from portal hypertension chronically stresses the splenic artery wall. Splenomegaly, which accompanies portal hypertension, further amplifies splenic artery flow and aneurysm growth. Pancreatitis — both acute and chronic — causes splenic artery pseudoaneurysms through enzymatic digestion of the arterial wall, making the pancreatic vicinity a key anatomic region to evaluate on every upper abdominal MRI. Abdominal aortic aneurysm coexists with splenic artery aneurysm more commonly than chance would predict, and both should be characterized when either is found.
Causes
Vascular degeneration and fibromuscular dysplasia.
Most true splenic artery aneurysms develop from medial degeneration of the splenic artery wall — a process driven by the chronic high-volume, pulsatile blood flow the splenic artery delivers to the spleen, combined with the natural tortuosity of the vessel that creates repetitive mechanical stress at curves and bifurcations. Fibromuscular dysplasia (FMD) — a non-inflammatory, non-atherosclerotic arteriopathy producing abnormal fibrous and muscular cell growth within arterial walls — is an important and underappreciated cause, particularly in younger women. Unlike the atherosclerosis-driven degenerative aneurysms of older men, FMD-related aneurysms occur in pre-menopausal women and are strongly associated with multiparity. Each pregnancy subjects the splenic artery to dramatically increased blood flow (splenic blood flow increases by 50% during pregnancy from portal blood flow augmentation), progressive estrogen-driven arterial wall softening (estrogen inhibits collagen cross-linking in arterial walls), and mechanical stress — these factors combine to produce a recognized pattern of aneurysm formation and growth during pregnancy, with the highest rupture risk in the third trimester.
Other contributing factors.
Portal hypertension — from cirrhosis, schistosomiasis, or other causes — increases splenic arterial blood flow to supply the enlarged, hypertrophic spleen, creating a high-flow state that stresses the splenic artery wall and promotes aneurysm dilation. Pancreatitis (both acute and chronic) causes splenic artery pseudoaneurysms through direct enzymatic erosion of the arterial wall by activated pancreatic proteases — these pseudoaneurysms are not true aneurysms (the wall is absent or breached) and carry a higher rupture risk than true aneurysms of equivalent size. Trauma, vasculitis (polyarteritis nodosa, systemic lupus), and infection (mycotic aneurysm from bacterial endocarditis or Salmonella) are less common causes. Women are affected 3–4 times more often than men overall, and multiparous women have the highest individual risk.
Symptoms
The majority of splenic artery aneurysms produce no symptoms and are discovered incidentally on abdominal CT or MRI performed for other indications. When symptoms occur before rupture, they are typically vague — upper abdominal or left-sided discomfort, often with radiation to the left shoulder (from diaphragmatic irritation) or left back. Larger aneurysms may cause early satiety from gastric compression. Rarely, a pulsatile left upper quadrant mass is palpable. A bruit may be audible on auscultation over the left upper abdomen.
Rupture produces sudden, severe left upper quadrant pain radiating to the left shoulder and back, followed by hemodynamic instability from intraperitoneal or retroperitoneal hemorrhage. A characteristic "double rupture" phenomenon occurs in approximately 25% of cases — initial hemorrhage is temporarily contained within the lesser sac (producing transient pain and hemodynamic stabilization), followed hours later by free rupture into the peritoneal cavity with catastrophic hemodynamic collapse. This false sense of initial improvement can delay recognition and is a key clinical pitfall. Rupture during pregnancy is the most catastrophic presentation — fetal mortality approaches 95% and maternal mortality is 70–75%, making elective treatment before or early in pregnancy the appropriate strategy for known aneurysms in women of childbearing age.
Diagnosis
Splenic artery aneurysms are most commonly discovered incidentally on CT or ultrasound. On CT, calcification within the aneurysm wall (eggshell calcification) is a classic appearance. Ultrasound with Doppler demonstrates the swirling blood flow within the aneurysm sac. For complete characterization and treatment planning, more detailed vascular imaging is required.
An MRI of the abdomen with MR angiography (MRA) provides comprehensive radiation-free evaluation of the splenic artery and its aneurysm. MRA precisely measures aneurysm maximum diameter (the primary determinant of treatment decisions), characterizes the aneurysm neck (broad-based vs. narrow-necked, which determines endovascular approach), identifies the relationship to the splenic hilum and branch vessels, and distinguishes true aneurysm (intact wall layers with characteristic flow signal) from pseudoaneurysm (irregular margins, surrounding inflammation, adjacent pancreatic pathology). Time-resolved MRA demonstrates dynamic filling and flow patterns. MRI simultaneously evaluates the liver for cirrhosis, the portal venous system for portal hypertension, and the pancreas for associated pancreatitis or pancreatic mass — providing the complete abdominal context that CT with iodinated contrast requires radiation and nephrotoxic contrast to achieve. For patients requiring serial surveillance, MRI eliminates cumulative radiation from repeated CT angiograms.
Classification
Splenic artery aneurysms are classified by wall composition, location, and size.
- True aneurysm: Involves all three layers of the arterial wall (intima, media, adventitia). The most common type. Associated with medial degeneration, FMD, portal hypertension, and multiparity. Calcification of the wall is common. Rupture risk approximately 2–3% lifetime for asymptomatic true aneurysms; higher for larger lesions.
- Pseudoaneurysm: Disruption of the arterial wall with hematoma contained by perivascular tissue rather than true arterial layers. Most often from pancreatitis (splenic artery erosion by pancreatic enzymes), trauma, or post-procedural. Higher rupture risk than true aneurysm regardless of size — treatment is recommended for all pseudoaneurysms regardless of diameter.
- By location — Proximal: Aneurysm in the proximal third of the splenic artery near the celiac origin. More accessible endovascularly; coil embolization or covered stent placement typically possible.
- By location — Distal/Hilar: Aneurysm near the splenic hilum or involving branch vessels. More complex anatomy — may require splenectomy at the time of surgical repair; endovascular approach technically demanding.
- By size: <2 cm — observation with periodic MRI in most patients; ?2 cm or any pseudoaneurysm — treatment recommended. Symptomatic aneurysms of any size and aneurysms in women of childbearing age planning pregnancy treated regardless of size.
Treatments
Treatment decisions are based on aneurysm size, morphology (true vs. pseudo), symptoms, rate of growth, pregnancy plans, and procedural risk.
Observation with surveillance imaging: True aneurysms under 2 cm in asymptomatic patients without plans for pregnancy are observed with MRI or CT angiography at 6–12 month intervals initially, extending to annual surveillance if stable. The goal is to detect growth exceeding 0.5 cm/year or absolute size reaching 2 cm — either of which triggers treatment planning. Cardiovascular risk factor modification (hypertension control, smoking cessation) reduces aneurysm growth rate.
Endovascular treatment.
Transcatheter endovascular repair has become the preferred treatment for most splenic artery aneurysms given its low procedural morbidity and rapid recovery. Catheter angiography is performed to map the splenic artery anatomy, after which one of several techniques is applied depending on aneurysm location and morphology. For proximal and mid-artery aneurysms, coil embolization of the aneurysm sac and/or the parent artery (with or without stent assistance for wide-necked aneurysms) is the most common approach — the spleen is typically preserved through collateral blood supply from short gastric arteries. Covered stent-grafts (exclusion of the aneurysm while preserving flow through the vessel) are used when distal splenic artery flow must be maintained. For pseudoaneurysms, direct sac embolization or covered stent placement achieves immediate hemostasis. Technical success rates exceed 90%; splenic infarction rates are approximately 5–15% with proximal coil embolization. Post-procedure MRI confirms aneurysm exclusion and assesses for splenic complications.
Surgical treatment.
Open or laparoscopic surgery is reserved for aneurysms not amenable to endovascular repair — particularly distal hilar aneurysms requiring splenectomy, failed endovascular attempts, infected (mycotic) aneurysms requiring debridement, and emergency rupture when endovascular resources are unavailable. Operative options include aneurysm ligation, resection with arterial reconstruction, and distal splenectomy. When splenectomy is performed, vaccination against encapsulated organisms is required as for any elective splenectomy.
Emergency treatment of rupture.
Ruptured splenic artery aneurysm requires immediate resuscitation and either emergency endovascular embolization (if anatomy permits and an experienced interventional team is immediately available) or emergency surgery. The double-rupture phenomenon — transient stability followed by catastrophic collapse — means that even patients who appear to stabilize after initial hemorrhage require urgent definitive treatment. Permissive hypotension is maintained until arterial control is achieved.
Get an MRI to Confirm Your Diagnosis
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