SAAs are the most common splanchnic arterial aneurysm, accounting for approximately 60% of all true splanchnic aneurysms. Women are affected four times more frequently than men. SAAs typically are saccular and occur at arterial bifurcations. They are multiple in approximately 20% of cases.

Three known factors are associated with the development of SAAs. The first factor relates to the effects of repeated pregnancy on the vessel wall. Approximately 40% of women with SAAs are grand multiparas, having completed six or more pregnancies. Aneurysm formation in these patients may be due to hormonal effects on elastic tissue and the marked increase in splenic artery
blood flow occurring with pregnancy. The second factor is systemic arterial dysplasia. This receives support from the observation that 2% of patients having renal artery fibrodysplasia also have SAA. The third factor associated with SAA formation is the presence of portal hypertension, with 10% to 15% of these patients exhibiting these aneurysms. Both hyperdynamic flow and hormonal consequences of end-stage cirrhosis cause increased splenic artery diameters in portal hypertension and may result in SAA.

Although many SAAs exhibit extensive calcific arteriosclerosis, this is considered a secondary event rather than the primary cause of most of these aneurysms. Additional causes of SAAs and pseudoaneurysms include trauma, as well as inflammatory diseases, particularly pancreatitis with associated pseudocyst formation.

SAAs are most often asymptomatic. Vague epigastric or left upper quadrant discomfort is a nonspecific symptom attributed to these lesions. Roentgenographic demonstration of left upper quadrant, curvilinear, signet ring-like calcification may reveal the presence of an SAA (Fig. 1). However, most are recognized as incidental findings during imaging studies, including computed tomographic (CT) angiography (CTA), magnetic resonance angiography (MRA), and arteriography for unrelated diseases.

Rupture of SAA occurs in less than 2% of patients. SAA rupture in nonpregnant patients is fatal in less than 25%. Rupture has been reported in more than 90% of aneurysms recognized during pregnancy, with a maternal mortality approaching 75% and fetal mortality exceeding 95%. However, many unruptured SAAs exist during pregnancy and go unrecognized clinically. Rupture often presents with hemorrhage contained within the lesser sac. Hemodynamic collapse occurs as blood escapes through the foramen of Winslow. Lesser sac tamponade that postpones catastrophic intraperitoneal bleeding accounts for the so-called double-rupture presentation.

Surgical treatment of SAA is warranted in all patients with symptomatic aneurysms, as well as in pregnant patients and women of childbearing age who might conceive at a later time. Elective treatment, by means of either open surgical procedure or endoluminal approach, should be considered for asymptomatic SAAs 2 cm or greater in diameter. Importantly, percutaneous SAA embolization provides a therapeutic option for the historically poor operative candidates. Given the amount of radiation involved with endoluminal treatment of SAAs, open surgical aneurysmectomy or aneurysm exclusion is preferred in pregnant patients, especially those in the first trimester. Open repair is recommended only when percutaneous treatment has failed or is not appropriate for that patient, and in those circumstances operative mortality should be less than 0.5% to justify its performance.