Embolization Therapy: Principles and Clinical Applications, 1 Ed.

Splenic and Gastrointestinal Aneurysms

Daniel C. Brown • Constantino S. Peña • James F. Benenati


Visceral abdominal aneurysms (VAAs) are rare, accounting for less than 1% of all arterial aneurysms, but can be life threatening, with reports of morbidity and mortality ranging up to 100% in the setting of aneurysm rupture.1,2 The treatment options vary depending on the vessels involved, aneurysm type (true aneurysm or pseudoaneurysm), etiology, and size.

The incidence of VAAs has been reported to be between 0.1% and 2% of the population, although autopsy studies have demonstrated much higher rates, up to 10%.35 An increased incidence in visceral aneurysms in recent years likely corresponds to the detection of asymptomatic aneurysms seen on the simultaneously increased number of cross-sectional imaging (computed tomography [CT] and magnetic resonance imaging [MRI]) examinations obtained over this time. Additionally, the higher prevalence of interventional procedures in the treatment of various abdominal pathologies has led to a concomitant increase in the incidence of iatrogenic pseudoaneurysms.1,3,4

True aneurysms are defined as a vessel diameter expansion of at least 50% that involves all three vessel wall layers: the intima, media, and adventitia.3 A pseudoaneurysm (or false aneurysm) fails to involve all three vessel layers but instead represents a form of vessel wall disruption allowing a plane of blood flow that is usually only contained by the adventitia3 or surrounding tissues, explaining its higher mortality compared to true aneurysms. Pseudoaneurysms (PAs) are usually iatrogenic or related to trauma and inflammatory conditions such as pancreatitis.6 Unfortunately, determining the type of aneurysm is not always possible from imaging characteristics alone, requiring a complete evaluation of the patient’s history, physical, and other vascular anatomy. The splenic (60%) and hepatic (20%) arteries account for the largest distribution of visceral aneurysms followed by the superior mesenteric (5%) and celiac (4%) arteries3,7 (Table 46.1). Interestingly, more than one visceral aneurysm is found in greater than a third of patients.

The possible etiologies of visceral aneurysms can be extensive (Table 46.2). However, attempting to determine their specific cause may be helpful in establishing the risk of rupture and developing successful treatment options. Degenerative and atherosclerotic aneurysms are commonly seen in the splenic, celiac, and superior mesenteric arteries. The presence of vessel wall calcifications usually suggests a stable, chronic process, whereas eccentric aneurysms without thrombus or calcification may be more concerning for rupture. In the setting of inflammatory or infectious processes, it may be best to ameliorate the process with systemic therapies before proceeding with nonemergent therapy.

As with other peripheral aneurysms, the strict use of a size criteria to guide the decision to treat is controversial and likely too simplistic. There are several factors that should determine the need for treatment. Several nonspecific guidelines have reported the use of a 2-cm threshold for the treatment of large vessel, asymptomatic visceral aneurysms such as those associated with the hepatic and splenic arteries.8,9However, the decision to treat and how to do so should likely include many factors, including the patient’s symptoms, aneurysm location and type, etiology, presence of calcification or thrombus, and particular visceral vessel hemodynamics. The potential treatment options will be based on these factors, and the possible complications from those various treatment options must also be considered. Generally speaking, PAs and symptomatic aneurysms should be treated regardless of their size. In contrast, over the last decade, most interventionalists have chosen to follow stable true visceral aneurysms that are less than 2.5 cm in diameter and lack concerning features, such as interval growth, which is considered a reason for treatment. It must be stated that the data on when to treat VAA is based on a limited experience primarily derived from single center and retrospective evaluations of ruptured aneurysms over the last three decades.

Treatment Options

Given the high morbidity and mortality observed with visceral aneurysm rupture, treatment to prevent rupture is paramount. Traditionally, surgical management was the primary treatment option, whereas endovascular options were initially only considered when patients were deemed too high risk for surgery. However, endovascular treatment offers a multitude of therapeutic options, with high technical success rates and minimal morbidity and mortality.1012As a result, endovascular treatment is now the first option, with surgery typically reserved for instances of acute large vessel ruptures, rebleeding, or growth after intervention and aneurysms that are not amenable to primary or repeat endovascular therapy.

VAA treatment should begin with a careful assessment of the patient’s history and physical examination to assess the etiology and chronicity of the aneurysm. The evaluation of cross-sectional imaging is also crucial for planning a successful treatment strategy. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) evaluation allows for the assessment of an aneurysm neck and the number and size of afferent and efferent vessels. The amount and extent of at-risk end organ tissue should also be evaluated. The presence of other visceral vessel stenosis and collateral pathways should be considered in deciding possible embolization techniques, locations, and agents. Additionally, thought and attention should be made to the endovascular access and treatment vessels to help determine potential treatment options, including puncture site location (femoral, upper extremity, direct puncture), sheath, catheter and microcatheter size, landing zone, coil or plug size, and delivery. Along with standard axial images, we also reformat CTA into thick (12 × 2 mm) maximum intensity projections (MIPs) in coronal and sagittal planes or used real time three-dimensional volume–rendered reconstructions to aid us in making these decisions before undertaking treatment.

Devices and Techniques

At an elementary level, VAA treatment involves prevention of subsequent aneurysm rupture by stopping blood flow to the aneurysmal or weakened portion of the artery. Treatment techniques attempt to prevent or minimize downstream or end organ effects by preserving collaterals or some form of end organ perfusion.1 The use of embolization coils to block flow has been the primary treatment tool. Recent advances include retrievable and gel expanding coils that achieve great success in obstructing inflow and outflow vessels or in the filling of an aneurysm sac with coils. Additionally, metallic expandable plugs have been used to similarly block efferent and afferent vessels.13 The use of liquid embolics (N-butyl cyanoacrylate [NBCA (glue)] and ethylene vinyl alcohol [Onyx; Covidien, Irvine, California]) to fill and mold to the size of the aneurysm sac has also been a useful technique in excluding flow to the aneurysm sac. However, although effective, these liquid embolics require delivery in an extremely controlled fashion.14 In VAA, the collateral pathways can be a double-edged sword that may protect end organ flow but may also revascularize the aneurysm by providing collateral or backflow into the aneurysm from other vessels that were not initially evident. For this reason, careful evaluation of VAA hemodynamics must be performed. Additionally, these pathways may limit the use of particle embolics as the potential for end organ damage may be great.

The development of covered stents has allowed for the possibility of preventing vessel rupture by strengthening or reinforcing the weakened vessel segment but also allowing continued end organ flow. These devices allow for the traditional blood flow patterns to continue within the visceral vessels. Unfortunately, the size of the covered stent delivery systems relative to the treatment vessel size as well as vessel tortuosity have limited their application to proximal splenic and hepatic arteries. Additionally, the vessel diameter proximal and distal to the aneurysm must be relatively equivalent.7 Stent-assisted coiling can also be performed to treat VAA. This is a technique that uses a bare metal stent by placing it across an aneurysm neck where it serves as a support or scaffold through which a catheter is then used to deploy coils into the aneurysm. The bare stent preserves distal flow while the coils are positioned through and around the stent into the aneurysm sac.


Splenic artery aneurysms (SAAs) are the most common true visceral artery aneurysm. They are most often saccular and located in the mid to distal splenic artery. The etiology of true SAA is varied including atherosclerosis, high-flow states such as pregnancy and portal hypertension, and liver transplantation.4,15,16 Traditionally, the splenic artery represents the single inflow and the single outflow vessel. This allows for coil embolization of the outflow segment first, followed by the inflow segment, a technique known as the sandwich technique, the isolation technique, or the coil-trapping technique. This may or may not also involve coil packing of the aneurysm sac itself (Fig. 46.1). This technique can also be performed with vascular plugs. The potential for collateral flow back to the SAA should be excluded by occluding both the inflow and outflow vessels adjacent to the aneurysm.

The rich small gastric and gastroepiploic collaterals usually protect the spleen from infarction. However, the possibility of covering the SAA with a covered stent is another potential treatment option2 that would preserve flow through the splenic artery (Fig. 46.2). As previously mentioned, the size of the splenic vessel and its tortuosity may limit this treatment. SAA with relatively small or narrow necks projecting from the splenic artery can be coiled primarily (Fig. 46.3) to maximize distal flow. In wide-necked aneurysms, bare metal stent–assisted aneurysm coiling may be employed; however, it is rarely used in the splenic artery as there is usually rich collateral blood flow.

Splenic artery PAs are rare and often associated with pancreatitis or trauma.6 Intraparenchymal splenic artery PAs are often observed in the setting of blunt abdominal trauma. The injury to the spleen in these instances often includes parenchymal laceration in addition to PA formation. There is some variability in the techniques used to treat these types of splenic injuries. Distal arterial embolization with or without adjunctive proximal splenic artery embolization17,18 has been described, whereas others have advocated that proximal splenic artery embolization may be an appropriate stand-alone option in hemodynamically stable patients, depending on severity of splenic injury.19

As with all embolization, consideration must be made to the possibility of collateral blood flow back into the PA as well as end organ perfusion when embolizing the splenic artery. Distal splenic artery coil embolization will result in focal parenchymal ischemia and/or infarction. In contrast, a small series demonstrated only a modest splenic artery pressure decrease after proximal balloon occlusion.20 This is likely due to the vast collateral network present resulting in perfusion to the splenic hilum via short gastric and gastroepiploic arteries as well as superior mesenteric artery filling of the dorsal pancreatic, pancreatica magna, transverse pancreatic, and pancreaticoduodenal arteries.21 In the setting of bleeding splenic PA, however, care must be taken to completely embolize the source of bleeding by excluding antegrade, retrograde, and collateral pathways (Fig. 46.4).


Hepatic artery aneurysms (HAAs) are the second most common type of VAA. Most occur in the extraparenchymal hepatic artery segment and are degenerative in nature, whereas intrahepatic aneurysms are mostly false aneurysms. Over the last two decades, there has been a rise in iatrogenic PA involving the hepatic arteries, gastroduodenal artery, and the vessels of the pancreaticoduodenal arcades, which are derived from the growth of percutaneous and surgical procedures in this area.3,10

The dual blood supply to the liver from the hepatic artery and the portal vein allows for aggressive treatment of HAA. However, the patency of the portal vein and its particular branches should be assessed before undergoing embolization of the hepatic artery. During treatment, the presence of transhepatic as well as extrahepatic collaterals should be considered. Treatment of these aneurysms typically includes the embolization of the outflow and inflow arteries (Fig. 46.5). Loss of distal perfusion is usually well tolerated because of portal venous flow, especially in patients who are free of underlying liver disease. Even with a dual blood supply to the liver, proximal HAA can be challenging to treat due to the amount of hepatic tissue placed at risk with complete arterial occlusion (Fig. 46.6).


In contrast to other VAA, superior mesenteric artery (SMA) aneurysms are usually symptomatic, presenting with abdominal pain.22 The proximal SMA is more commonly associated with aneurysm formation. These are usually degenerative or atherosclerotic true aneurysms, whereas PAs occur mostly commonly from infectious (septic emboli), inflammatory, and hereditary causes.22 Because of the number of essential vessels supplying the small bowel and right colon, treatment of these aneurysms can be difficult as maximal distal blood flow preservation is the goal. Unfortunately, these aneurysms have a high risk for rupture as well as a risk of distal embolization.23 Treatment options include surgical ligation with distal revascularization or transcatheter embolization, usually using a covered stent or a bare stent to trap the coils within the aneurysm (stent-assisted coiling). Liquid embolics have been used, but the delicate distal bed favors larger, more controlled devices. There have been recent publications and accounts of using multilayered stents in this region to maintain distal flow while diverting flow away from the aneurysms.21 This technology does not yet carry an “on label” indication in the United States.


The short and angled nature of the celiac artery with its usual three main branches makes treatment of celiac artery aneurysms (CAAs) difficult. CAAs are usually of atherosclerotic etiology; however, infectious, traumatic, and inflammatory conditions such as polyarteritis nodosa, fibromuscular dysplasia, and Behcet disease also occur. CAAs are relatively rare, but the mortality from rupture has been reported at nearly 100%. These aneurysms are usually long saccular aneurysms that involve two or more of the distal celiac vessels. Traditional surgical treatment for these aneurysms has been resection or ligation with distal revascularization. In patients who are high risk for surgery, transcatheter embolization of the branches and the aneurysms can be considered as a treatment option. The development of collateral pathways between the SMA and celiac may favor stepwise occlusion to strengthen these collateral pathways and minimize distal bed ischemia. Additionally, the liver (dual blood supply), spleen, and stomach are protected by their rich collateral pathway; however, the distal extent of the aneurysms that need to be occluded to prevent retrograde perfusion of the aneurysm may be distal to these collateral pathways24 (Fig. 46.7).


Aneurysms and PAs in this region are commonly related to prior procedures and pancreatitis. They usually present with bleeding and associated pain. The deep location of these small structures is usually seen in the setting of large hematomas, and pancreatitis-related collections makes transcatheter localization and embolization favorable. The rich collateral supply of the pancreaticoduodenal arcade makes these aneurysms difficult to treat without completely isolating the area of bleeding and carefully assessing for possible collateral flow (Fig. 46.8).


The need for evaluation after treatment and continued follow-up is controversial. Usually, an initial follow-up is performed to document exclusion of the aneurysm sac. Unfortunately, the follow-up of treated VAA can be difficult because of the artifact created by coils as well as other agents. The final angiogram at the time of embolization is important to document sac exclusion as well as collateral flow. Doppler ultrasound and CTA may be limited in many patients, but it may help identify flow within the aneurysm and continued aneurysm growth prompting repeat treatment. Recently, the use of MRI in patients who have undergone treatment with platinum-based coils has been explored. The post gadolinium images have been helpful at identifying residual flow within the treated aneurysm sac.25 The need for follow-up is necessary because of the risk for coil compaction and recanalization that may allow flow back into the visceral aneurysm sac. A single-site study of over 45 true VAA with a mean follow-up of 37 months found coil compaction and recanalization in almost 30% of patients. Larger aneurysms (>2 cm) typically had less coil density after their treatment; both factors were associated with an increased risk of recanalization of flow when compared to smaller VAA and those with a higher coil density.26 Recurrent or persistent VAA flow may also occur from collateral vessels and partial thrombosis.

There is no accepted or mandated posttreatment imaging follow-up protocol; however, it can be performed at 3 months, 12 months, and annually thereafter. The need for an earlier imaging follow-up may be adapted especially when treating a PA or if occlusion was not clear on the final treatment angiogram.3



• When possible, optimize imaging to visualize aneurysm neck and inflow and outflow vessels. This may include both preintervention cross-sectional and angiographic imaging.

• Consider collateral circulation before beginning embolization. In many cases, it will be easier to cross aneurysm and treat distal and proximal.

• Ensure embolization catheter is well seated before attempting to deploy coils to ensure the coils do not back up and/or migrate to nontarget sites.

• Guide catheters can provide additional stability and more secure access for microcatheters in tortuous vessels or otherwise tenuous positions.


• Large, detachable framing coils can shorten procedure time when coil embolizing an aneurysm sac.

• Use of vascular plugs can also shorten procedure time when embolizing an inflow and/or outflow vessel.

• Liquid embolics can be an excellent alternative to coils in select cases.

• Preserve distal flow to an end organ by using stent-assisted coiling. A bare metal stent is placed across an aneurysm neck where it serves as a support or scaffold through which a catheter is then used to deploy coils into the aneurysm.

• When preservation of distal flow is not as vital or not possible, the “sandwich” technique can be employed where coils are first placed in the distal vessel and then in then proximally, often across the PA neck to ensure no retrograde or collateral flow is maintained to the PA.

• When the anatomy allows, covered-stent placement across the aneurysm neck can provide a quick, durable treatment option.


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