| | The endovascular management of visceral artery aneurysms and pseudoaneurysmsPresented at the 2006 Vascular Annual Meeting, Philadelphia, Pa, Jun 1 to 3, 2006. Received 26 June 2006; accepted 30 October 2006. ObjectiveVisceral artery aneurysms may be treated by aneurysm exclusion, excision, revascularization, and endovascular techniques. The purpose of this study was to review the outcomes of the management of visceral artery aneurysms with catheter-based techniques. MethodsBetween 1997 and 2005, 90 patients were identified with a diagnosis of visceral artery aneurysm. This was inclusive of aneurysmal disease of the celiac axis, superior mesenteric artery (SMA), inferior mesenteric artery, and their branches. Surveillance without intervention occurred in 23 patients, and 19 patients underwent open aneurysm repair (4 ruptures). The endovascular treatment of 48 consecutive patients (mean age 58, 60% men) with 20 visceral artery aneurysms (VAA) and 28 visceral artery pseudoaneurysms (VAPA) was the basis for this study. Electronic and hardcopy medical records were reviewed for demographic data and clinical variables. Original computed tomography (CT) scans and fluoroscopic imaging were evaluated. ResultsThe endovascular treatment of visceral artery aneurysms was technically successful in 98% of 48 procedures, consisting of 3 celiac axis repairs, 2 left gastric arteries, 1 SMA, 12 hepatic arteries, 20 splenic arteries, 7 gastroduodenal arteries, 1 middle colic artery, and 2 pancreaticoduodenal arteries. Of these, 29 (60%) were performed for symptomatic disease (5 ruptured aneurysms). Procedures were performed in the endovascular suite under local anesthesia with conscious sedation (94%). The femoral artery was used as the preferential access site (90%). Coil embolization was used for aneurysm exclusion in 96%. N-butyl-2-cyanoacrylate (glue) was used selectively (19%) using a triaxial system with a 3F microcatheter for persistent flow or multiple branches. The 30-day mortality was 8.3% (n = 4). One patient died from recurrent gastrointestinal bleeding after gastroduodenal embolization, and the remaining died of unrelated causes. All perioperative deaths occurred in patients requiring urgent or emergent intervention in the setting of hemodynamic instability. No patients undergoing elective intervention died in the periprocedural period. Postprocedural imaging was performed after 77% of interventions at a mean of 16 months. Complete exclusion of flow within the aneurysm sac occurred in 97% interventions with follow-up imaging, but coil and glue artifact complicated CT evaluation. Postembolization syndrome developed in three patients (6%) after splenic artery embolization. There was no evidence of hepatic insufficiency or bowel ischemia after either hepatic or mesenteric artery aneurysm treatment. Three patients required secondary interventions for persistent flow (n = 1) and recurrent bleeding from previously embolized aneurysms (n = 2). ConclusionVisceral artery aneurysms and pseudoaneurysms can be successfully treated with endovascular means with low periprocedural morbidity; however, the urgent repair of these lesions is still associated with elevated mortality rates. Aneurysm exclusion can be accomplished with coil embolization and the selective use of N-butyl-2-cyanoacrylate. Current catheter-based techniques extend our ability to exclude visceral artery aneurysms, but imaging artifact hampers postoperative CT surveillance. Aneurysmal degeneration of the visceral branches of the abdominal aorta is a rare and potential life-threatening disease entity1, 2 with a documented prevalence of 0.1% to 2%.3, 4 The augmented use of ultrasonography and cross-sectional body imaging for intra-abdominal pathology, coupled with increased instrumentation of the biliary tract, has raised the prevalence and incidental identification of visceral artery aneurysms (VAA) and pseudoaneurysms (VAPA). Although small VAA generally remain asymptomatic, they follow an insidious course and the risk for aneurysm rupture and death remains real. Shanley et al5 reviewed cases of VAA from 1985 to 1995 in the English literature, reporting a mortality rate of 21% for ruptured hepatic artery aneurysms and 100% for ruptured celiac artery aneurysms. VAA have been historically managed with either close surveillance or open surgical intervention. Current open surgical therapeutic options for VAA and VAPA include aneurysm resection with revascularization, aneurysm ligation, or end-organ resection (ie, splenectomy). Endovascular approaches to managing VAA and VAPA (Fig 1, Fig 2, Fig 3) offer an alternative to conventional open surgery with the benefit of low procedural morbidity and mortality. Endoluminal ablation of VAA and VAPA have been shown to be highly technically successful,6 but concern of aneurysm reperfusion during follow-up persists.7 Furthermore, because ablative endoluminal therapy of VAA and VAPA often requires highly radiodense materials, such as glue and coils, postoperative surveillance for aneurysm reperfusion and parent vessel patency may be suboptimal. The purpose of this study was to describe our single-center experience with the endovascular ablative management of VAA and VAPA. Specific focus was given to procedural techniques, rates of technical success, perioperative morbidity and mortality, durability of repair, and adequacy of postoperative imaging modalities. Patients and methods  A retrospective review was performed of patients who underwent endovascular treatment of VAA or VAPA at The Cleveland Clinic Foundation from January 1, 1997, to July 31, 2005. During the study interval, 90 patients were identified with VAA. Endoluminal ablation of a VAA or VAPA was performed in 48 patients (51 procedures), representing 53.5% of all patients diagnosed with aneurysms of the visceral vessels. Three patients required an additional endoluminal procedure. Demographic and clinical data were obtained through review of physician and hospital records. Preoperative and postoperative imaging consisted of computed tomography (CT), magnetic resonance imaging (MRI) and angiography (MRA), duplex scanning, or a combination of these. Preoperative imaging was reviewed from captured and stored electronic images (MagicView program, Siemens, Erlangen, Germany) to confirm the diagnosis of VAA/VAPA. Patients with symptomatic or asymptomatic aneurysms of the celiac axis, superior mesenteric artery (SMA), and inferior mesenteric artery, and their respective branches, were included in the analysis. Patients with VAA in the setting of aortic dissection or concomitant aortic aneurysm were excluded. Pseudoaneurysms were distinguished from true aneurysms by clinical and imaging criteria. Clinically, patients with VAPA typically presented with an antecedent history of arterial trauma, intra-abdominal or retroperitoneal inflammation or malignancy, or biliary tract manipulation. Imaging of VAPA demonstrated evidence of focal arterial disruption in the setting of an otherwise normal artery. Evidence of surrounding inflammation in the setting of an irregular aneurysmal wall was also present. Patients who underwent diagnostic angiography without the intention of endovascular treatment were excluded. Preoperative demographic data included age, sex, and cardiovascular risk factors (Table I). Specifically, risk factors assessed included hypertension, hyperlipidemia, coronary artery disease, renal insufficiency, diabetes mellitus, and history of tobacco use. Patients were also assessed for whether their VAA/VAPA was symptomatic, ruptured, or hemodynamically stable at presentation. Operative technique Percutaneous interventions were performed by the faculty of The Cleveland Clinic Department of Vascular Surgery and Department of Interventional Radiology in dedicated endovascular suites with fixed imaging. The most common technique (81.3%) for endoluminal VAA/VAPA therapy was ablation with coils. In all cases, ablative therapy of the outflow tract, the VAA/VAPA itself, and the inflow artery was attempted. N-butylcyanoacrylate (N-BCA) glue (Cordis Neurovascular, Miami, Fla) or a combination of coils and N-BCA was used for ablation in 4.2% and 15% of cases, respectively. The United States Food and Drug Administration has approved N-BCA for the preoperative ablation of intracranial arteriovenous malformations, and we have found a benefit in extending its use to the treatment of VAA and endoleaks after endoluminal stent grafting. Depending on the desired rate of polymerization, N-BCA is diluted with ethiodized oil, a polymerization-retardant. Specifically, when embolizing a vessel with high rates of blood flow, we desired quick in vivo polymerization and a ratio of 1:1 oil to N-BCA was used. In situations where the microcatheter tip was positioned distant from the desired site of polymerization, a greater volume of ethiodized oil (ie, 2:1, 3:1 dilutions) was added to delay glue polymerization. Although the decision to use coils or N-BCA, or both, was physician-dependent, the glue was routinely used when access into the aneurysm’s outflow vessel was unattainable. Conscious sedation with local anesthetic was used in 45 of 48 interventions. Three patients required general anesthesia in the setting of hemodynamic instability secondary to blood loss from symptomatic disease. Endovascular access for all procedures was through the femoral artery (89.6%) or brachial artery (10.4%). A 5F (56.3%) or 6F sheath (29.2%) was used in most cases, and a 7F sheath was used in the rest. A shaped guiding catheter was used selectively in the ostia of the visceral vessel in instances in which a sheath could not successfully be engaged. Intravascular ultrasound was required in one patient to assist in identification of a celiac axis pseudoaneurysm that was not clearly demonstrated on selective angiography. A triaxial endovascular system with a 3F microcatheter was used in 64.6% of interventions and was specifically required for the deployment of N-BCA or 0.018-inch intravascular coils. We have also found a microcatheter system useful for interventions upon the distal aspect of an arterial bed and for the selective embolization of an aneurysm/pseudoaneurysm cavity with preservation of the proximal parent artery. An uncovered self-expanding nitinol stent was selectively placed to preserve flow within a visceral vessel and to exclude coils placed within aneurysmal artery from encroaching and compromising a nondiseased parent artery (n = 2) and to treat hemodynamically significant dissection resulting from visceral vessel cannulation (n = 1). Percutaneous mechanical thrombectomy of the celiac axis and femoral artery was required during two separate procedures to recanalize an acute procedure-related occlusion during hepatic artery embolization. Owing to the rich collateral network between the celiac axis and SMA, postembolization imaging through both arterial trees was routinely performed to confirm exclusion of the aneurysmal segment. All patients with elective repair underwent systemic anticoagulation with heparin to achieve an activated clotting time of >250 seconds. Patients with rupture received small doses (2 to 3000 units) of heparin after selective visceral cannulation. Three patients with hemodynamic instability received no anticoagulation. Technical success was defined as the successful deployment of coils or glue (or both) within the intended artery, exclusion of the aneurysmal arterial segment without evidence of contrast extravasation, and cessation of hemorrhage, if originally present. In instances of aneurysmal disease of second-order or third-order branches, technical success was further defined as exclusion of the aneurysm with preservation of flow within the intended parent artery. In three cases, VAA or VAPA with very sluggish flow in the fully anticoagulated state were considered successfully excluded. Data analysis and statistical methods Periprocedural data, associated morbidity, and mortality ≤30 days of the procedure were determined. Follow-up documentation of successful aneurysm ablation included resolution of gastrointestinal bleeding/hemobilia in such symptomatic cases and absence of flow on follow-up CT or MRI/MRA. Postoperative imaging was assessed for sac flow, aneurysm size change, adequacy of end-organ perfusion, and severity of coil or N-BCA artifact. Postprocedural imaging artifact was graded by severity: grade 1, minor with no radiopaque scatter; grade 2, moderate with mild radiopaque scatter beyond the region treated; and grade 3, severe with significant radiopaque scatter. The interval of follow-up at The Cleveland Clinic Foundation was recorded and averaged 15.6 months (range, 1 to 75 months). Results During the study period, 48 patients (mean age, 58 years) underwent endovascular management of VAA or VAPA. The anatomic distribution of aneurysms treated included 12 hepatic artery aneurysms (20%), 3 celiac axis aneurysms (6.3%), 2 left gastric aneurysms (4.2%), 2 SMA branch aneurysms (4.2%), 20 splenic artery aneurysms (41.7%), and 9 gastroduodenal/pancreaticoduodenal artery aneurysms (18.8%). Overall, 28 (58%) of the interventions were for pseudoaneurysmal pathology. In 65% of patients, treatment was required for symptomatic disease, including rupture, pain, gastrointestinal bleeding, and/or hemobilia. The symptoms at presentation and the distribution of lesions amongst the various arterial beds (Fig 4) were significantly different between VAA and VAPA. Of the 48 patients, 22 (46%) underwent urgent or emergent procedures. Treatment was for VAA in 42% of patients, and splenic artery aneurysms comprised 75% of true aneurysms in our study. The mean size of all VAA was 2.4 cm. At presentation, 30% of patients with VAA were symptomatic, and one third of these warranted urgent intervention. Only one case of hemodynamic instability secondary to a VAA was noted, however. Asymptomatic VAA (30%) were incidentally identified and treated on the basis of dimensional criteria. Two true aneurysms presented with rupture: one was a 2.5-cm hepatic artery aneurysm, and the other was a middle colic artery aneurysm of unknown size. Unlike true VAA, 89% of the pseudoaneurysms were symptomatic at presentation. Most of the visceral false aneurysms presented with gastrointestinal bleeding or hemobilia, such that 92% of these patients required urgent intervention. The mean size for all false aneurysms treated was 3.0 cm. Three pseudoaneurysms (1 SMA, 1 celiac, 1 splenic) presented with rupture. Technical success was achieved in 47 (98%) of 48 of procedures. One technical failure occurred during treatment of a celiac artery aneurysm distal to an ostial occlusion. Retrograde perfusion of a 2.8-cm aneurysm through the gastroduodenal arcade and splenic artery warranted intervention. Upon completion of the procedure, persistent flow through the aneurysm was identified. Follow-up imaging 3 weeks later demonstrated a slight decrease in aneurysm size. A secondary intervention was attempted to ablate the aneurysm sac, but was unsuccessful and aborted due to diminishing sac size. Interventions on the hepatic arterial tree, gastroduodenal/pancreaticoduodenal arteries, and left gastric artery were performed primarily for pseudoaneurysms related to percutaneous biliary catheters, intravascular chemoembolization catheters, local infectious and inflammatory processes, or iatrogenic operative injury. The 30-day operative mortality was 8.3%. Two unstable patients with extensive hepatobiliary surgery died after embolization: one died from recurrent bleeding in the setting of unresectable carcinoma. A third patient, treated for a ruptured hepatic artery aneurysm, died after a subarachnoid hemorrhage caused from a ruptured anterior cerebral artery aneurysm. A fourth patient died from complications from an underlying intra-abdominal malignancy after a technically successful endovascular treatment of an acutely ruptured 2-cm jejunal artery pseudoaneurysm. The four patients who died in the perioperative period were among the 22 patients who required urgent or emergent intervention because of hemodynamic instability attributable to a symptomatic VAA or VAPA (18% mortality rate). There were no deaths amongst patients electively treated for VAA/VAPA (Table II). | | |  | Arterial bed | Urgent vs elective | No. | Mean size (mm) | Technical success (%) | 30-day mortalityn (%) | End-organ ischemia | |
|---|
| Splenic | Urgent | 3 | 63 | 100 | 0 | 0 | | | | Elective | 17 | 28 | 100 | 0 | 5 (29) | | | Celiac axis branches⁎ | Urgent | 9 | 22 | 100 | 2(22) | 0 | | | | Elective | 5 | 32 | 80 | 0 | 1(20) | | | SMA | Urgent | 1 | 20 | 100 | 1(100) | 0 | | | | Elective | 1 | 22 | 100 | 0 | 0 | | | Hepatic | Urgent | 9 | 16 | 100 | 1(11) | 0 | | | | Elective | 3 | 53 | 100 | 0 | 0 | | | | |
Access-related complications developed in two patients. One sustained a documented groin hematoma not requiring transfusion. In the other patient, access-related femoral artery thrombosis occurred and was treated with percutaneous mechanical thrombectomy. This patient also developed a retroperitoneal hematoma ipsilateral to the access site. Both instances of access-related complications occurred during urgent therapy for symptomatic VAPA. There were no instances of femoral or brachial artery pseudoaneurysms. Excluding the four patients who died in the perioperative period, the mean length of stay for patients undergoing endovascular VAA or VAPA ablation was 5.3 days (range, 1 to 51 days). The mean lengths of stay were 1.8 days after intervention for VAA and 7.8 days after VAPA treatment. The length of stay for patients with VAPA was extended owing to complications attributable to recent surgeries or significant comorbidities warranting admission. Three patients (6.3%) required secondary interventions. One unsuccessful secondary intervention was attempted in the case of a celiac axis aneurysm, as previously described. A second patient, with Caroli disease and percutaneous biliary catheters, required coil embolization for hemobilia emanating from a third-order hepatic artery pseudoaneurysm. He presented 2 weeks later with recurrent gastrointestinal bleeding and hemobilia. Repeat angiography demonstrated migration of the recently placed coils into the pseudoaneurysm sac associated with sac growth. Successful recoiling proximal to the diseased segment was performed. Another secondary intervention was needed in a patient with a history of orthotopic hepatic transplantation who underwent coil embolization of a bleeding hepatic artery pseudoaneurysm. She presented 2 years later with rebleeding through the previously coiled segment that necessitated repeat endovascular ablation. No access site complications resulted from these reinterventions. Postprocedural imaging was available in 37 (77%) of the 48 patients. This consisted of angiography (n = 1), MRI/MRA (n = 3), and CT (n = 33). Two patients also underwent adjunctive duplex imaging. The mean length of radiologic follow-up was 15.6 months (range, 1 day to 75 months). Flow through the previously treated aneurysm sac was identified in only one patient 3 weeks after embolization; thus, aneurysm exclusion was confirmed in 36 (97.3%) of 37 postoperative studies. No patient demonstrated gross evidence of aneurysm sac growth or endoleak. In addition, no significant decrease in aneurysm sac size post-intervention was noted on follow-up. Six end-organ infarcts, all within the splenic bed, were identified. Volumetric analysis determined the mean infarct size was 19%. Two additional patients displayed evidence of splenic atrophy after embolization without evidence of splenic infarcts. Splenic size was preserved in all cases of splenic artery embolization with postintervention splenic infarct. Of note, all splenic changes were identified during the review of images for this retrospective study. None of these patients exhibited any hematologic or infectious complication or other evidence of clinical sequelae from the changes in spleen volume. No instances of hepatic infarction or bowel ischemia were identified during follow-up. No patients were identified with visceral artery aneurysms of other arterial beds. None of the 37 patients with postoperative follow-up had hepatic insufficiency or intestinal ischemia attributable to aneurysm ablation. Postembolization syndrome developed after endovascular ablation of a splenic artery aneurysm in three patients. In one case, there was evidence of distal embolization of N-BCA into the splenic hilum with the presence of multisegmental splenic infarction. Another patient had evidence of splenic atrophy without infarcts. The third patient demonstrated evidence of multiple underperfused segments of spleen. These patients had left-sided abdominal discomfort and diaphragmatic irritation that resolved over time. Despite evidence of splenic ischemia and postembolization syndrome in nearly 40% of patients with treated splenic VAA/VAPA, no patient demonstrated hematologic changes related to splenic insufficiency. Five of 33 CT scans were deemed to have grade 1 artifact, 11 had grade 2 artifact, and 17 had grade 3 artifact. Grade 1 artifact was noted in one MRI/MRA, and grade 3 artifacts were noted in two. No association could be identified between coils and N-BCA and the degree of artifact. Discussion Visceral artery aneurysms and pseudoaneurysms are rare but potentially lethal disease entities. The clinical significance of identifying and appropriately treating these pathologies stems from an effort to prevent aneurysm rupture into the peritoneal cavity or hepatobiliary and gastrointestinal tract. The increased application of high-resolution imaging techniques has resulted in increased identification of VAAs. In addition, increased manipulation of the biliary tree through percutaneous and endoscopic techniques, as well as placement of intravascular chemoembolization catheters, has resulted in a greater incidence of pseudoaneurysmal degeneration of the visceral vessels. Arterial trauma related to laparoscopic treatment of intra-abdominal and retroperitoneal pathologies has also contributed to the increasing incidence of VAPA. Although open surgical repair of these aneurysms remains the gold standard, endoluminal techniques may offer a viable alternative for therapy. Pseudoaneurysms of the splenic artery from pancreatic inflammation, mesenteric artery owing to abdominal sepsis or operative injury, and intrahepatic arterial tree from catheter or stent trauma pose a unique challenge to management: 1.Open surgical repair in these hostile environments is often fraught with technical difficulty and potentially elevates the associated morbidity of the repair. 2.This patient cohort often presents with significant comorbid conditions (pancreatitis, hepatobiliary disease) that elevate the risk of major operative vascular reconstruction. 3.Because many of these patients present acutely with bleeding or rupture, risk-stratification, and medical optimization may not be feasible. As such, minimally invasive endoluminal techniques may offer a distinct advantage to conventional repair. Most of the literature on open repair of visceral artery aneurysms is limited to small series and case reviews. Owing to the relative paucity of visceral artery aneurysms, outcomes for open repair are typically not distinguished by arterial bed. Furthermore, most of the existing studies have not made a distinction between true aneurysms and false aneurysms. This bears significance in assessing operative morbidity and mortality, because the risk of aneurysm rupture is a function of the visceral vessel involved as well as aneurysmal vs pseudoaneurysmal pathology. Mortality rates after the elective treatment of visceral artery aneurysms has been documented as approximately 5%.8 Conventional treatment of ruptured visceral artery aneurysms is associated with significant mortality. In the setting of splenic artery aneurysm rupture, open reconstruction is associated with operative mortality rates of 10% to 25%.9 Perioperative death rates may be even greater during conventional treatment of ruptured hepatic, SMA, and celiac axis aneurysms.3, 10 The use of minimally invasive techniques may provide a survival benefit not only for elective interventions but also for urgent procedures in patients presenting with visceral aneurysm rupture. Splenic artery aneurysms comprised 42% of aneurysms treated in this study. The preponderance of aneurysmal disease of the splenic bed is not unexpected. In fact, true splenic artery aneurysms account for 60% of all splanchnic aneurysms.11 Because variations in hormonal milieu are believed to contribute to extracellular matrix degeneration, it is not surprising that splenic artery aneurysms are more common in women than in men. Our study did not demonstrate the generally reported fourfold greater incidence of splenic artery aneurysms in women, but women did account for 60% of our cohort. A concern exists for splenic insufficiency after main splenic artery embolization. It was of interest that evidence of splenic ischemia, such as infarcts or significant atrophy, was noted in 40% of cases after splenic artery ablation, but it seemed to have minimal clinical sequelae. This was primarily noted after embolization of distal splenic artery or hilar/intrasplenic aneurysms. Conventional repair of these lesions, with its attendant morbidity, would typically require distal splenic artery ligation or splenectomy. Recently, stent graft repair of splenic artery aneurysms has received increasing attention.12, 13 It offers the potential benefit of maintaining splenic perfusion while excluding the aneurysm, thereby eliminating the risk of rupture. Our review of postoperative imaging suggested that the natural history of true splenic artery aneurysms may also involve elongation and increasing tortuosity of the vessel. In such instances, delivery of a covered stent to a mid-splenic or distal-splenic artery aneurysm may be technically unattainable because of existing device limitations. As such, endovascular stent grafting of these lesions may be confined to the proximal splenic artery. Further assessment of this mode of therapy is warranted for the treatment of splenic artery aneurysms and aneurysmal degeneration of other visceral beds. Technical success was achieved in 98% of our interventions. This is in concordance with other recent reports documenting the high rates of technical success attainable with the endovascular management of VAA.6 Our study is unique owing to the significant percentage of patients treated for distal extrahepatic, intrahepatic, gastroduodenal/pancreaticoduodenal, and intrasplenic/hilar lesions. To achieve such rates of technical success, aneurysmal exclusion requires intraoperative high-resolution imaging, technical expertise in visceral vessel cannulation, comfort with use of a triaxial system, and knowledge in the proper preparation and deployment of N-BCA. Although N-BCA is currently approved for the presurgical endoluminal ablation of cerebral arteriovenous malformations, we have found invaluable the extension of its use to treat endoleaks after endovascular aortic aneurysm repair and in the treatment of visceral artery aneurysms. Unlike coils, which are solid, N-BCA is deployed in liquid form before polymerization. This feature is beneficial in ablating aneurysms with multiple outflow vessels or in the setting of persistent aneurysm flow despite coiling. The use of N-BCA requires meticulous detail in preparation. Because it polymerizes on contact with tissue and blood, care must be exercised to reduce the risk of polymerization ex vivo or within the catheter system before deployment. Realizing the potential for microcatheter polymerization, we routinely use a triaxial system with a 3F microcatheter. In such a system, a sheath or guiding catheter is placed into the visceral vessel of interest. A 4F or 5F catheter is telescoped through the sheath or guiding catheter, through which a microcatheter is used for glue deployment. If the glue polymerizes within the microcatheter, rapid exchange of microcatheters is possible without losing visceral vessel access. A 3F microcatheter has also been useful in the exclusion of aneurysms of the intrahepatic circulation and distal arterial beds, where access with a 5F catheter may be unsafe or technically unattainable. We noted a perioperative mortality rate of 8.3%, which is higher than previously reported for the endoluminal ablation of visceral artery aneurysms.14 All patients who died in the perioperative period had required emergent intervention because of hemorrhage. No mortalities occurred after elective aneurysm ablation. This underscores a critical finding that the endovascular management of VAA/VAPA in the elective setting has a low rate of perioperative morbidity and mortality. However, the emergent treatment of these lesions, similar to open reconstruction, is associated with elevated rates of procedural morbidity. This study represents, to our knowledge, the largest review of endoluminally excluded visceral artery aneurysms. Radiologic surveillance after ablation highlights the mid-term durability of endovascular aneurysm ablation. No patient with VAA sustained a delayed aneurysm rupture during follow-up. In addition, no patient demonstrated evidence of aneurysm sac growth on postoperative surveillance. Conversely, aneurysm sac shrinkage was also not observed. The use of embolization materials to fill the aneurysm sac likely causes the aneurysm to mold itself to its internal contents. A dilemma is posed with current ablative techniques, however. Although a fluoroscopically identifiable agent is required for accurate deployment, current radiopaque agents create a significant amount of radiologic artifact on postoperative imaging. Assessment of aneurysm sac growth is thereby hampered. The development of fluoroscopically identifiable ablative agents that are not highly radiodense on noninvasive radiologic imaging is needed. In addition, investigation should be performed of alternative means of surveillance, such as color-flow duplex. Our study has various limitations. Inherent to its retrospective design, we are unable to draw conclusions about treatment paradigms for VAA or optimal modes of ablation. Guidelines for size criteria for intervention also cannot be extrapolated from our study. We generally treat all symptomatic aneurysms, visceral aneurysms in women of gestational age, and aneurysms sized >2 cm, but these guidelines have been extrapolated from literature specific to true splenic artery aneurysms. Just as the mortality after rupture of aneurysms of different arterial trees is different, the risk of rupture may also vary between visceral vessels. Pseudoaneurysms must also be evaluated separately from true aneurysms. Tessier et al15 reviewed their experience with splenic artery pseudoaneurysms during an 18-year period. They did not identify pseudoaneurysm size as being a predictor of risk for rupture because both small (0.3 cm) and large (17 cm) pseudoaneurysms had ruptured in their series. It has been our protocol to treat all visceral artery pseudoaneurysms irrespective of size. Ideally, randomized controlled trials comparing endovascular ablation with open reconstruction are required to make firm recommendations for protocols of therapy. Given the paucity of visceral artery aneurysms, however, the distinct behavior between aneurysms of different visceral vessels and the malignant natural history of pseudoaneurysms, such studies would likely be not be realistic or fulfilling. Longer-term follow-up with larger patient cohorts are necessary to elucidate the ultimate role of endoluminal therapy in the treatment of visceral artery aneurysms and pseudoaneurysms. Author contributions Conception and design: VSK, NT, RKG Analysis and interpretation: VSK, NT, RKG, TPS, DGC, GP, KO Data collection: VSK, NT Writing the article: VSK, NT Critical revision of the article: RKG, TPS, DGC, GP, KO Final approval of the article: VSK, NT, RKG, TPS, DGC, GP, KO Statistical analysis: VSK, NT Obtained funding: Not applicable Overall responsibility: VSK References 1. 1Venturini M, Angeli E, Salvioni M, De Cobelli F, Trentin C, Carlucci M, et al. Hemorrhage from a right hepatic artery pseudoaneurysm: endovascular treatment with a coronary stent-graft. J Endovasc Ther. 2002;9:221–224. MEDLINE |
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a Department of Vascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio. b Department of Interventional Radiology, The Cleveland Clinic Foundation, Cleveland, Ohio.  Reprint requests: Vikram S. Kashyap, MD, The Cleveland Clinic Foundation, Department of Vascular Surgery, S40, 9500 Euclid Ave, Cleveland, OH 44195.
Competition of interest: none. PII: S0741-5214(06)02025-8 doi:10.1016/j.jvs.2006.10.049 © 2007 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
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