Infrarenal Abdominal Aortic Aneurysm Complicated by Persistent Endotension After Endovascular Repair: Report of a Case

Endoleak and endotension may prevent the successful exclusion of an aneurysm after endovascular aortic aneurysm repair (EVAR). The pressurization in the excluded aneurysm sac caused by endotension may lead to rupture of the aneurysm; however, the cause of endotension and its underlying mechanisms remain unclear. We report a case of infrarenal abdominal aortic aneurysm (AAA) complicated by persistent endotension after EVAR. Although no endoleaks were found on conventional double-phase computed tomographic scans, a thrombosed endoleak existed in the side branch and attachment site of the endograft. After treating the undetectable thrombosed endoleaks, physical examination revealed that the pressure of the excluded aneurysm had diminished, with shrinkage of the aneurysm. This case report suggests that a high-pressure undetectable type I or type II endoleak could be a major cause of endotension. Thus, postoperative evaluation of the attachment site of an endograft is important after EVAR.     

The significance and management of different types of endoleaks

Development of endovascular abdominal aortic aneurysm repair (EVAR) has been accompanied by previously unencountered complications. The most challenging but least understood of these complications is the incomplete seal of the endovascular graft (endoleak), a phenomenon that has a variety of causes. An important consequence of endoleakage may be persistent pressurization of the aneurysm sac, which may ultimately lead to post-EVAR rupture. Data of 110 European centers were recorded in a central database (EUROSTAR). Patient, anatomic characteristics, and operative and device details were correlated with the occurrence of different types of endoleaks. Outcome events during follow-up, particularly expansion of the aneurysm, incidence of conversion to open repair, and post-EVAR rupture were assessed in the different categories of endoleaks and in a group of patients without any endoleak. Type I and III endoleak were associated with an increased frequency of open conversions or risk of rupture of the aneurysm. Device-related endoleaks also correlated with an increased need for secondary interventions. These types of endoleaks need to be treated without delay, and when no other possibilities are present, an open conversion to avert the risk of rupture should be considered. Type II endoleaks do not pose an indication for urgent treatment. However, they may not be harmless, because there was a frequent association with enlargement of aneurysm and reinterventions. Our findings suggest that more frequent surveillance examinations are indicated than in patients without collateral endoleak. The indication for intervention is primarily dictated by documented expansion of the aneurysm.     

Is a type II endoleak after EVAR a harbinger of risk? Causes and outcome of open conversion and aneurysm rupture during follow-up.

OBJECTIVE: There is still debate whether type II endoleaks represent a risk for the patient after EVAR. Treatment policies vary from fairly conservative to active intervention. In this analysis risk factors for type II endoleak and adverse events during follow-up were assessed. In addition, risk factors and causes for conversion to open repair and for rupture post-EVAR were studied. METHODS: The data of 3595 patients, who underwent operation between 1996 and 2002 in 114 European institutions that collaborated in the EUROSTAR Registry, were assessed. To accurately assess the influence of type II endoleaks patients with type I, III and combined endoleaks were excluded from the present study cohort. RESULTS: A combined adverse outcome event consisting of aneurysmal growth, transfemoral reintervention, and transabdominal secondary procedures (including laparoscopic branch vessel clipping) occurred in 55% in patients with type II endoleak at 3 years, compared to 15% in patients without any endoleak (p<0.0001). Conversion to open repair or post-EVAR rupture was not significantly associated with type II endoleaks. An independent association of device migration and expansion of the aneurysm with late conversion was observed. The cumulative incidence of aneurysm rupture at 3 years of follow-up was 1.2% for an annual rate of 0.4%. Variables that significantly and independently correlated with rupture were size of the aneurysm at preoperative measurement and device migration during follow-up. CONCLUSION: Endoleak type II may not be harmless as it was more frequently associated with enlargement of the aneurysm and reinterventions. Large aneurysms and migration of the device were the main risk factors for rupture. The clinical implications of these findings may involve more frequent surveillance visits for patients with type II endoleak. Aneurysm expansion is a clear indication for reintervention. Patients with large aneurysms, 65 mm or larger, may also benefit from a more comprehensive surveillance schedule.     

Endoleaks during follow-up after endovascular repair of abdominal aortic aneurysm. Are they all dangerous?

AIM: Development of endovascular abdominal aortic aneurysm repair (EVAR) has been accompanied by previously unencoutered complications. The most challenging but least understood of these complications is incomplete seal of the endovascular graft (endoleak), a phenomenon which has a variety of causes. An important consequence of endoleakage may be persistent pressurisation of the aneurysm sac, which may ultimately lead to post-EVAR rupture. METHODS: Data of 110 European centers were recorded in a central database (EUROSTAR). Patient, anatomic characteristics and operative and device details were correlated with the occurrence of different types of endoleaks. Outcome events during follow-up, notably expansion of the aneurysm, incidence of conversion to open repair and post-EVAR rupture were assessed in the different categories of endoleaks and in a group of patients without any endoleak. RESULTS: Type I and III endoleak were associated with an increased frequency of open conversions or risk of rupture of the aneurysm. Device-related endoleaks also correlated with an increased need for secondary interventions. These types of endoleak need to be treated without delay, and when no other possibilities are present, an open conversion to avert the risk of rupture should be considered. Endoleaks type II do not pose an indication for urgent treatment. However, they may not be harmless, as there was a frequent association with enlargement of aneurysm and reinterventions. CONCLUSION: Our findings suggest that more frequent surveillance examinations are indicated than in patients without collateral endoleak. The indication for intervention is primarily dictated by documented expansion of the aneurysm.     

腔内修复术治疗肾下型腹主动脉瘤的内漏防治：附43例报告

目的：总结应用腔内修复术治疗腹主动脉瘤的经验,探讨内漏的防治策略。方法：回顾性分析齐鲁医院及莱钢医院2007年1月—2012年12月接受腔内治疗的43例肾下型腹主动脉瘤患者临床资料,分析内漏的发生原因、预防和处理。结果：术后发生原发性内漏11例,其中I型8例,III型2例;植入分叉型支架发生9例,植入直管型支架发生2例。1例II型因漏血量小未处理;经一期经过球囊扩张、植入支架型血管或裸支架等处理后,除2例I型内漏仍有残留,其余I,III型内漏均消失。39例患者获随访4~50个月,发现迟发性Ib型、II型内漏各2例,继续随访1~2年,未见瘤体明显增大。3例残留原发性内漏自愈,术后半年复发Ia型内漏1例,导致动脉瘤复发破裂而再次接受腔内治疗。结论：内漏的发生与动脉瘤的解剖学条件、移植物缺陷和操作技术有关;防治内漏需要把握好手术适应证、合理选择支架,并有成熟的操作经验。

     

Significance of endoleaks after endovascular repair of abdominal aortic aneurysms: The EUROSTAR experience

OBJECTIVE: The purpose of this study was to assess the incidence, risk factors, and consequences of endoleaks after endovascular repair of abdominal aortic aneurysm. METHODS: Data on 2463 patients were collected from 87 European centers and recorded in a central database. Preoperative data were compared for patients with collateral retrograde perfusion (type II) endoleak (group A), patients with device-related (type I and III) endoleaks (group B), and patients in whom no endoleak was detected (group C). Only endoleaks observed after the first postoperative month of follow-up were taken into consideration. Regression analysis was performed to investigate statistical relationships between the occurrence and type of endoleak and preoperative patient and morphologic characteristics, operative details, type of device, and experience of the operating team. In addition, postoperative changes in aneurysmal morphology, the need for secondary interventions, conversions to open repair, aneurysmal rupture, and mortality during follow-up were compared between these study groups. RESULTS: Patients in group A had a higher prevalence of a patent inferior mesenteric artery compared with patients without endoleak. Patients in group B were treated more frequently than patients in group C by an operating team with experience of less than 30 procedures. The mean follow-up period was 15.4 months. Secondary interventions were needed in 13% of the patients. Rupture of the aneurysm during follow-up occurred in 0.52% (1/191) in group A, 3.37% (10/297) in group B, and 0.25% (5/1975) in group C. Life table analysis comparing the three study groups demonstrated a significantly higher rate of rupture in group B than in group C (P =.002). The incidence of conversion to open repair during follow-up was higher in group B than in the other two study groups (P <.01). Death was related to the aneurysm or to endovascular repair of the aneurysm in 7% of patients. Secondary outcome success, defined as absence of rupture and conversion, was significantly higher in group A and C compared with that in group B (P =.006 and P =.0001, respectively). CONCLUSIONS: The presence of device-related endoleaks correlated with a higher risk of aneurysmal rupture and conversion compared with patients without type I or III endoleaks. Type II endoleak was not associated more often with these events. Consequently, intervention in type II endoleak should only be performed in case of increase of aneurysm size.     

Influence of treatment of type II leaks on the aneurysm surface area.

OBJECTIVE: to determine whether interventional treatment of type II endoleaks leads to a decrease in aneurysm surface area. MATERIAL AND METHOD: type II endoleaks were detected in a group of 14 male patients (median age: 70.2 years) following endovascular repair of a total number of 160 infrarenal aneurysms of the abdominal aorta. The surface area of the aneurysm was determined by computed tomography (CT) pre- and postoperatively and at subsequent follow-up examinations. If type II endoleaks were documented at CT, patients underwent treatment by means of coil embolisation. RESULTS: interventional treatment resulted in successful occlusion of type II endoleaks in eight patients. One of the cases exhibited spontaneous occlusion. Occlusion was associated with an average decrease in aneurysm surface area of 3.3 cm(2)( p =0.01). In one of these patients, treatment resulted in a temporary occlusion of the endoleak, also with associated decrease in aneurysm size. After recurrence of the type II endoleak, however, the patient experienced an increase in aneurysm surface area. In the remaining four patients the type II endoleaks persisted, resulting in a non significant increase in aneurysm surface area. CONCLUSION: only complete occlusion of endoleaks results in decrease in the size of the aneurysm sac. Because of endotension and the risk of rupture we favour an early interventional treatment of type II endoleaks.     

Endoleak after endovascular repair of abdominal aortic aneurysm.

PURPOSE: We sought to assess the role of endovascular techniques in the management of perigraft flow (endoleak) after endovascular repair of an abdominal aortic aneurysm. METHOD: We performed endovascular repair of abdominal aortic aneurysm in 114 patients, using a variety of Gianturco Z-stent-based prostheses. Results were evaluated with contrast-enhanced computed tomography (CT) at 3 days, 3 months, 6 months, 12 months, and every year after the operation. An endoleak that occurred 3 days after operation led to repeat CT scanning at 2 weeks, followed by angiography and attempted endovascular treatment. RESULTS: Endoleak was seen on the first postoperative CT scan in 21 (18%) patients and was still present at 2 weeks in 14 (12%). On the basis of angiographic localization of the inflow, the endoleak was pure type I in 3 cases, pure type II in 9, and mixed-pattern in 2. Of the 5 type I endoleaks, 3 were proximal and 2 were distal. All five resolved after endovascular implantation of additional stent-grafts, stents, and embolization coils. Although inferior mesenteric artery embolization was successful in 6 of 7 cases and lumbar embolization was successful in 4 of 7, only 1 of 11 primary type II endoleaks was shown to be resolved on CT scanning. There were no type III or type IV endoleaks (through the stent-graft). Endoleak was associated with aneurysm dilation two cases. In both cases, the aneurysm diameter stabilized after coil embolization of the inferior mesenteric artery. There were two secondary (delayed) endoleaks; one type I and one type II. The secondary type I endoleak and the associated aneurysm rupture were treated by use of an additional stent-graft. The secondary type II endoleak was not treated. CONCLUSIONS: Type I endoleaks represent a persistent risk of aneurysm rupture and should be treated promptly by endovascular means. Type II leaks are less dangerous and more difficult to treat, but coil embolization of feeding arteries may be warranted when leakage is associated with aneurysm enlargement.     

Sac enlargement without endoleak: when and how to convert and technical considerations

The primary goal of endovascular treatment of abdominal aortic aneurysms (AAA) is prevention of death from rupture. Even in the absence of an endoleak, the AAA may continue to enlarge. The pathogenesis of this phenomenon remains unclear. Therefore, surveillance after endovascular AAA treatment must include regular evaluation of aneurysm size, or even better, aneurysm volume. Aneurysm sac enlargement without an endoleak is not a benign condition. Recurrent or persistent pressurization of the AAA sac will eventually result in rupture. Besides that, continued expansion of the AAA sac can result in dilatation of the infrarenal neck and/or iliac arteries, which may threaten the integrity of proximal and distal anastomotic seals. Many centers will take a pragmatic approach in case of endotension and a growing AAA, and convert to open surgery with removal of the endograft and placement of a regular vascular graft. Direct puncture and pharmacological intervention in the cause of sac enlargement by local instillation seems logical, but has failed so far. The third option for aneurysm sac enlargement without an endoleak is laparoscopic or open fenestration of the aneurysm. Until permanent solutions for endotension and endoleaks are found, endovascular aneurysm repair will remain an imperfect long-term treatment and continued follow-up will be mandatory.     

Management of a large intraoperative type IIIb endoleak in a bifurcated endograft-a case report

The purpose of this paper is to describe the intraoperative management of a type IIIb endoleak after deployment of a bifurcated endograft in a patient with narrow iliac access vessels. A 62-year-old man underwent elective endovascular repair (EVAR) of a 53 mm abdominal aortic aneurysm. After device deployment, a large IIIb endoleak, arising from the main body of the device, was visualized. Narrow iliac vessels precluded deployment of a second bifurcated graft, and the endoleak was successfully excluded with an aortomonoiliac device, followed by contralateral iliac occlusion and subsequent creation of a femorofemoral bypass. At 1-year follow-up, the aneurysm remains excluded and is decreasing in size. Type III endoleaks are a known complication of EVAR, requiring immediate treatment through their association with aneurysm enlargement and rupture. If an additional bifurcated graft cannot be used, aortomonoiliac conversion represents a feasible endovascular alternative treatment for type III endoleaks, other than conversion to open surgical repair. Therefore, aortomonoiliac converters with appropriate occluder devices should be readily available during deployment of bifurcated devices.     

Freedom from endoleak after endovascular aneurysm repair does not equal treatment success.

OBJECTIVE: To determine whether freedom from endoleak after endovascular repair of abdominal aortic aneurysm (EVAR) is a reliable guide to freedom from persistent or recurrent pressurisation of the aneurysm sac (endotension) and therefore freedom from risk of rupture. PATIENTS AND METHODS: The records of 55 patients followed for more than 3 months after EVAR were reviewed to correlate the presence or absence of endoleak on contrast-enhanced CT and/or angiography with changes in maximum aneurysm diameter (DMAX). RESULTS: in 22 (40%) patients there was no significant change in DMAX during follow-up. In 21 of these no endoleak was observed on CT or angiography. One patient developed a secondary side-branch endoleak which remains under observation. In 18 (33%) patients, DMAX decreased during follow-up. Thirteen of these remained free of endoleak. Four patients developed secondary endoleaks which were treated by secondary intervention. One patient with persistent primary endoleak suffered fatal aneurysm rupture three days before planned intervention. DMAX increased in 15 (27%) patients. In only five of these could an endoleak be identified on CT and/or angiography. One primary side-branch endoleak persists following failed embolisation. Four secondary endoleaks have been corrected by secondary intervention. Four of the remaining 10 patients died suddenly from unknown cause. All had DMAX greater than 65 mm at last follow-up. One patient underwent late conversion, which suggested continued pressurisation through thrombus at the site of a "sealed" primary proximal endoleak. Two patients are scheduled to undergo embolisation of patent side-branches revealed only by Levovist enhanced Duplex scanning and three patients remain under observation. CONCLUSION: Freedom from endoleak on conventional imaging incorrectly suggested freedom from endotension in 10 (18%) of our patients. Follow-up after endovascular repair must include regular measurement of DMAX and/or aneurysm sac volume to identify those patients who remain at risk of rupture.     

腹主动脉瘤腔内治疗并发症内漏的诊治

目的 探讨血管内技术治疗腹主动脉瘤时特有并发症内漏的诊断与处理方法。方法 对已施行腔内治疗37例腹主动脉瘤患者进行回顾性分析,讨论部分患者并发内漏的原因、诊断、处理、结果及预后。结果 37例支架型血管放置完成后,13例发现存在不同程度的内漏,其中I型6例,Ⅱ型3例,Ⅲ型2例,Ⅳ型1例,不明原因1例,1期经相关技术处理后I型、Ⅲ型内漏完全消失。手术结束时原发性内漏发生率13．5％（5／37）。随诊发现原发性内漏3例自愈,2例转化为持续性内漏;另发现2例继发性内漏发生率13．5％（5／37）。随诊发现原发性内漏3例自愈,2例转化为持续性内漏;另发现2例继发发现人漏。本组患者晚期内漏发生率10．8％（4／37）。结论 引起漏血的原因可能与瘤颈形态、长度、成角、钙化、移植物选择、分支血管血液倒流等因素有关。强调术中发现并一期处理,术后应密切随访。增强CT、血管超声和MRA检查是术检后检测内漏的主要手段。对漏血量及瘤体有增大趋势的内漏应积极处理。     

Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: significance of endotension from a "virtual," or thrombosed type II endoleak

Type II endoleaks, resulting from retrograde branch flow, after endovascular graft aneurysm exclusion are considered benign because they usually thrombose and are commonly associated with stable or shrinking aneurysm sacs. We report a hypogastric artery aneurysm rupture from endotension from an undetected, thrombosed Type II endoleak, associated with sac shrinkage. The patient had undergone an endovascular graft repair of a 4-cm right common iliac artery and 9-cm hypogastric artery aneurysm with distal hypogastric artery coil embolization. Serial computed tomography scans revealed no endoleak and a hypogastric aneurysm thrombosis with shrinkage. Eighteen months later, the aneurysm ruptured as a result of pressurization from backbleeding, patent branches.     

Endoleaks after endovascular repair of thoracic aortic aneurysms

OBJECTIVE: Endoleaks are one of the unique complications seen after endovascular repair of thoracic aortic aneurysms (TEVAR). This investigation was performed to evaluate the incidence and determinants of endoleaks, as well as the outcomes of secondary interventions in patients with endoleaks, after TEVAR. METHODS: Over a 6-year period, 105 patients underwent TEVAR in the context of pivotal Food and Drug Administration trials with the Medtronic Talent (n = 64) and Gore TAG (n = 41) devices. The medical and radiology records of these patients were reviewed for this retrospective study. Of these, 69 patients (30 women and 39 men) had follow-up longer than 1 month and were used for this analysis. The patients were evaluated for the presence of an endoleak, endoleak type, aneurysm expansion, and endoleak intervention. RESULTS: The mean follow-up in this patient cohort was 17.3 +/- 14.7 months (range, 3-71 months). Endoleaks were detected in 29% (20/69) of patients, of which 40% (8/20) were type I, 35% (7/20) were type II, 20% (4/20) were type III, and 5% (1/20) had more than one type of endoleak. Patients without endoleaks experienced greater aneurysm sac regression than those with endoleaks (-2.89 +/- 9.1 mm vs -0.13 +/- 7.2 mm), although this difference was not statistically significant (P = .232). All but 2 endoleaks (90%; 18/20) were detected on the initial postoperative computed tomographic scan at 30 days. Two endoleaks (10%; 2/20) developed late. The endoleak group had more extensive aneurysms with significantly larger aneurysms at the time of intervention (69.4 +/- 10.5 mm vs 60.6 +/- 11.0 mm; P = .003). Factors predictive of endoleak included male sex (P = .016), larger aneurysm size (P = .003), the length of aorta treated by stent grafts (P = .0004), and an increasing number of stents used (P < .0001). No open conversions were performed for treatment of endoleaks. Four (50%) of the eight type I endoleaks were successfully repaired by using endovascular techniques. None of the type II endoleaks was treated by secondary intervention. During follow-up, the maximum aneurysm diameter in the type II endoleak patients increased a mean of 2.94 +/- 7.2 mm (range, -4.4 to 17 mm). Spontaneous thrombosis has occurred in 29% (2/7) of the type II endoleaks. Patients with type III endoleaks experienced a decrease in mean maximal aneurysm diameter of 0.78 +/- 3.1 mm during follow-up. CONCLUSIONS: Endoleaks are not uncommon after TEVAR. Many type I endoleaks may be treated successfully by endovascular means. Short-term follow-up suggests that observational management of type II endoleaks is associated with continued sac expansion, and these patients should be monitored closely.     

EVAR reintervention management strategies in contemporary practice

It is known that following an endovascular aneurysm repair (EVAR) procedure, patients may experience endoleaks, device migration, stent fractures, graft deterioration, or aneurysm growth that might require a reintervention. In this review management strategies of reinterventions after EVAR in contemporary practice will be discussed. The current endovascular treatment options of Type I endoleak involve securing of the attachment site with percutaneous transluminal balloon angioplasty, stent-graft extension, or placement of a stent at the proximal attachment site. Moreover, the use of endostaples to secure the position of the proximal cuff to the primary endograft have been developed. Type II endoleaks can be managed conservatively if the aneurysm is shrinking or remains stable. Otherwise, reinterventions include transarterial embolization, translumbar embolization, transcaval embolization, direct thrombin injection, and endoscopic or open ligation of the lumbar and mesenteric arteries. There is little debate regarding the treatment of type III endoleaks, including deployement of additional stent graft components to bridge the defect. Endovascular treatment of endotension includes endovascular conversion stent or relining of the stent graft. Alternative options are puncture of the aneurysm sac and removal of the aneurysm sac content. In case of migration large balloon-expandable stents can be used to improve the seal between the components, or devices that deploy staples to secure endovascular grafts to the aortic wall to secure endovascular components together. In conclusion, the first treatment options for reinterventions after EVAR are catheter based nowadays.     

Nonoperative approach to endotension

OBJECTIVE: The necessity of operative treatment of endotension after endovascular grafting of abdominal aortic aneurysms (endovascular aneurysm repair; EVAR) is under debate. The proposed causes of endotension and related treatment protocols are controversial. We report the outcome of a nonoperative approach to five patients with endotension after EVAR. METHODS: From February 1997 to August 2004, 160 patients who underwent EVAR of an infrarenal abdominal aortic aneurysm were evaluated for the incidence of endotension. According to the endovascular protocol, plain radiographs, spiral computed tomography, and angiography were performed before and after surgery for follow-up. To detect endotension, spiral computed tomography was performed by using a delayed imaging technique after the infusion of contrast medium. Endotension was defined as an aneurysm sac enlargement after EVAR without evidence of endoleak. Aneurysm sac rupture was defined as discontinuity of the calcific rim of the aneurysmal sac and the presence of intra-aneurysmal fluid outside the sac. RESULTS: We found five (3.1%) patients with endotension. Three of these experienced aneurysmal sac rupture. Only one of the three was underwent operation on experiencing sudden intestinal occlusion due to intra-abdominal adhesions. This patient had no intra-abdominal or retroperitoneal bleeding or hematoma but died after intensive care as a result of non-aneurysm-related problems. Four patients with endotension are still being closely followed up according to our surveillance protocol, and they are doing clinically well. After rupture, clear shrinking of the aneurysm sac was seen in two patients. CONCLUSIONS: Endotension after EVAR may cause subsequent aneurysm rupture. Endotension is evidently not associated with endoleak I to III provided that the endovascular graft is maintained in appropriate position and that free endovascular flow is observed. We propose to consider a nonoperative approach in the clinically asymptomatic patient with aneurysm enlargement after EVAR if endoleak is excluded by well-performed imaging techniques.     

Endovascular repair of abdominal aortic aneurysm: current status

INTRODUCTION: Endovascular aneurysm surgery (EVAR) was introduced a decade ago. Early results are promising, however, there remain concerns regarding the longer-term durability of this technique. Consequently, the national multi-centre EVAR trial has been commenced to define the role of endovascular surgery in the management of abdominal aortic aneurysm. DISCUSSION: Successful EVAR requires accurate pre-operative assessment of aneurysm morphology. Current stent-grafts allow 60% of all infra-renal AAA to be treated. Reduced physiological stress and low peri-operative morbidity and mortality rates have been demonstrated with this technique when compared to open repair. Endoleak is an Achilles heel of EVAR, although in itself does not accurately predict outcome. First and second generation devices are estimated to have a 1% per year risk of rupture. CONCLUSIONS: Increased understanding of the issues surrounding aneurysm morphology and successful stent-grafting have allowed a major reduction of early type I endoleak. Late endoleak and graft migration remain problematic. Type I and III endoleaks are risk factors for subsequent rupture although the significance of type II endoleak remains uncertain. More robust indicators of outcome success/failure are required so that follow-up may be rationalised.     

Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: Significance of endotension from a “virtual,” or thrombosed type II endoleak

Type II endoleaks, resulting from retrograde branch flow, after endovascular graft aneurysm exclusion are considered benign because they usually thrombose and are commonly associated with stable or shrinking aneurysm sacs. We report a hypogastric artery aneurysm rupture from endotension from an undetected, thrombosed Type II endoleak, associated with sac shrinkage. The patient had undergone an endovascular graft repair of a 4-cm right common iliac artery and 9-cm hypogastric artery aneurysm with distal hypogastric artery coil embolization. Serial computed tomography scans revealed no endoleak and a hypogastric aneurysm thrombosis with shrinkage. Eighteen months later, the aneurysm ruptured as a result of pressurization from backbleeding, patent branches. (J Vasc Surg 2001;33:1271-4.)     

Transcaval embolization of a type I gutter endoleak after three-vessel chimney endovascular aneurysm repair

Chimney endovascular aneurysm repair provides an endovascular treatment for complex aortic aneurysms. However, type I gutter endoleaks can complicate this approach and prevent full aneurysm exclusion. Treatment of these leaks can be challenging. We report successful embolization of a type I gutter endoleak after (chimney endovascular aneurysm repair) via a transcaval approach.     

Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: the EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair

OBJECTIVE: The EUROSTAR (European Collaborators on Stent/graft techniques for aortic aneurysm repair) Registry was established in 1996 to collect data on the outcome of treatment of patients with infrarenal aortic aneurysms with endovascular repair. To date, 88 European centers of vascular surgery have contributed. The purpose of the study was to evaluate the results of this treatment in the medium term (up to 4 years) according to the analysis of "hard" or primary end points of rupture, late conversion, and death. PATIENTS AND METHODS: Patients with aortic aneurysms suitable for endovascular aneurysm repair were notified to the EUROSTAR Data Registry Centre before treatment to eliminate bias due to selective reporting. The following information was collected on all patients: (1) demographic details and the anatomic characteristics of their aneurysms, (2) details of the endovascular device used, (3) complications encountered during the procedure and the immediate outcome, (4) results of contrast enhanced computed tomographic imaging at 3, 6, 12, and 18 months after operation and at yearly intervals thereafter, and (5) all adverse events. Life table analysis was performed to determine the cumulative rates of (1) death from all causes, (2) rupture, and (3) late conversion to open repair. Risk factors for rupture and late conversion were identified through regression analysis. RESULTS: By March 2000, 2464 patients had been registered, and their mean duration of follow-up was 12.19 months (SD, 12.3 months). There were 14 patients with confirmed rupture of their aneurysms. The cumulative rate (risk) of rupture was approximately 1% per year. Emergency surgery was undertaken in 12 (86%) patients, of whom five (41.6%) survived. Two patients who were not treated surgically also died, which resulted in an overall death rate of 64.5% (9/14) of the patients. Significant risk factors for rupture were proximal type I endoleak (P =.001), midgraft (type III) endoleak (P =.001), graft migration (P =.001), and postoperative kinking of the endograft (P =.001). Forty-one patients underwent late conversion to open repair with a perioperative mortality rate of 24.4% (10/41). The cumulative rate (risk) of late conversion was approximately 2.1% per year. Risk factors (indications) for late conversion were proximal type I endoleak (P =. 001), midgraft (type III) endoleak (P =.001), type II endoleak (P =. 003), graft migration (P =.001), graft kinking (P =.001), and distal type I endoleak (P =.001). CONCLUSIONS: Endovascular repair of infrarenal aortic aneurysms with the first- and second-generation devices that predominated in this study was associated with a risk of late failure, according to an analysis of observed hard end points of 3% per year. Action taken to address the risk factors identified by the study may improve results in the future.