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。     

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。

     

A complication of open abdominal aortic aneurysm repair closely resembling a type II endoleak

Endoleak is a well-recognized complication of endovascular treatment of abdominal aortic aneurysms. Despite over 40 years of open transabdominal aortic aneurysm surgery, only in the last decade has endoleak as a complication of open surgery been described. Endoleak after conventional open surgery was first described by Chan et al in 2000 and remains a rare complication. We describe the first reported case of type II endoleak (back-bleeding inferior mesenteric artery) after open repair of abdominal aortic aneurysm, and its successful management by endovascular coil embolization.     

Management of endoleak after endovascular aneurysm repair: cuffs,coils, and conversion

OBJECTIVE: The effectiveness of endovascular treatment of abdominal aortic aneurysm (AAA) may be limited by persistent perfusion of the aneurysm sac (endoleak). Endoleak that results in persistent systemic pressurization of the aneurysm or in continued AAA expansion is believed to require treatment to prevent rupture. This report describes the results of three techniques used to treat endoleak. METHODS: Endovascular repair of AAA was performed in 597 patients between January 1996 and September 2002. Seventy-three endoleaks that required treatment developed in 70 patients (11.7%). These involved the graft attachment site (type I) or the graft junction site (type III) or originated from collateral side-branch vessels (type II) and were associated with an increase in aneurysm size. Endoleak type was confirmed at angiography in all cases. Average time between the initial endovascular procedure and endoleak treatment was 14.5 +/- 5.7 months. The techniques used for endoleak treatment were deployment of an endovascular extension graft or cuff (n = 44), coil embolization (n = 24,) and conversion to conventional open repair (n = 5). Configurations of endovascular grafts in which endoleak developed were bifurcated (n = 44), aortouniiliac (n = 15), and aortoaortic-tube (n = 11). Mean follow-up after endoleak treatment was 24.5 +/- 12.2 months (range, 1-60 months). RESULTS: Endovascular extension grafts or cuffs were used to treat 41 attachment site endoleaks and 3 graft junction endoleaks, with overall technical success rate of 97%. Embolic coils were used to treat 16 retrograde side-branch endoleaks and 8 attachment site endoleaks, with overall technical success rate of 87%. Conversion to open surgery was performed in 4 patients with attachment site endoleaks and 1 patient with a graft junction site endoleak, and was successful in all cases. After endoleak treatment, aneurysm size decreased (>5 mm) in 38% of patients, stabilized in 58% of patients, and increased (>5 mm) in 4% of patients. Major morbidity occurred in 7.0%, with no perioperative deaths. CONCLUSIONS: Endovascular extension grafts, coil embolization, and conversion to open surgery each may be used to effectively repair endoleak. Selection of the treatment method used is determined by the anatomic characteristics of the endoleak and the patient's ability to tolerate conventional repair. Conversion to open repair was uniformly successful. Deployment of an extension cuff was successful when complete closure of the endoleak was achieved. Embolic coils were effective for retrograde endoleaks and provided stabilization of AAA size in selected patients with attachment site endoleaks in limited follow-up.     

Type II endoleak after endovascular abdominal aortic aneurysm repair: a conservative approach with selective intervention is safe and cost-effective

OBJECTIVES: The conservative versus therapeutic approach to type II endoleak after endovascular repair of abdominal aortic aneurysm (EVAR) has been controversial. The purpose of this study was to evaluate the safety and cost-effectiveness of the conservative approach of embolizing type II endoleak only when persistent for more than 6 months and associated with aneurysm sac growth of 5 mm or more. METHODS: Data for 486 consecutive patients who underwent EVAR were analyzed for incidence and outcome of type II endoleaks. Spiral computed tomography (CT) scans were reviewed, and patient outcome was evaluated at either office visit or telephone contact. Patients with new or late-appearing type II endoleak were evaluated with spiral CT at 6-month intervals to evaluate both persistence of the endoleak and size of the aneurysm sac. Persistent (>or=6 months) type II endoleak and aneurysm sac growth of 5 mm or greater were treated with either translumbar glue or coil embolization of the lumbar source, or transarterial coil embolization of the inferior mesenteric artery. RESULTS: Type II endoleaks were detected in 90 (18.5%) patients. With a mean follow-up of 21.7 +/- 16 months, only 35 (7.2%) patients had type II endoleak that persisted for 6 months or longer. Aneurysm sac enlargement was noted in 5 patients, representing 1% of the total series. All 5 patients underwent successful translumbar sac embolization (n = 4) or transarterial inferior mesenteric artery embolization (n = 4) at a mean follow-up of 18.2 +/- 8.0 months, with no recurrence or aneurysm sac growth. No patient with treated or untreated type II endoleak has had rupture of the aneurysm. The mean global cost for treatment of persistent type II endoleak associated with aneurysm sac growth was US dollars 6695.50 (hospital cost plus physician reimbursement). Treatment in the 30 patients with persistent type II endoleak but no aneurysm sac growth would have represented an additional cost of US dollars 200000 or more. The presence or absence of a type II endoleak did not affect survival (78% vs 73%) at 48 months. CONCLUSIONS: Selective intervention to treat type II endoleak that persists for 6 months and is associated with aneurysm enlargement seems to be both safe and cost-effective. Longer follow-up will determine whether this conservative approach to management of type II endoleak is the standard of care.     

Mechanism of failure in the treatment of type II endoleak with percutaneous coil embolization

PURPOSE: Type II endoleak after endovascular abdominal aortic aneurysm repair is a failure of aneurysm sac exclusion with unknown long-term consequences. Elevated aneurysm sac pressures documented in these patients have led us to aggressively treat type II endoleaks with percutaneous transluminal coil embolization (PTCE). The purpose of this study was to evaluate the results and the mechanisms of failure of PTCE for type II endoleak. METHODS: One hundred ninety-one patients underwent endograft repair of infrarenal aortic aneurysms. Twenty-three of 28 patients with persistent primary (>3 months) or secondary (new-onset) endoleak underwent angiography; 14 of these patients had type II endoleaks. We reviewed our endovascular registry data, hospital charts, and radiologic studies of patients with type II endoleaks and analyzed the results in those treated with PTCE of the inflow vessel. RESULTS: All 14 patients with type II endoleaks were men, with a mean age of 76.7 years and a mean preoperative maximal aneurysm diameter of 5.7 +/- 1.0 cm. The type II endoleak was primary in 12 patients (86%) and secondary in two patients (14%) and iliolumbar in 11 patients (78%) and mesenteric in three patients (21%). Although a dominant affluent collateral channel (inosculation) was apparent in eight patients (57%), six patients (43%) showed a network of collateral vessels (retiform anastomosis). In six patients (43%), angiography revealed a second or "outflow" vessel indicative of a complex endoleak. In four patients with retiform iliolumbar type II endoleaks, PTCE was not attempted because of the retiform nature of the endoleak. The remaining 10 patients underwent PTCE, with coil deployment in all 10 and apparent initial technical success in nine patients. Follow-up computed tomographic scans revealed persistent endoleaks in six patients (60%). Mechanisms of failure included persistent flow through the coils in the treated vessel in two patients, development of a retiform anastomosis around the coiled vessel in three patients, and development of a new mesenteric endoleak after successful occlusion of an iliolumbar endoleak in one patient. Two patients underwent repeat PTCE with successful aneurysm sac exclusion in one. Internal iliac artery injury complicated one of the 12 PTCEs, and the resulting pseudoaneurysm was successfully treated with PTCE. Angiographic visualization of an outflow vessel (complex endoleak) was associated with PTCE failure (P =.008). CONCLUSION: PTCE of type II endoleaks has a high failure rate because of multiple anatomic mechanisms.     

Type II endoleaks: predictable,preventable, and sometimes treatable?

OBJECTIVE: The purpose of this study was to evaluate the effect of preoperative coil embolization of lumbar and inferior mesenteric arteries on the incidence of type II endoleak after endovascular abdominal aortic aneurysm repair. METHODS: The subjects were consecutive patients who underwent EVAR between January 1996 and January 2001. Patent aortic side branches were identified with preprocedural spiral computed tomographic scanning and calibrated angiography. Coil embolization was performed before EVAR. Patients were followed up with plain radiographs and ultrasound and dual phase spiral computed tomographic scans. Digital subtraction angiography was performed when endoleak was suspected. The outcome measures were the incidence of type II endoleaks and changes in maximum aortic sac diameter (Dmax). RESULTS: Forty patients underwent EVAR, with a median duration of follow-up of 24 months (range, 3 to 48 months). Before surgery, the inferior mesenteric artery was patent in 16 patients (45%) and the lumbar arteries in 21 patients (53%). Inferior mesenteric artery embolization was successful in 13 of 16 patients (81%). Lumbar embolization was attempted in 13 patients and was successful in eight (62%). During EVAR, successful sac exclusion was achieved in 38 patients (95%). None of the patients who underwent embolization before EVAR had type II endoleak develop, eight of 13 patients (62%) with patent lumbar arteries had endoleaks develop (P =.006), and three of these patients subsequently underwent successful coil embolization. Type II endoleak was associated with a 2.0-mm median increase in Dmax (P =.045). A 3.0-mm median reduction in Dmax was seen in the absence of type II endoleak (P =.002). CONCLUSION: Type II endoleaks are predictable, preventable, and sometimes treatable. Significant sac shrinkage occurs in the absence of lumbar endoleak but not in the presence of type II endoleak.     

Infected endovascular graft secondary to coil embolization of endoleak: a demonstration of the importance of operative sterility

A 60-year-old male underwent endovascular repair of a 5.4-cm enlarging abdominal aortic aneurysm with intraoperative recognition of a type I endoleak. The endoleak was demonstrated to be arising from the left limb of the bifurcated prosthesis. An intravascular stent was placed in the limb near the origin of the common iliac artery and it appeared that the endoleak had sealed. However, 1 month after operation a CT scan demonstrated a persistent, substantial size endoleak without aneurysm enlargement. Coil embolization of the endoleak was undertaken in the interventional radiology suite with apparent satisfactory result. Four days after embolization the patient developed abdominal pain and after 8 days fever and leukocytosis developed. Two weeks after embolization an abdominal CT and indium scan revealed an infected endovascular graft. By CT, the posterior wall of the aneurysm was destroyed and a peri-graft fluid collection with gas was present at the location of the coils. The patient was treated with graft and coil excision and autologous vein reconstruction. Endoluminal prostheses can be contaminated at the time of operative placement. However, an additional source of endoluminal graft infection can arise from secondary endovascular procedures for endoleaks and other graft complications. Since we began placing endovascular grafts at our institution in 1993, most coil embolizations have been performed in the interventional radiology suite. This experience of coil-induced infection causes us to consider performing this type of secondary intervention in the operating room environment.     

Type 1A endoleak detachable coil embolization after endovascular aneurysm sealing: Case report

IntroductionEndovascular aneurysm sealing (EVAS) with the Nellix system was introduced to reduce endovascular aneurysm repair (EVAR) perioperative complications, especially endoleaks. Herein we report a case of successful type 1A endoleak managed with detachable coils embolization after EVAS.Presentation of caseA 77-year-old male was referred for abdominal pain. The angio-CT scan confirmed the previous EVAS procedure and showed a type Is2 endoleak below the right renal artery resulting in a 2.5 cm aortic blister with contrast medium filling the space between the aortic wall and the endobags. The patient was considered unfit for conventional open surgery and an endovascular approach with coil embolization Concerto Helix Detachable Coil System was chosen under local anesthesia. After intervention, a complete abdominal pain regression was registered. The 12- month CT follow-up showed endoleak sealing and Nellix system stability.DiscussionEVAS has been associated to a high endoleaks and complications incidence when compared to EVAR. The EVAS different device concept led to a different endoleak classification and management. Endoleak management main options include the Nellix system explantation or the Nellix in Nellix application, however these are nearly always not applicable, respectively, due to the high surgical risk condition and the Nellix system availability, especially in emergent setting. Despite the use of coil embolization is controversial, this tool is off-the-shelf and leads to a disease resolution in most of patients without other surgical options.ConclusionProximal type Is2 embolization after EVAS is feasible with limited invasiveness.     

腹主动脉腔内修复术后II型内漏的栓塞治疗：附3例报告

目的:探讨腹主动脉腔内修复术(EVAR)后Ⅱ型内漏的治疗方法。方法:回顾性分析2011—2016年中南大学湘雅医院血管外科治疗的3例EVAR术后比较严重的Ⅱ型内漏患者的临床资料,1例胸腹主动脉瘤行杂交手术(开放手术重建内脏血管+EVAR)后瘤体继续增大,检查发现为腹腔干动脉反流性内漏;另外2例均为腹主动脉瘤行EVAR术后肠系膜下动脉反流性内漏。结果:腹腔干动脉反流性内漏患者用Interlock可解脱弹簧圈系统栓塞,另外2例采用普通弹簧圈栓塞。3例栓塞均获得成功,内漏消失。结论:EVAR术后Ⅱ型内漏采用不同的入路栓塞是行之有效的方法。     

Laparoscopic transperitoneal clipping of the inferior mesenteric artery for the management of type II endoleak after endovascular repair of an aneurysm

We report the case of a high risk patient with an abdominal infrarenal aortic aneurysm (AAA) who was treated by endovascular technique and the subsequent management of a type II endoleak by the laparoscopic approach. In this case, a 74-year-old woman with a 6-cm infrarenal AAA underwent endovascular repair using a bifurcated stent-graft device. Surveillance CT scan showed a persistent type II endoleak at 1 week and 3 months after the operation. Angiography confirmed retrograde flow from the inferior mesenteric artery (IMA). Attempted transarterial embolization of the IMA via the superior mesenteric artery was not successful. Laparoscopic transperitoneal IMA clipping was performed. Subsequent aortic duplex scan and CT scan confirmed complete elimination of the type II endoleak. We conclude that a combination of endovascular and laparoscopic procedures can be used to manage AAA successfully.     

What is the significance of endoleaks and endotension

Endovascular repair has been used over a decade as a treatment of abdominal aortic aneurysm, and has become a widely accepted treatment method with a low rate of perioperative complications. Endoleak, perigraft blood flow outside endograft but within aneurysmsac, has been intensively studied during the last 10 years of endovascular aneurysm repair (EVR). The natural history of aneurysms with endoleak and the true clinical significance of various types of endoleaks remains unclear. Type I/III endoleak has been found to be associated with aneurysm rupture, while the risk of rupture of aneurysms with type II endoleak and endotension appears very small. In endotension, the aneurysm sac remains pressurized, even if there is no evidence of an endoleak. Currently,it is accepted that type I/III endoleaks should be corrected, preferably by endovascular means, due to the risk of rupture. If endovascular repair is not possible, then open conversion should be considered. The risk of conversion should be weighed against the risk of aneurysm rupture. Treatment of type II endoleaks and endotension is more controversial. In those with aneurysm enlargement,secondary interventions are often performed.     

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.     

主动脉腔内修复术后中远期并发症与二次处理策略

目的探讨主动脉腔内修复术后中远期并发症的处理方法与效果。方法1999年5月至2007年6月对21例主动脉病变腔内修复术后中远期并发症进行了再次处理。其中腹主动脉瘤（AAA）15例,胸主动脉动脉瘤（TAA）3例,主动脉夹层（TAD）3例。并发症：Ⅰ型内漏11例,Ⅱ型内漏4例,Ⅲ型内漏2例;移植物阻塞4例。应用延长支架型血管技术处理Ⅰ、Ⅲ型内漏（6例）,应用“侧孔”、“凹口”、“分叉”支架型血管结合颈部血管旁路手术重建主动脉弓处理Ⅰ型内漏（3例）,应用栓塞技术处理Ⅱ型内漏（4例）,应用取栓和旁路手术技术处理移植物阻塞（4例）,应用开放手术技术处理动脉瘤破裂（1例）。结果20例（95．2％）应用腔内技术作为二次处理主要手段,二次处理30d内死亡1例（4．7％）,因技术需要而修改器材结构者3例。二次术后仍存在内漏者5例（29．4％,5／17）。二次干预瘤体相关性死亡3例（14．3％）。结论内漏和移植物阻塞是腔内修复术后主要中远期并发症,其主要原因是原发性内漏的延续和移植物移位。腔内技术可作为二次处理的主要手段。主动脉弓部病变进行二次干预有更大的挑战性。     

Colonic necrosis subsequent to catheter-directed thrombin embolization of the inferior mesenteric artery via the superior mesenteric artery: A complication in the management of a type II endoleak

The optimal management of endoleaks after endovascular repair of abdominal aortic aneurysms remains to be established. In this report, we describe a persistent side-branch, or type II, endoleak 1 year after endograft implantation treated with catheter-directed embolization of the aneurysm sac and the inferior mesenteric artery via the superior mesenteric artery, with embolization agents including thrombin, lipiodol, and gelfoam powder. Shortly after the embolization procedure, colonic necrosis developed in the patient, manifested by peritonitis, which necessitated a partial colectomy. This case underscores the devastating complication of colonic ischemia as a result of catheter-directed embolization of the inferior mesenteric artery in the management of an endoleak.     

Clinical Significance of Type II Endoleak after Endovascular Repair of Abdominal Aortic Aneurysm

Type II endoleaks after endovascular repair of abdominal aortic aneurysm (EVAR) are a result of retrograde flow from arterial branches (e.g., lumbar and inferior mesenteric) refilling the aneurysm sac, which has been excluded by the stent graft. Controversy continues with regard to the clinical significance and treatment of type II endoleaks. To develop recommendations for management, we analyzed outcome data from 10 EVAR trials completed over the last 5 years involving a total of 2,617 cases. The incidence of type II endoleak at discharge or 30 days was 6-17%, at 6 months 4.5-8%, and at 1 year 1-5%. Successful resolution of endoleak following secondary interventions was observed in 11-100% of cases. There were 10 conversions to open repair and no ruptures related to type II endoleak. In patients observed for 12 months with computed tomography and/or ultrasound, approximately one-half of type II endoleaks disappeared spontaneously. In the absence of a type I endoleak, our analysis of the current literature suggests that intervention for type II endoleak should be undertaken for abdominal aortic aneurysm sac enlargement occurring after 6 months, persistence for >12 months without abdominal aortic aneurysm sac enlargement, or an aneurysm sac pressure >20% of systolic blood pressure; translumbar aneurysm sac thrombosis and intra-arterial feeding vessel occlusion appear to be prudent management options. Presented at the Twenty-second Annual Meeting of the Southern California Vascular Surgery Society, San Diego, CA, May 1, 2004.     

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.     

Endoleaks after endovascular graft treatment of aortic aneurysms: Classification,risk factors,and outcome

Purpose: Incomplete endovascular graft exclusion of an abdominal aortic aneurysm results in an endoleak. To better understand the pathogenesis, significance, and fate of endoleaks, we analyzed our experience with endovascular aneurysm repair. Methods:Between November 1992 and May 1997, 47 aneurysms were treated. In a phase I study, patients received either an endovascular aortoaortic graft (11) or an aortoiliac, femorofemoral graft (8). In phase II, procedures and grafts were modified to include aortofemoral, femorofemoral grafts (28) that were inserted with juxtarenal proximal stents, sutured endovascular distal anastomoses within the femoral artery, and hypogastric artery coil embolization. Endoleaks were detected by arteriogram, computed tomographic scan, or duplex ultrasound. Classification systems to describe anatomic, chronologic, and physiologic endoleak features were developed, and aortic characteristics were correlated with endoleak incidence. Results: Endoleaks were discovered in 11 phase I patients (58%) and only six phase II patients (21%; p < 0.05). Aneurysm neck lengths 2 cm or less increased the incidence of endoleaks (p < 0.05). Although not significant, aneurysms with patent side branches or severe neck calcification had a higher rate of endoleaks than those without these features (47% vs 29% and 57% vs 33%, respectively), and patients with iliac artery occlusive disease had a lower rate of endoleaks than those without occlusive disease (18% vs 42%). Endoleak classifications revealed that most endoleaks were immediate, without outflow, and persistent (71% each), proximal (59%), and had aortic inflow (88%). One patient with a persistent endoleak had aneurysm rupture and died. Conclusions: Endoleaks complicate a significant number of endovascular abdominal aortic aneurysm repairs and may permit aneurysm growth and rupture. The type of graft used, the technique of graft insertion, and aortic anatomic features all affect the rate of endoleaks. Anatomic, chronologic, and physiologic classifications can facilitate endoleak reporting and improve understanding of their pathogenesis, significance, and fate. (J Vasc Surg 1998;27:69-80.)     

Endoleak after endovascular aneurysm repair: current concepts

Endoleak remains the most common complication following endovascular aneurysm repair. Over the past few years the classification of endoleaks has been defined and appropriate treatment identified for most endoleaks. The treatment of type II and type V endoleaks remains controversial. This article reviews the current knowledge relating to endoleak.     

Translumbar treatment of type II endoleaks after endovascular repair of abdominal aortic aneurysm

The modality of treatment and the appropriate time point to treat type II endoleaks after endovascular repair of abdominal aortic aneurysms (EVAR) remain controversial issues. The purpose of the present study was to assess the efficacy of translumbar embolization of type II endoleaks after endovascular repair of aortic aneurysm repair. Eighty-four consecutive patients after EVAR were analyzed for the onset of type II endoleaks. Of these, five patients had experienced translumbar embolization after ineffective intraartrial approach to exclude the endoleak. A combination of several liquid embolic agents was used as sealant. Post-procedural contrast-enhanced ultrasound (CEUS) was used to document the outcome of the embolization. Translumbar embolization was successful in four patients. Complete sealing of the nidus was seen on CEUS 24 h after the procedure. In one patient with a duplication of the inferior vena cava, the procedure was aborted because an additional type Ib endoleak was found. The procedure was well tolerated by all patients. The translumbar approach to treat growing aneurysm sacs in patients with persistent type II endoleaks is safe and well tolerated. The immediate post-interventional outcome as documented on CEUS is promising. Long-term follow-ups are yet to be performed.