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Outcomes of type II endoleaks after endovascular abdominal aortic aneurysm (AAA) repair: a single-center, retrospective study
Clinical Imaging 40 (2016) 875–879
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
Outcomes of type II endoleaks after endovascular abdominal aortic aneurysm (AAA) repair: a single-center, retrospective study☆,☆☆ Kaley Pippin a,⁎, Jacqueline Hill a, Jianghua He b, Philip Johnson a a b
Department of Radiology, University of Kansas Medical Center, 3901 Rainbow Blvd, Mailstop 4032, Kansas City, KS, 66160, USA Department of Biostatics, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS, 66160, USA
a r t i c l e
i n f o
Article history: Received 1 November 2015 Received in revised form 16 March 2016 Accepted 12 April 2016 Available online xxxx Keywords: Aortic aneurysm Abdominal Endovascular procedure Endoleak Aortic stent grafts
a b s t r a c t Purpose: This study aims to determine incidence and outcomes of type II endoleaks (T2E) after endovascular abdominal aortic aneurysm repair (EVAR). Methods: A retrospective review of procedural angiograms, computed tomography angiography, and medical records of 202 patients who underwent EVAR with the Gore Excluder stent graft was performed to determine presence and outcomes of T2E. Results: Median follow-up time for 163 patients meeting inclusion criteria [136 males (83%)] was 24.7 months (range=0.5–85.2 months). T2E occurred in 66/163 patients (40.5%). Aneurysm sac size was unchanged in 32/ 66 patients (48.5%), decreased in 22/66 (33.3%), and increased in 12/66 (18.2%). No aneurysm ruptures, conversion to open repair, or aneurysm-related deaths occurred. Conclusion: T2E are a common occurrence after EVAR, often with benign outcome. However, routine surveillance should be performed, particularly in patients with persistent endoleak or sac growth. © 2016 Elsevier Inc. All rights reserved.
1. Introduction Endovascular abdominal aortic aneurysm repair (EVAR) has become a widely accepted alternative to open surgical repair of abdominal aortic aneurysms (AAAs) since it was first described in 1991 [1]. When compared to open surgical repair, EVAR has significantly lower 30-day morbidity and mortality. This can largely be attributed to the minimally invasive technique of EVAR with 30-day mortality rates after EVAR reported as 1.2–2.1%, less than half the rate of open repair [2–4]. However, long-term morbidity and survival of patients undergoing EVAR have been shown to be no better than, or even inferior to, patients who have undergone open surgical repair [5–8]. This increased long-term morbidity and mortality following EVAR can be attributed to the presence of endoleaks, which have been associated with aneurysm sac expansion and rupture [9]. Endoleaks are caused by persistent blood flow into the native aortic aneurysm sac due to incomplete sealing or exclusion by the stent graft and are classified into five types (types I–V) based on the source of blood flow into the aneurysm sac [9]. Type II endoleaks are the most common, occurring in 3–43% of patients who have undergone EVAR, and occur when blood flows retrograde into the aneurysm sac through ☆ Conflicts of Interest: None. ☆☆ Preliminary data from this study were presented by P. Johnson at the 2014 Society of Interventional Radiology Annual Meeting. ⁎ Corresponding author. E-mail address: [email protected] (K. Pippin). http://dx.doi.org/10.1016/j.clinimag.2016.04.004 0899-7071/© 2016 Elsevier Inc. All rights reserved.
branch vessels and anastomotic connections [9]. Although common, there is no consensus on the optimal management of type II endoleaks once discovered [9–25]. Most physicians advocate that type II endoleaks have a benign course and practice a conservative approach of serial monitoring with computed tomography angiography (CTA) or ultrasound [10–21]. Other physicians believe that type II endoleaks lead to aneurysm sac rupture and practice a more aggressive approach of embolization of the endoleak [22–26]. The primary aim of this study was to determine the incidence and outcomes of type II endoleaks after EVAR utilizing a single brand of stent graft, Excluder (W. L. Gore and Associates, Flagstaff, Arizona). Because previous research has been limited to 4.8 years of follow-up, this study gathered data over an 8-year period with the intention of evaluating midterm outcomes of type II endoleaks [9]. We hypothesized that type II endoleaks are a common complication following EVAR, but most frequently have a benign outcome. 2. Materials and methods 2.1. Study design A retrospective study was conducted on a cohort of patients 18 years of age or older who underwent EVAR utilizing the Excluder stent graft at a tertiary care academic institution between April 1, 2005 and March 31, 2013. A vast majority of EVAR procedures at our institution in the chosen time period were performed using the Excluder stent graft. Therefore, we elected to evaluate the incidence and outcomes of type II
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K. Pippin et al. / Clinical Imaging 40 (2016) 875–879
Fig. 1. (a) Axial CTA image from a 74-year-old male demonstrates stent graft in the abdominal aorta with contrast opacification in the native aneurysm sac (arrow), compatible with a type II endoleak. (b) Axial CTA image from a different level in the same patient illustrates the method used to measure aneurysm sac (x=5.3 cm).
endoleaks with this commonly used device. Type II endoleaks were chosen as the focus of this study because it is the most controversial type of endoleak in terms of outcome and management. Evaluation of other types of endoleaks was beyond the scope of this study. Institutional review board approval was obtained to review patient records. 2.2. Inclusion and exclusion criteria All patients who underwent Gore Excluder stent graft placement for AAA by one of three board-certified interventional radiologists and/or vascular surgeons were eligible for inclusion in the study. Patients were excluded if they had ruptured, anastomotic, inflammatory, or infectious AAAs, as documented in the electronic medical record. Additionally, patients were excluded if they did not have at least one follow-up CTA of the abdomen/pelvis performed at our institution postprocedure. Patients who received follow-up imaging at outside institutions were excluded from the study due to the inability to review the images. Patients who were lost to clinical follow-up were included in this study if they had at least one follow-up CTA at our institution. Patients meeting inclusion criteria were identified through our institutional electronic medical record, utilizing CPT codes to select desired exams within the specified dates. 2.3. Image review Conventional angiograms and CTA abdomen/pelvis images for patients meeting inclusion criteria were independently reviewed by two board-certified radiologists to determine the presence or absence of type II endoleak. Any discrepant cases were adjudicated by a third board-certified radiologist. CTAs were performed according to standard of care at the time of acquisition and included precontrast images using 5 mm slices, arterial and venous phase images using 5 mm and 1.25 mm slices, and delayed images using 5 mm slices. The aneurysm sac was measured by a board-certified radiologist in a single plane at the point of maximum diameter using electronic calipers on axial CT images using Centricity PACS software (GE Medical Systems; Fig. 1). At our institution, standard imaging follow-up after EVAR is serial CTA at 30 days, 6 months, and annually thereafter. 2.4. Outcomes The primary outcome was to identify the incidence of type II endoleaks after EVAR. For this study, type II endoleaks were defined as
endoleaks that developed at the time of the postprocedural angiogram or were present on a follow-up CTA. Endoleaks were further divided into transient type II endoleaks (resolved in b180 days) and persistent type II endoleaks (persisted ≥ 180 days). Secondary study outcomes included endoleak persistence, aneurysm sac growth, secondary intervention, conversion to open repair, aneurysm rupture, and aneurysmrelated death. Aneurysm sac growth, shrinkage, or stability was determined using 5 mm as the cutoff value for significant change in size. Significant change of 5 mm was chosen because it is the most commonly used value in the literature [10–11,13–14]. Patient medical charts were reviewed by three medical students and a senior radiology resident to determine secondary clinical outcomes. Additional patient information, including demographics, tobacco use, comorbid clinical conditions, anticoagulation or antiplatelet medication use, patent lumbar and inferior mesenteric arteries, and presence of iliac artery aneurysm, was compared between patients who developed type II endoleaks and those who did not. While many of these factors are associated with AAA, we collected this information to determine if an association with type II endoleaks exists in order to better predict which patients might develop a type II endoleak.
Table 1 Demographic characteristics Characteristic
Patients Age in years (mean±SD) Follow-up months (mean±SD) Male Caucasian Tobacco users Hypertension Hyperlipidemia Diabetes Renal insufficiency COPD PVD CAD Anticoagulation medication Antiplatelet medication
P value+
Type II endoleak
No type II endoleak
n
%
n
%
66 72.5 ±9.7 26.9 ±21.7 55 59 53 54 51 11 9 11 14 43 6 57
40.5 − − 85.9 92.2 89.8 87.1 83.6 17.7 14.3 18.3 23.3 69.4 9.8 89.1
97 71.1±9.0 22.3±22.8 81 80 75 75 57 24 18 21 24 45 13 64
59.5 − − 81.8 86.9 94.9 90.4 72.1 30.8 23.1 27.3 30.7 56.7 16.7 76.2
.356 b.001 .490 .434 .325 .535 .110 .077 .187 .220 .332 .132 .245 .045
+ Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
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Fig. 2. Flowchart of patient selection and exclusion.
2.5. Statistical analysis Patient characteristics at baseline were summarized using descriptive statistics (mean and standard deviation for continuous variables and count and percentage for categorical variables) and compared between patients with and without type II endoleaks (Table 1). Preprocedural anatomic characteristics (patent lumbar and inferior mesenteric arteries, presence of iliac artery aneurysm) were also compared between the two groups (Table 1). For patients with type II endoleaks and follow-up length ≥ 180 days, comparison between patients with transient and persistent type II endoleaks was conducted for length of stay, total number of scans, aneurysm sac size, resolution of endoleaks, and time to resolution. The nonparametric Wilcoxon rank sum test was used to evaluate continuous variables due to the violation of normality assumption. The chi-square test or Fisher's Exact Test was used to evaluate categorical variables. Statistical analyses were performed using STATA 11.1 (StataCorp LP, College Station, TX) and statistical significance was determined using P value b.05. 3. Results Of the 202 patients who underwent EVAR with the Gore Excluder stent graft at our institution, 39 were excluded because follow-up imaging was not obtained at our institution (Fig. 2). Of the 163 patients meeting inclusion criteria, 66/163 (40.5%) experienced a type II
endoleak. Of the 66 patients with type II endoleaks, 41/66 patients (62.1%) had type II endoleaks identified on procedural angiograms, while 23/66 patients (34.8%) developed type II endoleaks by the first follow-up CTA (Table 2). One case was discrepant between the initial two radiologists who interpreted the images. Upon review by the third radiologist, it was determined that this one patient (1.5%) developed a type II endoleak at baseline. This patient also subsequently developed a delayed proximal type I endoleak, defined as failure of graft seal at the proximal attachment site, by the first follow-up visit. Two patients (3.0%) developed delayed type II endoleaks that were not present at baseline or on the first follow-up CTA but were seen on subsequent scans. Median follow-up time for all patients was 24.7 months (range = 0.5–85.2 months), with patients who experienced a type II endoleak having significantly longer mean follow-up time of 26.9±21.7 months compared to patients without type II endoleaks at 22.3 ± 22.8 months (P b.001). Patients were lost to follow-up in this study when imaging was not available in our institution's PACS. Additional comparisons were performed on patients with type II endoleaks by resolution time (transient vs. persistent endoleaks; Table 3). Eight patients with type II endoleaks were excluded from this analysis due to follow-up time less than 180 days. Of the 58 patients included, 41/58 patients (70.7%) experienced persistent type II endoleaks lasting longer than 180 days. Aneurysm sac size decreased or remained stable in most patients, regardless of resolution time. More patients with persistent type II endoleaks (10/58 patients,
Table 2 Type II endoleak characteristics Characteristic
Type II endoleak identification Diagnosed at baseline, resolved by first follow-up CTA Diagnosed at baseline, without resolution at first follow-up CTA Diagnosed on first follow-up CTA Diagnosed after first follow-up CTA Change in sac size Patients with stable sac size (≤5 mm) Patients with decreased sac size (≥5 mm) Patients with increased sac size (≥5 mm) Prophylactic aneurysm sac embolization Aneurysm diameter in mm (mean±SD) Number of patent lumbar arteries per patient (mean±SD) Patients with patent inferior mesenteric artery Iliac artery aneurysm a +
Type II endoleak (n=66)
P value+
No type II endoleak (n=97)
n
%
n
%
18 23 23 2
27.3a 34.8a 34.8a 3.0a
− − − −
− − − −
32 22 12 4 53.8 ±8.1 3.9±1.4 31 9
48.5a 33.3a 18.2a 6.1a − − 48.4 14.1
− − − − 51.8±9.1 2.5±1.6 40 10
− − − − − − 40.4 10.1
Percentage calculated out of patients with type II endoleaks. Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
.059 b.001 .312 .442
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Table 3 Transient vs. persistent type II endoleaks Characteristic
Patients Follow-up months (mean±SD) Total number of follow-up scans (mean±SD) Sac size in mm (mean±SD) Sac size change status Sac size change b5 mm Sac size decrease ≥5 mm Sac size increase ≥5 mm Endoleak resolution Days to resolution (mean±SD, censored for unresolved cases) +
P value+
Transient type II endoleak
Persistent type II endoleak
n
%
n
%
17 21.2±21.7 3.5±3.1 56.2±8.7
29.3 − − −
41 34.3±18.5 4.3±2.0 53.4±8.1
70.7 − − −
7 9 1 17 54.8±40.3
41.1 52.9 5.9 100.0 −
19 12 10 20 793.7±549.9
46.3 29.3 24.4 48.8 −
− .007 .047 .179 .145 − − − − −
Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
24.4%) experienced increase in sac size than patients with transient type II endoleaks (1/17 patients, 5.9%). However, the number of patients with change in aneurysm sac size was not significantly different between the transient type II endoleak and persistent type II endoleak groups (P=.145), possibly due to the small sample size. Of the patients with type II endoleaks, 32/66 patients (48.5%) experienced no change in aneurysm sac size, while the sac decreased in 22/66 patients (33.3%) and increased in 12/66 patients (18.2%). Spontaneous resolution of type II endoleaks occurred in 37/66 patients (56.1%). Four of the 66 patients (6.1%) underwent prophylactic sac embolization for asymptomatic growth. The decision to treat these patients was at the clinical discretion of the treating vascular surgeon and interventional radiologist on a case-by-case basis based on the location and size of the endoleak, the degree of sac enlargement, patient comorbidities, and patient preference. All embolizations were performed using a fluoroscopic and cone-beam CT-guided, direct puncture sac embolization technique with a combination of coils and N-butyl-2-cyanoacrylate-ethiodol. All procedures were successful, resulting in complete embolization of the leak. There were no aneurysm ruptures, conversion to open repair, or aneurysm-related deaths in either group. Of the 163 patients meeting inclusion criteria, 136 patients (83%) were male with a mean age of 71.7 years. A higher rate of antiplatelet medication use was present among patients who developed type II endoleaks (57/66 patients, 89.1%) compared with those who did not (64/97 patients, 76.2%; P=.045). There were no additional statistically significant differences in demographics, comorbidities, or anticoagulation use between patients with and without type II endoleaks (Table 1). Preprocedural anatomic characteristics were reviewed and compared between patients with and without type II endoleaks. Patients who developed type II endoleaks had more patent lumbar arteries preprocedure than those who did not develop type II endoleaks (3.9±1.4 vs. 2.5±1.6, respectively; Pb .001). No significant differences were found in preprocedure aneurysm diameter (P=.059), patent inferior mesenteric arteries (P=.312), or concomitant iliac artery aneurysms (P=.442) between the two groups (Table 2). 4. Discussion The results of this study confirm the common occurrence of type II endoleaks in patients who have undergone EVAR. In our patient population, 40.5% developed type II endoleaks. Although the incidence of type II endoleaks was high, associated adverse outcomes were rare; 12 of 66 patients (18.2%) with type II endoleaks experienced aneurysm sac growth, though there were no aneurysm ruptures, conversion to open repair, or aneurysm-related deaths. Additionally, 37/66 (56.1%) of the type II endoleaks spontaneously resolved and only 4/66 patients (6.1%) underwent prophylactic sac embolization for asymptomatic sac growth. These data further demonstrate that, while type II endoleaks are relatively common after EVAR, they most often have a benign clinical course.
There is some disagreement in the literature regarding the natural history of type II endoleaks, with some studies demonstrating a benign course and others reporting aneurysm ruptures due to type II endoleaks. Incidence of type II endoleaks in prior studies has ranged from 3% to 43%, with an overall incidence in a recent systematic review of 10.2% [9–25]. The incidence in our study was much higher than this finding at 40.5% but fell within the range of previously reported incidence. The high incidence could be related to the brand of stent graft, though a prior study failed to demonstrate a statistically significant difference in type II endoleak occurrence between stent graft brands [27]. It is also likely that the incidence was higher in our study because we included type II endoleaks that were identified on the completion angiogram at the time of the original procedure, as opposed to diagnosis only on follow-up CTA or ultrasound [9]. Despite the high incidence in our study, however, the complication rate remained low with spontaneous resolution observed in 37/66 patients (56.1%). There was no statistically significant difference in spontaneous resolution of type II endoleaks or change in AAA sac size between those who had transient and persistent type II endoleaks. Additionally, in a systematic review, open conversion was documented in 0–6% of patients and aneurysm sac rupture was observed in 0–2% [9]. Patients in our study did not experience either of these complications nor any aneurysm-related deaths. The aim of this study was to obtain longer term follow-up of type II endoleaks than has previously been reported in the literature. EVAR has not shown long-term superiority to open repair of AAAs due to the presence of endoleaks, and our goal was to demonstrate that the most common type of endoleak often exhibits a benign course. Although the study period was originally chosen to obtain long-term results, most patients with type II endoleaks did not receive imaging follow-up at our institution after an average of 2.2 years, limiting the length of our outcome evaluation. It is important to note that our institution is a tertiary care academic medical center with a wide referral base and patients often receive long-term follow-up imaging at outside institutions due to patient convenience factors. The patients were followed in coordination with their outside physician and the treating vascular surgeon. Because our data were limited only to imaging available in our institution's PACS archive, many patients were lost to follow-up. Our initial sample size was also small compared to other studies, limiting reliability of results. However, our study contains the largest patient population with type II endoleaks repaired using a single brand of stent graft. Additionally, this was a retrospective, single-institution study, utilizing a single stent graft, which may limit the generalizability of our findings. Despite these limitations, however, the results of this study are concordant with other research demonstrating the common occurrence and typically benign course of type II endoleaks. Routine surveillance of type II endoleaks should be performed as the benefit of identifying early aneurysm sac expansion outweighs the risk of long-term radiation effects. Selective intervention in persistent type II endoleaks or in patients with expanding aneurysm sac may be necessary. Further prospective trials are needed to determine the best management strategies for
K. Pippin et al. / Clinical Imaging 40 (2016) 875–879
type II endoleaks, particularly persistent ones lasting longer than 180 days. Finally, long-term outcomes of type II endoleaks need to be established to demonstrate true superiority of EVAR over open repair. 5. Conclusion Type II endoleaks are a common occurrence after EVAR utilizing the Gore Excluder stent graft, often with a benign outcome. However, routine surveillance should be performed for the life of the patient to assess for native aneurysm sac growth due to lack of data regarding long-term outcomes of type II endoleaks. Acknowledgments The authors acknowledge Scott Penny and Joseph Loeb, medical students at the University of Kansas School of Medicine, for their assistance with data acquisition. References [1] Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5:491–9. [2] Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG, EVAR trial patients. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomized controlled trial. Lancet 2004;364:843–8. [3] Blankensteijn JD, deJong SE, Prinssen M, van der Ham AC, Buth J, van Sterkenburg SM, et al. Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med 2005;352:2398–405. [4] Prinssen M, Verhoeven EL, Buth J, Cuypers PW, van Sambeek MR, Balm R, et al, DREAM Trial Group. A randomized trial comparing conventional and endovascular repair of aneurysms. N Engl J Med 2004;351:1607–18. [5] Goerich J, Rilinger N, Sokiranski R, Kraemer SC, Ermis C, Schuetz A, et al. Treatment of leaks after endovascular repair of aortic aneurysms. Radiology 2000;215:414–20. [6] Lederle FA, Freischlag JA, Kyriakides TC, Padberg FT, Matsumura JS, Kohler TR, et al, OVER Veterans Affairs Cooperative Study Group. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA 2009;302:1535–42. [7] De Bruin JL, Baas AF, Buth J, Prinssen M, Verhoeven EL, Cuypers PW, et al, DREAM Study Group. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med 2010;362:1881–9. [8] Becquemin JP, Pillet JC, Lescalie F, Sapoval M, Goueffic Y, Lermusiaux P, et al, ACE trialists. A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg 2011;53:1167–73. [9] Sidloff DA, Stather PW, Choke E, Bown MJ, Sayers RD. Type II endoleak after endovascular aneurysm repair. Br J Surg 2013;100:1262–70.
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[10] Rayt HS, Sandford RM, Salem M, Bown MJ, London NJ, Sayers RD. Conservative management of type 2 endoleaks is not associated with increased risk of aneurysm rupture. Eur J Vasc Endovasc Surg 2009;38:718–23. [11] Silverberg D, Baril DT, Ellozy SH, Carroccio A, Greyrose SE, Lookstein RA, et al. An 8year experience with type II endoleaks: natural history suggests selective intervention is a safe approach. J Vasc Surg 2006;44:453–9. [12] Sheehan MK, Ouriel K, Greenberg R, McCann R, Murphy M, Fillinger M, et al. Are type II endoleaks after endovascular aneurysm repair endograft dependent? J Vasc Surg 2006;43:657–61. [13] Tolia AJ, Landis R, Lamparello P, Rosen R, Macari M. Type II endoleaks after endovascular repair of abdominal aortic aneurysms: natural history. Radiology 2005;235:683–6. [14] Steinmetz E, Rubin BG, Sanchez LA, Choi ET, Geraghty PJ, Baty J, et al. Type II endoleak after endovascular abdominal aneurysm repair: a conservative approach with selective intervention is safe and cost-effective. J Vasc Surg 2004;39:306–13. [15] Parent FN, Meier GH, Godziachvili V, LeSar CJ, Parker FM, Carter KA, et al. The incidence and natural history of type I and II endoleak: a 5-year follow-up assessment with color duplex ultrasound scan. J Vasc Surg 2002;35:474–81. [16] Buth J, Harris PL, van Marrewijk C. Causes and outcomes of open conversion and aneurysm rupture after endovascular abdominal aortic aneurysm repair: can type II endoleaks be dangerous? J Am Coll Surg 2002;194:S98–S102 [Suppl]. [17] Tuerff SN, Rockman CB, Lamparello PJ, Adelman MA, Jacobowitz GR, Gagne PJ, et al. Are type II (branch vessel) endoleaks really benign? Ann Vasc Surg 2002;16:50–4. [18] Haulon S, Tyazi A, Willoteaux S, Koussa M, Lions C, Beregi JP. Embolization of type II endoleaks after aortic stent-graft implantation: technique and immediate results. J Vasc Surg 2001;34:600–5. [19] Chuter TA, Faruqi RM, Sawhney R, Reilly LM, Kerlan RB, Canto CJ, et al. Endoleak after endovascular repair of abdominal aortic aneurysm. J Vasc Surg 2001;34:98–105. [20] Conrad MF, Adams AB, Guest JM, Paruchuri V, Brewster DC, LaMuraglia GM, et al. Secondary intervention after endovascular abdominal aortic aneurysm repair. Ann Surg 2009;250:383–9. [21] Cassagnes L, Perignon R, Amokrane F, Petermann A, Becaud T, Saint-Lebes B, et al. Aortic stent-grafts: endoleak surveillance. Diagn Interv Imaging 2016. http://dx. doi.org/10.1016/j.diii.2014.12.014. [22] Jones JE, Atkins MD, Brewster DC, Chung TK, Kwolek CJ, LaMuraglia GM, et al. Persistent type 2 endoleak after endovascular repair of abdominal aortic aneurysm is associated with adverse late outcomes. J Vasc Surg 2007;46:1–8. [23] Van Marrewijk CJ, Fransen G, Laheij RJ, Harris PL, Buth J. Is a type II endoleak after EVAR a harbinger of risk? Causes and outcome of open conversion and aneurysm rupture during follow-up. Eur J Vasc Endovasc Surg 2004;27:128–37. [24] Liewald F, Ermis C, Goerich J, Halter G, Scharrer-Pamler R, Sunder-Plassmann L. Influence of treatment of type II leaks on the aneurysm surface area. Eur J Vasc Endovasc Surg 2001;21:339–43. [25] Solis MM, Ayerdi J, Babcock GA, Parra JR, McLafferty RB, Gruneiro LA, et al. Mechanism of failure in the treatment of type II endoleak with percutaneous coil embolization. J Vasc Surg 2002;36:485–91. [26] Kasirajan K, Matteson B, Marek JM, Langsfeld M. Technique and results of transfemoral superselective coil embolization of type II lumbar endoleak. J Vasc Surg 2003;38:61–6. [27] Haider SE, Najjar SF, Cho JS, Rhee RY, Eskandari MK, Matsumura JS, et al. Sac behavior after aneurysm treatment with the gore excluder low-permeability aortic endoprosthesis: 12-month comparison to the original excluder device. J Vasc Surg 2006;44:694–700.
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
Outcomes of type II endoleaks after endovascular abdominal aortic aneurysm (AAA) repair: a single-center, retrospective study☆,☆☆ Kaley Pippin a,⁎, Jacqueline Hill a, Jianghua He b, Philip Johnson a a b
Department of Radiology, University of Kansas Medical Center, 3901 Rainbow Blvd, Mailstop 4032, Kansas City, KS, 66160, USA Department of Biostatics, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS, 66160, USA
a r t i c l e
i n f o
Article history: Received 1 November 2015 Received in revised form 16 March 2016 Accepted 12 April 2016 Available online xxxx Keywords: Aortic aneurysm Abdominal Endovascular procedure Endoleak Aortic stent grafts
a b s t r a c t Purpose: This study aims to determine incidence and outcomes of type II endoleaks (T2E) after endovascular abdominal aortic aneurysm repair (EVAR). Methods: A retrospective review of procedural angiograms, computed tomography angiography, and medical records of 202 patients who underwent EVAR with the Gore Excluder stent graft was performed to determine presence and outcomes of T2E. Results: Median follow-up time for 163 patients meeting inclusion criteria [136 males (83%)] was 24.7 months (range=0.5–85.2 months). T2E occurred in 66/163 patients (40.5%). Aneurysm sac size was unchanged in 32/ 66 patients (48.5%), decreased in 22/66 (33.3%), and increased in 12/66 (18.2%). No aneurysm ruptures, conversion to open repair, or aneurysm-related deaths occurred. Conclusion: T2E are a common occurrence after EVAR, often with benign outcome. However, routine surveillance should be performed, particularly in patients with persistent endoleak or sac growth. © 2016 Elsevier Inc. All rights reserved.
1. Introduction Endovascular abdominal aortic aneurysm repair (EVAR) has become a widely accepted alternative to open surgical repair of abdominal aortic aneurysms (AAAs) since it was first described in 1991 [1]. When compared to open surgical repair, EVAR has significantly lower 30-day morbidity and mortality. This can largely be attributed to the minimally invasive technique of EVAR with 30-day mortality rates after EVAR reported as 1.2–2.1%, less than half the rate of open repair [2–4]. However, long-term morbidity and survival of patients undergoing EVAR have been shown to be no better than, or even inferior to, patients who have undergone open surgical repair [5–8]. This increased long-term morbidity and mortality following EVAR can be attributed to the presence of endoleaks, which have been associated with aneurysm sac expansion and rupture [9]. Endoleaks are caused by persistent blood flow into the native aortic aneurysm sac due to incomplete sealing or exclusion by the stent graft and are classified into five types (types I–V) based on the source of blood flow into the aneurysm sac [9]. Type II endoleaks are the most common, occurring in 3–43% of patients who have undergone EVAR, and occur when blood flows retrograde into the aneurysm sac through ☆ Conflicts of Interest: None. ☆☆ Preliminary data from this study were presented by P. Johnson at the 2014 Society of Interventional Radiology Annual Meeting. ⁎ Corresponding author. E-mail address: [email protected] (K. Pippin). http://dx.doi.org/10.1016/j.clinimag.2016.04.004 0899-7071/© 2016 Elsevier Inc. All rights reserved.
branch vessels and anastomotic connections [9]. Although common, there is no consensus on the optimal management of type II endoleaks once discovered [9–25]. Most physicians advocate that type II endoleaks have a benign course and practice a conservative approach of serial monitoring with computed tomography angiography (CTA) or ultrasound [10–21]. Other physicians believe that type II endoleaks lead to aneurysm sac rupture and practice a more aggressive approach of embolization of the endoleak [22–26]. The primary aim of this study was to determine the incidence and outcomes of type II endoleaks after EVAR utilizing a single brand of stent graft, Excluder (W. L. Gore and Associates, Flagstaff, Arizona). Because previous research has been limited to 4.8 years of follow-up, this study gathered data over an 8-year period with the intention of evaluating midterm outcomes of type II endoleaks [9]. We hypothesized that type II endoleaks are a common complication following EVAR, but most frequently have a benign outcome. 2. Materials and methods 2.1. Study design A retrospective study was conducted on a cohort of patients 18 years of age or older who underwent EVAR utilizing the Excluder stent graft at a tertiary care academic institution between April 1, 2005 and March 31, 2013. A vast majority of EVAR procedures at our institution in the chosen time period were performed using the Excluder stent graft. Therefore, we elected to evaluate the incidence and outcomes of type II
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Fig. 1. (a) Axial CTA image from a 74-year-old male demonstrates stent graft in the abdominal aorta with contrast opacification in the native aneurysm sac (arrow), compatible with a type II endoleak. (b) Axial CTA image from a different level in the same patient illustrates the method used to measure aneurysm sac (x=5.3 cm).
endoleaks with this commonly used device. Type II endoleaks were chosen as the focus of this study because it is the most controversial type of endoleak in terms of outcome and management. Evaluation of other types of endoleaks was beyond the scope of this study. Institutional review board approval was obtained to review patient records. 2.2. Inclusion and exclusion criteria All patients who underwent Gore Excluder stent graft placement for AAA by one of three board-certified interventional radiologists and/or vascular surgeons were eligible for inclusion in the study. Patients were excluded if they had ruptured, anastomotic, inflammatory, or infectious AAAs, as documented in the electronic medical record. Additionally, patients were excluded if they did not have at least one follow-up CTA of the abdomen/pelvis performed at our institution postprocedure. Patients who received follow-up imaging at outside institutions were excluded from the study due to the inability to review the images. Patients who were lost to clinical follow-up were included in this study if they had at least one follow-up CTA at our institution. Patients meeting inclusion criteria were identified through our institutional electronic medical record, utilizing CPT codes to select desired exams within the specified dates. 2.3. Image review Conventional angiograms and CTA abdomen/pelvis images for patients meeting inclusion criteria were independently reviewed by two board-certified radiologists to determine the presence or absence of type II endoleak. Any discrepant cases were adjudicated by a third board-certified radiologist. CTAs were performed according to standard of care at the time of acquisition and included precontrast images using 5 mm slices, arterial and venous phase images using 5 mm and 1.25 mm slices, and delayed images using 5 mm slices. The aneurysm sac was measured by a board-certified radiologist in a single plane at the point of maximum diameter using electronic calipers on axial CT images using Centricity PACS software (GE Medical Systems; Fig. 1). At our institution, standard imaging follow-up after EVAR is serial CTA at 30 days, 6 months, and annually thereafter. 2.4. Outcomes The primary outcome was to identify the incidence of type II endoleaks after EVAR. For this study, type II endoleaks were defined as
endoleaks that developed at the time of the postprocedural angiogram or were present on a follow-up CTA. Endoleaks were further divided into transient type II endoleaks (resolved in b180 days) and persistent type II endoleaks (persisted ≥ 180 days). Secondary study outcomes included endoleak persistence, aneurysm sac growth, secondary intervention, conversion to open repair, aneurysm rupture, and aneurysmrelated death. Aneurysm sac growth, shrinkage, or stability was determined using 5 mm as the cutoff value for significant change in size. Significant change of 5 mm was chosen because it is the most commonly used value in the literature [10–11,13–14]. Patient medical charts were reviewed by three medical students and a senior radiology resident to determine secondary clinical outcomes. Additional patient information, including demographics, tobacco use, comorbid clinical conditions, anticoagulation or antiplatelet medication use, patent lumbar and inferior mesenteric arteries, and presence of iliac artery aneurysm, was compared between patients who developed type II endoleaks and those who did not. While many of these factors are associated with AAA, we collected this information to determine if an association with type II endoleaks exists in order to better predict which patients might develop a type II endoleak.
Table 1 Demographic characteristics Characteristic
Patients Age in years (mean±SD) Follow-up months (mean±SD) Male Caucasian Tobacco users Hypertension Hyperlipidemia Diabetes Renal insufficiency COPD PVD CAD Anticoagulation medication Antiplatelet medication
P value+
Type II endoleak
No type II endoleak
n
%
n
%
66 72.5 ±9.7 26.9 ±21.7 55 59 53 54 51 11 9 11 14 43 6 57
40.5 − − 85.9 92.2 89.8 87.1 83.6 17.7 14.3 18.3 23.3 69.4 9.8 89.1
97 71.1±9.0 22.3±22.8 81 80 75 75 57 24 18 21 24 45 13 64
59.5 − − 81.8 86.9 94.9 90.4 72.1 30.8 23.1 27.3 30.7 56.7 16.7 76.2
.356 b.001 .490 .434 .325 .535 .110 .077 .187 .220 .332 .132 .245 .045
+ Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
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Fig. 2. Flowchart of patient selection and exclusion.
2.5. Statistical analysis Patient characteristics at baseline were summarized using descriptive statistics (mean and standard deviation for continuous variables and count and percentage for categorical variables) and compared between patients with and without type II endoleaks (Table 1). Preprocedural anatomic characteristics (patent lumbar and inferior mesenteric arteries, presence of iliac artery aneurysm) were also compared between the two groups (Table 1). For patients with type II endoleaks and follow-up length ≥ 180 days, comparison between patients with transient and persistent type II endoleaks was conducted for length of stay, total number of scans, aneurysm sac size, resolution of endoleaks, and time to resolution. The nonparametric Wilcoxon rank sum test was used to evaluate continuous variables due to the violation of normality assumption. The chi-square test or Fisher's Exact Test was used to evaluate categorical variables. Statistical analyses were performed using STATA 11.1 (StataCorp LP, College Station, TX) and statistical significance was determined using P value b.05. 3. Results Of the 202 patients who underwent EVAR with the Gore Excluder stent graft at our institution, 39 were excluded because follow-up imaging was not obtained at our institution (Fig. 2). Of the 163 patients meeting inclusion criteria, 66/163 (40.5%) experienced a type II
endoleak. Of the 66 patients with type II endoleaks, 41/66 patients (62.1%) had type II endoleaks identified on procedural angiograms, while 23/66 patients (34.8%) developed type II endoleaks by the first follow-up CTA (Table 2). One case was discrepant between the initial two radiologists who interpreted the images. Upon review by the third radiologist, it was determined that this one patient (1.5%) developed a type II endoleak at baseline. This patient also subsequently developed a delayed proximal type I endoleak, defined as failure of graft seal at the proximal attachment site, by the first follow-up visit. Two patients (3.0%) developed delayed type II endoleaks that were not present at baseline or on the first follow-up CTA but were seen on subsequent scans. Median follow-up time for all patients was 24.7 months (range = 0.5–85.2 months), with patients who experienced a type II endoleak having significantly longer mean follow-up time of 26.9±21.7 months compared to patients without type II endoleaks at 22.3 ± 22.8 months (P b.001). Patients were lost to follow-up in this study when imaging was not available in our institution's PACS. Additional comparisons were performed on patients with type II endoleaks by resolution time (transient vs. persistent endoleaks; Table 3). Eight patients with type II endoleaks were excluded from this analysis due to follow-up time less than 180 days. Of the 58 patients included, 41/58 patients (70.7%) experienced persistent type II endoleaks lasting longer than 180 days. Aneurysm sac size decreased or remained stable in most patients, regardless of resolution time. More patients with persistent type II endoleaks (10/58 patients,
Table 2 Type II endoleak characteristics Characteristic
Type II endoleak identification Diagnosed at baseline, resolved by first follow-up CTA Diagnosed at baseline, without resolution at first follow-up CTA Diagnosed on first follow-up CTA Diagnosed after first follow-up CTA Change in sac size Patients with stable sac size (≤5 mm) Patients with decreased sac size (≥5 mm) Patients with increased sac size (≥5 mm) Prophylactic aneurysm sac embolization Aneurysm diameter in mm (mean±SD) Number of patent lumbar arteries per patient (mean±SD) Patients with patent inferior mesenteric artery Iliac artery aneurysm a +
Type II endoleak (n=66)
P value+
No type II endoleak (n=97)
n
%
n
%
18 23 23 2
27.3a 34.8a 34.8a 3.0a
− − − −
− − − −
32 22 12 4 53.8 ±8.1 3.9±1.4 31 9
48.5a 33.3a 18.2a 6.1a − − 48.4 14.1
− − − − 51.8±9.1 2.5±1.6 40 10
− − − − − − 40.4 10.1
Percentage calculated out of patients with type II endoleaks. Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
.059 b.001 .312 .442
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Table 3 Transient vs. persistent type II endoleaks Characteristic
Patients Follow-up months (mean±SD) Total number of follow-up scans (mean±SD) Sac size in mm (mean±SD) Sac size change status Sac size change b5 mm Sac size decrease ≥5 mm Sac size increase ≥5 mm Endoleak resolution Days to resolution (mean±SD, censored for unresolved cases) +
P value+
Transient type II endoleak
Persistent type II endoleak
n
%
n
%
17 21.2±21.7 3.5±3.1 56.2±8.7
29.3 − − −
41 34.3±18.5 4.3±2.0 53.4±8.1
70.7 − − −
7 9 1 17 54.8±40.3
41.1 52.9 5.9 100.0 −
19 12 10 20 793.7±549.9
46.3 29.3 24.4 48.8 −
− .007 .047 .179 .145 − − − − −
Wilcoxon rank sum test was used for continuous variables; chi-square or Fisher's Exact Test was used for categorical variables.
24.4%) experienced increase in sac size than patients with transient type II endoleaks (1/17 patients, 5.9%). However, the number of patients with change in aneurysm sac size was not significantly different between the transient type II endoleak and persistent type II endoleak groups (P=.145), possibly due to the small sample size. Of the patients with type II endoleaks, 32/66 patients (48.5%) experienced no change in aneurysm sac size, while the sac decreased in 22/66 patients (33.3%) and increased in 12/66 patients (18.2%). Spontaneous resolution of type II endoleaks occurred in 37/66 patients (56.1%). Four of the 66 patients (6.1%) underwent prophylactic sac embolization for asymptomatic growth. The decision to treat these patients was at the clinical discretion of the treating vascular surgeon and interventional radiologist on a case-by-case basis based on the location and size of the endoleak, the degree of sac enlargement, patient comorbidities, and patient preference. All embolizations were performed using a fluoroscopic and cone-beam CT-guided, direct puncture sac embolization technique with a combination of coils and N-butyl-2-cyanoacrylate-ethiodol. All procedures were successful, resulting in complete embolization of the leak. There were no aneurysm ruptures, conversion to open repair, or aneurysm-related deaths in either group. Of the 163 patients meeting inclusion criteria, 136 patients (83%) were male with a mean age of 71.7 years. A higher rate of antiplatelet medication use was present among patients who developed type II endoleaks (57/66 patients, 89.1%) compared with those who did not (64/97 patients, 76.2%; P=.045). There were no additional statistically significant differences in demographics, comorbidities, or anticoagulation use between patients with and without type II endoleaks (Table 1). Preprocedural anatomic characteristics were reviewed and compared between patients with and without type II endoleaks. Patients who developed type II endoleaks had more patent lumbar arteries preprocedure than those who did not develop type II endoleaks (3.9±1.4 vs. 2.5±1.6, respectively; Pb .001). No significant differences were found in preprocedure aneurysm diameter (P=.059), patent inferior mesenteric arteries (P=.312), or concomitant iliac artery aneurysms (P=.442) between the two groups (Table 2). 4. Discussion The results of this study confirm the common occurrence of type II endoleaks in patients who have undergone EVAR. In our patient population, 40.5% developed type II endoleaks. Although the incidence of type II endoleaks was high, associated adverse outcomes were rare; 12 of 66 patients (18.2%) with type II endoleaks experienced aneurysm sac growth, though there were no aneurysm ruptures, conversion to open repair, or aneurysm-related deaths. Additionally, 37/66 (56.1%) of the type II endoleaks spontaneously resolved and only 4/66 patients (6.1%) underwent prophylactic sac embolization for asymptomatic sac growth. These data further demonstrate that, while type II endoleaks are relatively common after EVAR, they most often have a benign clinical course.
There is some disagreement in the literature regarding the natural history of type II endoleaks, with some studies demonstrating a benign course and others reporting aneurysm ruptures due to type II endoleaks. Incidence of type II endoleaks in prior studies has ranged from 3% to 43%, with an overall incidence in a recent systematic review of 10.2% [9–25]. The incidence in our study was much higher than this finding at 40.5% but fell within the range of previously reported incidence. The high incidence could be related to the brand of stent graft, though a prior study failed to demonstrate a statistically significant difference in type II endoleak occurrence between stent graft brands [27]. It is also likely that the incidence was higher in our study because we included type II endoleaks that were identified on the completion angiogram at the time of the original procedure, as opposed to diagnosis only on follow-up CTA or ultrasound [9]. Despite the high incidence in our study, however, the complication rate remained low with spontaneous resolution observed in 37/66 patients (56.1%). There was no statistically significant difference in spontaneous resolution of type II endoleaks or change in AAA sac size between those who had transient and persistent type II endoleaks. Additionally, in a systematic review, open conversion was documented in 0–6% of patients and aneurysm sac rupture was observed in 0–2% [9]. Patients in our study did not experience either of these complications nor any aneurysm-related deaths. The aim of this study was to obtain longer term follow-up of type II endoleaks than has previously been reported in the literature. EVAR has not shown long-term superiority to open repair of AAAs due to the presence of endoleaks, and our goal was to demonstrate that the most common type of endoleak often exhibits a benign course. Although the study period was originally chosen to obtain long-term results, most patients with type II endoleaks did not receive imaging follow-up at our institution after an average of 2.2 years, limiting the length of our outcome evaluation. It is important to note that our institution is a tertiary care academic medical center with a wide referral base and patients often receive long-term follow-up imaging at outside institutions due to patient convenience factors. The patients were followed in coordination with their outside physician and the treating vascular surgeon. Because our data were limited only to imaging available in our institution's PACS archive, many patients were lost to follow-up. Our initial sample size was also small compared to other studies, limiting reliability of results. However, our study contains the largest patient population with type II endoleaks repaired using a single brand of stent graft. Additionally, this was a retrospective, single-institution study, utilizing a single stent graft, which may limit the generalizability of our findings. Despite these limitations, however, the results of this study are concordant with other research demonstrating the common occurrence and typically benign course of type II endoleaks. Routine surveillance of type II endoleaks should be performed as the benefit of identifying early aneurysm sac expansion outweighs the risk of long-term radiation effects. Selective intervention in persistent type II endoleaks or in patients with expanding aneurysm sac may be necessary. Further prospective trials are needed to determine the best management strategies for
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type II endoleaks, particularly persistent ones lasting longer than 180 days. Finally, long-term outcomes of type II endoleaks need to be established to demonstrate true superiority of EVAR over open repair. 5. Conclusion Type II endoleaks are a common occurrence after EVAR utilizing the Gore Excluder stent graft, often with a benign outcome. However, routine surveillance should be performed for the life of the patient to assess for native aneurysm sac growth due to lack of data regarding long-term outcomes of type II endoleaks. Acknowledgments The authors acknowledge Scott Penny and Joseph Loeb, medical students at the University of Kansas School of Medicine, for their assistance with data acquisition. References [1] Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5:491–9. [2] Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG, EVAR trial patients. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomized controlled trial. Lancet 2004;364:843–8. [3] Blankensteijn JD, deJong SE, Prinssen M, van der Ham AC, Buth J, van Sterkenburg SM, et al. Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med 2005;352:2398–405. [4] Prinssen M, Verhoeven EL, Buth J, Cuypers PW, van Sambeek MR, Balm R, et al, DREAM Trial Group. A randomized trial comparing conventional and endovascular repair of aneurysms. N Engl J Med 2004;351:1607–18. [5] Goerich J, Rilinger N, Sokiranski R, Kraemer SC, Ermis C, Schuetz A, et al. Treatment of leaks after endovascular repair of aortic aneurysms. Radiology 2000;215:414–20. [6] Lederle FA, Freischlag JA, Kyriakides TC, Padberg FT, Matsumura JS, Kohler TR, et al, OVER Veterans Affairs Cooperative Study Group. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA 2009;302:1535–42. [7] De Bruin JL, Baas AF, Buth J, Prinssen M, Verhoeven EL, Cuypers PW, et al, DREAM Study Group. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med 2010;362:1881–9. [8] Becquemin JP, Pillet JC, Lescalie F, Sapoval M, Goueffic Y, Lermusiaux P, et al, ACE trialists. A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg 2011;53:1167–73. [9] Sidloff DA, Stather PW, Choke E, Bown MJ, Sayers RD. Type II endoleak after endovascular aneurysm repair. Br J Surg 2013;100:1262–70.
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