Early Post-EVAR Rupture in a Patient with Early Type II Endoleak: A Borderline Treatment

Early Post-EVAR Rupture in a Patient with Early Type II Endoleak: A Borderline Treatment

Journal Pre-proof Early post – EVAR rupture in a patient with early type II endoleak: A borderline treatment Christiana Anastasiadou, M.D, Sotiris Gia...

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Journal Pre-proof Early post – EVAR rupture in a patient with early type II endoleak: A borderline treatment Christiana Anastasiadou, M.D, Sotiris Giannakakis, M.D, PhD, Anastasios Papapetrou, M.D, PhD, George Galyfos, M.D, Msc, PhD, George Kastrisios, M.D, Chrisostomos Maltezos, M.D, PhD PII:

S0890-5096(19)30963-X

DOI:

https://doi.org/10.1016/j.avsg.2019.10.099

Reference:

AVSG 4766

To appear in:

Annals of Vascular Surgery

Received Date: 15 September 2019 Revised Date:

30 October 2019

Accepted Date: 31 October 2019

Please cite this article as: Anastasiadou C, Giannakakis S, Papapetrou A, Galyfos G, Kastrisios G, Maltezos C, Early post – EVAR rupture in a patient with early type II endoleak: A borderline treatment, Annals of Vascular Surgery (2019), doi: https://doi.org/10.1016/j.avsg.2019.10.099. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Elsevier Inc. All rights reserved.

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Early post – EVAR rupture in a patient with early type II endoleak: A borderline

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treatment

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Christiana Anastasiadou M.D, Sotiris Giannakakis M.D, PhD, Anastasios Papapetrou M.D,

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PhD, George Galyfos M.D, Msc, PhD, George Kastrisios M.D, Chrisostomos Maltezos M.D,

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PhD

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Department of Vascular Surgery, General Hospital of Attica “KAT”

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Corresponding author: Anastasiadou Christiana

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Email address: [email protected]

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14561, Greece

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Fax: +302132086455 tel: +302132086069

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Email addresses (rest authors):

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[email protected]

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[email protected] [email protected]

Address: Nikis 2, Kifisia, Athens, P.O

[email protected]

[email protected]

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Abstract:

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Purpose: The detection of type II endoleak one month after endovascular aneurysm

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repair (EVAR) is usually neglected or considered benign. Aim of this report is to present a

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case of post-EVAR rupture, due to type II endoleak, and discuss on pathophysiology and

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differential diagnosis.

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Case report: We present a case of a 67-year old male who was treated with EVAR for

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an asymptomatic abdominal aortic aneurysm and four months later, he presented with a

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contained rupture due to a type II endoleak. The patient was treated conservatively without

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any intervention with satisfying result.

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Conclusion: We are demonstrating conservative management as a valid therapeutic option for patients presenting with a contained post-EVAR rupture.

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Keywords: type V endoleak, endotension, type ii endoleak, post-evar, rupture, post-

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implantation syndrome, conservative

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Acknowledgement: Informed consent has been obtained from the patient for publication of

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the case report and accompanying images. This case report was also presented at L.I.V.E

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Symposium which was held in Larissa (Greece) 9-11 May 2019.

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Conflict of interest: None

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Introduction:

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Despite recent improvements in technology, and familiarization with endovascular

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techniques, endovascular aneurysm repair (EVAR) is still associated with complications that

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may either require re-intervention or lead to rupture. Persistent sac pressurization may occur

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from high-flow endoleaks (type I or III) or transmission of systemic pressure through the

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intraluminal thrombus (endotension or type V endoleak). However, type II endoleaks remain

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the most common type, and they are usually attributed to backfilling of the aneurysmal sac

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from patent aortic branches such as lumbar arteries or the inferior mesenteric artery. Type II

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endoleaks seem to appear in 10-20% of all post-EVAR CT-scans although they resolve

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spontaneously within six to twelve months in 80% of the cases.

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suggest an intervention when a type II endoleak causes sac expansion of more than 10mm.

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(SVS 2017 recommendation 2C, ESVS 2018, recommendation 2B) [3,4] In case of a contained

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rupture, however, the clinical presentation is not definitive, and a misdiagnose is possible.

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Aim of this report is to demonstrate that in rare cases of post-EVAR rupture with adequate

[2]

Current recommendations

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proximal and distal graft sealing and no active extravasation, conservative therapy may be

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considered as a valid strategy.

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Case report:

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A 67-year old male patient with an asymptomatic abdominal aortic aneurysm

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(maximum diameter 6.2cm) underwent an EVAR procedure using an Anaconda endograft

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(Vascutek Corporation). His medical history included diabetes mellitus and chronic

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prostatitis. Postoperatively, he presented a post-implantation syndrome (PIS), including fever

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(temperature of 38ºC) and an increase in serum inflammation markers (White blood cells

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[WBC] 14000x103/ul, C-reactive protein [CRP] 7,6 mg/dl). The patient was discharged four

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days later being afebrile and under single antiplatelet therapy.

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One month later, a computed tomography angiography (CTA) revealed: (i) a small

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type II endoleak, (ii) inferior mesenteric artery (IMA) patency (proximal diameter 2.2mm),

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(iii) patency of three lumbar arteries (proximal diameter 0.9-1.1mm) and (iv) stable size of

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aneurysm sac (maximum diameter 6.2cm). (Fig.1) Three months later, the patient presented at

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the emergency department of another hospital with fever (temperature of 39 ºC) and lower

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abdominal pain radiated to the back. At the time of the presentation, the laboratory tests were

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indicative of urinary tract infection (positive urinalysis, erythrocyte sedimentation rate [ESR]:

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99ml/h, WBC: 6800x103/ul

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Hematocrit [Ht]: 36.6%). As a result, he was admitted to a urology department and was

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treated with fosfomycin (3g/daily). The patient was discharged a few days later being afebrile

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and under fosfomycin therapy for four weeks.

57%Neu, procalcitonin [PCT]: 0.03 ng/ml, CRP 5.72 mg/dl,

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However, the patient presented again at our vascular surgery department two days

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after the previous discharge complaining of a residual vague lumbar pain. A new CTA was

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performed revealing not only an aneurysm sac expansion (maximum diameter 6.5cm) but also

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a contained rupture adjacent to the left psoas. (Fig 2, video 1, video 2). Since the patient was

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haemodynamically stable without any hemoglobin decrease (compared to the previous

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admission) we decided to admit the patient for observation and withdraw aspirin. Further

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laboratory assessment included measurement of serum inflammation markers, blood cultures

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and urinalysis which were all negative. Repeated haemoglobin measurements did not show

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any significant variation. Therapy with fosfomycin3g/daily and meropenem 6g/daily was

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extended for one week based on the recent urinary tract infection and the history of chronic

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prostatitis.

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Additionally, the patient underwent a digital subtraction angiography (DSA) after

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three days in order to exclude any occult endoleak. However, in the delayed phase, a small

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type II endoleak was demonstrated arising from a patent lumbar artery. (Fig. 3, Video 3).

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Finally, the patient was discharged one week later, after complete resolution of symptoms and

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with stable hemoglobin levels. One year later, the patient remains in good health,

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asymptomatic, with total regression of the aneurysm sac (Figure 4, Video 4),

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Discussion:

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Considering disease progression, we assume that a pressurization of the aneurysm sac

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occurred during the first month in this case which led to contained rupture. Differential

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diagnosis included urinary tract infection, renal colic, pancreatitis, psoas abscess and post-

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EVAR rupture. Labaratory tests (negative blood cultures, positive urinalysis) were indicative

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of urinary tract infection and vascular imaging was not performed at that time. However,

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CTA was performed a few days later in our department under the indication of persistent back

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pain.

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Regarding pathophysiology, type II endoleak was the most obvious risk factor in this

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case. Literature suggests that factors increasing the risk of a persistent or “malignant” type II

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endoleak include a patent IMA, a large number or diameter of patent lumbar arteries

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(especially L3 and L4 lumbar arteries), a large endoleak cavity between inflow and outflow

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[5]

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arteries combined with ongoing anticoagulation.

In the present case, there was more than

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one branch patent although no aneurysm sac expansion was observed after the first

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postoperative month. Given that ruptures from type II endoleak are rare, we decided to

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perform DSA in order to exclude an occult type I endoleak. In addition, DSA would facilitate

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transarterial superselective catheterization of the IMA or any embolization. Eventually, IMA

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was not visualized, and the remaining lumbar artery was considered small and insignificant.

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[3,4,5]

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which could have contributed to contamination of the endograft. However, none of the

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laboratory tests or imaging was suggestive of endograft infection.

Other aggravating factor for rupture could be the inflammation (urinary tract infection)

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Another speculation is that the rupture was somewhat correlated with a type V

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endoleak (endotension) in the contect of PIS. According to literature, the Anaconda endograft

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is associated with more intense PIS compared to other endografts.

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suggested that the volume of new-onset thrombus is significantly correlated with the peak

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postoperative temperature (P < 0.05). the increase in WBC count (P < 0.05), CRP level (P <

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0.001), and IL-6 level (P < 0.05).

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new-onset thrombus and that transmission of systemic pressure through this thrombus

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(videlicet type V endoleak) could lead to rupture cannot be proved in this patient and thus,

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this is a limitation of the present case report.

[6]

[6]

Kakisis et al, have

However, the theory that this syndrome can produce

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Conclusion:

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Clinical presentation of post-EVAR rupture is not typical in the absence of high-flow

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endoleak and it may occult. We demonstrate conservative management and close observation

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as valid option in such patients presenting with contained rupture. Finally, we highlight the

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need for further studies to identify a possible correlation of PIS with type V endoleak as well

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as early identification of high-risk type II endoleak.

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References:

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1. Panagiotis Kougias, Jean Bismuth, Tam T. Huynh et al. Symptomatic Aneurysm

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Rupture Without Bleeding Secondary to Endotension 4 Years After Endovascular

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Repair of an Abdominal Aortic Aneurysm J ENDOVASC THER 2008;15:702–705

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2. Brewster DC, Jones JE, Chung TK et al. Long-term outcomes after endovascular abdominal aortic aneurysm repair: the first decade. Ann Surg. 2006;244(3):426–438.

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3. F.L. Moll J.T. Powell, G. Fraedrich et al Management of Abdominal Aortic

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Aneurysms Clinical Practice Guidelines of the European Society for Vascular

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Surgery Eur J Vasc Endovasc Surg (2011) 41, S1-S58

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4. Elliot L. Chaikof Dalman, Mark K. Eskandari et al. The Society for Vascular

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Surgery practice guidelines on the care of patients with an abdominal aortic

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aneurysm. J Vasc Surg 2018; 67:2-77.

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5.

Andrew Brown, Greta K Saggu, Matthew J Bown et al. Type II endoleaks:

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challenges and solutions. Vascular Health and Risk Management 2016:12 53–63

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6. John D. Kakisis, Konstantinos G. Moulakakis, Constantine N. Antonopoulos

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et al. Volume of new-onset thrombus is associated with the development of

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postimplantation syndrome after endovascular aneurysm repair J Vasc Surg

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2014;60:1140-5.

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Figure legends:

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Fig. 1. CT angiography (one month postoperatively) which reveals a type II endoleak (note

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the patency of three lumbar arteries and inferior mesenteric artery)

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Fig. 2. CT angiography (four months postoperatively) which reveals rupture of the aortic wall

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without extravasastion. Please notice that there is no aortic-wall thickening, no air around the

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graft and no soft tissue greater than 5 mm between psoas and the stent graft, fluid collection.

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Fig. 3. Digital subtraction angiography revealed a small type II endoleak in delayed phase.