De Novo Periaortic Fibrosis after Endovascular Aortic Repair

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De Novo Periaortic Fibrosis after Endovascular Aortic Repair Faris Alomran, Romain de Blic, Alexandros Mallios, Alessandro Costanzo, Benoit Boura, and Myriam Combes, Paris France

We report a case of a 63-year-old man presenting with abdominal pain and hydronephrosis secondary to periaortic fibrosis (PAF) 8 months after an endovascular aortic repair (EVAR) using a woven polyester bifurcated graft. De novo delayed PAF after open repair is rare and even more infrequent after EVAR. All 3 previously reported cases occurred after woven polyester grafts and no reported cases after polytetrafluorethylene grafts. Management included steroidal anti-inflammatory treatment and bilateral double J tube placement. Satisfactory results were obtained.

Periaortic fibrosis (PAF) with or without aortic aneurysmal change is most commonly idiopathic but can also occur secondary to use of certain medications, malignant diseases, infections, and surgery.1 In the presence of an abdominal aortic aneurysm (AAA) of inflammatory origin both endovascular aortic repair (EVAR) and open surgical intervention are feasible options. De novo delayed PAF after open surgery is rare,1 although less frequent after EVAR, with only 3 cases having been reported in the literature.2e4

CASE REPORT A 63-year-old man presented with a non-inflammatory, 51-mm abdominal aortic aneurysm. Standard preoperative work-up was unremarkable, showing a leukocyte count of 7700 mm3 and a C-reactive protein (CRP) of 8 mg/L. The patient underwent conventional EVAR with a bifurcated graft (Endurant; Medtronic, Santa Monica, CA, USA). Postoperatively, he was well beyond a 24-hr period of hyperthermia that occurred, which spontaneously resolved without treatment. The Department of Vascular Surgery, Institute Mutualiste Montsouris, Paris, France. Correspondence to: Faris Alomran, MD, Department of Vascular Surgery, Institute Mutualiste Montsouris, 46 Boulevard Jourdain, Paris 75014, France; E-mail: [email protected] Ann Vasc Surg 2014; 28: 493.e1–493.e3 http://dx.doi.org/10.1016/j.avsg.2013.06.019 Ó 2014 Elsevier Inc. All rights reserved. Manuscript received: May 9, 2013; manuscript accepted: June 11, 2013; published online: November 25, 2013.

hyperthermia was attributed to postimplantation syndrome and the patient was discharged on day 5 as per protocol after a satisfactory computed tomography (CT) scan showing no evidence of periaortitis, endoleak, or device migration (Fig. 1). At 3-month follow-up, the patient complained of vague abdominal discomfort and constipation. Work-up included a standard blood panel, colonoscopy, and a CT scan, all of which were unremarkable. At 8 months postoperatively, he underwent a standard blood test that revealed acute-onset renal failure with a serum creatinine of 124 mmol/L and an inflammatory syndrome with a CRP of 124 mg/L. At this stage, CT imaging revealed PAF engulfing the ureters causing hydronephrosis, but no graft abnormalities (Fig. 2). The patient was urgently hospitalized and underwent ureter drainage by placement of double J catheters in both ureters. Prednisolone therapy was initiated at 1 mg/kg and reduced by 5 mg bimonthly. There was an immediate reduction in biologic inflammatory markers and renal function returned to baseline 2 weeks later. CT scan 3 months after commencement of steroidal therapy revealed a significant reduction in PAF and correct placement of both double J catheters (Fig. 3).

DISCUSSION PAF is a rare, mostly idiopathic, inflammatory condition that ranges from inflammatory AAA to isolated retroperitoneal fibrosis.1 The clinical signs and symptoms signaling onset of PAF are nonspecific, such as lower back or abdominal pain; later signs include localized compressive mass effect and a systemic inflammatory disease expression. The 493.e1

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Fig. 1. CTA 1 week postoperatively showing good device placement and no endoleak.

Fig. 2. Nine-month CTA showing major PAF, engulfing both ureters and causing hydronephrosis. Steroidal anti-inflammatory treatment was initiated at this stage.

nonspecific nature of the presenting clinical manifestations often lead to a considerable delay between the onset of symptoms and diagnosis, resulting in significant complications such as ureteral obstruction with secondary acute or chronic renal failure. Positron emission tomography (PET) may provide an earlier diagnosis for cases in which PAF is suspected, showing increased metabolic activity prior to the onset of morphologic changes.5 Ureter involvement has been reported in >80% of idiopathic cases.1,6 In our opinion, the nonspecificity of the symptoms indicates a possible underreporting of de novo onset of PAF after both open surgery and EVAR. The histopathology underlying PAF post-EVAR is poorly understood with an absence of any tissue biopsies due to the effective nonsurgical treatment of this disease. Initially, chronic periaortitis was considered a localized inflammatory response to severe aortic atherosclerosis, and recent findings suggest a systemic autoimmune origin. In idiopathic PAF the inflammatory infiltrate consists of mainly lymphocytes.7 The infiltrate can be both diffuse and nodular with transmural infiltration and fibrinoid necrosis of small- and medium-sized retroperitoneal vessels in some cases.6,7 The fibrous tissue often has a perivascular or perineural disposition but the pathogenesis is still unclear.

Annals of Vascular Surgery

Fig. 3. Three-month CTA after the diagnosis and ongoing treatment of PAF showing a marked reduction in the inflammation and the correct positioning of the nephrostomy tubes.

We carefully reviewed the patient’s medical history, biologic markers, and CT scans prior to EVAR and found no evidence of preexistent aortitis or PAF. One hypothesis that may explain this finding is that PAF is an insidious extension of the postimplantation syndrome that is widely observed after EVAR. Interestingly, of the 4 cases reported to date, all were woven polyester bifurcated grafts and none were expanded polytetrafluorethylene (ePTFE) grafts. Three were Medtronic devices (AneuryX, Talent, and Endurant; Medtronic) and one was a Zenith device (William Cook, Brisbane, Australia). Vo^ ute et al. observed a stronger, statistically significant inflammatory response after implantation of stent grafts when comparing woven polyester versus ePTFE composition.8 Ex vivo, researchers also found that woven polyester triggered a significantly greater release of proinflammatory markers than ePTFE grafts.9 The interval to diagnosis and age at presentation of PAF post-EVAR ranges from 5 to 17 months and 59 to 76 years, respectively. Aggressiveness of the disease has been shown to vary, with 1 case resulting in major thickening of 1.5 cm of the aortic wall, involvement of the inferior vena cava, and requiring almost 1 year of steroid treatment.2 In another report, nephrectomy was performed for renal failure with persistent flank pain, and the springs of the EVAR device could be palpated through the aortic wall.3 Idiopathic retroperitoneal fibrosis is usually treated with initial high-dose corticosteroids, followed by tapering to low-dose maintenance therapy, especially if there is a hydro-ureteronephrosis. We treated this patient using prednisone as it has been shown to induce resolution of symptoms and ureteral obstruction and to decrease erthyrocyte sedimentation rate in inflammatory AAAs.10 In the 3 cases of PAF post-EVAR in the literature,

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tamoxifen therapy was used in addition to prednisolone, with efficacious results.2e4 In conclusion, PAF post-EVAR remains a very rare complication. The pathophysiology may be suggestive of a progression of PIS post-EVAR into PAF, but there is little evidence to support this claim. REFERENCES 1. Vaglio A, Salvarani C, Buzio C. Retroperitoneal fibrosis. Lancet 2006;367:241e51. 2. Jetty P, Barber GG. Aortitis and bilateral ureteral obstruction after endovascular repair of abdominal aortic aneurysm. J Vasc Surg 2004;39:1344e7. 3. Simons PC, van Overhagen H, Bruijninckx CMA, et al. Periaortitis with ureteral obstruction after endovascular repair of an abdominal aortic aneurysm. AJR Am J Roentgenol 2002;179:118e20. 4. Vijaynagar H, McMahon GS, McCarthy MJ. Periaortic inflammation after endovascular aneurysm repair. Ann Vasc Surg 2011;25:558.e5e7.

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5. van Bomel EF, Siemes C, van der Veer SJ, et al. Clinical value of gallium-67 SPECT scintigraphy in the diagnositic and therapeutic evaluation of retroperitoneal fibrosis: a prospective study. J Intern Med 2007;262: 224e34. 6. Vaglio A, Corradi D, Manenti L, et al. Evidence of autoimmunity in chronic periaortitis: a prospective study. Am J Med 2003;114:454e62. 7. Gilkeson GS, Allen NB. Retroperitoneal fibrosis: a true connective tissue disease. Rheum Dis Clin N Am 1996;22: 23e38. 8. Vo^ ute M, Bastos Gonc¸alves F, van de Luijtgaarden K, et al. Stent graft composition plays a material role in the postimplantation syndrome. J Vasc Surg 2012;56:1503e9. 9. Swartbol P, Truedsson L, P€arsson H, et al. Tumor necrosis factor-alpha and interleukin-6 release from white blood cells induced by different graft materials in vitro are affected by pentoxifylline and iloprost. J Biomed Mater Res 1997;36: 400e6. 10. Baskerville PA, Browse NL. The diagnosis and treatment of peri-aortic fibrosis. Br J Surg 1983;70:381e5.

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