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Inflammatory Aneurysms Treated with EVAR
Inflammatory Aneurysms Treated with EVAR William M. Stone, MD, and Grant T. Fankhauser, MD Inflammatory abdominal aortic aneurysms (IAAA) are being treated more frequently by endovascular aneurysm repair (EVAR). Some authors caution against treating IAAA by EVAR because retroperitoneal inflammation may not subside post-operatively. A recent experience of 69 IAAA treated by open and endovascular methods is presented with results supporting the use of EVAR for IAAA. Several other studies evaluating EVAR in the treatment of IAAA are discussed. Semin Vasc Surg 25:227-231 © 2012 Elsevier Inc. All rights reserved.
A
S EARLY AS 1935, the entity of inflammatory aortic aneurysms was apparent. James reported the findings in a patient with uremia secondary to renal involvement from a retroperitoneal inflammatory process.1 The patient was also noted to have a large abdominal aortic aneurysm. In 1955, Schumacker and Garrett2 reported the case of a 13-cm abdominal aortic aneurysm presenting with fibrosis and retroperitoneal inflammation. The patient also had ureteral obstruction. In 1972, Walker et al reported a series of 19 patients who had abdominal aortic aneurysms and retroperitoneal fibrosis.3 They were the first to use the term inflammatory aneurysms. Approximately 3% to 10% of abdominal aortic aneurysms are characterized by increased inflammation surrounding the aneurysm.4 This finding is classically described as a white glistening fibrotic surface with a thickened aneurysmal wall. The inflammatory process frequently involves neighboring structures, such as the ureters, duodenum, or vena cava. This reaction leads to significant adhesion formation within the retroperitoneum and increases the morbidity of open surgical repair. In inflammatory abdominal aortic aneurysms (IAAA), histologically, the elastic and muscular fibers of the aortic media have been replaced by fibrotic tissue. Plasma cells and inflammatory cells such as lymphocytes are also present.5 Patients clinically present with symptoms of abdominal and or back pain; fatigue and weight loss are also common. Frequently noted is an elevated erythrocyte sedimentation rate. The key to diagnosis is the degree of retroperitoneal fibroses. The fibrotic changes represent an increased risk of morbidity during open surgery. This surgical challenge has been
Mayo Clinic, Phoenix, AZ. Address reprint requests to William M. Stone, Mayo Clinic College of Medicine, 5777 E. Mayo Boulevard, Phoenix, AZ 85254. E-mail: stone. [email protected]
0895-7967/$-see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1053/j.semvascsurg.2012.09.008
reported numerous times in the literature, with suggestions of higher morbidity, higher mortality, longer operating time, and increased need for transfusions.6 It has been theorized that endovascular aneurysm repair (EVAR) could offer an advantage in the treatment of IAAAs. There are numerous reports with conflicting opinions on the advantages and disadvantages of treating IAAA with EVAR.7-10
Open Repair Although IAAA can be approached through a midline incision, many surgeons elect to utilize a retroperitoneal approach. This affords direct access to the aorta while minimizing the manipulation of fibrotic tissues. Preoperative ureteral stent placement is a common strategy for ureteral identification with extensive inflammation. Encountering an unanticipated inflammatory aneurysm is becoming less common with the increased use of preoperative computed tomography (CT). Ruptured IAAA are a subset where the inflammation is still often unexpected and preoperative imaging is unavailable. The morbidity of open repair or IAAA most frequently involves injury to adjacent structures. The inflammatory process obscures normal tissue planes and tends to bleed more than normal tissue. These are compelling reasons to attempt endovascular repair.
Endovascular Repair Avoiding an inflamed, fibrotic retroperitoneum is the driving force behind the desire to repair IAAA endovascularly. Aneurysms that are anatomically suitable are tempting to treat with a stent-graft, but there has been debate as to the regression of the inflammatory process after repair. Some surgeons believe that the inflammation might persist de227
W.M. Stone and G.T. Fankhauser
228 Table 1 Preoperative Age and Aneurysm Size EVAR Age (y) n Mean (SD) SEM Median Range Preoperative size (cm) n Mean (SD) SEM Median Range
10 72.2 (8.02) 2.54 71.5 62.0-82.0
Open 59 66.2 (10.43) 1.36 68.0 23.0-83.0
10 5.9 (1.24) 0.39 6.0 (4.0-8.3)
56 6.3 (1.57) 0.21 6.0 (3.4-11.3)
Total 69 67.1 (10.29) 1.24 68.0 23.0-83.0 66 6.2 (1.52) 0.18 6.0 (3.4-11.3)
P Value
.09
.51
Abbreviations: SD, standard deviation; SEM, standard error of mean.
spite aneurysm exclusion and eventual open repair could be necessary.
ative death (1.4%) in a patient undergoing open repair for a ruptured suprarenal IAAA.
Recent Experience
Results of Open Repair
We recently performed a retrospective review on all patients with the diagnosis of IAAA undergoing repair from January 1, 1999 through July 31, 2011 in the Mayo Clinic System. This included all patients from Mayo Clinic in Rochester, MN, Phoenix, AZ, and Jacksonville, FL. The diagnosis of IAAA was made by the operating surgeon at the time of intervention in those patients undergoing open repair and was dependent on the clinical judgment of the vascular surgeon. In patients undergoing EVAR, the diagnosis of IAAA was made by radiologic interpretation of CT. Excluded from review were those patients who had inflammation noted on radiographic imaging but were not deemed by the surgeon to have a true inflammatory aneurysm at the time of surgery. Also excluded were those patients with infectious etiologies.
Fifty-nine of the 69 patients (85.5%) with IAAA underwent conventional open aneurysm repair during the study period. Three patients (5.0%) presented with ruptured aneurysm. Ureteral involvement with inflammation was present in 21 (34.4%) and preoperative ureteral stent placement was performed in 19 of these patients. Four patients (6.7%) were administered perioperative steroids for treatment of comorbid conditions but not for resolution of the inflammatory process. Suprarenal aortic cross-clamping was required for repair in 36 (61%) of these patients to attain adequate control of the aorta. Preoperative mean aneurysm size was 6.3 cm (range, 3.4 to 11.3 cm). A midline abdominal incision was performed in 52 patients (88%), a retroperitoneal approach was utilized in 6 patients (10%), and bilateral subcostal incision was performed in 1 patient (1.6%). Twenty-two major postoperative complications occurred in these 59 patients (37.9%) undergoing open repair. These complications included renal insufficiency in 5 patients (8.3%) needing postoperative dialysis. Ischemic colitis was present in 2 patients (3.3%), but no patient required colonic resection. Postoperative ureteral obstruction requiring intervention occurred in 3 patients (4.9%). There was one death (1.6%) in the 30-day postoperative period in a patient presenting with a ruptured suprarenal IAAA. There were no aneurysm-related deaths identified during follow-up. Mean follow-up was 42.6 months (median, 29.0 months) with a range of 1 to 144 months. Seventeen patients (28.3%) were lost during the follow-up period. Of 42 patients (71.1%) who had postoperative imaging, all had resolution of the aneurysm sac. Hydronephrosis was found to resolve in 7 of 12 patients (58.3%).
Overall Results During the 12-year study period, 69 patients underwent intervention for repair of IAAA and were included for review (Table 1). During the same time period, approximately 3,500 noninflammatory AAAs were repaired. The mean age of patients undergoing intervention for IAAA was 67.1 years (range, 23 to 83 years) including 53 males (77%) and 16 (23%) females. The majority of patients experienced symptoms of pain (36 of 69 [52%]). Four patients (5.6%) presented with ruptured IAAA. Ureteral involvement in the inflammatory process by CT imaging was seen in 23 patients (32.3%) and 21 of the 23 (91.3%) underwent preoperative ureteral stent placement. Mean preoperative aneurysm size in the overall group was 6.2 cm in maximum diameter (range, 3.4 to 11.3 cm) and did not include the rind. Follow-up ranged from 1 to 144 months with a mean of 41.1 months. Eighteen patients (25.7%) were lost to follow-up. There was one postoper-
Results of Endovascular Repair There were 10 patients (14%) that underwent EVAR for management of their IAAA during the study period. The mean age
Inflammatory aneurysms treated with EVAR was 72.2 years. Preoperatively, eight patients (80%) experienced abdominal pain and, one of these (10%) presented with a ruptured aneurysm. Two patients (20%) had ureteral involvement in the inflammatory process and one of those required preprocedural stenting. Preoperative mean aneurysm size was 5.9 cm (range, 4.0 to 8.3 cm). Postoperative aneurysm size decreased in seven patients (70%), with two patients (20%) showing no change in aneurysm size and one patient lost during the follow-up period. Mean follow-up was 33.6 months. Postoperative mean aneurysm size was 4.73 cm. The mean change in size was a decrease of 1.12 cm. Of all patients with postoperative imaging, there was a mean decrease in aneurysm size of 17.8% (range, 57.6% to 0%). The inflammatory rind preoperatively measured 5.4 mm in mean thickness in patients with IAAA undergoing EVAR. Postoperatively, the mean size of inflammatory rind was 2.7 mm. One patient had an increase in the size of the inflammatory rind but had no change in the size of the aneurysm sac. All other patients had decrease in the size of the inflammatory rind. Mean decrease in the thickness of the inflammatory rind was 50.8% (range, 92.1% to 0%). Postoperative abdominal pain was resolved in 6 of 7 patients (85.7%) after EVAR. Two patients (20%) developed atrial fibrillation postoperatively, but there were no other significant complications reported. No patient required subsequent intervention for repair of the aneurysm and no endoleaks were identified in follow-up. There was no perioperative mortality and no patient died of aneurysm-related causes during the follow-up period.
Published Reports on Endovascular Repair of Inflammatory Aneurysms Outcomes of open surgery for management of inflammatory aneurysms are noted with an increased complication rate compared with noninflammatory aneurysms. In a large series, it was demonstrated that operative mortality increased threefold when comparing inflammatory to noninflammatory aneurysms.6 In addition, there is a significant increase in major morbidity between open surgery for inflammatory aneurysms compared with noninflammatory aneurysms.11 In the early years of vascular surgery, extensive retroperitoneal adhesiolysis was routinely performed.12 This practice led to major complications, including enterotomies and duodenal injury. In addition, there was a significant rate of ureteral injury due to this extensive dissection. In order to decrease the perioperative complications, it was suggested in the late 1970s to avoid extensive adhesiolysis.13 In light of the morbidity and mortality from open repair of IAAA, the option of endovascular aneurysm repair seems intuitive. However, the benefit from endovascular intervention is still unproven. Does the endovascular approach reduce not only the risk of aneurysmal rupture, but also the long-term risk of periaortic fibrosis? Not only are
229 the ureters potentially involved in the inflammatory process, but the duodenum and kidneys might be at risk due to the inflammatory process. Certain groups, such as the one from Liverpool,14 would suggest that EVAR is not suitable for IAAA repair due to the persistence of perianeurysmal fibrosis after endograft placement. Other publications, such as the meta-analysis from the EUROSTAR (European Collaborators on Stent-Graft Techniques for Abdominal Aortic Aneurysm Repair) and other meta-analyses, provide mixed results.8-10,15 The technical success of EVAR in our study was 100%. All of the aneurysms undergoing attempt at endovascular repair were treated successfully. Aneurysm size was significantly reduced in this group of patients. The amount of periaortic fibrosis was significantly reduced in 6 of 7 patients who had follow-up imaging. One of those 7 patients demonstrated stable inflammatory thickness in follow-up. Aneurysm sac shrinkage was present in seven of nine patients. The two remaining patients had no change in the size of the aneurysm sac. There were no endoleaks identified in any patient undergoing endovascular repair during periprocedural imaging or during long-term follow-up. In a series involving nine patients from Modena, Italy, the long-term results of endovascular repair are discussed.16 They reported good survival rates with follow-up as long as 60 months. Technical success was achieved in a significant number with low mortality. Aneurysm sac shrinkage occurred in 89% of their patients. There was no aneurysm rupture or aneurysm-related death. A 55% reduction in the inflammatory process was seen by measuring the periaortic fibrosis thickness in this group of patients. This finding is similar to our results of the Mayo Clinic series (Table 2). One of the most extensive series of EVAR for IAAA to date would be the report from the EUROSTAR database.8 This study compares the results of inflammatory abdominal aortic aneurysms versus noninflammatory aortic aneurysms managed with EVAR. This series includes 52 patients with IAAA, which represents 1.4% of the EUROSTAR data. All patients had the diagnosis of inflammatory aneurysm made by CT imaging. The mean age of patients with inflammatory aneurysm was approximately 6 years younger than noninflammatory aneurysms. Other
Table 2 Current Results and Comparison to Published Data Coppi et al16 IAAA treated with EVAR, n Aneurysm-related deaths, n (%) Patients with decreased periaortic inflammation postoperatively (%) Patients with decreased aneurysm size postoperatively (%)
Lange Mayo et al8 Clinic
9 0 78
52 1 (1.8) —
10 0 86
89
87
70
Abbreviations: EVAR, endovascular aneurysm repair; IAAA, inflammatory abdominal aortic aneurysms.
W.M. Stone and G.T. Fankhauser
230 significant differences found in this series and identified by other large series of inflammatory aneurysms are that the risk of smoking was significantly greater in inflammatory aneurysm and the instance of hypertension was significantly less. Also, cardiac and pulmonary disease is less common. Perhaps the younger age of patients with inflammatory aneurysms relates to fewer cardiac and pulmonary comorbidities. Operating time for inflammatory aneurysms when placing endografts in comparison to noninflammatory aneurysms was not significantly different. There was a significant increase in the rate of limb stenosis or occlusion in patients with inflammatory aneurysms. This problem might be related to the severe inflammatory reaction surrounding the aneurysm. However, this result was not found in our series, but might be related to the endograft used. Overall, morbidity and mortality were not significantly different between inflammatory and noninflammatory aneurysms. Minor complications, such as access-site infections, were likewise not statistically different. The EUROSTAR data also provide results for long-term outcomes.8 It is interesting to note that there was no significant difference in the rate of endoleaks. There was no difference in device migration, kinking, or thrombosis. There was also no difference in aneurysm shrinkage between the two groups. What was significantly different was that worsening of renal function in the IAAA group. If patients were followed long-term, renal function deteriorated in 27% of all IAAA patients. The effect of EVAR on the amount of inflammatory fibrosis is less clear. EVAR demonstrated a significant reduction in the amount of inflammation in approximately half of the patients. The results published by Puchner et al from Vienna parallel the results of the EUROSTAR data.10 This metaanalysis of the treatment of inflammatory aortic aneurysms by EVAR had a mean follow-up of 18 months. Results are quite similar to both ours and the EUROSTAR data. Periaortic fibrosis was reduced by approximately 51% in this group; in 42% there was no significant change in periaortic fibrosis; and in 7% there was an increase in the periaortic fibrosis. In this series, in comparison with our reported results, there was a large male predominance, similar to EUROSTAR, with 98% of the patients being male. In another large meta-analysis, Paravastu and coworkers presented a review of open versus endovascular repair for IAAA.15 They again demonstrated a significantly higher mortality rate with open repair (6.2% v 2.4%). They suggest that there is no significant difference in open versus EVAR on the resolution of the inflammatory process. Patients demonstrating significant reduction in fibrosis were 73% in the open group versus 65% with use of EVAR (P ⫽ NS). In the open group, hydronephrosis and hydroureter was improved in 69% of the patients, and only 38% in the EVAR group (P ⫽ .01). In addition, the hydronephrosis or hydroureter progressively worsened in 9% of the open group versus 21% of the patients in the EVAR group. However, the all-cause 1-year mortality was significantly greater in the open group versus the EVAR group (P ⫽ .01).
Arguments Against EVAR EVAR itself produces inflammation in the aorta. This reaction is not as immediate a response as in open repair; however, over time it can be significant.17 It has been hypothesized that this increase in inflammation might be due to reaction to the Dacron in the endograft, however, similar results have been demonstrated in grafts using polytetrafluoroethylene. The possibility that EVAR generates its own inflammatory reaction adds to the skepticism that endovascular repair will promote the resolution of inflammation in IAAA. This skepticism is unfounded based on our results in which inflammation improved in all cases of EVAR. Numerous reports demonstrate, similar to our present series, that EVAR for inflammatory aneurysm successfully reduces the size of the aortic aneurysm in a majority of patients. It also reduces the amount of periaortic fibrosis, but not to the extent that open aneurysm repair does. Endovascular repair outcomes are achieved with a lower morbidity and 1-year mortality. The Achilles’ heel of EVAR for inflammatory abdominal aortic aneurysms revolves around renal and ureter involvement. The improvements in hydroureter and hydronephrosis are inferior with EVAR compared with open repair. We hypothesize that this difference in renal improvement might be related to the fact that the periaortic fibrosis resolves at a slower rate compared with open repair. Based on our results and results in the literature, one would suggest that EVAR is appropriate treatment for inflammatory aortic aneurysms where there is no renal or ureter involvement in the inflammation. It might also be successful treatment for a proportion of patients with renal or ureter involvement if they are poor open surgical risks.
Conclusions Endovascular repair is an effective treatment for inflammatory aneurysms, but there may be less resolution of the inflammatory process. Follow-up imaging in necessary to monitor the involvement of the ureters and resolution of any hydronephrosis. Additional intervention might be necessary after EVAR repair. Open surgical repair is always an option. The suitability of the patient for a major operation must be balanced with the possibility that endovascular repair might not resolve all of the inflammatory process.
References 1. James TGI: Uremia due to aneurysm of the abdominal aorta. Br J Urol 7:157, 1935 2. Schumacker HB Jr, Garrett R: Obstructive uropathy from abdominal aortic aneurysm. Surg Gynecol Obstet 100:758-761, 1955 3. Walker DI, Bloor K, Williams G, et al: Inflammatory aneurysms of the abdominal aorta. Br J Surg 59:609-614, 1972 4. Sueyoshi E, Sakamoto I, Uetani M: Endovascular repair of inflammatory abdominal aortic aneurysm: serial changes of periaortic fibrosis demonstrated by CT. Abdom Imaging 34:523-526, 2009 5. van Bommel EF, van der Veer SJ, Hendriksz TR, et al: Persistent chronic peri-aortitis (’inflammatory aneurysm’) after abdominal aortic aneurysm repair: systematic review of the literature. Vasc Med 13:293-303, 2008
Inflammatory aneurysms treated with EVAR 6. Pennell RC, Hollier LH, Lie JT, et al: Inflammatory abdominal aortic aneurysms: a thirty-year review. J Vasc Surg 2:859-869, 1985 7. Hechelhammer L, Wildermuth S, Lachat ML, et al: Endovascular repair of inflammatory abdominal aneurysm: a retrospective analysis of CT follow-up. J Vasc Interv Radiol 16:737-741, 2005 8. Lange C, Hobo R, Leurs LJ, et al: Results of endovascular repair of inflammatory abdominal aortic aneurysms. A report from the EUROSTAR database. Eur J Vasc Endovasc Surg 29:363-370, 2005 9. Hinchliffe RJ, Macierewicz JA, Hopkinson BR: Endovascular repair of inflammatory abdominal aortic aneurysms. J Endovasc Ther 9:277-281, 2002 10. Puchner S, Bucek RA, Rand T, et al: Endovascular therapy of inflammatory aortic aneurysms: a meta-analysis. J Endovasc Ther 12:560567, 2005 11. Sultan S, Duffy S, Madhavan P, et al: Fifteen-year experience of transperitoneal management of inflammatory abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 18:510-514, 1999 12. Ruppert V, Verrel F, Kellner W, et al: Endovascular repair of inflam-
231
13. 14.
15.
16.
17.
matory abdominal aortic aneurysms: a valuable alternative?— case report and review of literature. Ann Vasc Surg 18:357-360, 2004 Goldstone J, Malone JM, Moore WS: Inflammatory aneurysms of the abdominal aorta. Surgery 83:425-430, 1978 Vallabhaneni SR, McWilliams RG, Anbarasu A, et al: Perianeurysmal fibrosis: a relative contra-indication to endovascular repair. Eur J Vasc Endovasc Surg 22:535-541, 2001 Paravastu SC, Ghosh J, Murray D, et al: A systematic review of open versus endovascular repair of inflammatory abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 38:291-297, 2009 Coppi G, Rametta F, Aiello S, et al: Inflammatory abdominal aortic aneurysm endovascular repair into the long-term follow-up. Ann Vasc Surg 24:1053-1059, 2010 Abdelhamid MF, Davies RS, Adam DJ, et al: Changes in thrombin generation, fibrinolysis, platelet and endothelial cell activity, and inflammation following endovascular abdominal aortic aneurysm repair. J Vasc Surg 55:41-46, 2012
A
S EARLY AS 1935, the entity of inflammatory aortic aneurysms was apparent. James reported the findings in a patient with uremia secondary to renal involvement from a retroperitoneal inflammatory process.1 The patient was also noted to have a large abdominal aortic aneurysm. In 1955, Schumacker and Garrett2 reported the case of a 13-cm abdominal aortic aneurysm presenting with fibrosis and retroperitoneal inflammation. The patient also had ureteral obstruction. In 1972, Walker et al reported a series of 19 patients who had abdominal aortic aneurysms and retroperitoneal fibrosis.3 They were the first to use the term inflammatory aneurysms. Approximately 3% to 10% of abdominal aortic aneurysms are characterized by increased inflammation surrounding the aneurysm.4 This finding is classically described as a white glistening fibrotic surface with a thickened aneurysmal wall. The inflammatory process frequently involves neighboring structures, such as the ureters, duodenum, or vena cava. This reaction leads to significant adhesion formation within the retroperitoneum and increases the morbidity of open surgical repair. In inflammatory abdominal aortic aneurysms (IAAA), histologically, the elastic and muscular fibers of the aortic media have been replaced by fibrotic tissue. Plasma cells and inflammatory cells such as lymphocytes are also present.5 Patients clinically present with symptoms of abdominal and or back pain; fatigue and weight loss are also common. Frequently noted is an elevated erythrocyte sedimentation rate. The key to diagnosis is the degree of retroperitoneal fibroses. The fibrotic changes represent an increased risk of morbidity during open surgery. This surgical challenge has been
Mayo Clinic, Phoenix, AZ. Address reprint requests to William M. Stone, Mayo Clinic College of Medicine, 5777 E. Mayo Boulevard, Phoenix, AZ 85254. E-mail: stone. [email protected]
0895-7967/$-see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1053/j.semvascsurg.2012.09.008
reported numerous times in the literature, with suggestions of higher morbidity, higher mortality, longer operating time, and increased need for transfusions.6 It has been theorized that endovascular aneurysm repair (EVAR) could offer an advantage in the treatment of IAAAs. There are numerous reports with conflicting opinions on the advantages and disadvantages of treating IAAA with EVAR.7-10
Open Repair Although IAAA can be approached through a midline incision, many surgeons elect to utilize a retroperitoneal approach. This affords direct access to the aorta while minimizing the manipulation of fibrotic tissues. Preoperative ureteral stent placement is a common strategy for ureteral identification with extensive inflammation. Encountering an unanticipated inflammatory aneurysm is becoming less common with the increased use of preoperative computed tomography (CT). Ruptured IAAA are a subset where the inflammation is still often unexpected and preoperative imaging is unavailable. The morbidity of open repair or IAAA most frequently involves injury to adjacent structures. The inflammatory process obscures normal tissue planes and tends to bleed more than normal tissue. These are compelling reasons to attempt endovascular repair.
Endovascular Repair Avoiding an inflamed, fibrotic retroperitoneum is the driving force behind the desire to repair IAAA endovascularly. Aneurysms that are anatomically suitable are tempting to treat with a stent-graft, but there has been debate as to the regression of the inflammatory process after repair. Some surgeons believe that the inflammation might persist de227
W.M. Stone and G.T. Fankhauser
228 Table 1 Preoperative Age and Aneurysm Size EVAR Age (y) n Mean (SD) SEM Median Range Preoperative size (cm) n Mean (SD) SEM Median Range
10 72.2 (8.02) 2.54 71.5 62.0-82.0
Open 59 66.2 (10.43) 1.36 68.0 23.0-83.0
10 5.9 (1.24) 0.39 6.0 (4.0-8.3)
56 6.3 (1.57) 0.21 6.0 (3.4-11.3)
Total 69 67.1 (10.29) 1.24 68.0 23.0-83.0 66 6.2 (1.52) 0.18 6.0 (3.4-11.3)
P Value
.09
.51
Abbreviations: SD, standard deviation; SEM, standard error of mean.
spite aneurysm exclusion and eventual open repair could be necessary.
ative death (1.4%) in a patient undergoing open repair for a ruptured suprarenal IAAA.
Recent Experience
Results of Open Repair
We recently performed a retrospective review on all patients with the diagnosis of IAAA undergoing repair from January 1, 1999 through July 31, 2011 in the Mayo Clinic System. This included all patients from Mayo Clinic in Rochester, MN, Phoenix, AZ, and Jacksonville, FL. The diagnosis of IAAA was made by the operating surgeon at the time of intervention in those patients undergoing open repair and was dependent on the clinical judgment of the vascular surgeon. In patients undergoing EVAR, the diagnosis of IAAA was made by radiologic interpretation of CT. Excluded from review were those patients who had inflammation noted on radiographic imaging but were not deemed by the surgeon to have a true inflammatory aneurysm at the time of surgery. Also excluded were those patients with infectious etiologies.
Fifty-nine of the 69 patients (85.5%) with IAAA underwent conventional open aneurysm repair during the study period. Three patients (5.0%) presented with ruptured aneurysm. Ureteral involvement with inflammation was present in 21 (34.4%) and preoperative ureteral stent placement was performed in 19 of these patients. Four patients (6.7%) were administered perioperative steroids for treatment of comorbid conditions but not for resolution of the inflammatory process. Suprarenal aortic cross-clamping was required for repair in 36 (61%) of these patients to attain adequate control of the aorta. Preoperative mean aneurysm size was 6.3 cm (range, 3.4 to 11.3 cm). A midline abdominal incision was performed in 52 patients (88%), a retroperitoneal approach was utilized in 6 patients (10%), and bilateral subcostal incision was performed in 1 patient (1.6%). Twenty-two major postoperative complications occurred in these 59 patients (37.9%) undergoing open repair. These complications included renal insufficiency in 5 patients (8.3%) needing postoperative dialysis. Ischemic colitis was present in 2 patients (3.3%), but no patient required colonic resection. Postoperative ureteral obstruction requiring intervention occurred in 3 patients (4.9%). There was one death (1.6%) in the 30-day postoperative period in a patient presenting with a ruptured suprarenal IAAA. There were no aneurysm-related deaths identified during follow-up. Mean follow-up was 42.6 months (median, 29.0 months) with a range of 1 to 144 months. Seventeen patients (28.3%) were lost during the follow-up period. Of 42 patients (71.1%) who had postoperative imaging, all had resolution of the aneurysm sac. Hydronephrosis was found to resolve in 7 of 12 patients (58.3%).
Overall Results During the 12-year study period, 69 patients underwent intervention for repair of IAAA and were included for review (Table 1). During the same time period, approximately 3,500 noninflammatory AAAs were repaired. The mean age of patients undergoing intervention for IAAA was 67.1 years (range, 23 to 83 years) including 53 males (77%) and 16 (23%) females. The majority of patients experienced symptoms of pain (36 of 69 [52%]). Four patients (5.6%) presented with ruptured IAAA. Ureteral involvement in the inflammatory process by CT imaging was seen in 23 patients (32.3%) and 21 of the 23 (91.3%) underwent preoperative ureteral stent placement. Mean preoperative aneurysm size in the overall group was 6.2 cm in maximum diameter (range, 3.4 to 11.3 cm) and did not include the rind. Follow-up ranged from 1 to 144 months with a mean of 41.1 months. Eighteen patients (25.7%) were lost to follow-up. There was one postoper-
Results of Endovascular Repair There were 10 patients (14%) that underwent EVAR for management of their IAAA during the study period. The mean age
Inflammatory aneurysms treated with EVAR was 72.2 years. Preoperatively, eight patients (80%) experienced abdominal pain and, one of these (10%) presented with a ruptured aneurysm. Two patients (20%) had ureteral involvement in the inflammatory process and one of those required preprocedural stenting. Preoperative mean aneurysm size was 5.9 cm (range, 4.0 to 8.3 cm). Postoperative aneurysm size decreased in seven patients (70%), with two patients (20%) showing no change in aneurysm size and one patient lost during the follow-up period. Mean follow-up was 33.6 months. Postoperative mean aneurysm size was 4.73 cm. The mean change in size was a decrease of 1.12 cm. Of all patients with postoperative imaging, there was a mean decrease in aneurysm size of 17.8% (range, 57.6% to 0%). The inflammatory rind preoperatively measured 5.4 mm in mean thickness in patients with IAAA undergoing EVAR. Postoperatively, the mean size of inflammatory rind was 2.7 mm. One patient had an increase in the size of the inflammatory rind but had no change in the size of the aneurysm sac. All other patients had decrease in the size of the inflammatory rind. Mean decrease in the thickness of the inflammatory rind was 50.8% (range, 92.1% to 0%). Postoperative abdominal pain was resolved in 6 of 7 patients (85.7%) after EVAR. Two patients (20%) developed atrial fibrillation postoperatively, but there were no other significant complications reported. No patient required subsequent intervention for repair of the aneurysm and no endoleaks were identified in follow-up. There was no perioperative mortality and no patient died of aneurysm-related causes during the follow-up period.
Published Reports on Endovascular Repair of Inflammatory Aneurysms Outcomes of open surgery for management of inflammatory aneurysms are noted with an increased complication rate compared with noninflammatory aneurysms. In a large series, it was demonstrated that operative mortality increased threefold when comparing inflammatory to noninflammatory aneurysms.6 In addition, there is a significant increase in major morbidity between open surgery for inflammatory aneurysms compared with noninflammatory aneurysms.11 In the early years of vascular surgery, extensive retroperitoneal adhesiolysis was routinely performed.12 This practice led to major complications, including enterotomies and duodenal injury. In addition, there was a significant rate of ureteral injury due to this extensive dissection. In order to decrease the perioperative complications, it was suggested in the late 1970s to avoid extensive adhesiolysis.13 In light of the morbidity and mortality from open repair of IAAA, the option of endovascular aneurysm repair seems intuitive. However, the benefit from endovascular intervention is still unproven. Does the endovascular approach reduce not only the risk of aneurysmal rupture, but also the long-term risk of periaortic fibrosis? Not only are
229 the ureters potentially involved in the inflammatory process, but the duodenum and kidneys might be at risk due to the inflammatory process. Certain groups, such as the one from Liverpool,14 would suggest that EVAR is not suitable for IAAA repair due to the persistence of perianeurysmal fibrosis after endograft placement. Other publications, such as the meta-analysis from the EUROSTAR (European Collaborators on Stent-Graft Techniques for Abdominal Aortic Aneurysm Repair) and other meta-analyses, provide mixed results.8-10,15 The technical success of EVAR in our study was 100%. All of the aneurysms undergoing attempt at endovascular repair were treated successfully. Aneurysm size was significantly reduced in this group of patients. The amount of periaortic fibrosis was significantly reduced in 6 of 7 patients who had follow-up imaging. One of those 7 patients demonstrated stable inflammatory thickness in follow-up. Aneurysm sac shrinkage was present in seven of nine patients. The two remaining patients had no change in the size of the aneurysm sac. There were no endoleaks identified in any patient undergoing endovascular repair during periprocedural imaging or during long-term follow-up. In a series involving nine patients from Modena, Italy, the long-term results of endovascular repair are discussed.16 They reported good survival rates with follow-up as long as 60 months. Technical success was achieved in a significant number with low mortality. Aneurysm sac shrinkage occurred in 89% of their patients. There was no aneurysm rupture or aneurysm-related death. A 55% reduction in the inflammatory process was seen by measuring the periaortic fibrosis thickness in this group of patients. This finding is similar to our results of the Mayo Clinic series (Table 2). One of the most extensive series of EVAR for IAAA to date would be the report from the EUROSTAR database.8 This study compares the results of inflammatory abdominal aortic aneurysms versus noninflammatory aortic aneurysms managed with EVAR. This series includes 52 patients with IAAA, which represents 1.4% of the EUROSTAR data. All patients had the diagnosis of inflammatory aneurysm made by CT imaging. The mean age of patients with inflammatory aneurysm was approximately 6 years younger than noninflammatory aneurysms. Other
Table 2 Current Results and Comparison to Published Data Coppi et al16 IAAA treated with EVAR, n Aneurysm-related deaths, n (%) Patients with decreased periaortic inflammation postoperatively (%) Patients with decreased aneurysm size postoperatively (%)
Lange Mayo et al8 Clinic
9 0 78
52 1 (1.8) —
10 0 86
89
87
70
Abbreviations: EVAR, endovascular aneurysm repair; IAAA, inflammatory abdominal aortic aneurysms.
W.M. Stone and G.T. Fankhauser
230 significant differences found in this series and identified by other large series of inflammatory aneurysms are that the risk of smoking was significantly greater in inflammatory aneurysm and the instance of hypertension was significantly less. Also, cardiac and pulmonary disease is less common. Perhaps the younger age of patients with inflammatory aneurysms relates to fewer cardiac and pulmonary comorbidities. Operating time for inflammatory aneurysms when placing endografts in comparison to noninflammatory aneurysms was not significantly different. There was a significant increase in the rate of limb stenosis or occlusion in patients with inflammatory aneurysms. This problem might be related to the severe inflammatory reaction surrounding the aneurysm. However, this result was not found in our series, but might be related to the endograft used. Overall, morbidity and mortality were not significantly different between inflammatory and noninflammatory aneurysms. Minor complications, such as access-site infections, were likewise not statistically different. The EUROSTAR data also provide results for long-term outcomes.8 It is interesting to note that there was no significant difference in the rate of endoleaks. There was no difference in device migration, kinking, or thrombosis. There was also no difference in aneurysm shrinkage between the two groups. What was significantly different was that worsening of renal function in the IAAA group. If patients were followed long-term, renal function deteriorated in 27% of all IAAA patients. The effect of EVAR on the amount of inflammatory fibrosis is less clear. EVAR demonstrated a significant reduction in the amount of inflammation in approximately half of the patients. The results published by Puchner et al from Vienna parallel the results of the EUROSTAR data.10 This metaanalysis of the treatment of inflammatory aortic aneurysms by EVAR had a mean follow-up of 18 months. Results are quite similar to both ours and the EUROSTAR data. Periaortic fibrosis was reduced by approximately 51% in this group; in 42% there was no significant change in periaortic fibrosis; and in 7% there was an increase in the periaortic fibrosis. In this series, in comparison with our reported results, there was a large male predominance, similar to EUROSTAR, with 98% of the patients being male. In another large meta-analysis, Paravastu and coworkers presented a review of open versus endovascular repair for IAAA.15 They again demonstrated a significantly higher mortality rate with open repair (6.2% v 2.4%). They suggest that there is no significant difference in open versus EVAR on the resolution of the inflammatory process. Patients demonstrating significant reduction in fibrosis were 73% in the open group versus 65% with use of EVAR (P ⫽ NS). In the open group, hydronephrosis and hydroureter was improved in 69% of the patients, and only 38% in the EVAR group (P ⫽ .01). In addition, the hydronephrosis or hydroureter progressively worsened in 9% of the open group versus 21% of the patients in the EVAR group. However, the all-cause 1-year mortality was significantly greater in the open group versus the EVAR group (P ⫽ .01).
Arguments Against EVAR EVAR itself produces inflammation in the aorta. This reaction is not as immediate a response as in open repair; however, over time it can be significant.17 It has been hypothesized that this increase in inflammation might be due to reaction to the Dacron in the endograft, however, similar results have been demonstrated in grafts using polytetrafluoroethylene. The possibility that EVAR generates its own inflammatory reaction adds to the skepticism that endovascular repair will promote the resolution of inflammation in IAAA. This skepticism is unfounded based on our results in which inflammation improved in all cases of EVAR. Numerous reports demonstrate, similar to our present series, that EVAR for inflammatory aneurysm successfully reduces the size of the aortic aneurysm in a majority of patients. It also reduces the amount of periaortic fibrosis, but not to the extent that open aneurysm repair does. Endovascular repair outcomes are achieved with a lower morbidity and 1-year mortality. The Achilles’ heel of EVAR for inflammatory abdominal aortic aneurysms revolves around renal and ureter involvement. The improvements in hydroureter and hydronephrosis are inferior with EVAR compared with open repair. We hypothesize that this difference in renal improvement might be related to the fact that the periaortic fibrosis resolves at a slower rate compared with open repair. Based on our results and results in the literature, one would suggest that EVAR is appropriate treatment for inflammatory aortic aneurysms where there is no renal or ureter involvement in the inflammation. It might also be successful treatment for a proportion of patients with renal or ureter involvement if they are poor open surgical risks.
Conclusions Endovascular repair is an effective treatment for inflammatory aneurysms, but there may be less resolution of the inflammatory process. Follow-up imaging in necessary to monitor the involvement of the ureters and resolution of any hydronephrosis. Additional intervention might be necessary after EVAR repair. Open surgical repair is always an option. The suitability of the patient for a major operation must be balanced with the possibility that endovascular repair might not resolve all of the inflammatory process.
References 1. James TGI: Uremia due to aneurysm of the abdominal aorta. Br J Urol 7:157, 1935 2. Schumacker HB Jr, Garrett R: Obstructive uropathy from abdominal aortic aneurysm. Surg Gynecol Obstet 100:758-761, 1955 3. Walker DI, Bloor K, Williams G, et al: Inflammatory aneurysms of the abdominal aorta. Br J Surg 59:609-614, 1972 4. Sueyoshi E, Sakamoto I, Uetani M: Endovascular repair of inflammatory abdominal aortic aneurysm: serial changes of periaortic fibrosis demonstrated by CT. Abdom Imaging 34:523-526, 2009 5. van Bommel EF, van der Veer SJ, Hendriksz TR, et al: Persistent chronic peri-aortitis (’inflammatory aneurysm’) after abdominal aortic aneurysm repair: systematic review of the literature. Vasc Med 13:293-303, 2008
Inflammatory aneurysms treated with EVAR 6. Pennell RC, Hollier LH, Lie JT, et al: Inflammatory abdominal aortic aneurysms: a thirty-year review. J Vasc Surg 2:859-869, 1985 7. Hechelhammer L, Wildermuth S, Lachat ML, et al: Endovascular repair of inflammatory abdominal aneurysm: a retrospective analysis of CT follow-up. J Vasc Interv Radiol 16:737-741, 2005 8. Lange C, Hobo R, Leurs LJ, et al: Results of endovascular repair of inflammatory abdominal aortic aneurysms. A report from the EUROSTAR database. Eur J Vasc Endovasc Surg 29:363-370, 2005 9. Hinchliffe RJ, Macierewicz JA, Hopkinson BR: Endovascular repair of inflammatory abdominal aortic aneurysms. J Endovasc Ther 9:277-281, 2002 10. Puchner S, Bucek RA, Rand T, et al: Endovascular therapy of inflammatory aortic aneurysms: a meta-analysis. J Endovasc Ther 12:560567, 2005 11. Sultan S, Duffy S, Madhavan P, et al: Fifteen-year experience of transperitoneal management of inflammatory abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 18:510-514, 1999 12. Ruppert V, Verrel F, Kellner W, et al: Endovascular repair of inflam-
231
13. 14.
15.
16.
17.
matory abdominal aortic aneurysms: a valuable alternative?— case report and review of literature. Ann Vasc Surg 18:357-360, 2004 Goldstone J, Malone JM, Moore WS: Inflammatory aneurysms of the abdominal aorta. Surgery 83:425-430, 1978 Vallabhaneni SR, McWilliams RG, Anbarasu A, et al: Perianeurysmal fibrosis: a relative contra-indication to endovascular repair. Eur J Vasc Endovasc Surg 22:535-541, 2001 Paravastu SC, Ghosh J, Murray D, et al: A systematic review of open versus endovascular repair of inflammatory abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 38:291-297, 2009 Coppi G, Rametta F, Aiello S, et al: Inflammatory abdominal aortic aneurysm endovascular repair into the long-term follow-up. Ann Vasc Surg 24:1053-1059, 2010 Abdelhamid MF, Davies RS, Adam DJ, et al: Changes in thrombin generation, fibrinolysis, platelet and endothelial cell activity, and inflammation following endovascular abdominal aortic aneurysm repair. J Vasc Surg 55:41-46, 2012