Inflammatory aneurysms of the abdominal aorta: Incidence, pathologic, and etiologic considerations☆☆☆★

Article Outline

• Abstract
• Material and methods
• Results
  • Clinical presentation
  • Diagnostic tests
  • Pathologic features
  • Operative management and clinical outcome
• Discussion
• Discussion
• References
• Copyright

Abstract 

Among 486 patients undergoing repair for abdominal aortic aneurysm (AAA) during a 12-year period, 30 (6.2%) had evidence of “inflammatory” AAA. One patient (3%) had acute rupture, and six patients (20%) had chronic contained rupture. Ureteral obstruction was evident in 20% of the patients. In the early period of the study there were two postoperative deaths and operative time and blood loss were significantly increased. In the last period of the study, no attempt was made to separate the duodenum and the ureters from the aneurysm; there was no operative mortality, and operative time and blood loss were similar to that of patients with atherosclerotic aneurysms. In 23 of 100 specimens of atherosclerotic AAA, microscopic findings resembling inflammatory AAA were found. On the basis of our study we conclude the following: (1) Inflammatory AAAs are simply atherosclerotic aneurysms that show an unusual accentuation of the chronic inflammation observed in relation to atherosclerotic aneurysms. (2) Operative technique should be modified to avoid excessive dissection and lysis of ureters and duodenum. (3) Excellent early and late results can be expected with proper surgical technique. (4) The causes of AAA are multiple, and chronic contained rupture of the aneurysm and reactive lymphatic hyperplasia might play a role of greater significance than previously thought. (J Vasc Surg 1989;9:643–50.)

Atherosclerotic abdominal aortic aneurysms (AAAs) constitute a common clinical entity for the vascular surgeon. Current surgical management of unruptured AAA is associated with low morbidity and mortality rates,¹ and the life expectancy of patients surviving operation approaches that of the general population. ², ³

Occasionally patients with AAA may have an unusual anatomic or pathologic picture with increased surgical risk. There is a form of AAA termed inflammatory aneurysm that has attracted relatively little attention in the past. Only recently several reports attempted to define the incidence and nature of this disease process. ⁴, ⁵, ⁶, ⁷, ⁸

Inflammatory AAAs are characterized by dense, fibrotic, perianeurysmal fibrosis. Although it seems to represent a distinct clinicopathologic entity, the cause, appropriate treatment, and natural history of the condition are controversial. The purpose of this study was to review our experience with the surgical treatment of patients with inflammatory aneurysms and to characterize the appearance, etiopathologic features, and incidence of this disease.

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Material and methods 

Of 486 patients who underwent AAA repair in the last 12 years, 30 were identified as having inflammatory aneurysm, for an incidence of 6.2%. The diagnosis was made from the gross appearance of the lesion, which was characterized by a dense perianeurysmal fibrous reaction and thickening of the aneurysm wall. The medical records of the patients were analyzed and form the basis of this report; associated risk factors, diagnostic tests performed, and clinical appearance of patients with inflammatory and ordinary atherosclerotic aneurysms were reviewed and compared.

To further delineate the histologic characteristics of inflammatory aneurysms, the microscopic sections of 100 randomly selected specimens from ordinary atherosclerotic AAAs were reviewed and compared to those of inflammatory aneurysms (21 specimens were available for comparison). We defined as ordinary atherosclerotic AAA, an aneurysm without gross signs of sclerosis, inflammation, and microscopic atherosclerotic changes. If the microscopic study showed severe inflammation, the aneurysm was still considered to be “ordinary atherosclerotic” on the basis of the intraoperative evaluation. The severity of the chronic inflammation and fibrosis related to each aneurysm was graded on a scale 0 to 3; 0 indicated no signs of inflammation, 1 indicated mild inflammation, 2 indicated moderate inflammation, and 3 indicated severe inflammation. Statistical significance between groups (p < 0.05) was determined by a two-tailed t test for continuous variables and chi-square test for categoric variables.

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Results 

Clinical presentation 

The 30 patients with inflammatory aneurysms consisted of 26 men and four women. Age ranged from 49 to 81 years (mean 62.2). Twenty-seven patients (90%) had symptoms referable to their aneurysm. Back pain and abdominal pain were the most common symptoms. Only 80 of the 456 patients (18%) with ordinary atherosclerotic AAAs had symptoms referable to their aneurysm (p < 0.001). Acute rupture was more common between ordinary atherosclerotic aneurysms (76/456, 17%) than between inflammatory aneurysms (1/30, 30%) (p < 0.001).

Significant weight loss was found in three patients (10%) with inflammatory AAAs and in 33 (7%) of the patients with atherosclerotic AAAs (p = NS). Table I shows the profile of patients with inflammatory and atherosclerotic aneurysms.

Table I. Patient profile

Smoking habitus was common in both groups. More than 40% of the patients have arterial hypertension. Multiple aneurysms occurred in three patients (10%) with inflammatory aneurysms and in 27 (6%) of those with atherosclerotic aneurysms. Occlusive arterial disease in other arterial segments was diagnosed in 47% of the patients with inflammatory aneurysms and in 48% of those with ordinary atherosclerotic aneurysms (p = NS) (Table II).

Table II. Associated arterial occlusive disease

Patients with inflammatory AAAs had a lower incidence of coronary artery disease and diabetes; this difference was not statistically significant.

The size of the aneurysm was assessed preoperatively by clinical examination, abdominal roentgenography (five patients), ultrasonography (seven patients), or computed tomographic scan (six patients) or was measured at operation. In inflammatory aneurysms the maximum transverse diameter varied from 4 to 14 cm (mean 8.3 ± 1.2); in ordinary atherosclerotic aneurysms it ranged from 4.5 to 15 cm (mean 7.2 ± 2) (p < 0.05). Twenty percent (6/30) of patients with inflammatory aneurysms had symptoms of obstructive uropathy, whereas only 1% (6/456) of those with atherosclerotic aneurysms (p < 0.01) had symptoms.

A variety of previous abdominal operations had been performed in more than 40% of the patients. One patient with inflammatory aneurysm underwent ureterolysis for symptoms of ureteral obstruction 2 years previously; symptoms of obstructive uropathy recurred despite steroid therapy. It is interesting to note that after standard aneurysmectomy and bypass grafting, patients experienced complete relief from symptoms and had no recurrence 3 years after surgery.

Diagnostic tests 

A diagnosis of inflammatory aneurysm was suspected preoperatively in only four patients (13%); these four patients were operated on in a more recent period, when this clinical diagnosis was more frequently considered. Abdominal ultrasound was performed in seven patients, and in none was there suspicion of inflammatory aneurysm. However, in a retrospective review of each examination, thickening of the anterior and lateral aortic wall was present in three cases. Computed tomographic scan of the abdomen was performed in six patients; retrospective review showed periaortic soft tissue density and thick aortic wall in at least five cases (Table III).

Table III. Positive diagnostic tests for inflammatory AAA

Sixteen patients underwent angiography preoperatively, but the results of this study did not reveal the inflammatory nature of the aneurysm (Table III).

Ten patients underwent excretory pyelography. Some degree of ureteral obstruction was present in six cases. Medial deviation of one or both ureters was evident in five cases. Results of cultures of the aortic wall, performed in five cases, were negative. Serologic test results for syphilis (four patients) were negative (Table III).

The average white blood cell count in patients with inflammatory aneurysm was slightly higher than normal (mean 9500 cell/mm³). However, if we exclude patients with inflammatory aneurysm and contained chronic rupture, white blood cell count was in the normal range. The erythrocyte sedimentation rate was available in only four cases and in all it was elevated. However, because of the small number of patients in whom the test was performed, a meaningful comparison between inflammatory and ordinary atherosclerotic AAAs was not feasible.

Overall, out of 35 clinical variables evaluated to determine possible differences between patients with and without inflammatory AAAs, seven variables resulted in statistically significant difference: age, sex, incidence of symptoms referable to the AAA, incidence of acute rupture, presence of ureteral obstruction, transverse diameter, and incidence of chronic contained rupture.

Pathologic features 

There was a characteristic appearance at laparotomy. The aneurysm was encased in a thick, shiny, dense, whitish fibrotic process. The fibrotic reaction was contiguous with the aneurysm and extended in all directions. Depending on the extent of the fibrosis, it may vary so as to occupy the entire retroperitoneum. Various anatomic structures were involved. In all of the patients the fourth portion of the duodenum was incorporated into the fibrotic process, and in most of the patients the vena cava and the left renal vein were also involved. Also incorporated were the small bowel (six cases) and the sigmoid colon (six cases); in the most advanced cases the pancreas (two cases) and the stomach (three cases) were incorporated.

The anterior and lateral walls of the aneurysm were thick, whereas the posterior wall appeared grossly normal. Six patients had evidence of a chronic rupture that was walled off by the inflammatory process.

Twenty-one specimens were available for review. In all cases there was evidence of atherosclerotic disease of the aorta, with intimal fibrosis and extensive mural thrombosis. The media was extensively involved by a degenerative process, characterized by loss of smooth muscle cells and elastic fibers and development of replacement fibrosis (Figs. 1 and 2).

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• Fig. 1. 

  Specimen from inflammatory aneurysm. Border of adventitia and retroperitoneum. Note perivascular lymphocytic infiltrate. The retroperitoneal adipose tissue is infiltrated by chronic inflammatory cells and fibroblasts. (Hematoxylin-eosin stain; original magnification × 100.)

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• Fig. 2. 

  Specimen from inflammatory aneurysm. Photomicrograph at border of adventitia and retroperitoneum. The upper part of the photograph shows considerable inflammatory cell infiltrate and red cell debris. Note the striking fibrosis. (Hematoxylin-eosin stain; original magnification × 100.)

The adventitia and periadventitial tissue were the site of marked chronic inflammation. The inflammatory process consisted of lymphocytes, plasma cells, and mononuclear cells, with varying degrees of concomitant fibrosis.

Adventitial endarteritis was common.

The inflammatory process was usually diffuse; however, in some areas it consisted of localized perivascular aggregates. Lymphoid follicles with germinative centers were frequently seen. In several cases hyperplastic lymph nodes were incorporated in the fibrous process. In all these cases the inflammatory process showed varying degrees of infiltrative fibrosis. Entrapment of nerve tissue in the periaortic fibrous tissue was frequently seen.

It is interesting to note that periadventitial inflammation was present in 23 out of 100 specimens from ordinary atherosclerotic AAAs. In 10 cases the inflammation was mild, with scant numbers of lymphocytes and plasma cells in the adventitia. Hyperplastic lymph nodes and lymphoid aggregates were seen in some cases. In eight cases the inflammation was considered moderate. In five cases there was a severe inflammation similar to that observed in cases of “inflammatory” aneurysm (Fig. 3).

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• Fig. 3. 

  Specimen from ordinary atherosclerotic aneurysm. External border of adventitia. Note loose fibroconnective tissue with few inflammatory cells. (Hematoxylin-eosin stain; original magnification × 40.)

Operative management and clinical outcome 

Experience and anatomic conditions dictate certain modifications in the surgical treatment of inflammatory aneurysms. Proximal aortic control is obtained with minimal dissection; usually the iliac arteries are clamped with minimal dissection. The aneurysm is opened longitudinally and laterally to the duodenum. The adherent duodenum is not separated. By working inside the aneurysmal cavity, a synthetic graft is inserted. To avoid excessive dissection if the iliac arteries are involved by the disease, it is preferable to oversew the common iliac arteries from inside the sac, and to anastomize the graft to the proximal external iliac artery. The aneurysmal wall is then approximated over the prosthesis. To facilitate this maneuver it is convenient to perform an extensive endarterectomy of the aneurysmal wall.

Ureterolysis was performed in two patients. However, in the current management it is seldom performed.

During a mean follow-up of 60 months, none of the patients operated on complained of symptoms of the ureteral or duodenal obstruction. None received steroid therapy. The patient who had acute rupture died from renal failure 12 days after surgery. Of 29 patients without acute rupture, one died after surgery. This patient was operated on in a more remote period. In the initial experience (12 cases), troublesome dissection of adherent structures was often attempted with increased morbidity, mortality, operative time, and blood loss. In the last period of the study (18 cases), dissection was kept minimal and operative time and blood loss were similar to that in patients with ordinary atherosclerotic aneurysm.

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Discussion 

The cause of so-called inflammatory aneurysms of the abdominal aorta remains obscure. Walker et al.⁴ believed that they were distinct clinical entities different from atherosclerotic aneurysms. The clinical and pathologic findings in our study favor the hypothesis that inflammatory aneurysms represent an exaggerated accentuation of the chronic inflammation and fibrosis that may be observed in relation to atherosclerotic aneurysms.⁹

Review of specimens from ordinary atherosclerotic aneurysms showed varying degrees of chronic inflammation and adventitial fibrosis. In some cases the inflammatory response was minimal or absent, in others it was diffuse and resembled inflammatory aneurysms. There was a gradual passage, in terms of inflammatory response, from ordinary atherosclerotic to inflammatory response.

The cause of this inflammatory response is uncertain. An attractive hypothesis is that inflammation is the result of an autoimmune response to the components of the atherosclerotic plaque. Lymphocytic infiltrates have been correlated to the severity of atherosclerosis.¹⁰ However, the reason some patients experience this exaggerated response is unclear. The hypothesis that the inflammatory response results from subclinical retroperitoneal leakage of blood has been rejected because hemosiderin-laden macrophages have been rarely found in the retroperitoneal fibrosis. In our series 20% of the patients had chronic contained rupture of the AAA as assessed intraoperatively. Pennell et al.¹¹ reported gross evidence of blood extravasation in 15 out of 127 patients (12%) with inflammatory aneurysm. Crawford et al.¹² reported only one case of chronic contained rupture among 30 patients. It should be noted that in some instances an old chronic contained rupture can be missed at operation. In a certain group of patients the unusual inflammatory response seems to be related to the chronic retroperitoneal hematoma. A particular finding in our study was the presence of numerous hyperplastic periaortic lymph nodes; this might represent a secondary response to an inflammatory process. However, the hypothesis that the enlarging aneurysm can compress the lymphatic vessels with stasis and edema and secondary fibrosis is suggestive. In fact, the posterior wall of the aneurysm, where the lymphatic network is absent or poorly developed, is seldom involved by the fibrotic process. The periaortic fibrosis can represent a protective mechanism, and lower rupture rate for inflammatory AAA has been reported.,,However, rupture of the aneurysm can still occur through the thin posterior wall.

The low mortality and morbidity after appropriate surgical treatment justify operative repair of these aneurysms, without delay. Operative technique should be modified with minimal dissection of the periaortic tissue.

Infrarenal aortic cross-clamping is feasible and safe, and suprarenal clamping should be reserved for selected cases. Steroid therapy has been recommended before surgery to reduce periaortic inflammation.¹⁴ In our opinion, preoperative steroid treatment should be avoided, because if it really lessens the retroperitoneal inflammatory changes, theoretically it can favor the acute rupture of the AAA, reducing the resistance of the periaortic tissue.

Preoperative diagnosis of inflammatory aneurysm is important so that appropriete preoperative and intraoperative maneuvers can be planned.

Angiography is of no benefit in the diagnosis. Ultrasound may show a sonolucent area separate from the aorta. CT scan, with its ability to show variable amounts of soft tissue surrounding the aorta, is the most reliable diagnostic test.¹⁵

Excretory pyelography should be performed in patients with obstructive uropathy.

Symptoms can assist in the diagnosis. The triad of chronic abdominal pain, weight loss, and elevated erythocyte sedimentation rate was highly suggestive of inflammatory aneurysm in a previous report.¹¹ In our study we noted that a diagnosis of inflammatory AAA was seldom made preoperatively even if symptoms were clearly present. Abdominal pain was the most common symptom associated with the presence of inflammatory AAA; the presence of symptoms of ureteral obstruction was highly suggestive for inflammatory AAA. The combination of abdominal pain and ureteral obstruction was almost peculiar to the presence of an inflammatory aneurysm.

In patients with ureteral obstruction, preoperative ureteral catheterization can be useful to facilitate identification of the ureter if ureterolysis seems necessary. However, in none of the patients in our series were ureteral stents inserted before surgery. Since ureterolysis can complicate aneurysm repair, it should be performed in selected cases such as in patients with bilateral ureteral obstruction. In the remaining cases it is preferably a conservative attitude, awaiting spontaneous resolution of the problem with serial pyelographic studies. In such a case, steroid therapy may be advantageous.

It is important to note that none of our patients complained of late symptoms of the ureteral obstruction, and rare cases have been reported in the literature. ¹¹, ¹², ¹³ Two patients had associated ureterolysis and both are free of symptoms at late follow-up.

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Discussion 

Dr. Jonathan B. Towne (Milwaukee, Wis.). I essentially agree with the surgical approach to inflammatory aneurysms described in this report. We have become more aware of the importance of noninvasive evaluation and imaging of these aneurysms, and we have been especially pleased with their detection by either ultrasound or computed tomographic (CT) scanning. When inflammatory aneurysms are suspected preoperatively, it is important to document the course of the ureters by means of either delayed films after angiography or formal intravenous pyelography.

Although 20% of the patients in this series had ureteral involvement, we have not made it a point to dissect the ureters in such cases at our center. Since you seem to have followed this same policy, do you have any objective follow-up data indicating that ureteral obstruction resolves once the aneurysm has been corrected? Also, what then are your indications for ureterolysis, or at least for the placement of indwelling ureteral catheters? Finally, do you have any idea why this tremendous inflammatory reaction occurs in the first place?

Dr. Sterpetti. Our review covered a 15-year study period, so Dr. Schultz must answer some of your questions concerning our surgical approach during that time. However, with regard to the incidence of late ureteral obstruction, none of our patients experienced this complication during a mean follow-up interval of 6 years. While preparing this work, I was able to find only two examples of late ureteral obstruction after aortic grafting without ureterolysis, published in the surgical literature. Routine lysis does not seem to be necessary, but if stents are in place, it may occasionally be warranted in the presence of known bilateral obstruction.

My own hypothesis concerning the cause of these aneurysms is based on the fact that their posterior walls usually are quite normal despite extensive fibrosis laterally and anteriorly. Since the lymphatic network along the posterior wall is not well developed, I suspect that compression of the lymphatics associated with the lateral and anterior walls may lead to lymphatic stasis and reactive fibrosis. The problem, of course, is why some aneurysms develop this kind of inflammation and others do not. It may be that the rate of expansion of the aneurysm is important. In other words, if an aneurysm enlarges very suddenly, it may compress the lymphatic network more severely.

Dr. Schultz. Actually, Dr. Sterpetti already has answered most of your questions. I believe our surgical approach to these aneurysms has improved as we have come to recognize the importance of minimal dissection. If one attempts to lyse either the ureter or the duodenum, it may cause a great deal of difficulty, and probably is responsible for some of the increased morbidity and mortality that is reported for inflammatory aneurysms in the literature. However, it must be remembered that this is not the type of retroperitoneal fibrosis that may be anticipated but instead is an inflammatory process specific to aneurysms that occurs to an unpredictable degree in different patients.

Dr. John H. Hageman (Toledo, Ohio). One of the interesting features of this type of inflammatory process is that it may not necessarily be confined to the aneurysm, but may also involve the suprarenal aorta and especially the left renal vein. It appears that the ureteral problems resolve after the aneurysm is removed, but have you actually monitored any of these patients with follow-up pyelograms or CT scans to confirm that impression?

Dr. Schultz. First of all, we often consult a urologist to assist us with these problems, but I am not aware of any chronic ureteral complications related to chronic fibrosis. I should also mention that we have not used steroids although they have been reported to have some success in the past.

Dr. Richard Pennell (St. Louis, Mo.). When I was a fellow in Rochester, we reviewed about 130 patients who had come to the Mayo Clinic with inflammatory aneurysms. We found that this diagnosis often is overlooked despite the fact that it usually can be established by ultrasonography or CT scanning. It is important that the radiologists at your centers be aware of this phenomenon because it usually may be recognized radiographically. Second, a number of physical findings in conjunction with inflammatory aneurysms seem to be relatively specific. They include either abdominal or back pain, anorexia and weight loss reflecting almost a systemic disease, and finally, an elevation in the erythrocyte sedimentation rate.

Using immunofluorescent staining techniques, we investigated the possibility that an immune response caused by an infiltration of lymphoplasma cells might be responsible for the inflammatory features. Whereas we found a lot of plasma cells, we could not identify any specific immune complexes. From the perspective of the pathologist, there are many similarities between inflammatory aneurysms and both giant cell arteritis and retroperitoneal fibrosis.

Dr. Schultz. I am sure that the sedimentation rates in our patients would have been elevated, but they unfortunately were not routinely obtained in our series. I agree with you that the diagnosis generally can be made on the basis of a preoperative CT scan. The CT findings may confuse even radiologists, and at our institution they occasionally have been mistaken for evidence of rupture or dissection.

Dr. James J. Schuler (Chicago, Ill.). You mentioned that there were two factors in your preoperative evaluation that seemed to have some value in predicting that you were dealing with an inflammatory aneurysm. They included thickening and an increased density of the wall of the aneurysm discovered on CT scanning, and “characteristic signs” on excretory pyelography. Just what are those signs?

Dr. Schultz. Obstruction is the one that was seen most frequently when we had the benefit of a preoperative pyelogram.

Dr. Jonathan E. Hasson (Madison, Wis.). During the past year Dr. Charles Acher and I have repaired six of these aneurysms using the retroperitoneal approach. Provided the diagnosis is established preoperatively, we found that exposure through the flank with the patient in the full lateral position greatly expedites the resection and simplifies dissection, simply because one is posterior to the ureter and the duodenum never enters the field. As already has been mentioned, the inflammatory response generally is restricted to the anterior and lateral walls of the aorta and usually does not involve the retroperitoneum itself.

Dr. Schultz (closing). That is an extremely interesting observation, and I am glad that you brought it to our attention.

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