Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 9  |  Issue : 5  |  Page : 418-420

Giant femoral aneurysm in giant cell arteritis


1 Department of Cardiovascular Surgery, Istanbul Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Training and Research Hospital, Istanbul, Türkiye
2 Department of Cardiovascular Surgery, Cizre State Hospital, Şırnak, Türkiye
3 Department of Pathology, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul, Türkiye
4 Department of Cardiovascular Surgery, Istanbul Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, Istanbul, Türkiye

Date of Submission11-Feb-2022
Date of Acceptance14-Mar-2022
Date of Web Publication13-Jan-2023

Correspondence Address:
Dr. Zihni Mert Duman
Department of Cardiovascular Surgery, Cizre State Hospital, Şırnak
Türkiye
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijves.ijves_12_22

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  Abstract 


Giant cell arteritis (GCA) which mostly causes thoracic aortic aneurysm is the most common vasculopathy of medium and large vessels, especially in people over 50 years of age. A 63-year-old male patient presented with pain and swelling in the right inguinal region. On examination, a pulsatile mass was palpable in the right femoral region. Computed tomographic angiography showed aneurysm enlargement reaching 70.9 mm in diameter at the level of the right common femoral artery (CFA). Aneurysm excision and Dacron graft interposition surgery was performed for the patient with local pain symptoms. The patient who had no postoperative complication was discharged 3 days later. Two weeks later, the pathology result of the aneurysm was obtained. Pathological examination of the aneurysm was GCA, and also, temporal artery biopsy was also performed to clarify the diagnosis. In this case report, we report the first defined CFA aneurysm caused by GCA and its surgical treatment. In the patient whom we did not think of as inflammatory arteritis at the first stage, we reached the actual diagnosis with pathology examination. Therefore, we recommend that all surgically removed aneurysm tissues be sent for pathology examination.

Keywords: Aneurysm, common femoral artery, giant cell arteritis


How to cite this article:
Bayram M, Duman ZM, Devecioglu EG, Timur B. Giant femoral aneurysm in giant cell arteritis. Indian J Vasc Endovasc Surg 2022;9:418-20

How to cite this URL:
Bayram M, Duman ZM, Devecioglu EG, Timur B. Giant femoral aneurysm in giant cell arteritis. Indian J Vasc Endovasc Surg [serial online] 2022 [cited 2023 Jan 29];9:418-20. Available from: https://www.indjvascsurg.org/text.asp?2022/9/5/418/367714




  Introduction Top


Giant cell arteritis (GCA) is the most common vasculopathy of medium and large vessels, especially in people over 50 years of age.[1] In the early phase of the disease, large-vessel involvement is typically asymptomatic. In advanced stages, GCA can cause symptoms related to thoracic aortic aneurysm, aortic syndrome, abdominal aortic aneurysm, and stenosis of peripheral large arteries.[2]

Most peripheral aneurysms result from weakening of the arterial wall caused by atherosclerosis. Familial syndromes such as Marfan, Ehlers–Danlos, and Loeys–Dietz syndrome, as well as Behçet's disease, GCA, and other vasculitides involving large vessels can cause arterial enlargement and aneurysm formation.[3]

Common femoral artery (CFA) aneurysms are defined as 50% enlargement of the normal diameter of the artery. True aneurysms of the femoral artery are rare. They are bilateral in one-third of patients, and usually, the patient has other accompanying aneurysms in the abdominal aorta or popliteal artery. Femoral artery aneurysms were classified as two types by Cutler and Darling in 1973. They defined type 1 as an aneurysm containing CFA and ending proximal to the bifurcation and type 2 as an aneurysm containing CFA and profunda femoris artery (PFA).[4]

In this case report, we describe the first CFA aneurysm caused by GCA. The aneurysm is also the largest of the type 1 CFA aneurysms described in the literature.


  Case Report Top


A 63-year-old male patient presented with pain and swelling in the right inguinal region. He had been treated for diabetes mellitus and hypertension for over 20 years. Percutaneous coronary intervention had been performed on the right coronary artery 1 month ago for anginal symptoms. He was an ex-smoker who had smoked 30 years. The drugs used by the patient are 20 mg atorvastatin, 81 mg aspirin, and 75 mg clopidogrel daily. On examination, a pulsatile mass was palpable in the right femoral region. Duplex ultrasound revealed a thrombus surrounding the lumen in the enlarged right CFA. Computed tomographic angiography (CTA) was performed. CTA showed aneurysm enlargement reaching 70.9 mm in diameter at the level of the right CFA [Figure 1]. There was a thrombus surrounding the lumen of the aneurysm, and the actual lumen was measured as 22 mm. As the accompanying aneurysm, the left common iliac artery was measured as 22 mm. The aneurysm terminated before bifurcation. There was no other accompanying aneurysm. In laboratory data, creatinine was measured as 1.36 mg/dL. White blood cells count was 9.6 × 109/L, hemoglobin was 12.3 g/dL, platelet was 188 × 109/L, and international normalized ratio (INR) was 0.82 within normal limits. Aneurysm excision and graft interposition surgery was planned for the patient with local pain symptoms.
Figure 1: Aneurysm enlargement reaching 70.9 mm in diameter at the level of the right common femoral artery

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Operative technique

The patient was placed supine on the operating table. A longitudinal incision was made from the groin fold. After the aneurysm sac was found [Figure 2]a, the proximal CFA was taken under control. After systemic heparinization (80 IU/Kg), the proximal CFA was clamped and the aneurysm was opened. No atherosclerotic changes were observed in the intima of the aneurysm tissue. Aneurysm was excised. PFA and superficial femoral artery (SFA) proximal orifices were made suitable for anastomosis. Both had adequate retrograde flow. Dacron graft interposition was performed from CFA to SFA. PFA was anastomosed to the Dacron graft end-to-side [Figure 2]b. The incisions were closed.
Figure 2: (a) Operative view of the aneurysm sac. (b) Dacron graft interposition

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Postoperative follow-up

The patient who had no postoperative complication was discharged 3 days later. Two weeks later, the pathology result of the aneurysm was obtained. Pathological examination of the aneurysm wall showed infiltration of the vessel wall by giant cells, lymphocytes, and plasma cells and fragmentation of the internal elastic lamina [Figure 3]a and [Figure 3]b. We questioned the patient's preoperative history in more detail; the patient also had complaints of weight loss and jaw claudication.
Figure 3: (a) Common femoral artery biopsy showing infiltration of vessel wall by giant cells, lymphocytes, and plasma cells and fragmentation of the internal elastic lamina (H and E, ×100). (b) Giant cell (H and E, ×400)

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In the patient whose clinical and pathological results were consistent with GCA, temporal artery biopsy was also performed to clarify the diagnosis. The new biopsy was also reported as GCA. Two milligrams prednisone daily and methotrexate 10 mg once a week were started by the rheumatology clinic. The patient did not have any clinical complaints and additional problems on CTA 1 year after the operation.


  Discussion Top


GCA is a type of vasculitis with a granulomatous infiltration mostly affecting the aorta and its main branches.[5] Histologically, GCA aortas are characterized by granulomatous infiltrates in the media, dominated by macrophages that can form giant cells and adaptive immune cells (interferon and interleukin-17–producing T cells).[6] Macrophages in the media cause damage to the arterial wall through secretion of metalloproteinases and reactive oxygen intermediates. These processes lead to fragmentation of the internal elastic lamina and weaken the arterial wall. Compared to the general population, patients with GCA were 17.3 times more likely to develop a thoracic aortic aneurysm and 2.4 times more likely to develop an abdominal aortic aneurysm.[7]

Assie et al. showed that the vasculitic involvement in CFA was 13.9% in a 36-patient study covering the long-term follow-up of upper and lower extremity vasculitis due to GCA.[8] In addition, Lensen et al. showed that the rate of femoral artery involvement was found between 12% and 53% in patients with cranial GCA involvement.[9] However, both studies consisted of patients presenting with symptoms related to embolism or stenosis, and there were no patients with femoral artery aneurysms.

True femoral aneurysms are less common than femoral pseudoaneurysms due to the increasing number of percutaneous interventions. Most peripheral aneurysms result from weakening of the arterial wall caused by atherosclerosis. Familial syndromes such as Marfan, Ehlers–Danlos, and Loeys–Dietz syndrome, as well as Behçet's disease, GCA, and other vasculitides involving large vessels can cause arterial enlargement and aneurysm formation.[3] One-third of isolated true femoral aneurysms are asymptomatic. Symptoms caused by the mass effect of the aneurysm are mostly localized pain, leg edema, femoral vein thrombosis, or neuropathic pain. Most common presentation of CFA aneurysms is lower extremity ischemia from embolization. Rupture is rarely seen in 4% of cases.

The clinic of CFA aneurysms has not been well studied because of their low frequency. Therefore, many authors base their treatment guidelines on popliteal artery aneurysms. In addition, there is no separate recommendation for aneurysms due to GCA. It is usually treated according to the same recommendations as for arteriosclerotic aneurysms. Surgery is not recommended during active inflammation, as the anastomotic line is fragile and tends to get occluded when vascular anastomoses are performed during active disease. Complications are rare in asymptomatic femoral aneurysms smaller than 2.5 cm and can be followed conservatively. Open and endovascular techniques of CFA aneurysm repair have been described in the literature.[10] Open surgery is the preferred method in the treatment of large CFA aneurysms.

In this case report, we describe the first CFA aneurysm caused by GCA. The aneurysm is also the largest of the type 1 CFA aneurysms described in the literature. Due to the large size of the aneurysm, we preferred open surgery to endovascular surgery. We performed Dacron graft interposition safely. Further, the patient had another accompanying aneurysm in the left common iliac artery. It was a small aneurysm that did not require surgery.


  Conclusion Top


We showed that GCA, which is known to cause mostly thoracic aortic aneurysm or abdominal aortic aneurysm, can also cause femoral artery aneurysms. In this patient whom we did not think of as inflammatory arteritis at the first stage, we reached the actual diagnosis with pathology examination. Therefore, we recommend that all surgically removed aneurysm tissues be sent for pathology examination.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Mahr A, Belhassen M, Paccalin M, Devauchelle-Pensec V, Nolin M, Gandon S, et al. Characteristics and management of giant cell arteritis in France: A study based on national health insurance claims data. Rheumatology (Oxford) 2020;59:120-8.  Back to cited text no. 1
    
2.
Berti A, Campochiaro C, Cavalli G, Pepe G, Praderio L, Sabbadini MG, et al. Giant cell arteritis restricted to the limb arteries: An overlooked clinical entity. Autoimmun Rev 2015;14:352-7.  Back to cited text no. 2
    
3.
Attenhofer Jost CH, Greutmann M, Connolly HM, Weber R, Rohrbach M, Oxenius A, et al. Medical treatment of aortic aneurysms in Marfan syndrome and other heritable conditions. Curr Cardiol Rev 2014;10:161-71.  Back to cited text no. 3
    
4.
Cutler BS, Darling RC. Surgical management of arteriosclerotic femoral aneurysms. Surgery 1973;74:764-73.  Back to cited text no. 4
    
5.
Weyand CM, Goronzy JJ. Immune mechanisms in medium and large-vessel vasculitis. Nat Rev Rheumatol 2013;9:731-40.  Back to cited text no. 5
    
6.
Graver JC, Boots AM, Haacke EA, Diepstra A, Brouwer E, Sandovici M. Massive B-cell infiltration and organization into artery tertiary lymphoid organs in the aorta of large vessel giant cell arteritis. Front Immunol 2019;10:83.  Back to cited text no. 6
    
7.
Nuenninghoff DM, Hunder GG, Christianson TJ, McClelland RL, Matteson EL. Incidence and predictors of large-artery complication (aortic aneurysm, aortic dissection, and/or large-artery stenosis) in patients with giant cell arteritis: A population-based study over 50 years. Arthritis Rheum 2003;48:3522-31.  Back to cited text no. 7
    
8.
Assie C, Janvresse A, Plissonnier D, Levesque H, Marie I. Long-term follow-up of upper and lower extremity vasculitis related to giant cell arteritis: A series of 36 patients. Medicine (Baltimore) 2011;90:40-51.  Back to cited text no. 8
    
9.
Lensen KD, Voskuyl AE, Comans EF, van der Laken CJ, Smulders YM. Extracranial giant cell arteritis: A narrative review. Neth J Med 2016;74:182-92.  Back to cited text no. 9
    
10.
Rancic Z, Pecoraro F, Pfammatter T, Mayer D, Veith FJ, Lachat M. Less invasive (common) femoral artery aneurysm repair using endografts and limited dissection. Eur J Vasc Endovasc Surg 2013;45:481-7.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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