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Rare Case of Bilateral Common Iliac Vein Compression by Arterial Stents and Calcification
Abstract
May–Thurner syndrome is a rare condition involving compression of the left iliac vein by the right common iliac artery. Rarely, iliac vein compression syndromes are found to be right-sided and even more rarely bilateral. We present a rare case of bilateral iliac vein compression treated percutaneously with excellent results.
VASCULAR DISEASE MANAGEMENT 2012:9(11):E186-E188
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Case Report
An 88-year-old African American male, with history of peripheral arterial disease status post bilateral common iliac artery stents 2 years prior, presented with worsening left lower extremity edema and calf discomfort. He first presented 1 year earlier with similar symptoms and was found to have an acute left lower extremity deep venous thrombosis (DVT). At that time, his left femoral vein DVT was successfully treated with mechanical thrombectomy and thrombolysis and short-term anticoagulation. Follow-up evaluation revealed resolution of his lower extremity edema and thrombosis, which was confirmed by venous ultrasound. He now presented with recurrence of symptoms progressing over the previous week, and repeat ultrasound confirmed recurrent acute left femoral DVT.
Venography via left popliteal vein access revealed a hazy filling defect in the left femoral vein. Selective venogram of the left external iliac vein was performed with the use of a glide catheter and revealed compression of the left common iliac vein at the level of the previously stented right common iliac artery (Figure 1). Intravascular ultrasound imaging of the left common iliac vein confirmed extrinsic compression (Figure 2), and identified the likely etiology of DVT.
Access was then obtained in the right femoral vein to position a catheter at the inferior vena cava-common iliac vein bifurcation to accurately position the left common iliac vein stent. However, selective venography of the right femoral vein revealed compression of the right common iliac vein (Figure 3) at the level of a calcified nodule adjacent to the vein that was suspicious of arterial calcification. Access was then obtained in the right common femoral artery to further evaluate this finding.
Simultaneous angiogram of the right common femoral artery and vein revealed compression in the right common iliac vein at the origin of the right internal iliac artery as the calcified vessel coursed around the common iliac vein (Figure 4). This finding of extrinsic venous compression was also confirmed by intravascular ultrasound imaging of the right common iliac vein.
The patient was treated for bilateral iliac vein compression with deployment of self-expanding 14 mm Protégé stents (Covidien) in bilateral iliac veins with good angiographic result and brisk flow (Figure 5). He was discharged home the following day on dual antiplatelet therapy with aspirin and clopidogrel. He has been followed in clinic for 6 months with no recurrence of symptoms.
Discussion
May–Thurner syndrome is a rare condition in which the left common iliac vein becomes compressed by the overlying right common iliac artery, which may cause left lower extremity edema with discomfort and thrombus formation. In contrast to the right common iliac vein, which ascends almost vertically to the inferior vena cava, the left common iliac vein has a more horizontal course and may underlie the right common iliac artery, causing compression against the lumbar spine.1,2 Occasionally, the iliac vein compression can occur on the right side due to anatomical variants resulting in right-sided symptoms.3 Several other variants have been described, including a rare case of right common iliac vein compression by the right internal iliac artery.4 Although the true prevalence of May–Thurner syndrome is unknown, authors have reported 49% to 62% prevalence in patients with DVT.5
Compression of the venous system causes stasis of blood, which may precipitate DVT formation.1 The vein may also develop fibrosis from the repetitive pulsatility of the artery, which may further precipitate thrombus formation. Diagnosis is made with venography and angiography showing venous compression by the artery.6 Intravascular ultrasound can also aid in the diagnosis. Management of the underlying venous compression is imperative to prevent further exacerbations. Treatment includes stent implantation at the site of venous compression.7 If the patient has extensive thrombosis, pharmacologic thrombolysis and/or mechanical thrombectomy may be performed to decrease the incidence of post-thrombotic syndrome.2
Conclusion
We present a rare case of bilateral iliac vein compression presenting late in life, likely secondary to extrinsic arterial stent compression of the left iliac vein, and calcified right internal iliac artery compression of the right iliac vein. This bilateral iliac vein compression was managed successfully with bilateral iliac vein stenting.
References
- May R, Thurner J. The cause of the predominantly sinistral occurrence of thrombosis of the pelvic veins. Angiology. 1957;8(5):419-427.
- Fazel R, Froehlich JB, Williams DM, Saint S, Nallamothu BK. Clinical problem-solving. A sinister development –a 35-year-old woman presented to the emergency department with a history of progressive swelling and pain in her left leg, without antecedent trauma. N Engl J Med. 2007;357(1):53-59.
- Al-Nouri O, Milner R. May-Thurner syndrome. Vasc Disease Manag. 2011;8(3):E53-E56.
- Molloy S, Jacob S, Buckenham T, Khaw KT, Taylor RS. Arterial compression of the right common iliac vein: an unusual anatomic variant. Cardiovasc Surg. 2002;10(3):291-292.
- Juhan C, Cornillon B, Tobiana F, Schlama S, Barthelemy P, Denjean-Massia JP. Patency after iliofemoral and iliocaval venous thrombectomy. Ann Vasc Surg. 1987;1(5):529-533.
- Heuser RR, Henry M, eds. Textbook of Peripheral Vascular Interventions, 2nd Edition. London: Informa Healthcare; 2008.
- VanHise A, Gilbert D, George JC. Endovascular management of chronic left iliac vein occlusion in May-Thurner syndrome. Vasc Disease Manag. 2012;9(8):E139-E142.
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Editor’s Note: Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr. Rosen reports no conflicts regarding the content herein. Dr. George reports consultancy for Covidien. Dr. Groben reports no conflicts regarding the content herein.
Manuscript submitted September 20, 2012, provisional acceptance given October 15, 2012, final version accepted October 17, 2012.
Address for correspondence: Jon C. George, MD, Director of Clinical Research, Division of Cardiovascular Medicine, Deborah Heart and Lung Center, 200 Trenton Road, Browns Mills, NJ, 08015, USA. Email: georgej@deborah.org