CASE REPORT

Vascular Disease Management® March 2017 E78

Revascularization of Chronic Venous Occlusion in the Setting of Post-Thrombotic Syndrome

Jon George, MD; Deepakraj Gajanana; Sean Janzer; Vincent Figueredo; Dennis MorrisFrom the Einstein Heart and Vascular Institute, Einstein Medical Center, Philadelphia, Pennsylvania

Post-thrombotic syndrome (PTS), often the

sequelae of deep vein thrombosis (DVT) in

lower extremities, carries high morbidity and

often mortality. Timely intervention is critical for

preventing complications and salvaging the extremity.

Of late, there is growing interest in endovascular

techniques, including percutaneous angioplasty with

stent placement. We describe a unique case of May-

Thurner syndrome complicated by PTS that was

successfully treated using an endovascular approach.

Figure 1. Venous duplex showing occlusive thrombus in the left common femoral vein (CFV), near-total occlusion of the left superficial femoral (SFV) with non-compressibility of left greater saphenous vein (GSV).

ABSTRACT: Post-thrombotic syndrome is a complication that may follow deep vein thrombosis, and is

associated with significant morbidity. There is growing interest in endovascular techniques to treat this

complication. We present a case of May-Thurner syndrome complicated by post-thrombotic syndrome

that was successfully treated using an endovascular approach.

VASCULAR DISEASE MANAGEMENT 2017;14(3):E78-E84

Key words: post-thrombotic syndrome, endovascular technique

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CASE PRESENTATIONA 66-year-old male with past medical history of

colon cancer with subtotal colectomy and ileostomy,

left atrial myxoma with resection 4 months prior, and

concurrent left lower-extremity DVT, presented for

routine office visit. He was found to have persistent

bilateral lower-extremity edema, left greater than right

for 4 months despite appropriate anticoagulation with

warfarin and compression stockings. Upon evaluation,

his initial vital signs revealed blood pressure of 109/90

mm Hg, heart rate of 71 bpm, and pulse oximetry of 99%

on room air. He had unremarkable cardiopulmonary

and abdominal examination. He was found to have

significant left lower-extremity edema, extending up

to the upper thigh level with chronic venous stasis skin

changes and varicose veins. His hemoglobin was 11.8

g/dL and international normalized ratio (INR) was 2.0.

Figure 2. Chronic total occlusion of the femoral vein with collateral branches filling the distal common femoral vein and proximal common femoral vein.

Figure 3. Intravascular ultrasound image confirming severe compression of the left common iliac vein up to 60.4% area compression.

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An echocardiogram revealed mild mitral regurgitation

and normal biventricular function, with left ventricular

ejection fraction of 55% without any pericardial

effusion. A computed tomography scan of abdomen

and pelvis 4 months prior showed no organomegaly

or lymphadenopathy.

The presentation was consistent with PTS, despite

being compliant with warfarin therapy and therapeutic

INR. Venous duplex of bilateral lower extremities

revealed occlusive thrombus in the left common femoral

vein (CFV), near-total occlusion of left superficial

femoral (SFV), and popliteal vein with thickening of

greater saphenous vein (Figure 1). The patient was

then referred for venography of left lower-extremity

for further assessment and definitive therapy.

Selective left lower-extremity venography was

performed with the patient placed in supine frog-legged

position and ultrasound-guided 6 Fr sheath placement

in left popliteal vein using micropuncture access kit.

Selective venogram confirmed left popliteal scarring

with 50%-60% stenosis, with 100% occlusion of the

femoral vein with collateral branches filling the distal

Figure 4. Stenting and postdilation of left common femoral vein, proximal and distal femoral vein.

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CFV above the femoral head (Figure 2). A TriForce

coaxial crossing system (Cook Medical) was then

advanced over a stiff Glidewire to cross the occlusion

in the femoral vein to enter the reconstituted segment

in the CFV. Intravascular ultrasound confirmed severe

compression of the left common iliac vein (CIV) up to

60.4% area compression (Figure 3). A 24 x 45 mm self-

expanding Wallstent (Boston Scientific) was deployed

in the left CIV and postdilated using a 16 x 40 mm

Mustang XXL balloon (Boston Scientific) with good

expansion (Figure 4). Following this, 14 x 80 mm, 10 x

80 mm, and 8 x 150 mm self-expanding Protégé stents

(Medtronic) were deployed in the left CFV, proximal

to mid femoral vein, and mid to distal femoral vein,

respectively. The CFV was postdilated using a 12 x 40

mm Mustang balloon and the remainder of the stented

segment was postdilated using a 6 x 200 mm EverCross

balloon (Medtronic) with good expansion. Final

venogram revealed excellent angiographic result with

brisk flow through the entire stented segment (Figure

5), with excellent stent apposition under intravascular

ultrasound imaging. Hemostasis was achieved using

manual compression and the patient was discharged

home the next day with marked improvement in his

symptoms. His medical regimen at discharge included

aspirin 81 mg indefinitely, clopidogrel 75 mg for 1

month, and warfarin for 3 months.

DISCUSSIONDVT of the lower extremities occurs in about 1 per

1000 people/year and is associated with significant

morbidity.1 PTS is the development of symptoms

and signs of chronic venous insufficiency following

DVT.2 Despite adequate anticoagulation, PTS occurs

Figure 5. Final venogram revealing excellent angiographic result with brisk flow through the entire stented segment with excellent stent apposition under intravascular ultrasound imaging.

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in 20%-50% of patients with history of DVT.3 PTS

might develop over a matter of a few months, and in

some instances a few years after symptomatic DVT.4

A few identified risk factors include older age, obesity,

recurrent ipsilateral DVT, extensive DVT, symptoms

beyond 1 month, and subtherapeutic anticoagulation.

It carries significant morbidity and mortality, with a

significant economic burden to health-care systems.5

Usually, patients present with pain, venous varicosities,

edema, skin pigmentation, and eventually venous ulcers.

The patient described above had a history of DVT,

was on therapeutic anticoagulation with warfarin, and

had persistent symptoms beyond 3 months; thereby,

he had PTS by definition. There was no discussion of

switching the mode of anticoagulation, since there was

no recurrence of DVT on warfarin therapy but rather

onset and progression of PTS related to occlusive DVT.

Presence of unilateral DVT and PTS should often raise

suspicion for any extrinsic compression of the iliofemoral

system. May-Thurner syndrome is an often unrecognized

etiology of DVT, due to left CIV compression from the

right common iliac artery, first described by May and

Thurner in 1956.6 There is lack of awareness regarding

this entity and if not treated in a timely fashion, ulceration

and possible infection may result in amputation of the

affected extremity.

Once PTS is suspected, there are several classification

systems to clinically stage the extent of the disease,

which in turn determines treatment strategy. One such

classification is the CEAP (clinical, etiological, anatomic,

pathophysiological) system.7 Our patient was CEAP class

4a (associated with pigmentation/eczema). Since PTS is

a clinical diagnosis, any imaging modality would provide

additional information with regard to management.

Doppler ultrasound and plethysmography have been used

to measure venous reflux, venous obstruction, and calf

muscle dysfunction. However, it is limited in its assessment

of iliac veins. Thus, an additional imaging modality such

as intravascular ultrasound during venography is essential

to rule out May-Thurner syndrome. Our patient had

significant thrombus burden on ultrasound and changes

consistent with chronic inflammation of the affected veins

with significant secondary skin changes. The patient

described above had intravascular ultrasound imaging

during venography, which confirmed May-Thurner

syndrome. Treatment for May-Thurner syndrome has

evolved over the years, from conservative approach

with compression stockings8 to surgical veno-venous

bypass.9 The advancement of endovascular techniques,

including percutaneous iliac vein angioplasty with stent

placement, has revolutionized the treatment for May-

Thurner syndrome.10

Despite adequate anticoagulation, nearly one-half of

the cases develop PTS due to mechanisms less clearly

understood, as mentioned above. Treatment of PTS

and chronic DVT has evolved over years, with greater

emphasis on mechanical thrombectomy, thus focusing

on restoration of normal flow over anticoagulation.

One of the arguments for pharmacological thrombolysis

or surgical thrombectomy is the fact that residual

thrombus11 is a strong risk factor for recurrent DVT

and hence PTS. In a study comparing systemic

thrombolysis to heparin, PTS developed less frequently

in those treated with plasminogen activators rather than

heparin. However, at the cost of increased bleeding

risk (risk ratio, 2.9; 95% confidence interval, 1.1–8.1;

P=.04) than in those treated with heparin alone.12 In

another randomized trial comparing anticoagulation to

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surgical thrombectomy, improved venous patency and

a reduction in PTS was demonstrated in the surgical

arm,13 at the expense of surgical and anesthetic risks.

Other preventive strategies that have been proven to

be beneficial are elastic compression stockings and

exercise therapy.

In chronic DVT with persistent PTS, standard

endovascular chronic total occlusion revascularization

techniques are employed to traverse the occlusion. One

such catheter is the Wildcat catheter system, which

has been successfully used to cross the chronic venous

occlusion and has been reported previously.14 In our

patient, we used the TriForce Peripheral Crossing

system to successfully traverse the chronically occluded

venous segment. Thrombolysis has no perceived role

in chronic DVT due to the chronic nature of the

coagulation cascade; however, its role in acute DVT will

be dictated by the results of the pending ATTRACT

(Acute Venous Thrombosis: Thrombus Removal

with Adjunctive Catheter-Directed Thrombolysis)

multicenter, randomized, phase 3 trial.

In a study by Raju et al,15 chronic occlusion affecting

ilio-femoral segments treated with large-caliber, self-

expanding stents extending below the groin crease

were studied for the ease of deployment and long-

term patency. Actuarial primary, primary-assisted,

and secondary patency rates of stents at 24 months

were 49%, 62%, and 76%, respectively. The stented

group had significant symptomatic improvement with

minimal morbidity. The same group in another review

reported excellent results with iliac vein interventions

with better long-term patency results. Thus, our

patient underwent stenting of the chronically occluded

venous segments in order to mitigate the symptoms of

PTS, with excellent result post procedure. The patient

was seen in the follow-up clinic and had excellent

symptom improvement.

This case highlights endovascular management of

May-Thurner syndrome complicated with PTS. We

describe the technique of crossing chronic venous

occlusion and revascularization with stenting. The

importance of post-interventional care including an-

tiplatelet therapy, anticoagulation, and early ambula-

tion, should not be underestimated. n

Editor’s Note

Disclosures: Manuscript submitted July 17, 2016; pro-

visional acceptance given August 2, 2016; final acceptance

given November 8, 2016.

Address for correspondence: Jon C. George, MD, Einstein

Medical Center, Interventional Cardiology and Endovascular

Medicine, 5501 Old York Road, Philadelphia, PA 19141.

Email: jcgeorgemd@gmail.com

REFERENCES1. White RH. The epidemiology of venous thromboembolism. Circulation.

2003;107(23 Suppl):I4-I8.

2. Kahn SR, Partsch H, Vedantham S, et al. Definition of post-thrombotic

syndrome of the leg for use in clinical investigations: a recommendation

for standardization. J Thromb Haemost. 2009;7:879.

3. Schulman S, Lindmarker P, Holmstrom M, et al. Post-thrombotic

syndrome, recurrence, and death 10 years after the first episode of venous

thromboembolism treated with warfarin for 6 weeks or 6 months. J

Thromb Haemost. 2006;4:734-742.

4. Prandoni P, Lensing AWA, Cogo A, et al. The long-term clinical course of

acute deep venous thrombosis. Ann Intern Med. 1996;125:1-7.

5. Grosse SD, Nelson RE, Nyarko KA, et al. The economic burden of

incident venous thromboembolism in the United States: a review of

estimated attributable healthcare costs.Thromb Res. 2016;137:3-10. Epub

2015 Nov 24.

6. May R, Thurner J. The cause of the predominately sinistral occurrence of

thrombosis of the pelvic veins. Angiology. 1957;8:419-427.

7. Porter JM, Moneta GL; International consensus committee on chronic

venous disease. Reporting standards in venous disease: an update. J Vasc

Surg. 1995;21:635-645.

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HMP Com

munica

tions

For Pers

onal

Use O

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CASE REPORT

Vascular Disease Management® March 2017 E84

8. Cockett FB, Thomas ML. The iliac compression syndrome. Br J Surg.

1965;52:816-821.

9. Taheri SA, Williams J, Powell S, et al. Iliocaval compression syndrome. Am

J Surg. 1987;154:169-172.

10. Heniford BT, Senler SO, Olsofka JM, Carrillo EH, Bergamini TM. May-

Thurner syndrome: management by endovascular surgical techniques.

Ann Vasc Surg. 1998;12:482-486.

11. Hull RD, Marder VJ, Mah AF, Biel RK, Brant RF. Quantitative assessment

of thrombus burden predicts the outcome of treatment for venous

thrombosis: a systematic review. Am J Med. 2005;118:456-464.

12. Goldhaber SZ, Meyerovitz MF, Green D, et al. Randomised controlled

trial of tissue plasminogen activator in proximal deep venous thrombosis.

Am J Med. 1990;88:235-240.

13. Plate G, Eklof B, Norgren L, et al. Venous thrombectomy for iliofemoral

vein thrombosis – 10 year results of a prospective randomised study. Eur J

Vasc Endovasc Surg. 1997;14:367-374.

14. Smeds MR, Jacobs DL. Treatment of chronic venous stent occlusion with

a Wildcat catheter. Vasc Endovascular Surg. 2011;45:453-456.

15. Raju S, McAllister S, Neglen P. Recanalization of totally occluded iliac

and adjacent venous segments. J Vasc Surg. 2002;36:903-911.

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