Iliofemoral Deep Venous Thrombosis

Treating a unique DVT case with rheolytic mechanical thrombectomy and infusion thrombolysis.

By George H. Meier, MD, RVT, FACS
 

The treatment of iliofemoral thrombophlebitis has changed little since the initiation of heparin use in the 1930s. Whereas current management strategies focus on the outpatient use of low-molecular-weight heparin, treatment relies on the prevention of clot propagation rather than any effort to resolve the clot burden present. As a result, preservation of valve function is unusual, with most patients resolved to lifelong postphlebitic syndrome, often leading to chronic debilitating swelling and ulceration in the leg. If practitioners are to make a difference in the chronic debilitating outcomes associated with thrombophlebitis and valve destruction, they must obviously develop a treatment strategy that prevents venous reflux and obstruction. To this end, if the patient presents with a first-time venous thrombosis in the proximal lower-extremity veins, more aggressive treatment in an effort to preserve valve function may be warranted. Modern therapy with percutaneous mechanical thrombectomy and thrombolysis may allow preservation of valve function and avoid the sequelae of chronic venous insufficiency.1 Although this hypothesis is not yet definitively proven, several studies suggest improved outcomes associated with thrombolysis in deep venous thrombosis (DVT).2-7 Left-leg DVT is nearly twice as common as DVT in the right leg. The etiology of this is related to the anatomic compression of the left common iliac vein by the right common iliac artery, known as May-Thurner syndrome.8 Therefore, particularly in the proximal venous segments, DVT may be secondary to the anatomic compression that is readily treatable with modern endovascular techniques.9-17 For this reason, left iliofemoral DVT warrants aggressive early treatment to prevent valve destruction and possibly relieve anatomic venous compression.18 In this case report, we review the treatment of iliofemoral thrombophlebitis in a young male physician with a second episode of left lower-extremity DVT with pulmonary embolus. HISTORY A 38-year-old male physician presented with a second episode of shortness of breath associated on this occasion with significant swelling of his left leg. Three years earlier, he had suffered a pulmonary embolus with hemodynamic compromise treated by systemic thrombolytic therapy. A CT scan at that time revealed a saddle embolus in his main pulmonary artery (Figure 1). Subsequent workup revealed left calf and popliteal vein DVT without proximal extension. He was treated with low-molecular-weight heparin followed by warfarin for 6 months. Workup for hypercoagulable disorders was negative, and a family history for clotting disorders was absent. Warfarin was continued for 6 months and then discontinued, and he was placed on 325 mg of aspirin daily. The patient did well for the intervening period of 3 years, with a convalescent CT scan demonstrating complete resolution of his pulmonary emboli. No further episodes of shortness of breath occurred, and his exercise tolerance was normal. He did notice mild intermittent swelling of the left lower extremity, which resolved with elevation. On the morning of presentation, the patient noted increased shortness of breath on arising, associated with significant swelling of the left lower extremity. Recognizing the symptoms of recurrent pulmonary embolus, he was sent for an emergency CT scan that once again demonstrated pulmonary emboli (Figure 2), smaller than the previous episode. Duplex ultrasound of the left leg revealed complete occlusion of his left leg venous system, including the left iliac veins. His inferior vena cava appeared to be patent. The patient was systemically placed on heparin. After careful discussion with the patient concerning the short- and long-term risks of catheter-directed thrombolytic therapy and rheolytic mechanical thrombectomy, he asked to proceed secondary to the debilitating swelling and pain with ambulation associated with his left-leg phlegmasia. This procedure was scheduled for the next morning. On the second hospital day, the patient was taken to the angiography suite for his procedure. He was placed in a prone position under conscious sedation, and access to his thrombosed popliteal vein was achieved using ultrasound guidance (Figure 3). A 6-F sheath was placed, and a Berenstein catheter (AngioDynamics, Inc., Queensbury, NY) was passed over a Bentson wire. Venography confirmed occlusive DVT from the popliteal to the iliac veins (Figures 4 through 6). A 6-F AngioJet DVX catheter (Possis Medical) was prepared, and thrombolysis was initiated using the Power-Pulse spray technique. A total of 5 mg of tissue plasminogen activator (tPA) was mixed in 50 mL of saline and infused into the clot with the suction port of the AngioJet turned off. An 8-mm X 4-cm angioplasty balloon was inflated repeatedly during a 30-minute dwell period to mix the tPA thoroughly with the clot. No attempt was made to cross the proximal occlusion because this natural cap served to prevent proximal embolization and avoided the need for an inferior vena cava filter. After 30 minutes, the AngioJet catheter was reinserted, and suction was reactivated. Multiple passes were made in the area of thrombosis with dramatic improvement (Figures 7 and 8). Nonetheless, proximal chronic clot remained, and because we felt this was likely due to May-Thurner compression chronically, the decision to perform extended catheter-directed thrombolysis was made. A 90-cm UniFuse infusion catheter with 50 cm of side holes (AngioDynamics, Inc.) was placed from the popliteal vein to the common iliac vein, and an infusion of tenecteplase at .5 mg/h was begun. During this infusion, the heparin dose was decreased to 300 U/h and was continued overnight. The next morning, repeat venography was performed (Figures 9 through 12). An inferior vena cavogram showed a widely patent IVC and proximal common iliac vein. Surprisingly, a bifid external iliac vein was seen, which created a flow abnormality in the left leg and appeared to be the cause of the left-leg recurrent DVT. Residual chronic thrombus was seen in this bifid vein, and a decision was made to stent the segment. Two 10-mm X 40-mm Smart stents (Cordis Corporation, Warren, NJ) were placed in a kissing configuration with excellent results (Figures 13 and 14). The patient was recommended for lifelong warfarin given his anatomic variation. Follow-up duplex scan at 2 months demonstrated normal venous flow patterns, normal valve closure times in the iliofemoral segment, and widely patent iliac veins. DISCUSSION This is the first report of a bifid external iliac vein as a cause for recurrent iliofemoral DVT and pulmonary embolus. Although compression of the left iliac vein by the right common iliac artery (May-Thurner syndrome) is common even in a normal population,9,15,19 its association with DVT has been well described. Presumably, this flow abnormality increases blood stagnation and leads to a left-sided predilection for all lower-extremity DVT. In this patient, a flow abnormality was created by a bifid external iliac vein. This anatomic variant has not been previously described in association with DVT or pulmonary embolus. Nonetheless, a flow abnormality from this anatomy clearly would predispose the individual to an increased risk of ipsilateral DVT. Perhaps the bigger question is why to treat this patient with thrombolysis and rheolytic mechanical thrombectomy in the first place. Clearly, this is a young patient with a long life expectancy. Although anticoagulation alone is likely to prevent further pulmonary emboli, the left-sided veins will likely be obstructed to flow because recanalization is less common in the proximal veins.15,20 Similarly, the valves in the left-leg veins are unlikely to be functional, leading to chronic reflux and further venous hypertension in the lower leg. Postphlebitic syndrome would be expected in the majority, resulting in a chronic debilitating outcome for this patient. With thrombolysis, valve function can be preserved,13,21,22 although long-term prospective data are unavailable. The addition of percutaneous mechanical thrombectomy speeds the clot resolution, hopefully decreasing the time to restoration of normal flow and preventing irreversible valve damage. This adjunct also lowers the dose of thrombolytic necessary to restore flow and decreases the duration of treatment, both hopefully limiting overall bleeding risk. In this way, risk of thrombolysis seems small compared to the benefit of valve preservation, especially in young patients with first-time episodes of DVT. Many interventionists believe that the time is right for a new treatment paradigm in proximal DVT.1,4,10,12,23-25 This case exemplifies the results that can be achieved and supports a more aggressive approach to DVT management, particularly in first-time iliofemoral thrombosis. If we can preserve valve function, then the chronic sequelae of DVT can hopefully be avoided. With this more aggressive management, these patients should be able to lead a normal healthy life without the chronic complications of lower-extremity venous insufficiency. George H. Meier, MD, RVT, FACS, is Professor and Chief, Vascular Surgery, University of Cincinnati College of Medicine, in Cincinnati, Ohio. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Meier may be reached at (513) 558-5367; george.meier@uc.edu. 1. Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology. 1999;211:39-49. 2. Semba CP, Razavi MK, Kee ST, et al. Thrombolysis for lower extremity deep venous thrombosis. Tech Vasc Interv Radiol. 2004;7:68-78. 3. Peden E, Wei Z, Bush RL, et al. The case for thrombolysis for iliofemoral venous thrombosis. Semin Vasc Surg. 2005;18:139-147. 4. Kim HS, Patra A, Paxton BE, et al. Catheter-directed thrombolysis with percutaneous rheolytic thrombectomy versus thrombolysis alone in upper and lower extremity deep vein thrombosis. Cardiovasc Intervent Radiol. 2006;29:1003-1007. 5. Casella IB, Presti C, Aun R, et al. Late results of catheter-directed recombinant tissue plasminogen activator fibrinolytic therapy of iliofemoral deep venous thrombosis. Clinics. 2007;62:31-40. 6. Comerota AJ, Paolini D. Treatment of acute iliofemoral deep venous thrombosis: a strategy of thrombus removal. Eur J Vasc Endovasc Surg. 2007;33:351-360; discussion 361-362. 7. Enden T, Sandvik L, Klow NE, et al. Catheter-directed venous thrombolysis in acute iliofemoral vein thrombosis—the CaVenT study: rationale and design of a multicenter, randomized, controlled, clinical trial (NCT00251771). Am Heart J. 2007;154:808-814. 8. May R, Thurner J. The cause of the predominately sinistral occurrence of thrombosis of the pelvic veins. Angiology. 1957;8:419-427. 9. Wolpert LM, Rahmani O, Stein B, et al. Magnetic resonance venography in the diagnosis and management of May-Thurner syndrome. Vasc Endovasc Surg. 2002;36:51-57. 10. Shebel ND, Whalen CC. Diagnosis and management of iliac vein compression syndrome. J Vasc Nurs, 2005;23:10-17; quiz 18-19. 11. Seidensticker D, Wilcox J, Gagne P. Treatment of May-Thurner syndrome with catheter-directed thrombolysis and stent placement, complicated by heparin-induced thrombocytopenia. Cardiovasc Surg. 1998;6:607-613. 12. Patel NH, Stookey KR, Ketcham DB, et al. Endovascular management of acute extensive iliofemoral deep venous thrombosis caused by May-Thurner syndrome. J Vasc Interv Radiol. 2000;11:1297-1302. 13. Laiho M, Oinonen A, Sugano N, et al. Preservation of venous valve function after catheter-directed and systemic thrombolysis for deep venous thrombosis. Eur J Vasc Endovasc Surg. 2004;28:391-396. 14. Kim JY, Choi D, Ko YG, et al. Percutaneous treatment of deep vein thrombosis in May-Thurner syndrome. Cardiovasc Intervent Radiol. 2006;29:571-575. 15. Fraser DG, Moody AR, Morgan PS, et al. Iliac compression syndrome and recanalization of femoropopliteal and iliac venous thrombosis: a prospective study with magnetic resonance venography. J Vasc Surg. 2004;40:612-619. 16. Comerota AJ. Quality-of-life improvement using thrombolytic therapy for iliofemoral deep venous thrombosis. Rev Cardiovasc Med. 2002;3(suppl2):S61-S67. 17. Berger A, Jaffe JW, York TN. Iliac compression syndrome treated with stent placement. J Vasc Surg, 1995;21:510-514. 18. Vedantham S, Millward S, Cardella J, et al. Society of Interventional Radiology position statement: treatment of acute iliofemoral deep vein thrombosis with use of adjunctive catheter-directed intrathrombus thrombolysis. J Vasc Interv Radiol. 2006;17:613-616. 19. Kibbe MR, Ujiki M, Goodwin AL, et al. Iliac vein compression in an asymptomatic patient population. J Vasc Surg. 2004;39:937-943. 20. Singh H, Masuda EM. Comparing short-term outcomes of femoral-popliteal and iliofemoral deep venous thrombosis: early lysis and development of reflux. Ann Vasc Surg. 2005;19:74-79. 21. Shull KC, Nicolaides AN, Fernandes J, et al. Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg. 1979;114:1304-1306. 22. Elsharawy M, Elzayat E. Early results of thrombolysis vs anticoagulation in iliofemoral venous thrombosis. A randomised clinical trial. Eur J Vasc Endovasc Surg. 2002;24:209-214. 23. Verhaeghe R, Stockx L, Lacroix H, et al. Catheter-directed lysis of iliofemoral vein thrombosis with use of rt-PA. Eur Radiol. 1997;7:996-1001. 24. Vedantham S, Vesely TM, Sicard GA, et al. Pharmacomechanical thrombolysis and early stent placement for iliofemoral deep vein thrombosis. J Vasc Interv Radiol. 2004;15:565-574. 25. Semba CP, Dake MD. Iliofemoral deep venous thrombosis: aggressive therapy with catheter-directed thrombolysis. Radiology. 1994;191:487-494.
 

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Endovascular Today is a publication dedicated to bringing you comprehensive coverage of all the latest technology, techniques, and developments in the endovascular field. Our Editorial Advisory Board is composed of the top endovascular specialists, including interventional cardiologists, interventional radiologists, vascular surgeons, neurologists, and vascular medicine practitioners, and our publication is read by an audience of more than 22,000 members of the endovascular community.