A 36-year-old previously healthy man presents with a swollen and painful right calf 1 week after returning from a trip to Europe. On examination, the affected calf is tender, slightly warm, and swollen. A venous duplex ultrasound documents acute occlusive deep venous thrombosis (DVT) involving the posterior tibial, popliteal, and femoral veins. The common femoral vein is patent. The patient has no history of bleeding problems. In order to reduce the lifelong risk of the post-thrombotic syndrome (PTS), percutaneous endovenous intervention is undertaken.

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  The pathophysiology of sequelae of DVT excluding those related to embolization is due to venous obstruction and reflux.

  
  
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  Persistence of thrombus has been shown to be associated with valvular damage and resultant reflux.¹

  
  
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  Thrombus acts as a nidus for further propagation.²

  
  
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  Anticoagulation alone does not dissolve the formed thrombus but merely reduces new thrombus formation and the risk of embolization.

  
  
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  The body’s fibrinolytic system has to dissolve the formed thrombus, a process that may take weeks to months, hence the ineffectiveness of anticoagulation alone to prevent permanent valvular damage.

  
  
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  In a recent randomized trial of acute iliofemoral DVT patients who were treated with regional thrombolysis within 3 weeks of symptom onset, reflux continued to develop in 60% of patients at 6 months.³

  
  
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  There is a limited time window to intervene to prevent venous reflux beyond which permanent valvular would occur.

  
  
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  The combination of venous obstruction and reflux work in synergy to initiate a cascade of acute and chronic inflammatory changes at the microcellular level.

  
  
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  Ambulatory venous hypertension leads to edema, inflammatory cellular mobilization and activation, hemosiderin deposition, hypoxic injury, fibrosis, lipodermatosclerosis, loss of muscle pump function, venous claudication, and ultimately ulceration.^4,5

  
  
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  Rarely phlegmasia cerulea dolens may occur with a high mortality and morbidity.⁶

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  The majority of the interventional literature has focused on treatment of iliac DVT with caudal extension to the common femoral vein.

  
  
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  There is a paucity of data on percutaneous endovenous intervention (PEVI) in the femoropopliteal vein alone.

  
  
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  Approximately half of the patients who present with “first-time” acute femoropopliteal DVT exhibit venographic evidence of previous and often recurrent DVT without even knowing about it.⁷

  
  
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  The “20% rule” applies to patients with femoropopliteal DVT: 20% have a known history of previous DVT, 20% have concomitant symptomatic PE on admission, 20% have asymptomatic DVT on the contralateral side (if unprovoked), and 20% have DVT in the iliac veins.⁷

  
  
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  The currently available thromboreductive modalities are applicable in both femoropopliteal and iliofemoral DVT.

  
  
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  The efficacy and success of treatment depends on several factors: (1) extent of thrombus, (2) chronicity of thrombus, (3) presence of venous stenosis or sclerosis, and (4) preservation of venous anatomy.

  
  
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  There is a spectrum in the venographic appearance of DVT with important clinical implications. On one side of the spectrum is the first-time DVT with preserved venous anatomy, which is quite responsive to regional thrombolysis and thrombectomy (Figure 54-1). On the other side of the spectrum is distorted venous anatomy with venosclerosis and stenosis and minimal thrombus burden, which is highly resistant to thrombolysis. Here a “venous conduit” needs to be reconstructed, often times with the use of stents. Balloon venoplasty alone is less effective due to the high elastic recoil and perivenous fibrosis. Frequently, in-between forms exist, that is, acute on chronic DVT (Figure 54-2).

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  A number of devices are currently available that may be used in the femoropopliteal vein. They use a combination of thrombolysis and aspiration. Use of ultrasound has been claimed to accelerate the process of clot dissemination.

  
  
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  The available devices include (1) Angiojet (Possis Medical, Minneapolis, MN), (2) Trellis (Covidien, Mansfield, Mass), (3) Ekos Endowave (Ekos, Bothell, WA), (4) Helix Clot Buster (ev3, Plymouth, MN), (5) Hydrolyser (Cordis, Warren, NJ), (6) Eliminator (IDev Technologies, Houston, TX), and (7) Arrow Trerotola (Teleflex, Limerick, PA). The first two have been used more frequently (Figure 54-3).

  
  
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  In general, acute DVT responds favorably to any of the above modalities, whereas chronic DVT and venosclerosis are highly resistant. The color of the aspirate in the suction tubing of the Angiojet device is a predictor of success. Effective clot lysis is expected when the aspirate color is dark as compared to bright red (Figure 54-4).