Venous Intervention

Venous intervention

There has been a steady advancement in the treatment of venous diseases from the early 1920s from basic attempts on venous thrombectomy to the evolution of intravenous and catheter directed thrombolysis (CDT) for venous thrombosis and then to the placement of endovascular stents. In this review, attempts have been made to discuss the advanced interventional therapy for the management of venous diseases in the present era.

Options to reduce thrombus burden

Options available to reduce the thrombus burden include mechanical thrombectomy (MT), CDT, or combination of pharmacological and mechanical thrombectomy (PMT).

CDT selectively administers the thrombolytic agent into the thrombus and is usually the first line of the treatment.^[1-3]

Catheter-directed pharmacologic thrombolysis

It is an important advancement for iliocaval venous occlusion and proximal DVT. Main benefit is direct delivery of the drug through a catheter into the thrombus at that site. This therapy is successful most likely during an acute event (<14 days old) and is less effective in chronic condition (>4 weeks old).^[4] The thrombolytic agents used are streptokinase, reteplase, tenecteplase, alteplase, and urokinase. However, none has specific FDA approval for their use in DVT. However, small studies show that CDT may reduce post-thrombotic syndrome (PTS). National Venous Thrombolysis Registry shows a strong point of a relationship between the degree of thrombolysis and patency of the vessel. In this multicenter study, the use of CDT with agent urokinase in 303 limbs of 287 patients was evaluated. In this study, iliofemoral DVT was most common and 25% of the patients had isolated femoropopliteal DVT. On venography, complete lysis of the clot defined as grade III lysis was seen in only 31% of cases and partial lysis of the clot, that is, >50% of resolution of clot (Grade II lysis) was seen in 52% of the cases. Moreover, venous patency also showed improved valvular function. In this study, 72% of patients who had optimal lysis of the clot maintained normal function of the valve but in 62% of patients who had incomplete lysis of the clot had valvular incompetence. Major bleeding was seen in 11% of patients and was seen at venous access sites.^[5]

In patients presenting with symptoms of massive swelling of limbs associated with severe pain, intervention helps reduce mortality and prevention to venous gangrene. In the CAVNET study, in CDT group, the incidence of PTS was reduced to 14.4%, and venous patency rate at 6 months was 65.9% versus 47.4% in control group (P = 0.012).^[6] However, in large studies, it was not seen. In the ATTRACT study which was a randomized and multicenter trial, at 2 years, there was no reduction of overall PTS (48.0% vs. 47.4%), but there was a significant overall difference of 6% decline in moderate to severe degree of PTS (P = 0.04).^[7]

Thrombolysis is started with an initial bolus dose of 2–4 mg tPA. For pulse spray CDT with rtPA, weight-based dosing is started at the rate of 0.01 mg/kg/h with maximum of 1.0 mg/h.^[8] Low-dose heparin is administered concurrently (500 units/h) to prevent thrombosis of the access sheath.

Dose of urokinase is started as infusion of 1−2.5 lac IU of urokinase over 15 min and followed by 5–10 lac IU in 24 h, for 48–72 h.

[Table 1] shows the summary of trials of CDT.

After CDT, the thrombus will become soft and can be easily aspirated through a larger catheter with mechanical suction, using a syringe. In recent years, the AngioJet Rheolytic catheter System (MEDRAD Interventional, Minneapolis, MN) and an ultrasound-emitting thrombolytic infusion catheter (EKOS Corporation, Bothell, WA) are available [Figure 1]. However, due to its high-cost, they both are reserved only for those patients who do not respond well with PMT.

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Figure 1:

AngioJet catheter system.

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Percutaneous transluminal angioplasty and stenting

After successful PMT, the patency of proximal venous pathway should be demonstrated by angiography. If significant residual stenosis is present, serial dilatation is done with increasing balloon size, after crossing the lesion with wire, up to the size appropriate to the size of the vein. After this, self-expanding stent of sufficient size and length may be deployed, most commonly, the wall stent. Post-dilatation may be required to overcome the stent under expansion due to venous fibrosis, common in chronic venous occlusion. In follow-up, technical success of procedure is demonstrated by DSA which should have residual stenosis of <30%.^[9,10]

Inferior vena cava (IVC) occlusion

Thrombotic occlusion of IVC mostly occurs due to propagation of iliofemoral vein thrombosis or IVC filter thrombosis [Figure 2]. Most of the patients present with unilateral or bilateral lower limb swelling. However, some patients have good collateral pathways and so may not manifest classical symptoms of IVC obstruction. Standard treatment for IVC thrombosis involves surgical thromboembolectomy.^[11,12] Initial endovascular treatment consists of CDT [Figure 3], for acute occlusion followed by PMT [Figures 4 and 5]. Usually, large sheaths are required, through femoral vein approach. Underlying stenosis requires angioplasty with or without stent placement. Self-expanding stents are used which can be oversized to prevent stent migration. If IVC obstruction is chronic [Figure 6], the role of CDT is limited. The occlusion is difficult to cross. Mostly, terumo wire is used to cross and the serial dilatations are given with increasing sized balloons. These lesions are very fibrotic and require high pressures to dilate [Figure 7], which may cause significant pain to the patient.^[13] Sizes most often used are up to 14 mm for iliacs and may be up to 24 mm for IVC [Figures 8 and 9].

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Figure 2:

Acute occlusion of inferior vena cava, with thrombus.

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Figure 3:

Partial recanalization of inferior vena cava after catheter directed thrombolysis.

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Figure 4:

Thrombus extracted manually.

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Figure 5:

Complete recanalization of inferior vena cava after catheter directed thrombolysis and mechanical thrombus extraction.

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Figure 6:

Chronic occlusion of inferior vena cava.

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Figure 7:

Fibrotic lesion of inferior vena cava, difficult to dilate with 7 mm balloon.

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Figure 8:

Dilatation of inferior vena cava with 18 mm balloon.

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Figure 9:

Recanalization of inferior vena cava after balloon dilatation.

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Endovascular management of May–Thurner syndrome (MTS)

MTS is defined as compression of the left iliac vein by the right common iliac artery against lumber spine, resulting in thrombosis of iliac vein or iliofemoral vein. Risk factors include female gender, especially, postpartum period, multiparous women, or who are using oral contraceptives. Scoliosis can also predispose to MTS. Other risk factors include dehydration, hypercoagulable states, and radiation exposure. Among patients who present with a symptomatic lower extremity venous disorder, MTS is estimated to be the etiology in 2–5% of patients, although some retrospective reviews have reported much higher rates.^[14] Majority of individuals who are having a MTS anatomy are usually asymptomatic, but can have progression to venous thrombosis due to venous hypertension. Patients who are symptomatic due to MTS anatomy can have swelling with severe debilitating acute extremity pain, venous claudication, or chronic symptoms of venous insufficiency. A significant number of patients (up to 85%) with MTS experience venous claudication.^[15,16] This phenomenon is due to venous outflow obstruction.

Non-invasive venous imaging

In the absence of thrombosis, in MTS, non-invasive vascular imaging can be done to identify the lesion. Options include duplex ultrasound, CT venography, and MR venography.

Although venous ultrasound has high sensitivity and specificity for the detection of proximal DVT using B-mode using compressibility criterion, the deep location of the proximal iliac vein along with other factors (e.g., obesity) may limit ultrasound for making an accurate diagnosis of MTS. B-mode will help to compare the reduction in the diameter of the vein at the smallest area to that of normal diameter of the vein. Peak vein velocity is the measurement of post-stenotic segment to that of the pre-stenotic segment and gradient >2.0 is considered significant.^[17]

Both CT and MR venograms have more than 95% specificity and sensitivity for diagnosing MTS, but these imaging modalities require adequate technical protocols for imaging acquisition.^[18,19]

The treatment of this syndrome (MTS) depends on whether DVT is present or not. The treatment is usually conservative in patients with non-thrombotic MTS with no or mild symptoms, whereas in patients with non-thrombotic MTS with moderate to severe symptoms (leg swelling, skin discoloration and pain), the treatment is usually angioplasty and stenting. In thrombotic MTS, initial treatment consists of anticoagulants, CDT or PMT. Then, USG is done to assess venous stenosis; and if found, angioplasty and stenting of iliocaval segment are done. Extending the stent into the IVC has no negative impact.^[20]

Axillosubclavian vein thrombosis (ASCT)

Upper limb DVT is rare and accounts for 2–4% of all DVT.^[21] It is mostly secondary to indwelling catheters or pacemaker leads. Most patients can be managed anticoagulants of short duration and may or may not require catheter removal. In presence of severe symptoms, CDT may be required.

Primary ASVT (Paget-Schroetter Syndrome) is less common than secondary ASVT. It affects people of younger age group which is healthy otherwise. Repetitive activity of the upper extremity predisposes susceptible individuals to ASCT in the presence of an underlying abnormality of the thoracic outlet. The subclavian vein is usually compressed between the first rib and a hypertrophied scalene muscle and subclavius tendon. Medical therapy usually fails in this subgroup of patients. An effective treatment is resection of this first rib. Initial therapy is Catheter-based treatment, which begins with basilic vein access, followed by CDT. Then, the early first rib resection is performed in the same hospital sitting.

Superior vena cava (SVC) syndrome

SVC syndrome occurs as a result of obstruction of flow through SVC. There are multiple causes of SVC syndrome [Table 2], but most common cause is intra-thoracic malignancy, responsible for 60–85% cases.^[22] Signs of SVC syndrome include swelling of face, neck, and upper limb with distension of jugular vein. Symptoms include breathlessness, chest discomfort, cough, difficulty in swallowing, hoarseness of voice, and fullness of head due to facial plethora. Severe headache, delirium, and coma suggest the presence of associated cerebral edema. Anticoagulation is given in these conditions to prevent formation of thrombus and subsequent propagation and to reduce the risk of pulmonary embolism (PE). Revascularization is done only in the presence of significant symptoms. In SVC syndrome, palliative therapy is advocated if life expectancy is <6 months. SVC stenting for malignant disease carries an excellent technical success rate of 95–100% and primary and secondary patency rates of 85% and 93%, respectively, at 3 months.^[23] Before planning endovascular intervention, bilateral upper limb venography is required to see the extent of disease. CDT is usually required followed by angioplasty with large balloons. Stents are required in most cases as the lesions are mostly fibrotic. Stents are oversized by 10–20% to prevent stent migration. If there are pacing leads, which cannot be extracted, stenting across the leads can be done and is safe.^[24]