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Endovenous intervention for thoracic central venous obstruction

Endovenous intervention for thoracic central venous obstruction
Literature review current through: Jan 2024.
This topic last updated: May 25, 2022.

INTRODUCTION — Thoracic central venous obstruction (TCVO) is a common venous outflow condition defined as more than 50 percent stenosis or thrombosis of a thoracic central vein. TCVO can be asymptomatic or present with variable degrees of edema and pain involving the upper extremity, chest, head or neck, respiratory symptoms, or neurologic manifestations from cerebral edema. TCVO encompasses a broad spectrum of diseases and may be related to central venous access and devices, hemodialysis arteriovenous access, anatomic abnormalities associated with venous thoracic outlet syndrome, malignancy, or prothrombotic states, among others.

Advancements in endovascular techniques have revolutionized the options for treating TCVO and are reviewed here. The clinical features, diagnosis, and approach to management of TVCO are reviewed separately. (See "Overview of thoracic central venous obstruction".)

INDICATIONS — Endovascular intervention has revolutionized treatment of TCVO and has evolved to become the standard of care and the initial approach for treating patients with moderate-to-severe symptoms associated with thrombotic TCVO, as well as for a subset of patients with nonthrombotic TCVO. Patient populations who may benefit from endovenous intervention for TCVO include:

Moderate-to-severe symptoms associated with superior vena cava obstruction (ie, superior vena cava syndrome). (See "Malignancy-related superior vena cava syndrome".)

Moderate-to-severe symptoms associated with venous thoracic outlet syndrome. (See "Overview of thoracic outlet syndromes", section on 'Venous TOS' and "Primary (spontaneous) upper extremity deep vein thrombosis".)

Venous outflow lesions associated with hemodialysis access, provided clinical/physiological abnormalities are present. (See "Central vein obstruction associated with upper extremity hemodialysis access".)

Contraindications — Asymptomatic venous lesions associated with central venous catheters generally do not merit endovascular treatment.

Patients with mildly symptomatic thrombotic venous lesions are treated with anticoagulation, while asymptomatic or mildly symptomatic nonthrombotic lesions are observed with serial imaging. (See "Overview of thoracic central venous obstruction", section on 'Management'.)

Other contraindications include concurrent systemic infection, local infection at the proposed access site, and coagulopathy.

APPROACH TO INTERVENTION — For TCVO, data to guide management and guidelines or expert consensus are lacking. Thus, intervention is guided primarily by clinical experience and in particular experience with iliocaval venous obstruction.

The general approach to endovascular intervention for TCVO depends upon the etiology and acuity of the obstruction, severity of symptoms, and the presence or absence of thrombus (ie, nonthrombotic versus thrombotic TCVO). Among these, the severity of symptoms is the primary driver for intervention. The main benefit of endovascular intervention is rapid resolution of acute symptoms with overall high initial technical success rates and low procedural complications [1,2].

A multidisciplinary treatment approach is important, particularly when treating patients with superior vena cava (SVC) obstruction (ie, SVC syndrome). (See "Malignancy-related superior vena cava syndrome", section on 'General principles'.)

When endovascular therapy is elected for TCVO, understanding the underlying anatomy is imperative, as placement of a stent or even angioplasty alone can compromise future options secondary to complications such as stent fracture, occlusion, or even intimal hyperplasia [3].

Endovascular intervention can be performed in conjunction with other therapies (eg, chemotherapy, radiation therapy), as needed.

Primary versus secondary etiology — Patients with primary etiology for TCVO may benefit to a greater degree compared with a secondary etiology (eg, catheter related, malignancy related). Secondary etiologies are associated with a greater incidence of recurrent obstruction, particularly thrombosis [4].

Central versus peripheral obstruction — The approach to endovascular intervention is affected by the location of the obstruction. Treatment of more centrally located lesions (eg, brachiocephalic, SVC) is associated with potentially serious complications; however, these present more often with severe symptoms and an urgent need for successful intervention. (See 'Acute/subacute versus chronic obstruction' below.)

For patients with SVC obstruction, we treat aggressively using balloon angioplasty alone with every effort to avoid stenting, if possible. Stenting may be required but is associated with inherent complications such as vena cava rupture or stent migration/embolization.

For patients with subclavian or brachiocephalic obstruction, we treat aggressively with initial balloon angioplasty. If the results of angioplasty are suboptimal, we proceed with stenting.

Acute/subacute versus chronic obstruction — The acuity of TCVO can be classified based on the duration of symptoms as acute (1 to 14 days), subacute (15 to 28 days), and chronic (>28 days) [5]. (See "Clinical features, diagnosis, and classification of thoracic central venous obstruction", section on 'Clinical classifications'.)

When acute symptoms of venous obstruction are severe and cause life-threatening symptoms, venous intervention needs to be performed expeditiously to relieve obstruction. (See "Malignancy-related superior vena cava syndrome", section on 'Urgency of diagnosis and treatment'.)

For less severe presentations, there is less urgency. There are few data evaluating the timing of treatment relative to the onset of symptoms related to TCVO, and management is largely extrapolated from studies of the lower extremity. For lower extremity iliocaval venous thrombosis, studies of the efficacy for thrombolytic therapy have used ≤14 days as a limit for treating acute thrombus [6-15], but symptoms, rather than the absolute duration of thrombosis, are probably more important. In most interventional practices, clinicians will intervene for thrombotic obstruction up to four weeks from the onset of acute symptoms. We agree with guidelines from the Society for Vascular Surgery that state "on balance, recommendations for consideration of early thrombus removal strategies in patients with symptoms of <14 days of duration would seem fairly secure, although a benefit in patients with a duration of symptoms of >14 days cannot be excluded" [6]. Thus, clinicians may extend thrombolytic therapy to the subacute period and pursue thrombolysis up to eight weeks from the initial presentation depending upon etiology (eg, primary upper extremity deep venous thrombosis). Treatment of longer-duration thrombus (chronic period) and chronic venous disease (eg, post-thrombotic syndrome) is associated with worse results.

PROCEDURE OVERVIEW — Endovascular procedures used to treat TCVO are typically performed in an interventional suite or hybrid operating room using monitored conscious sedation. Advanced anesthetic techniques may be appropriate in selected cases (eg, patients with airway edema). (See "Considerations for non-operating room anesthesia (NORA)".)

Patients must be informed through a well-balanced discussion of all risks, including the risk of bleeding, compared with the benefits of relieving obstruction and potential future benefits such as a decreased chance of post-thrombotic syndrome.

Intervention for TCVO is undertaken in a stepwise fashion, including:

Gaining initial access to the venous circulation. (See 'Venous access' below.)

Performing initial venography to confirm the obstruction and define the presence and extent of any thrombus. For those who underwent ultrasound, the ability to fully characterize the obstruction can be limited due to a variety of factors (eg, body habitus, vein depth, overlying bowel gas). (See "Clinical features, diagnosis, and classification of thoracic central venous obstruction", section on 'Ultrasound'.)

Administering intravenous heparin (weight-based dosing: 50 units/kg). Full-dose heparin is administered to achieve a therapeutic activated clotting time. In the absence of thrombus, administer heparin as a bolus of 3000 to 5000 units prior to angioplasty or deploying the stent. If bleeding is a concern, an initial bolus of low-dose heparin may be used until access is established, the lesion is crossed, and intraluminal positioning is confirmed. For heparin allergy, alternative parenteral anticoagulants can be used (eg, direct thrombin inhibitor). If heparin is contraindicated as with heparin-induced thrombosis, argatroban may be used [16,17].

Reducing the burden of thrombus from the venous system, with mechanical thrombectomy alone or a combined approach with pharmacologic thrombolysis and mechanical thrombectomy (ie, pharmacomechanical thrombolysis). (See 'Reducing thrombus burden' below.)

Using intravascular ultrasound (ideal if available) to confirm and characterize the degree of stenosis and for determining measurements for stent placement. (See 'Venous access' below.)

Performing angioplasty/stenting of stenotic venous lesions and completion venography to confirm unobstructed venous patency and optimal stent positioning. (See 'Treating venous stenosis' below and 'Venous access' below.)

VENOUS ACCESS — Venous access can be obtained from the upper or lower extremity or both (dual access), depending upon the veins to be treated. Dual access may be useful in treating longer chronic lesions.

Much less commonly used percutaneous access to the vena cava includes translumbar [18], transrenal [19], or transhepatic [20] access sites. These unconventional accesses are less well tolerated compared to peripheral access sites, may require general anesthesia, are technically demanding, and are usually associated with higher rate of dysfunction with or without complications [21].

Site selection and access technique — The selected access site depends upon the location of the lesion to be treated, with an upper extremity site (eg, cephalic, basilic vein, distal brachial vein, internal jugular vein, or axillary vein) used to treat many brachiocephalic or subclavian lesions (image 1) and a femoral site often selected when treating superior vena cava lesions or if attempts accessing upper extremity veins have failed. A single venous access site is usually adequate, but dual access can provide more options for imaging and improved support for device delivery. In the author's experience, dual access may be needed in up to 25 percent of cases and is useful for treating long chronic lesions.

The access site is sterilely prepared and draped. A micropuncture needle is used to access the selected vein using ultrasound guidance. The micropuncture sheath is upsized to a 7 French sheath, and the patient is systemically anticoagulated (typically intravenous unfractionated heparin).

Crossing the lesion — Once venous access is achieved, venography is performed to confirm the diagnosis of TCVO. A 4 or 5 French hydrophilic guidewire and catheter (eg, Glidewire, Glide catheter) are used to navigate to the occluded segment (image 2). Subsequently, a 0.018 or 0.035 guiding or support catheter (eg, Navicross) can be used to cross the lesion.

If the venous lesion cannot be easily crossed, more aggressive techniques can be used; however, these risk vessel rupture. Methods include using a hydrophilic wire to initiate a subintimal track or using total occlusion guidewires or crossing devices that use various forms of energy.

Following catheter placement across a lesion, venography is performed to confirm intraluminal positioning of the catheter prior to any further intervention.

REDUCING THROMBUS BURDEN — Reducing thrombus burden using catheter-directed techniques quickly alleviates symptoms, is necessary to uncover venous stenosis, and helps to achieve proper stent sizing. With thrombotic TCVO, there is often an urgency to thrombus removal (eg, superior vena cava [SVC] syndrome), favoring mechanical methods to reduce thrombus burden quickly. Mechanical methods are often combined with pharmacologic lytic agents in those without contraindications to their use (table 1). (See 'Aspiration mechanical thrombectomy' below.)

Catheter-directed thrombolysis is beneficial for patients with thrombotic SVC syndrome, primary upper extremity thoracic/upper extremity deep venous thrombosis (ie, venous thoracic outlet syndrome [vTOS]), and for treatment of outflow lesions in patients with hemodialysis arteriovenous access, as well as for treatment of occluded venous stents. Thrombolytic therapy can uncover the area of severe stenosis and may decrease the number of stents needed.

Catheter-directed thrombolysis has been instrumental in improving outcomes in patients with vTOS, particularly among patients with thrombotic obstruction. However, it is important to note that after completion of thrombolysis for vTOS, no further endovenous interventions should be performed [16,22-25]. Decompression of the thoracic outlet (eg, surgical rib resection) is undertaken first. Depending upon the nature of any adjunctive open vascular procedures (eg, venous angioplasty), venous angioplasty and stenting may be needed (intraoperatively, postoperatively) to manage a residual venous stenosis. (See "Primary (spontaneous) upper extremity deep vein thrombosis".)

Agents and devices — For venous interventions, a limited number of agents and a variety of devices have been used to manage venous obstruction.

Agents – Recombinant tissue plasminogen activator (alteplase, reteplase, tenecteplase) is the most common agent used for thrombolysis in the United States. An alternative agent is urokinase.

Devices – A variety of devices can be used to deliver thrombolytic agents. Thrombolysis catheters (eg, Unifuse, EKOS, Trellis, ClotTriever catheters) have a series of side holes along the treating end that are available in several lengths. The catheter can be used alone or in conjunction with a delivery system to provide additional energy and that may or may not include suction (eg, ClotTriever, Indigo, AngioJet, EKOS, Trellis systems) [26].

Techniques

Pharmacologic thrombolysis — To perform pharmacologic thrombolysis, an infusion catheter with side holes that will span the length of the occlusion (12 to 30 cm) is placed over the wire within the thrombus and the infusion initiated (eg, alteplase 0.01 mg/kg/hr). We generally start alteplase at 1 mg/hour and maintain for 12 to 48 hours depending upon the thrombus burden. Venography is repeated to evaluate for residual thrombus and to identify any underlying venous lesions.

Prior to catheter-directed thrombolysis, we obtain baseline fibrinogen and activated partial thromboplastic time (aPTT). During the infusion, the patient is closely monitored for bleeding complications. Fibrinogen and aPTT values are monitored every six to eight hours to titrate the infusion to minimize bleeding. For fibrinogen <150 mg/dL or a drop in fibrinogen greater than one-half of the previous level, we generally reduce the rate of infusion by one-half, and if the fibrinogen falls below 100 mg/dL, we hold the infusion for one hour and then recheck fibrinogen levels. If fibrinogen levels are low and there is concern for bleeding, fresh frozen plasma or cryoprecipitate can be transfused, but this is rarely needed. This approach is predominantly based on clinical experience managing these patients.

There are a few scenarios in which pharmacologic thrombolysis might be needed following angioplasty and stenting, such as for persistent symptomatic thoracic/upper extremity thrombus, or for thrombus that remains and will not be covered by a stent, or for thrombus that is protruding through stent struts [22,27,28]. However, in general, even in these situations, once the thoracic central veins are recanalized, the thrombolytic agent can be discontinued, and full systemic anticoagulation can be initiated.

Pharmacomechanical thrombolysis — Some interventionists prefer pharmacomechanical thrombolysis (eg, AngioJet, EKOS, Trellis system), rather than pharmacologic thrombolysis alone. Using these systems, thrombus is fragmented, increasing the surface on which the pharmacologic agents can act, thereby reducing clot burden more quickly and minimizing the total time of thrombolysis and the amount of thrombolytic agent required [29].

Aspiration mechanical thrombectomy — Aspiration mechanical thrombectomy has emerged as an option for patients in whom there is concern for using thrombolysis (eg, malignancy, hemodialysis, other increased risk for bleeding (table 1)) [30], or if the anticoagulation alone is not sufficient to resolve the thrombosis [6,31]. In these patients, aspiration of acute thrombus without the need for administration of thrombolytic medication can reduce the length of vein that requires treatment and reduces pulmonary embolism [32]. A variety of devices are available in a range of catheter sizes and lengths. For thrombus aspiration in venous structures, commonly used devices approved for use in the venous vasculature without using thrombolytic medication include (but are not limited to) the following:

ClotTriever – ClotTriever catheter has a coring element that separates thrombus from the vessel wall and a collection bag. Once micropuncture access is obtained using ultrasound guidance, a 0.035-inch 260-cm hydrophilic wire (eg, Glidewire) is advanced through the thrombus into the inferior vena cava. A 13 French specialty sheath (part of the ClotTriever system) is advanced over the wire followed by the ClotTriever catheter with its integrated funnel. Once the catheter is beyond the thrombus, the catheter is deployed. A few passes may be required to suction all the clot burden [33].

Indigo – The Indigo continuous aspiration mechanical thrombectomy system is comprised of a catheter, a separator, and a vacuum pump [34]. Among the available catheter sizes, the 8 French catheter is commonly used for venous indications and can aspirate up to 160 mL/s. The catheter has an angulated tip for rotational use to clear large thrombus burdens. The separator allows thrombus fragmentation and mobilization as well as cleaning of the catheter when it gets clogged by thrombus. The catheter is attached to a vacuum pump that provides continuous negative suction -29 mmHg.

AngioVac – The AngioVac system uses a large (26 French) sheath and requires venovenous bypass and an activated clotting time of >300 seconds [35,36].

TREATING VENOUS STENOSIS — Venography with adjunctive intravascular ultrasound, if available, is used to aid in positioning devices, measure the vein to ensure proper stent sizing, and evaluate the results of intervention. Venous angioplasty is indicated for venous stenosis >50 percent the luminal diameter, provided there are associated hemodynamic (pressure drop, associated collateral veins) or clinical abnormalities (moderate to severe symptoms consistent with lesion location).

Angioplasty alone is preferred for most lesions; however, central venous lesions often exhibit elastic recoil requiring supplemental stenting to maintain patency. Some have argued for the placement of stents or stent-grafts as primary rather than rescue therapy. (See 'Stenting as primary therapy' below.)

About 11 percent of patients with cardiac leads may develop TCVO [37]. For patients with pacemaker wire-related TCVO, angioplasty alone is usually sufficient to manage the venous stenosis; however, restenosis is likely to occur, and close follow-up for those patients is warranted. When stenting is needed, the pacemaker leads need to be temporarily removed to prevent them from becoming entrapped within the stent [38].

Venous angioplasty technique — Depending upon the diameter of the target venous segment, after crossing the lesion(s) and confirming intraluminal cannulation, a noncompliant, high-pressure balloon with a diameter usually between 10 to 14 millimeters is positioned and deployed. Our preference is to inflate to the balloon's rated pressure for three to five minutes (image 3). Such prolonged inflation may counteract the significant recoil and nonelastic nature of venous lesions. Following angioplasty, completion venography is performed (image 4). Technical success is defined as regaining an adequate lumen with residual stenosis less than 30 percent. The degree of residual stenosis generally determines whether the use of a stent is warranted. (See 'Stenting for failed angioplasty' below.)

Efficacy of primary angioplasty — Technical success rates for primary angioplasty range between 70 and 90 percent. With angioplasty alone, repeated interventions with close surveillance are generally needed to maintain patency over the long term.

Studies evaluating angioplasty for the treatment of TCVO generally consist of small observational studies [39-41]. The effectiveness of primary angioplasty depends upon the etiology and location of the venous lesion. Overall primary and cumulative patency rates for angioplasty vary widely, with 12-month primary patency rates ranging from 12 to 50 percent and cumulative patency rates ranging from 13 to 100 percent.

Occlusion following treatment of TCVO is often related to treatment of lesion classified as elastic but can also be related to intimal hyperplasia. In one series, 100 percent of lesions classified as elastic occluded in an average of 2.9 months [42]. When these lesions are identified following angioplasty, the authors proposed primary stenting [42].

There is growing evidence that using drug-eluting balloons, which are commonly used to treat arterial lesions [43], may be beneficial to decrease intimal hyperplasia/restenosis in patients with TCVO [44-46].

Venous stenting — Venous stenting may be used as rescue therapy for failed angioplasty or as primary therapy. The indications for these and efficacy of stenting is reviewed below. (See 'Stenting for failed angioplasty' below and 'Stenting as primary therapy' below.)

Stent types and selection — Both balloon-expandable (stainless steel, cobalt chromium) and self-expanding (stainless steel, nitinol) stents, as well as self-expanding covered stents (polytetrafluoroethylene [PTFE]-coated nitinol) and stent-grafts, have been used for treating TCVO. Most of these stents have been adapted from their use in the arterial circulation. Dedicated venous stents (eg, Venovo, Vici, Zilver Vena) have been approved for use in the US, demonstrating efficacy and safety in pivotal trials (eg, iliocaval placement) [47].

Balloon-expandable bare stents (eg, Palmaz, Gianturco Z-stent, stainless steel Wallstent) allow precise placement with less migration and high radial force to resist recoil.

Self-expanding bare stents (eg, Venovo, Wallstent) are made from nitinol, a shape memory alloy, and may offer some advantages, such as ease of positioning and deployment, and greater flexibility [48]. Self-expanding stents also resist "two-point compression" and compensate for anatomic changes caused by respiration [2].

Covered stents (eg, Viabahn [self-expanding], iCast [balloon expandable]) can be used to manage rupture. However, the use of covered stents may obstruct collateral venous drainage.

Stent-grafts are covered stents (PTFE, Dacron) that are partly self-expanding and partly balloon expandable and fully covered except at points of fixation. Stent-grafts can also be used to manage rupture and may improve patency rates when used to treat TCVO [49]. A hybrid venous stent-graft with a covered central portion and uncovered ends (ie, Viatorr TIPS) is also available.

Stent selection depends upon many factors, including the diameter of the affected vein, length and severity of the venous lesion, and degree of resistance to dilation.

For the brachiocephalic and subclavian veins, the author prefers to use a self-expanding stent.

For the superior vena cava, the author prefers to use a balloon-expandable bare stainless-steel stent, specifically the Palmaz stent. Most reported series involve use of stainless-steel stents [22,48,50-58].

Although there is a general impression on the part of many interventionalists that results have progressively improved with successive generations of stents (stainless-steel to nitinol to covered stents), the available data have shown considerable overlap in patency rates, and comparisons of stainless steel with nitinol stents have failed to detect any meaningful differences [16,59-62].

Stenting techniques — Once venous access has been established and the appropriate wires and sheaths are in place, the selected stent is placed over the wire and positioned across the venous stenosis. Stent-grafts are typically placed over a wire and deployed through a dedicated sheath. For patients with thrombotic occlusion of the superior vena cava (SVC) (image 5), thrombolysis may be needed before proceeding with stenting [27,63,64]. (See 'Reducing thrombus burden' above.)

Predilation – Prior to placing a stent, it may be necessary to predilate the lumen with an undersized balloon to a diameter that is large enough to accommodate the delivery device and place the stent [27]. For larger stent diameters (eg, SVC), sequential dilation with increasing angioplasty balloon diameters facilitates subsequent stent deployment and expansion [65]. The patient (eg, pain, blood pressure changes, arrhythmia) and the response of the vein are assessed with each dilation.

Reconstruction of brachiocephalic confluence – For patients with bilateral involvement of the brachiocephalic veins, treatment of one rather than both may be associated with lower complication rates. Severe symptoms are often relieved after treating only one of the brachiocephalic veins. Bilateral stenting is generally avoided if the SVC diameter is <15 mm [66,67].

When treatment of both brachiocephalic veins is deemed necessary, the confluence of the brachiocephalic veins can be reconstructed using "kissing stents" (ie, "double barrel" technique) [68,69]. Some interventionalists deliver balloon-expandable stents inside initially deployed self-expanding stents to improve radial strength.

For patients with concurrent SVC/brachiocephalic obstruction, a separate stent may first be deployed into the SVC into which each of the brachiocephalic stents are positioned ("pants leg approach").

Another approach passes one stent through the wall of another stent ("Y approach"), which may reduce the potential for stent migration and reocclusion, but the stent structure may be weakened [70].

If complications occur during stenting (eg, vein rupture), maintaining the wire across the lesion is important to immediately deploy a balloon to the site of rupture and tamponade bleeding. A covered stent or stent-graft can then be deployed at the site of rupture.

Stenting for failed angioplasty — For most patients, we suggest no stenting unless angioplasty has immediately failed or there is recurrent stenosis/occlusion. Observational data suggest that stenting does not improve patency rates and likely promotes additional intervention.

Stenting following failed angioplasty for TCVO may be appropriate in the following situations:

Acute elastic recoil (>50 percent) following angioplasty

Recurrent stenosis within three months of angioplasty alone

While stenting can provide additional mechanical support at the site of intervention, stenting is associated with a variety of complications, including stent fracture, stent migration, stent foreshortening, and coverage of significant collateral veins. Stents can also be problematic when deployed near the confluence of veins. In addition, reintervention is often needed for in-stent stenosis.

Because of these issues, stents are generally avoided, particularly in patients with TCVO associated with hemodialysis arteriovenous access. According to Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines, angioplasty without stent placement is the preferred treatment approach for TCVO [71]. (See "Central vein obstruction associated with upper extremity hemodialysis access", section on 'Treatment'.)

The outcomes for stenting for the treatment of TCVO have also been quite variable [72].

Among the various case series, primary and cumulative patency rates, respectively, at varying time intervals are below [42,59,62,73-81]. All of these series used a stainless-steel stent.

3 months – 63 to 100 percent; 72 to 100 percent

6 months – 42 to 89 percent; 55 to 100 percent

12 months – 14 to 73 percent; 31 to 91 percent

It should be noted that in most instances, comparison with angioplasty results is not appropriate since stenting procedures should be classified as rescue procedures, assuming that the cases were done for the recommended indications.

Stenting as primary therapy — Stenting as primary therapy may be appropriate for obstruction related to venous compression (ie, no stenotic venous lesion; eg, venous compression from malignant SVC syndrome) provided the etiology is not related to venous thoracic outlet syndrome. Another use for stenting as primary therapy is following vein recanalization for which the stent is placed to reconstitute a vascular lumen [82]. Lastly, while the high rate of recurrent stenosis following angioplasty has led some investigators to suggest primary stent placement for treating elastic lesions [42], we generally prefer primary angioplasty with rescue stenting only when needed.

There is considerable overlap when comparing patency rates of primary angioplasty versus primary stent placement for treating central venous stenosis, suggesting no advantage. In addition, secondary interventions appear to be the rule even for stenting, and assisted primary patency rates are generally comparable. These results are similar regardless of whether a stent or stent-graft has been used as the primary intervention [41,83,84]. However, few studies have focused on TCVO.

One study reported higher long-term, cumulative patency rates for covered stent-grafts compared with uncovered stents, although there were no differences in clinical success rate or patient survival [55]. These findings warrant further confirmation in large series.

In a review of 30 patients with TCVO, a prior angioplasty or stent had been performed in 23 patients [83]. Primary patency rates following stent-graft placement were 97, 81, 67, and 45 percent at 3, 6, 12, and 24 months, respectively. Primary assisted patency rates were 100, 100, 80, and 75 percent at 3, 6, 12, and 24 months, respectively. The time to repeat intervention was significantly shorter for patients who had not undergone a prior angioplasty or bare stenting compared with those who had. Patients presenting with occlusion had a significantly shorter primary patency interval after stent-grafting compared with those presenting with stenosis. Twelve patients required further stent-grafting to maintain patency.

POSTPROCEDURE CARE AND FOLLOW-UP — Following the intervention, the access sheath is removed, and pressure is applied for hemostasis. Most patients can be discharged the same day or after overnight observation in the absence of significant complications.

In the immediate postprocedure period, the patient should be carefully monitored for cardiac and pulmonary symptoms. While rare, the increase in venous return that occurs after relieving central venous obstruction can precipitate pulmonary edema [85].

Following endovenous intervention for TCVO, surveillance includes close clinical follow-up usually every three months and a repeat venography if symptoms recur. The patient is advised to contact their clinician immediately if symptoms recur.

Antithrombotic therapy — Short-term antithrombotic therapy is recommended following endovenous treatment of central venous obstruction. However, data guiding antithrombotic therapy for TCVO are lacking, and practices vary. Our approach is extrapolated from experience with iliocaval venous obstruction.

There is no consensus on the optimal type and duration of antithrombotic regimen after angioplasty and stenting for venous occlusive disease. There are no data from randomized trials to guide decisions on antithrombotic therapy, and as a result, clinical practice varies widely [86-88]. Our general approach is as follows:

Patients with thrombotic TCVO should receive therapeutic anticoagulation with dosing and duration as per venous thromboembolism guidelines [6,89,90]. We continue systemic anticoagulation for six months. Anticoagulation options and dosing for patients with thoracic central/upper extremity deep venous thrombosis are reviewed separately. (See "Overview of thoracic central venous obstruction", section on 'Anticoagulation'.)

In addition:

For patients who undergo venous angioplasty but no stent has been deployed, we suggest aspirin (81 mg) daily.

For those who undergo venous stenting at low risk for bleeding, we suggest clopidogrel for a period of four to six weeks, then aspirin indefinitely.

Some have suggested a brief period of triple therapy (anticoagulation and dual antiplatelet therapy) for patients with thrombotic central venous obstruction. However, we do not support this approach and suggest not using triple antithrombotic therapy because of its inherent increased risk of major bleeding.

For patients with nonthrombotic TCVO, after a stent has been deployed, we suggest dual antiplatelet therapy with clopidogrel in addition to aspirin for four to six weeks, then aspirin indefinitely. Antiplatelet therapy should be sufficient [17,91]. Some have suggested systemic anticoagulation for a period of one to nine months to decrease subsequent thrombosis in patients treated for malignant obstruction [25,51,52,56]. However, there are no reliable studies and little consensus [48,51,92]. For patients thought to have a hypercoagulable state related to their malignancy, we may use a low molecular weight heparin (eg, enoxaparin) or a direct oral anticoagulant such as apixaban instead of clopidogrel. (See "Cancer-associated hypercoagulable state: Causes and mechanisms" and "Anticoagulation therapy for venous thromboembolism (lower extremity venous thrombosis and pulmonary embolism) in adult patients with malignancy".)

For patients with an increased risk for bleeding, antiplatelet therapy following intervention is individualized but often consists of aspirin alone.

Timing of adjunctive therapy

For patients with primary upper extremity venous thrombosis (venous thoracic outlet syndrome; ie, Paget Schrotter syndrome), surgical decompression is recommended as soon as possible following thrombolysis to reduce the incidence of recurrent thrombosis [93-95]. Ideally, decompression surgery is performed during same admission or within four to six weeks (image 6). The patient should remain on full anticoagulation until decompression surgery is completed.

For patients with malignancy, radiation or chemotherapy can be initiated or resume as needed. (See "Malignancy-related superior vena cava syndrome", section on 'Radiation therapy' and "Malignancy-related superior vena cava syndrome", section on 'Chemotherapy sensitive malignancy (small cell lung cancer, lymphoma, germ cell tumor)'.)

COMPLICATIONS — The overall complication rate following endovenous intervention for TCVO is overall low [2,65,66,96]. Minor procedural complications (eg, hematoma, access site infection) occur in less than 5 percent of cases. Major procedural complications such as vessel rupture, cardiac tamponade, and pulmonary embolism are relatively uncommon but can be fatal if the diagnosis is delayed [51,97,98].

Late stent-related complications include reocclusion, in-stent restenosis, and stent migration.

Reocclusion Reocclusion can also be caused by intimal hyperplasia (in-stent stenosis) or rethrombosis. For patients with malignancy-related occlusion, recurrent occlusion is often related to tumor growth (ingrowth to stent, stent compression). However, the stent usually remains patent until the patient's death, since patients with malignancy-related TCVO often have a short life expectancy [50]. (See "Malignancy-related superior vena cava syndrome".)

If reocclusion occurs, it can generally be treated with reintervention with good secondary patency rates [17,50,99].

Stent migration Stent migration can occur because of stent foreshortening or stent undersizing. The displaced stent can usually be retrieved using endovascular techniques (eg, snare).

Complications occur in up to 7 percent of patients treated for superior vena cava (SVC) syndrome [92]. There is some evidence that use of stents over 16 mm in diameter may be associated with higher increased risk of SVC rupture, dysrhythmias, pericardial tamponade, or cardiac arrest [48]. Patients who have undergone radiation therapy for treatment of malignancy prior to endovenous intervention may have an increased risk of SVC rupture.

PATENCY RATES — Overall, patency rates of endovascular intervention for TCVO are better, in general, for patients with primary compared with secondary (eg, catheter-related, malignancy-related) TCVO.

Venous thoracic outlet syndrome – For venous thoracic outlet syndrome, multiple experts have reported recanalization rates up to 80 percent with early catheter-directed thrombolysis (ie, ≤14 days from onset of symptoms) [100,101]. Delayed presentation is associated with chronic fibrotic obstruction of subclavian/axillary veins, with patency rates dropping significantly after two weeks (29 percent in one study [94]). Delayed presentations are associated with poor outcomes even when surgical decompression and interposition/vein patch angioplasty are performed [102]. (See "Primary (spontaneous) upper extremity deep vein thrombosis".)

Catheter-associated disease – For patients with hemodialysis-associated disease, primary patency rates range from 23 to 55 percent at 6 months and 12 to 50 percent at 12 months [39,40,84]. One study comparing angioplasty with angioplasty/stenting reported similar results for both groups at 30 days and one year [41]. Assisted primary patency rates at one year were 73 percent for angioplasty and 46 percent for stenting. Other studies have reported improved results with bare metal stenting, with primary patency rates ranging from 42 to 89 percent at 6 months and 14 to 73 percent at 12 months compared with angioplasty [41,73]. (See "Catheter-related upper extremity venous thrombosis in adults".)

Malignancy-associated disease – Retrospective, observational data suggest technical success rates of 80 to 98 percent, with relief of symptoms in >90 percent of patients [99]. Superior vena cava stenting appears durable, with restenosis rates of about 12 percent (range: 4.3 to 29.5 percent) and recurrence rates of 11 percent (range: 1.2 to 20.5 percent). (See "Malignancy-related superior vena cava syndrome".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Superficial vein thrombosis, deep vein thrombosis, and pulmonary embolism" and "Society guideline links: Venous access" and "Society guideline links: Chronic venous disorders" and "Society guideline links: Dialysis".)

SUMMARY AND RECOMMENDATIONS

Thoracic central venous obstruction – Thoracic central venous obstruction (TCVO) is defined as more than 50 percent stenosis or thrombosis of a thoracic central vein including any, or all of, the subclavian or brachiocephalic veins, and superior vena cava (SVC). (See 'Introduction' above.)

Indications – The severity of symptoms is the primary driver for endovenous intervention for TCVO, with the main benefit being rapid resolution of acute symptoms and a low rate of procedural complications. Patient populations who may benefit from endovenous intervention for TCVO include (see 'Indications' above):

Moderate-to-severe symptoms associated with SVC obstruction (ie, SVC syndrome)

Moderate-to-severe symptoms associated with venous thoracic outlet syndrome

Symptomatic, hemodynamically significant venous outflow lesions associated with hemodialysis access

Approach to intervention – The approach to endovenous intervention for TCVO depends upon acuity and etiology, severity of symptoms, and the presence or absence of thrombus (ie, nonthrombotic versus thrombotic TCVO). Patients with primary etiology for TCVO may benefit to a greater degree compared with a secondary etiology (eg, catheter related, malignancy related). A multidisciplinary treatment approach is important, particularly when treating patients with malignancy-associated TCVO. (See 'Approach to intervention' above.)

Procedure overview – Intervention for TCVO is undertaken in a stepwise fashion, including gaining access to the venous circulation, performing initial venography, administering intravenous heparin, reducing thrombus burden, performing angioplasty/stenting of any stenotic venous lesions, and completion venography to confirm unobstructed venous patency and optimal stent positioning. (See 'Procedure overview' above.)

Thrombolysis – For most patients with thrombotic TCVO and appropriate indications for treatment, we suggest initial pharmacomechanical thrombolysis rather than catheter-directed thrombolysis alone or percutaneous mechanical thrombectomy alone (Grade 2C). The addition of mechanical methods to pharmacologic thrombolysis quickly reduces thrombus burden and reduces the dose of the thrombolytic agent needed. For patients in whom pharmacologic thrombolysis is not desirable because of an increased bleeding risk, aspiration mechanical thrombectomy alone may be sufficient for clearing thrombus burden. (See 'Reducing thrombus burden' above.)

Angioplasty and stenting – For most patients, we suggest no stenting unless angioplasty has immediately failed due to acute elastic recoil (>50 percent) or there is recurrent stenosis/occlusion within a three-month period of angioplasty. Patency rates for primary angioplasty and primary stent placement using a variety of stent types (material, configuration) are overall similar. While stenting provides additional mechanical support, it is associated with potential complications (eg, vein rupture, stent migration/embolization) and potential covering of significant collateral veins. Reintervention is often needed for in-stent stenosis. (See 'Treating venous stenosis' above.)

For patients with subclavian or brachiocephalic obstruction, we treat aggressively with initial balloon angioplasty. If the results of angioplasty are suboptimal, we proceed with stenting using a self-expanding dedicated venous stent.

For patients with SVC obstruction, we treat aggressively using balloon angioplasty alone with every effort to avoid stenting, if possible. Stenting may be required but is associated with potential serious complications (eg, SVC rupture, stent migration/embolization). When stenting is needed, we use a balloon-expandable bare stainless-steel stent.

Antithrombotic therapy — Our approach to antithrombotic therapy following endovenous intervention for TCVO is as follows. (See 'Antithrombotic therapy' above.)

Patients with acute thrombotic TCVO should receive therapeutic anticoagulation with dosing and duration as per venous thromboembolism guidelines. (See "Overview of thoracic central venous obstruction", section on 'Anticoagulation'.)

In addition:

-For patients who undergo venous angioplasty, but no stent has been deployed, we suggest aspirin (81 mg) daily, rather than no antiplatelet therapy (Grade 2C).

-For patients at low risk for bleeding, after stenting we suggest monotherapy using clopidogrel alone for a period of four to six weeks, rather than no therapy or dual antiplatelet therapy (Grade 2C). Thereafter, we suggest aspirin indefinitely, rather than no antiplatelet therapy (Grade 2C).

For patients with nonthrombotic TCVO at low risk for bleeding, after stenting we suggest dual antiplatelet therapy using clopidogrel and aspirin for four to six weeks, rather than monotherapy or no therapy (Grade 2C). Thereafter, we suggest aspirin indefinitely, rather than no antiplatelet therapy (Grade 2C).

For patients treated for malignant venous obstruction, some have suggested prolonged systemic anticoagulation (eg, low molecular weight heparin, direct oral anticoagulant) to decrease subsequent thrombosis. However, there are no reliable studies and little consensus.

For patients with an increased risk for bleeding, antiplatelet therapy after thoracic central venous stenting is individualized but often consists of aspirin alone. For all patients, we avoid triple antithrombotic therapy (ie, anticoagulation and dual antiplatelet therapy) because of its inherent increased risk of major bleeding.

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Topic 120732 Version 6.0

References

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