Catheter-directed thrombectomy with the JETi8 in the treatment of acute superior vena cava syndrome.

Superior vena cava syndrome can lead to significant morbidity and mortality, particularly in acute settings. We report a case of an acute Port-a-Cath-associated thrombosis of the superior vena cava. Percutaneous catheter-directed thrombectomy was performed using the JETi8 thrombectomy device with additional angioplasty and stenting, allowing rapid flow restoration and rapid clinical recovery. Postoperative anticoagulation was initiated and pursued lifelong. This report is unique in illustrating how JETi8 thrombectomy seems to be a safe and effective therapy, allowing rapid flow restoration, rapid clinical improvement, and persistent patency at 6 months.

Increased use of intravenous devices has led to a higher rate of superior vena cava syndrome (SVCS). Although malignant causes remain the most frequent etiology, intravenous device-related SVCS accounts for approximately 30% of cases. SVCS can lead to significant morbidity and mortality, particularly in acute life-threatening SVC obstruction. We report a case of acute severe SVCS, treated with JETi8 thrombectomy followed by angioplasty and stenting of the SVC. The patient consented to the procedure and the publication of this case report.

Case report

We present the case of a 56-year-old woman with a history of breast cancer treated surgically followed by radiochemotherapy through a Port-a-Cath (PAC) placed in the left subclavian vein 3 years ago; currently taking hormone therapy (anastrozole). She presented to the emergency with severe upper body edema, facial cyanosis, and mild consciousness alteration. She reported intermittent upper body edema after receiving the second dose a severe acute respiratory syndrome coronavirus 2 vaccine 3 months earlier. Computed tomography angiography (CTA) was performed 1 month ago showing patent SVC and well-placed PAC (Fig 1) No other measures were taken; however, intermittent facial edema persisted.

Fig 1

Coronal (A) and axial (B) computed tomography (CT) images showing patent superior vena cava (SVC) and a well-placed Port-a-Cath (PAC) 1 month before admission.

At admission, she was hemodynamically stable (137/74 mm Hg) with mild tachypnea (25/min) and patent airways. Anaphylaxis was initially suspected and clemastine, methylprednisolone, and ephedrine were administered. CTA showed complete SVC occlusion over 5 cm (Fig 2), with the tip of the PAC in the right subclavian vein. Ultrasound examination revealed no extremity deep vein thrombosis (DVT), but the absence of blood flow in the subclavian, axillar, and jugular veins owing to upstream SVC occlusion.

Fig 2

Coronal (A), sagittal (B) and axial (C) computed tomography (CT) images showing a superior vena cava (SVC) occlusion. Port-a-Cath (PAC) in the left subclavian vein with its distal extremity in the right subclavian vein (A).

She became hemodynamically unstable presenting hypotension (89/67 mm Hg) and tachycardia (100/min). A massive pulmonary embolism was suspected, which warranted administration of systemic thrombolysis and ephedrine. A transthoracic echocardiogram showed no signs of massive pulmonary embolism. The instability was short-lived and needed no further acute interventions. She was then transferred to the intensive care unit for surveillance. Intravenous unfractionated heparin was initiated. An endovascular thrombectomy was planned for the next day because the necessary inventory was not immediately available.

Intervention was performed in supine position under general anesthesia. Venous access was achieved through a left femoral central venous catheter. A hydrophile, 0.035-inch, stiff guidewire was inserted and the central venous catheter replaced with a 6F sheath. A pigtail catheter was placed in the SVC under fluoroscopy. Phlebography showed a complete venous thrombosis at the superior cavoatrial junction with patent innominate, jugular, and subclavian veins (Fig 3, A) The pigtail was replaced for a long steerable guiding sheath Oscor Destino Twist of 8.5F. The occlusion was passed using the guidewire and a vertebral catheter up to the right subclavian vein. We performed percutaneous catheter-directed thrombectomy of the SVC using the JETi 8F device (Abbott, Walk Vascular, LCC, Abbott Park, IL) inserted through the sheath allowing a rotational directed thrombectomy, without additional lysis. Phlebography showed flow restoration with residual stenosis (Fig 3, B and C) Angioplasty of the SVC was performed using a high-pressure AltoSa XL Percutaneous Transluminal Angioplasty balloon (AndraTec) of 14 mm followed by a 16-mm balloon, allowing deployment of an Abre stent of 16 × 60 mm (Medtronic, PLC, Dublin, Ireland). Phlebography showed total SVC recanalization without residual stenosis and complete stent deployment (Fig 3, D). The PAC was withdrawn over a guidewire under fluoroscopy. Immediate clinical improvement was seen with complete regression of facial cyanosis and edema. She returned to intensive care unit for surveillance and was extubated on postoperative day 2. Low-molecular-weight heparin followed by oral anticoagulation (rivaroxaban 20 mg/day) were introduced and pursued lifelong. Rapid clinical recovery allowed discharge after 9 days. Postoperative CTA at 1 (Fig 4) and 6 months showed persistent vessel patency without clinical complications. A screening for thrombophilia showed a heterozygote mutation of prothrombin (factor II) G20210A.

Fig 3

Intraoperative phlebography. A, Complete venous thrombosis of the superior cavoatrial junction. B, Phlebography after JETi8 thrombectomy. C, Residual stenosis of the superior vena cava (SVC). D, Successful deployment of the Abre stent and complete recanalization of the SVC.

Fig 4

Coronal (A) and axial (B) computed tomography (CT) images showing a patent stent in the superior vena cava (SVC).

Discussion

Severe SVCS is rare. However, its incidence is increasing owing to the use of indwelling catheters.

Complete SVC obstruction is only seen in 0.1% to 3.3% of patients, but can be life threatening and requires emergent treatment. Still, no official guidelines for the management of SVCS have been established. Although no randomized trials have been conducted, endovascular treatment of SVCS is currently considered as the first-line treatment. Catheter-directed thrombolysis has been described extensively as an efficient treatment for SVC obstruction with successful outcomes. However, it involves prolonged infusion of thrombolytic agents, which can lead to a high rate of hemorrhage., Also, the rates of rethrombosis can be significant and long-term patency compromised.

Another possibility is catheter-directed thrombectomy, allowing a single-session treatment. It is known that for prompt symptoms relief, rapid recanalization of the SVC is necessary., Catheter-directed thrombectomy minimizes the rate of catheter-directed thrombolysis-associated complications such as overnight thrombolytic infusions, hemorrhaging, or hemolytic complications. Only three cases were reported on the use of rheolytic thrombectomy in SVCS, all using the AngioJet thrombectomy device. Rapid relief of SVCS symptoms and SVC patency was achieved with effective short-term clinical success without complications.,, However, potentially life-threatening adverse effects have been described with the AngioJet device. A vacuum effect, created by its saline jet, leads to indirect clot aspiration with residual systemic clots fragments, possibly causing hemolysis. Other thrombectomy devices used in peripheral DVT such as end hole aspiration devices can be obstructed when large volumes of thrombi are crossed. The JETi8 thrombectomy system is a single lumen catheter that combines clot fragmentation through a pressurized saline jet with active clot aspiration, minimizing dissemination. It received US Food and Drug Administration clearance in October 2016 for the treatment of coronary and peripheral vessel thrombosis. Only a few studies describe its use, safety, and efficacy in the treatment of acute iliocaval and iliofemoral DVT and none in the SVC. As compared with the Angiojet, no hemolysis was reported with the JETi8.13, 14, 15, 16

In this case, the thrombus was removed efficiently and blood flow restored without additional thrombolysis. Residual stenosis was seen. Additional stenting in the treatment of SVC occlusion is often needed, especially in chronic lesions or extrinsic compression, and increases long-term patency., In this case, balloon angioplasty and anticoagulation could have sufficed. Still, we opted for stenting so as to ensure long-term patency. There are few dedicated venous stents on the market. A Wallstent (Boston Scientific, Marlborough, MA) of 24 × 70 mm was initially considered; however, because of its flexibility, deployment accuracy can be impaired and stent length can be variable. In this case, the stent would have protruded into the right atrium. Therefore, we chose the Abre (Medtronic, PLC) stent, a venous self-expandable nitinol stent, CE and US Food and Drug Administration approved (respectively in 2017 and 2020) for the treatment of symptomatic iliofemoral DVT. An ongoing investigational device exemption study (ABRE CSR v1.2 30/JUL/2020) shows easy and accurate stent deployment all the while ensuring radial strength and crush resistance without compromising flexibility. Although this case describes an off-label use of the Abre stent, deployment was precise with a satisfying venogram.

Prothrombin G20210A mutation increases the risk of DVT by two- to five-fold. Hormone therapy is also a known risk factor for venous thromboembolism. This patient combined several risk factors for acute SVCS. Considering these risk factors, despite successful SVC recanalization and PAC removal, there is an indication for life-long anticoagulation.

Conclusions

Urgent antegrade flow restoration is essential in acute life-threatening SVSC. The JETi8 thrombectomy system combined with angioplasty and stenting of the SVC seems to be an efficient and safe, percutaneous treatment of acute SVCS. It allows immediate flow restoration and clinical improvement with persistent patency at 6 months follow-up without complications.