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Bhatt DL, editor. Guide to Peripheral and Cerebrovascular Intervention. London: Remedica; 2004.

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Guide to Peripheral and Cerebrovascular Intervention.

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Venous stenosis

and .

Venous stenosis can manifest with swelling, pain, and superficial varicosities. Clinically significant venous stenosis is much more common in the upper than in the lower extremities. The most commonly affected sites include the axillary, brachial, cephalic, or brachiocephalic veins, or the SVC. Venous stenosis is due to intimal hyperplasia and fibrosis secondary to placement of central venous catheters, pacemaker leads, hemodialysis catheters, prior radiation, trauma, or extrinsic compression by musculoskeletal structures. Chronic intimal injury of the subclavian or axillary veins can occur as a result of compression between the first rib and costoclavicular ligament during strenuous shoulder activity, resulting in venous thrombosis (Paget–Schroetter disease, "effort" thrombosis, or the venous form of thoracic outlet syndrome) [57]. SVC syndrome is a life-threatening condition secondary to extrinsic compression or intrinsic obstruction (eg, thrombotic occlusion) of the SVC. Patients with SVC syndrome usually complain of a rapidly progressive headache and swelling in the head, neck, and upper extremities; jugular venous distention and plethora in the affected parts of the body are obvious. If left untreated, the patient may further develop confusion and obtundation as a result of cerebral hypoperfusion. Nearly half of the patients with a hemodialysis arteriovenous fistula develop subclavian vein stenosis due to prior temporary hemolysis catheter insertion and subsequent high venous outflow that propagates intimal hyperplasia and exaggerates the pressure gradient even in moderate stenosis. Iliofemoral venous stenosis may be due to extrinsic compression (eg, pelvic malignancy, retroperitoneal fibrosis), fibrotic healing after surgery, or irradiation (see Figure 4).

Figure 4. Severe iliac vein stenosis caused by extrinsic compression from a metastatic tumor, resulting in massive lower extremity edema.

Figure 4

Severe iliac vein stenosis caused by extrinsic compression from a metastatic tumor, resulting in massive lower extremity edema. (a) After initial recanalization. (b) The stenosis is resistant to balloon inflation. (c) Placement of a bare metal stent is (more...)

Treatment for upper extremity venous stenosis

Balloon angioplasty is the therapy of choice for symptomatic venous stenosis. Venous access can be established via the antecubital vein, dialysis fistula, or common femoral vein. Conservative balloon sizing should be adopted at the start because these vessels have less muscular tissue than the arterial system. Fibrotic stenosis that fails to yield to balloon angioplasty may be treated with cutting balloons or directional atherectomy. Stents should be used when significant residual angiographic stenosis or flow-limiting stenosis is present. Self-expanding stents (eg, WALLSTENT [Boston Scientific, Natick, MA, USA] or SMART [Cordis]) may be used for lesions located in highly mobile sites. The nominal size of the self-expanding stent should be 1–2 mm above the estimated reference diameter of the vein to ensure proper apposition and to minimize the risk of stent migration (8–12 mm for subclavian or axillary veins, 14–20 mm for SVC). Resolution of symptoms (eg, cyanosis, swelling, pain) begins almost instantaneously after successful revascularization. Stent placement across the ostia of other venous drainage should be avoided if possible. Stents are relatively contraindicated when the lesion is due to thoracic outlet syndrome.

Fibrotic adhesion of permanent pacemaker or defibrillator leads can occasionally result in venous obstruction (causing swelling and pain in the arm) or SVC syndrome, depending on the location of the obstruction. Traditionally, treatment involves surgical explantation of the device and the leads and replacement of the vessel with an artificial conduit. The feasibility of an endovascular strategy has been demonstrated [58]. First, a percutaneous telescoping excimer laser sheath with countering force is used to remove the leads (see Figure 5). The lumen can then be enlarged with standard balloon angioplasty and stent placement procedures. A new set of permanent pacemaker leads may then be implanted within the treated venous vessels. Most operators would favor anticoagulation with warfarin for a few weeks to a few months, with or without antiplatelet therapy (aspirin and clopidogrel).

Figure 5. (a,b) Serial cineangiograms demonstrate the advancement of an excimer laser sheath (arrow) over the right atrial lead (arrowhead) and to the distal tip of the right ventricular electrode (open arrow).

Figure 5

(a,b) Serial cineangiograms demonstrate the advancement of an excimer laser sheath (arrow) over the right atrial lead (arrowhead) and to the distal tip of the right ventricular electrode (open arrow). (ce) Venogram-confirmed severe stenosis in (more...)

Treatment for lower extremity venous stenosis

Symptomatic venous stenosis of the iliofemoral vein can be treated with endovascular techniques. Venous access can be established via the right internal jugular vein, ipsilateral popliteal vein, or contralateral femoral vein. Balloon predilation should be performed and self-expanding stents should be used, followed by optimal expansion of the stent by matching the diameter of the vein with a postdilating balloon catheter (usually 10–14 mm diameter). Similar to endovascular revascularization of the upper extremities, most physicians favor short-term warfarin, with or without dual antiplatelet therapy, after stent placement. Close surveillance with duplex ultrasound is recommended to assess patency within the first year.

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 2004, Remedica.
Bookshelf ID: NBK27375

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