Vein Valves

Valve leaflets comprise a thin fold of the intima, with a thin layer of collagen and a network of elastic fibers that extend toward the intima of the vessel wall. The space between the valve and the vessel wall is called the sinus of the valve. The wall of the vessel becomes thinner and slightly expanded just above the attachment of each valve cusp. Only the medium-size veins have valves. Their main function is to ensure the antegrade flow of blood, peripheral to central and superficial to deep, and to prevent the backflow of blood away from the heart. In general, the small and large veins have no valves. Valves have a bicuspid structure and are more numerous in the veins of the lower extremity, where the force of gravity is the greatest. Venous valves have cuplike endothelial flaps, which fill when there is retrograde flow of blood. When filled, the valves completely block the lumen, preventing flow reversal and transference of pressure.

Physiology

The venous system has a large capacity, accounting for approximately two-thirds of the systemic blood. Veins, because of their unique vascular structure, can undergo a large change in volume with minimal change in transmural pressure. This characteristic is called venous capacitance.

Because of their low elastic tissue content and prominent collagen-composed adventitia, the veins are actually stiffer than arteries when they are compared at the same distending pressure. A person in a resting upright position has significantly elevated venous pressures at the level of the feet and calves, accumulating a large volume of blood in the lower extremities. In similar cases, the calf muscles magnify the venous return by working as a pump system. During walking or exercise, calf muscle contraction pushes the accumulated blood toward the heart, decreasing the venous pressures close to zero. The venous pressure remains low even during calf muscle relaxation. At this time, the venous valves come into play, preventing the backflow of blood but allowing the inflow of blood to refill the system. It is imperative that the vein valves be competent for this pump system to work appropriately. The calf muscle pump works most efficiently when all venous valves are competent. A normal pump system reduces venous pressures and volume in the exercising muscle, increases venous return, and improves arterial perfusion.

Varicose Veins

Incompetent valves in the saphenous system permit reflux of blood from the central veins to the peripheral veins. As the vein dilates because of an excessive volume of blood, each valve becomes incompetent. This valve incompetence occurs in the deep and superficial systems, creating a standing column of blood with a constant increase in pressure transmitted through the systems and resulting in varicose veins.

Chronic Venous Disease

Chronic venous insufficiency is a significant problem in the United States, affecting as much as a quarter of the population. Venous valve incompetence is central to the underlying venous hypertension that appears to underlie most or all signs of chronic venous disease. Chronic venous disease affects a younger segment of the population; the resulting morbidity of edema, leg pain, and ulceration may then lead to lifestyle alterations, loss of work, and frequent hospitalizations. The prevalence of venous ulcerations is not restricted to the elderly but certainly increases with age.¹ It has been estimated that venous ulcers have had a major negative economic impact, with the loss of approximately 2 million working days and treatment costs of approximately $3 billion per year in the United States.² The chief clinical manifestations of chronic venous disease are aching, leg pain, heaviness, a sensation of swelling, itching, cramps, and restless legs. Chronic venous disease can be graded according to the descriptive clinical, etiological, anatomical, and pathophysiological (CEAP) classification, which provides an orderly framework for communication and decision making³ (Table 43-1). The pathophysiology of chronic venous disease in regard to its clinical expression has been well described, involving venous valve incompetence, structural changes in the vein wall (manifest as hypertrophy), and the role of elevated venous pressure and shear stress.⁴ There has been much newer work in understanding the pathophysiology of the skin changes of chronic venous disease. These studies have emerged to validate that chronic inflammation has a key role in the skin changes of chronic venous disease. Support for the role of chronic inflammation in chronic venous disease has come to be known as the microvascular leukocyte-trapping hypothesis, where elegant studies have shown elevated numbers of macrophages, T lymphocytes, and mast cells in skin biopsy specimens from lower limbs affected by chronic venous disease.⁵ The chronic inflammatory state in patients with chronic venous disease is related to the skin changes typical of the condition.⁴ Increased expression and activity of metalloproteinase (MMP, especially MMP2) has been reported in lipodermatosclerosis,⁶ venous leg ulcers,⁷ and wound fluid from nonhealing ulcers.⁸ The treatment of chronic venous disease is beyond the scope of this chapter but would be aimed at preventing venous hypertension, venous reflux, and chronic inflammation (Fig. 43-1). Compression stockings and devices are certainly the mainstay of controlling venous hypertension. New endovenous ablation procedures utilizing laser energy or radiofrequency are available to treat venous reflux. Clinical research is now being actively pursued seeking pharmacotherapy to alleviate the chronic inflammatory state of chronic venous disease, particularly targeting the interaction of leukocytes and endothelial cells.

TABLE 43-1 Revised Clinical Classification of Chronic Venous Disease of the Leg*

* Chronic Venous Disease grading system based on descriptive clinical, etiological, anatomical, and pathophysiological classification scheme.

Figure 43-1 Venous hypertension as the hypothetical cause of the clinical manifestations of chronic venous disease, emphasizing the importance of inflammation.

Diagnosis of Central Venous Stenosis

The clinical presentation of SVC syndrome is relatively consistent and can be verified with multiple diagnostic modalities. Computed tomography (CT) is helpful for the workup of SVC syndrome and often gives enough information to proceed directly to an endovascular procedure.¹⁵ An upper extremity venogram will reveal multiple collaterals if the obstruction is of long standing. With acute SVC obstruction, however, there are often surprisingly few collaterals. In most cases, the venogram will demonstrate the level of involvement, but it can still overestimate the length of involvement of the innominate veins and even the SVC because of the high resistance to flow. Magnetic resonance imaging (MRI) is helpful for the evaluation of SVC syndrome, and procedure planning can be based solely on MRI findings.¹⁶ MRI will give good information regarding the extent of occlusion and collateral flow. Ultrasound, on the other hand, is not accurate in locating the central obstruction. The Doppler signal will raise a suspicion of obstruction because of the flattened character of the waveform, but the level of obstruction is difficult or impossible to estimate with ultrasound, especially in the central portion of the SVC. Ultrasound with Doppler can, however, be a useful tool for follow-up after endovascular repair. Obstructive changes in the waveform will raise suspicion of recurrent narrowing or occlusion of the recanalized vessel.

Technique

Endovascular therapy has emerged as first-line treatment for central vein stenosis.¹⁷ It is important to have a plan of approach before attempting SVC recanalization or stent placement. Taking into account the patient’s clinical presentation and preprocedural noninvasive imaging is essential to a successful outcome. Many operators have used femoral vein access, but others have used jugular, subclavian,¹⁸ and arm vein access or even transhepatic venous approaches for stent delivery.¹⁹ One may use any combination of these approaches, but it is always paramount to have a guidewire “through and through,” especially when stenoses are severe and difficult to pass.^20,21 It certainly adds to the safety of the procedure to have a guidewire passing the right atrium into the inferior vena cava (IVC) during stent delivery and dilation. This is particularly important in preventing stent migration. This guidewire position will prevent the stent from migrating into the right side of the heart or pulmonary artery. The stent is thus more likely to stay on the wire and can be more safely manipulated, removed, or moved to a different location. Accessing the SVC from the right internal jugular vein or upper extremity veins has several benefits. Manipulation is easier because of the limited space in the internal jugular vein compared with the right atrium, which one has to work through in coming from a femoral vein access. The distance from the access site to the obstruction is also shorter, which can make it easier to cross chronic total occlusions. An upper extremity access, as via the brachial or basilic vein, is also a viable option. The entire venous intervention can be performed from this access, including thrombolysis, angioplasty, and stent placement in most cases.²² This is also comfortable and well tolerated by most patients. Hemostasis is not usually problematic, placing a pressure dressing for 20 minutes or holding pressure for 5 to 10 minutes is usually successful. If double-barrel stenting is required to treat the SVC, bilateral upper extremity access is ideal, with the stents each traversing the brachiocephalic veins. Several operators advocate using the common femoral vein for access, but it may be difficult to access an occluded or severely narrowed SVC from the femoral vein because of its anatomical relationship with the right atrium.^23,24 Some operators have therefore crossed the obstruction from the brachial veins, creating a through-and-through access from the femoral vein by snaring the wire and pulling it through the femoral vein.²⁵ In addition, double-barrel stents into each of the brachiocephalic veins can be easily placed from a bilateral common femoral vein access.

There is some experience in performing thrombolytic therapy prior to SVC stent placement as well as in conjunction with it. Isolated pharmacomechanical thrombolysis plus primary stenting is a combined procedure that opens an acutely thrombosed superior vena cava rapidly to alleviate symptoms in seriously ill patients with SVC syndrome. O’Sullivan²⁶ reported a case series where all patients received isolated pharmacomechanical thrombolysis with tissue plasminogen activator delivered in a Trellis Peripheral Infusion System (Bacchus Vascular, Santa Clara, CA) that removed obstructive clots in minutes versus the 24 to 48 hours required for traditional catheter-directed thrombolysis. In each patient, stents were deployed immediately following pharmacomechanical thrombolysis in a combined procedure lasting less than 1 hour. In the appropriate clinical setting, thrombolysis for SVC syndrome prior to endovascular therapy may have great utility. By resolving the acute thrombus, one need only stent the underlying stenosis, which most of the time is shorter than the occluded segment that was occupied by thrombus. Therefore a shorter segment of vessel has to be stented, thus reducing the number of stents utilized and ultimately also reducing the potential thrombogenic stent surface. Gray, et al.²⁷ reviewed the outcomes from thrombolysis of SVC thrombus in 16 patients; they had no major complications and complete success in 56% without stents. Thrombolysis was effective in 73%. Stents were not used in any of the patients, which may explain many of the poor clinical outcomes. Many patients with SVC syndrome have central venous catheters in place, on which they are dependent. Numerous reports describe pulling the catheters up from the SVC during the procedure and then placing the catheter down through the stent immediately after the procedure.²⁸

Stent Selection

Early reports of SVC stenting described the use of Gianturco (Cook, Incorporated, Bloomington, IN) stents. This was the first self-expanding stent in wide use and had diameters that were acceptable. There were few complications reported, but large sheath introducers are required for this stent, and it is used only in cases where inflow vessels must be covered because of the large spaces between the stent’s interstices. Next, the Palmaz stent (Cordis Corporation, Miami, FL) was released for use. This stent is balloon-expandable and is now rarely used in the SVC. It has a higher radial force than self-expanding stents and, on occasion, when extra radial force is needed, can be used either primarily or secondarily within a deployed self-expanding stent that cannot sustain the radial force of SVC recoil. In today’s era of endovascular therapy, self-expanding stent delivery systems are used mainly for SVC stenting (Fig. 43-2).^29,30 The newer self-expanding stent delivery systems are easily deployed and come on a small 6- to 7-Fr delivery system. The WALLSTENT (Boston Scientific Corporation, Natick, MA) was one of the earlier versions of a self-expanding stent and is still widely used for SVC intervention. Its main shortcoming is that it foreshortens significantly on delivery, which makes precise placement difficult. Recent generations of self-expanding stents are made of nitinol and do not have this problem. A few examples of self-expanding nitinol stents include the Smart Stent (Cordis Corporation, Miami, FL), Luminex (Angiomed/Bard, Karlsruhe, Germany), and Zilver (Cook Incorporated, Bloomington, IN). For the SVC, a stent 12 to 16 mm in diameter is usually adequate.

Figure 43-2 A. Venogram of significant SVC stenosis. B. Venogram of SVC after 12-mm PTA. C. Venogram after 14-mm WALLSTENT.

(Boston Scientific, Natick, MA.)

Complications

In a group of 59 patients with malignant disease, Lanciego reported 6 reocclusions, all of which were treated successfully with restenting in combination with thrombolysis.³¹ One of the patients in this series had stent migration to the right atrium, which was successfully treated.

Hemopericardium has been reported by several operators in the literature. This complication most commonly occurs during the procedure itself or immediately after stent placement,³² but delayed bleeding into the pericardium has also been described.³³ The pericardial reflection can extend very high in the mediastinum, and the position is unpredictable.³⁴ In this regard, it is advisable to place stents high in the SVC without compromising clinical results. If there is a high index of suspicion for hemopericardium, an echocardiogram or right heart catherization should be done immediately.