Historical Background

Treatment of this disorder has evolved from sclerotherapy to open radical surgery to the use of sophisticated technology such as laser, radiofrequency, or ultrasound-guided foam sclerotherapy.

The exact historical point in time when saphenous vein incompetence was recognized as a source of venous hypertension is unclear; however, Trendelenburg promulgated saphenofemoral ligation in 1891.¹ In the early 20th century, stripping of the saphenous veins was added to proximal ligation. Keller² described an internal stripper in 1905. Hence, high ligation of the great saphenous vein (GSV) at the saphenofemoral junction (SFJ) followed by GSV stripping from groin to knee, or ankle was the standard of care and was performed in the hospital setting for about 100 years.

The two methods of thermal ablation in comprehensive vein centers at present are the VNUS ClosureFAST procedure, which uses a catheter to direct radiofrequency (RF) energy from a dedicated generator (VNUS Medical Technologies, Inc., Sunnyvale, CA), and endovenous laser (EVL) ablation, which uses a laser fiber and generator to produce focused heat (multiple manufacturers). Both RF and EVL are catheter-based endovascular interventions that use electromagnetic energy to destroy the refluxing saphenous system.

RF catheters were the first devices to become available to venous surgeons for endovenous thermal ablation of the GSV after garnering Food and Drug Administration approval in 1999. In 2002, endovascular ablation of the GSV using laser energy became available in the United States.

Etiology and Natural History of Disease

The majority of patients (60% to 70%) with varicose veins have an incompetent SFJ and GSV reflux.³ It is critical to recognize that bulging varicose veins are usually associated with an underlying source of venous hypertension, and treatment of the source is as important as is treatment of the actual varicose vein.

Chronic venous disorders generally result from primary venous insufficiency or secondary processes, such as acute deep venous thrombosis (DVT) or trauma. An analysis of chronic venous disease indicated that primary valvular incompetence was present in 70% to 80% of cases; secondary valvular incompetence was due to trauma or DVT in 18% to 25%, and congenital anomaly was present in 1% to 3%.⁴

Patient Selection

Patients with chronic venous disease (CVD) will usually present to a physician with concerns referable to both medical symptoms and cosmetic appearance of their disease. Patient satisfaction results from identifying and properly treating the patient’s primary concerns, which may include medical and/or cosmetic issues. Not all symptomatic patients are aware of their symptoms because the onset may be insidious. Symptoms may include leg heaviness, pain or tenderness along the course of a vein, pruritus, burning, restlessness, night cramps, edema, skin changes, and paresthesias. After treatment, patients are often surprised to realize how much discomfort they had accepted as normal. Pain caused by CVD is often improved by walking or by elevating the legs. The pain of arterial insufficiency, conversely, is worsened by ambulation and elevation. Pain and other symptoms of venous disease may intensify with the menstrual cycle, pregnancy, and in response to exogenous hormonal therapy (i.e., oral contraceptives).

As is customary for any medical condition, the physician must begin with a careful history and physical examination. The primary purpose of the clinical examination of the patient presenting with chronic venous disease (CVD) is to classify the subject using the popular CEAP system^5,6—clinical (telangiectasias to skin damage), etiologic (primary, secondary, or congenital), anatomic (superficial, deep, or perforators), and pathophysiologic (reflux, obstruction, or both) patterns, forming the acronym CEAP. For each of these major classifications, there are subgroups. For the work described in this chapter, clinical signs emerge as the most important and are grouped as follows—C1: spider telangiectasias; C2, varicose veins (Fig. 4-1); C3, edema; C4, lipodermatosclerosis; C5, healed ulcer; and C6, active ulcer. Regarding treatment, the class (C) is the most important parameter to establish during the initial encounter. Treatment algorithms for chronic venous insufficiency (CVI) (i.e., patients with more severe disease [C4, C5, C6]) are discussed in other sections of this book. This chapter focuses on the treatment of C2 disease.

Fig 4–1 B, Typical varicose veins of the calf resulting from great saphenous vein (GSV) incompetence.

Endovascular Instrumentation

Device choice is a matter of physician preference. Our center and other investigators have compared the efficacy of RF and EVL. The ablation data are slightly better for EVL.^7,8 A few years ago, we published our 3-year data showing 94% success with RF and 98% success with laser⁹; however, in current practice, the results are closer to 98% success with either technology.

Figure 4-2 depicts the general layout of an office-based venous surgery suite. An operating table with a back table is prepared in the usual sterile manner. The laptop ultrasound system is mounted on a movable cart, and the thermal ablation equipment is in close proximity to allow easy viewing of the display panels by the operator. Hemodynamic monitoring equipment (heart rate, blood pressure, oxygen saturation) is available and is used during cases offering conscious sedation. If local anesthesia without sedation is used, hemodynamic monitoring is not required in most states.

Fig 4–2

Tumescent Anesthesia Delivery

A 30-ml syringe with a 25-gauge needle is preferred if anesthesia is delivered by the operator. Extension sets with three-way stopcocks are useful if an assistant is available to push the anesthetic solution. Alternatively, tumescent anesthesia infusion pumps are commercially available.

Imaging

Fig 4–3 C, Preparing for preprocedure ultrasound scan. This is referred to as “reading” the vein. The surgeon will create an image in his or her “mind’s eye” prior to beginning the procedure.

Access and Closure

The surgeon begins by placing a wheal of local anesthesia on the skin access site with a syringe and small (25- to 30-gauge) needle (Fig. 4-4). The access needle is then held at an approximately 45-degree angle 1 inch from the ultrasound probe, and the target vein will be located at the tip of an imaginary triangle where the ultrasound beam and the tip of the access needle meet under the skin. For large veins (>5-mm diameter), an 18-gauge needle is used. For smaller diameter veins (<5-mm diameter), a 21-gauge needle and micropuncture assembly are preferred (Fig. 4-5).

Fig 4–4

Fig 4–5 C, Cross-sectional ultrasound image of great saphenous vein (GSV) (the target vein) (arrow).

The needle tip is guided to the roof of the vein using ultrasound to visualize where the puncture will take place. Usually one will tent the roof of the vein with a gentle push, easily seen with ultrasound imaging, prior to a more forceful motion for entry. Aspiration of dark nonpulsatile blood into a connected syringe confirms venous entry (Fig. 4-6).

Fig 4–6

Hemostasis and Anticoagulation

Hemostasis at the entry site is obtained with manual pressure. As a general rule, thromboprophylaxis with anticoagulation is not required unless the patient has an underlying thrombophilia.

Patients should be stratified into mild-, moderate-, or high-risk classes to determine whether thromboprophylaxis (mechanical, pharmaceutical) is required perioperatively.

As demonstrated in Figure 4-7, we believe that on-table activation of the calf pump is very effective in preventing thromboembolic complications during thermal ablation procedures. After the ablation and before the ambulatory phlebectomy portion of the procedure (discussed in Chapter 9), we simply ask the patient to actively dorsiflex and plantarflex the foot 20 times.

Fig 4–7

Operative Steps

Once the patient has entered the operating suite, a brief examination of the leg is performed. The skin overlying all areas of bulging varicose veins is marked with a magic marker. The patient is then placed in the supine position on the operating table. A detailed duplex ultrasound report should be readily available so the operator can review it before beginning the procedure. Our preference is to then perform a rapid scan of the medial leg with the ultrasound probe for the purpose of obtaining a high-level understanding of the venous anatomy. The operator should note areas of tortuosity, aneurysmal dilatation, and location of tributaries and perforators prior to beginning the procedure. I call this “reading” the vein; its importance is discussed later.

The ultrasound scan begins at the groin, and the course of the vein is followed distally until the straight segment terminates as it begins to divide and produce varicosed tributaries. These varicosed tributaries are the escape points for saphenous incompetence. This transition zone is usually found just below the knee, although many anatomic variants exist. Therefore, percutaneous access is usually obtained immediately below the knee; however, the operator must be prepared to access anywhere from below the knee to the thigh.

Once the optimal access site is chosen, preparations for entry begin. The intraluminal space of the target vein must be accessed to place a guidewire. The preferred technique is percutaneous access under ultrasound guidance. The surgeon and patient must both be comfortable. The surgeon should rest both forearms somewhere in the operative field so that his or her hands are stable.

The ultrasound probe is held perpendicular to the skin to demonstrate the target vein in either the short or long access on the ultrasound screen. Once venous entry is confirmed, a guidewire is chosen. The micropuncture needle accepts a .018-inch wire followed by a 4-Fr coaxial microsheath and its intraluminal dilator. Usually a small stab incision with a No. 11 blade scalpel is required at the wire entry site to widen the incision for the microsheath. Confirmation that the .018-inch wire is in the endoluminal space is performed with ultrasound (Fig. 4-8).

Fig 4–8 C, Cross-sectional ultrasound image demonstrating intraluminal placement of .018 guidewire (arrow).

The microsheath assembly is placed, the microdilator and .018-inch guidewire are removed, and the remaining microsheath is used to place a .035-inch guidewire (Fig. 4-9, A). The .035-inch guidewire is then navigated to the SFJ using ultrasound control (Fig. 4-9, B and C).

Fig 4–9 A, A .018 guidewire and dilator will be removed, leaving microsheath in place.

B, A .035 guidewire inserted into microsheath. C, Cross-sectional ultrasound image demonstrating intraluminal placement of .035 guidewire (arrow).

Some operators prefer to deliver the wire with the J-tip at the lead, but we prefer to send the straight end of the wire up first, especially in smaller veins. J-tipped wires may cause distention of the vein and induce friction with the inner lining of the vein wall during passage. This generally will cause pain secondary to venous distention, which activates the adrenergic sympathetic nerve fibers residing in the adventitia (Fig. 4-10).

Fig 4–10 A, CFV, Common femoral vein; EPV, external pudendal vein; GSV, great saphenous vein; SCIV, superficial circumflex iliac vein; SEV, superficial epigastric vein; SFJ, saphenofemoral junction. C, Long-access ultrasound image of saphenofemoral junction (SFJ). Top arrow points to guidewire tip at SFJ. Bottom arrow points to common femoral vein (CFV).

Once the tip of the wire is positioned at the SFJ, a larger coaxial sheath is placed (Fig. 4-11).

Fig 4–11 B, Outside of the legs, the surgeon measures the estimated sheath length. C, Arrow points to tip of braided sheath at saphenofemoral junction (SFJ). Black dot to the left of arrow tip is the external pudendal artery.