The basic abnormality in patients with chronic venous insufficiency is elevation of venous pressure. With calf muscle pump dysfunction, valvular reflux, blood pools in the lower extremities and venous hypertension occurs, leading to venous hypertension. Outflow obstruction from proximal obstruction can also produce venous hypertension, resulting in “venous claudication” as the deep venous system fills with blood during exercise. The leg becomes painful, swollen, and heavy (especially with exercise), mimicking arterial insufficiency.
Valvular incompetence of the deep veins can be congenital or result from damage following phlebitis, varicose veins, or deep venous thrombosis. The best estimate for the incidence of chronic venous insufficiency is approximately 30%. Chronic venous stasis changes are centered in the “gaiter areas” around the ankles. This is the location of the commonly affected perforator veins and is a region with sparse soft tissue support to withstand elevated venous pressures. Brawny edema is produced by extravasation of plasma fluid, red blood cells, and plasma proteins. Lysis of red blood cells results in deposition of hemosiderin, which creates a brownish discoloration. Leukocytes become sequestered in the microcirculation, leading to capillary occlusion and release of superoxide radicals, proteolytic enzymes, and growth factors. Macrophages and lymphocytes are primary mediators of this inflammatory response, which results in fibroblast activation. Ultimately, this fibrosis results in compromised skin perfusion and ulceration.
Symptoms and Signs of Chronic Venous Insufficiency
The first symptom to develop is usually ankle and calf edema. Involvement of the foot suggests lymphedema. Long-standing disease is characterized by stasis dermatitis, hyperpigmentation, and ulceration. Venous ulcers are large, painful, and often accompanied by stasis dermatitis and stasis pigmentation changes.
Imaging and Other Diagnostic Studies
Duplex ultrasound can identify the presence and location of incompetent perforating veins. It has been used to evaluate the function of individual venous valves. However, it does not easily assess calf muscle pump function or the presence of proximal obstruction. These concerns are addressed with use of other tests, such as air plethysmography, which gives a quantitative assessment of venous reflux, calf muscle pump function (by the ejection fraction), and overall venous function (by residual volume function). These measurements help to stratify patients into treatment groups.
Determination of functional outflow obstruction requires venography with or without pressure measurement, although intravascular ultrasound is also very useful to determine the presence or absence of venous obstruction. Using descending phlebography, pathologic reflux can be identified in patients with postthrombotic damage.
Treatment of Chronic Venous Insufficiency
Patients respond well to a conservative treatment composed of intermittent leg elevation, regular exercise to improve calf muscle pump, and the use of surgical elastic compression stockings. Although the mechanism by which elastic compression improves the symptoms has not been clearly established, recent work suggests that external compression may restore competency of dilated valve cusps and affect venoarterial reflex. Most venous ulceration will improve with leg elevation, external compression, and local wound care. Compression can be achieved with either an inelastic bandage such as a Unna’s boot or with an occlusive wound dressing covered by ACE bandage wrapping or surgical support stockings.
Surgery is indicated for a small percentage of patients with nonhealing ulcers or disabling symptoms refractory to conservative management. The two main categories of procedures are antireflux procedures and bypass operations for obstruction. The pathology must be accurately characterized so that an appropriate operative strategy can be developed.
Perforating vein ligation is used in patients with recurrent or recalcitrant venous ulcers with demonstrated incompetence of perforating veins under the area of ulceration. It is performed to reverse the local wound complication of venous ulceration and does nothing to change the underlying deep venous hemodynamics of the leg. Therefore, patients must understand that for maximal effectiveness after perforator ligation, standard treatment for chronic venous insufficiency must be continued. Patients who have proximal venous obstruction should have this problem corrected prior to perforator interruption. The incidence of ulcer recurrence after perforator ligation is 15–20%, but the wound complication rate secondary to impaired incisional healing with severe stasis disease ranges from 12% to 55%. Wound complications have been reduced to 5% with the introduction of subfascial endoscopic perforator surgery, which achieves an ulcer recurrence rate of 12–28% at 2 years, equal to the rate following open surgery.
Venous reconstructive surgery is indicated for
failure to relieve symptoms after vein stripping or perforator ligation
venous reflux not amenable to a conservative treatment regimen
intractable disabling venous claudication associated with venous outflow obstruction.
Procedures for reflux include valvuloplasty, valvular transplantation, and venous segment transposition. The best results with valvuloplasty are achieved when it is combined with perforator ligation. The reported success rate is approximately 80% in one recent study of 155 extremities with a 1- to 13-year follow-up. Valvuloplasty can be performed by placement of external cuffs or bands, vein wall plication, angioscopic repair, or open valve repair. Venous valve transplantation involves replacing a refluxing segment of vein with a healthy segment of autologous axillary vein with functional valves. Transplantation of individual valves at the level of the popliteal vein is a technique with reported good clinical results in 60–70% of cases and an improvement in venous hemodynamics by air plethysmography. Alternatively, a competent segment of profunda vein can be used to replace an incompetent segment of superficial femoral or greater saphenous vein in a vein transposition. Although initial results of these procedures are good, the effect is apparently not long-lasting.
Bypasses and angiographic procedures can be performed for venous obstruction. The Palma procedure is a cross-femoral bypass first described in 1958 for iliac vein obstruction. In this procedure, the proximal saphenous vein from the contralateral leg is tunneled suprapubically to the femoral vein on the side of the iliac obstruction. This allows for venous flow to bypass across the pelvis and empty through the patent contralateral iliac vein. Prosthetic material has been used. Overall 5-year graft patency averages 75–80%. Historically, distal femoral arteriovenous fistulas were constructed to improve iliofemoral vein graft patency, but more current experience does not support their continued use in many cases. Patients with short-segment iliac vein obstruction from May-Thurner syndrome (left iliac vein compression) have been successfully treated by angioplasty and stenting.
Saphenopopliteal bypass (May-Husni procedure) can be considered for occlusion of the superficial femoral vein. In this procedure, calf blood flow is shunted around the obstructed superficial femoral vein through the patent saphenous vein. Approximately 75% of patients are reported to show clinical improvement postoperatively.