Superficial venous incompetence is an extremely common problem for which people may or may not seek medical treatment, depending on their cosmetic concerns, symptoms, or occurrence of complications. Primary varicose veins are the result of a polygenetic inheritance pattern resulting in structural weaknesses in the vein wall and of the venous valves. Munn et al reported that 80% of patients admitted for surgery for greater saphenous vein incompetence had a family history of varicose veins. Superficial valvular incompetence may be present for years prior to the development of large varicosities. The San Valentino epidemiologic study, with 20,000 patients and 10-year follow up, showed that incompetence at the saphenofemoral junction and at the saphenopopliteal junction was present in 9% of people ages 45 to 65, while varicose veins were present in only 6%. Several risk factors contribute to their development, including increased age, female gender, pregnancy, increased height and weight, and standing occupations. Secondary varicose veins are caused by post-thrombotic damage, pelvic tumors, congenital abnormalities (Klippel-Trenaunay-Weber syndrome, valvular agenesis), and acquired or congenital arteriovenous fistulae.

In their textbook, Varicose Veins (Mosby, 1939), Ochsner and Mahorner provide an early reference to the problem of reflux through incompetent valves as a cause for varicose veins:

“It is our opinion that most varicose veins of the lower extremity are associated with incompetence of valves, generally of the saphenous vein, but possibly, at times, of other veins which are of etiologic importance…”

“…When the communicating veins of the thigh have incompetent valves, some of the blood…passes back to the superficial system through the communicating channels.”

The historic methods of dealing with this abnormal reflux, either via the saphenous trunk or through perforating veins, provide an interesting background to what remains a controversy even today.

The deep and superficial veins of the lower extremities occupy two distinct compartments separated by the deep fascia. Perforator veins connect the superficial and deep veins in the two compartments. Communicating veins connect veins within the same compartment. The superficial compartment, by design, is a low-pressure chamber. The deep compartment is a high-pressure chamber, due to the pumping mechanism of the muscles in the deep posterior compartment of the calf, which generate pressure of 200 to 300 mmHg to pump venous blood proximally toward the heart. There is evidence that the muscles of the foot also play a role in this process.

The venous valves are designed to direct blood flow from the superficial compartment to the deep compartment of the leg, and then from the distal leg to the proximal leg. At the moment of calf muscle contraction, the perforator valves close to prevent the high deep compartment pressure from reaching the superficial compartment and the skin. If the perforator valves become incompetent, the calf pump pressure is transmitted from the deep compartment to the superficial compartment, converting it into a high-pressure compartment. This results in edema, pain, varicose veins, and all the manifestations of high pressure, the so-called “hypertensive leg.”

Browse and Burnand have clearly stated: “The absence of venous hypotension during exercise is the ultimate cause of almost all venous pathology.”

The controversy over the fundamental etiology of varicose veins has continued for decades. Most authors agree that valve reflux is the principal contributing factor to formation of varicose veins and chronic venous insufficiency. A body of knowledge claims that the initiating factor in vein dilatation is vein wall weakness and subsequent dilatation, thus creating secondary valve incompetence as the dilating vein wall pulls the valve open so it cannot properly close. This concept is countered by those who claim that primary valvular incompetence is the initiating event. Whichever hypothesis is correct, the end result is the same, with valve incompetence creating venous hypertension in the superficial compartment of the leg.

Thus, we believe that the fundamental cause of varicose veins is reflux, via incompetent valves in perforator veins throughout the leg, including the largest of the perforators, the greater and lesser saphenous veins. Our approach to varicose veins is to study each patient carefully to determine the sites of significant valve incompetence and to ligate these pathologic perforator veins, along with excision of enlarged superficial veins. The removal of the greater saphenous vein is not necessary unless the vein is so enlarged and bulbous that it is not of use as an arterial conduit, should the need arise.

The surgeon should remember that varicose vein surgery is not just for the relief of unsightly and painful varicose veins, with all of their complications; the operative procedure should also control the physiologic defect of valve incompetence, which ultimately leads to recurrence and further complications of the disease.

Table 74-1 displays the trends in our practice. Between January 1, 1996 and December 31, 2003, 1,119 procedures were performed by two vascular surgeons. Six hundred eighty-three consisted of ligation of the greater saphenous vein and excision of distal varicosities, with specific attention to ligation and division of incompetent perforating veins. A decreasing number of vein strippings was performed between 1996 and 1998. The dominant procedure between January 2001 and December 2003 was ligation of the incompetent greater saphenous vein and other incompetent perforating veins with excision of varicose veins. The percentage of lesser saphenous vein ligations has also been trending upward through the years. The shift away from vein stripping and away from simple vein excision toward the ligation of points of reflux (saphenofemoral junction, saphenopopliteal junction, and other incompetent perforating veins) has occurred for two equally important reasons. One is secondary to the advances made in the quality and interpretation of venous duplex ultrasound, and the other stems from recognizing the benefit of preserving a viable saphenous vein.

The pre-operative evaluation involves a thorough history and physical with attention to the venous and arterial status of the affected extremities. A detailed drawing that maps the distribution of varicosities is completed with the patient standing. This becomes the template on which all future treatments are charted. Digital photography greatly contributes to pretreatment documentation. Venous photoplethysmography can determine the severity of venous insufficiency and whether or not it is localized to the superficial or deep venous system. A venous refill time of less than 20 seconds is indicative of either superficial or deep venous insufficiency, and failure of the results to normalize after application of a tourniquet signifies deep venous incompetence.

A venous duplex imaging examination is performed in the office with the treating physician present. The patency of the deep and superficial veins is assessed, and incompetence within the venous system is evaluated. The deep veins, greater and lesser saphenous veins, saphenofemoral and saphenopopliteal junctions, and perforating veins are investigated. Reflux greater than 0.5 second at either the saphenofemoral or saphenopopliteal junction is considered significant. This is frequently associated with an enlarged greater or lesser saphenous vein. In our
own experience, saphenofemoral reflux is the most common cause of varicose veins, followed by distal incompetent perforating veins and, lastly, by saphenopopliteal reflux.