Varicose Veins: Evaluating Modern Treatments, With Emphasis on Powered Phlebectomy for Branch Varicosities

Frank Vandy; Thomas W Wakefield

Disclosures

Interv Cardiol. 2012;4(5):527-536. 

In This Article

Varicose Veins: Epidemiology, Risk Factors & Pathophysiology

Chronic venous insufficiency (CVI) is one of the most commonly reported medical conditions in the USA with healthcare costs of associated venous ulcers exceeding US$1 billion annually.[1] The underlying pathophysiology of CVI is venous hypertension of the lower extremities, which can lead to various clinical problems including pain, dilated or varicose veins, swelling, edema, skin changes and ulcerations. Although CVI-associated ulcers only affect up to 1% of the population, less severe manifestations of CVI, such as varicose veins, carry a prevalence of 2–56% worldwide.[2] Varicose veins should not be confused with reticular veins or telangiectasias as the treatment modalities differ. Varicose veins are dilated, palpable subcutaneous veins generally larger than 3 mm; reticular veins are dilated nonpalpable subdermal veins 1–3 mm in size; telangiectasias are dilated intradermal venules less than 1 mm.[3] While millions of individuals seek medical attention annually for cosmetic management of their varicose veins, as an early clinical finding on the continuum of CVI, treatment of symptomatic varicose veins is indicated for reasons other than appearance.

Risk factors associated with CVI and varicose veins have been well described. A strong familial relationship for varicose veins has been demonstrated in multiple studies.[2,4–8] However, with the exception of a few congenital disorders associated with varicose veins (e.g., Klippel–Trenaunay syndrome and Chuvash polycythemia), no specific gene has been identified with the development of varicose veins.[4] Increased age and female gender have also been demonstrated to be linked to the development of varicose veins in large epidemiological studies.[9,10] Furthermore, multiparous women have been shown to have a higher risk of developing varicose veins over time, independent of pregnancy-associated weight gain.[6,11] However, obese women are three-times more likely than nonoverweight women to develop and report varicose veins while no such relationship has been shown for men.[12] Finally, occupations that require long periods of standing have been associated with the development of varicose veins.[2,13,14]

The discomfort of varicose veins is often described as fatigue, heaviness or even itching, all of which can be exacerbated following prolonged standing and relieved by leg elevation. However, associated lower extremity edema and hyperpigmentation of the skin are common. In order to create a common objective language by which the clinical manifestations, distribution and underlying pathophysiology of CVI could be universally understood the Clinical, Etiology, Anatomic and Pathophysiology (CEAP) classification of CVI was developed (Table 1). CEAP was created by an international consensus to provide uniformity in reporting, diagnosing and treating CVI.[3]

The venous anatomy of the lower leg is made up of two axial systems, a superficial and a deep venous system. The superficial system lies above the muscle fascia in the subcutaneous tissues. The principal veins in the superficial system are the great saphenous vein (GSV) and the small saphenous vein (SSV). The GSV runs from the medial ankle to the groin, joining the common femoral vein at the saphenofemoral junction. The SSV runs from the lateral ankle to the level of the knee where it drains into the popliteal vein at the saphenopopliteal junction. The axial deep veins lie deep within the fascial compartments and run in parallel with the major named arterial structures. The below knee deep vein coalesce to form the popliteal vein, followed by the femoral vein, common femoral vein and iliac vein. In addition, the profunda femoris vein drains the upper leg and serves as a tributary to the common femoral vein. The deep and superficial systems are interconnected by fascial piercing perforator veins. It is generally regarded that the deep system is a system of high pressure as it is subject to the calf muscle pump responsible for pumping blood back to the heart. As pressure increases during calf muscle contraction, blood is forced upwards toward the heart. A series of one-way bicuspid valves prevents refluxing of blood back into the leg. As blood is ejected from the deep veins, venous pressure drops allowing blood to flow from the superficial system through the perforator veins, once again filling the deep system. During calf muscle contraction, one-way valves in the perforator veins prevent back flow of blood into the superficial system (Figure 1A).

Figure 1.

Pathophysiology of valvular reflux and chronic venous insufficiency. (A) The function of a normal valve, as opposed to a nonfunctional valve. (B) The relationship between the perforating veins and valves and the deep and superficial venous systems, both competent and incompetent valves.
Images courtesy of Section of Vascular Surgery University of Michigan with permission.

CVI occurs when this normal flow of blood back to the heart is disrupted secondary to venous valve incompetence or venous obstruction. Valvular incompetence can occur at all three levels, deep, superficial and perforator. When valvular reflux occurs at the saphenofemoral junction, saphenopopliteal junction or perforator veins, high pressure occurs in the superficial system. High pressure within the superficial system leads to venous dilation, which contributes to superficial valve incompetence. As a result of superficial valve incompetence, high pressure is transmitted to small subcutaneous veins, which become dilated tortuous clusters of varicose veins (Figure 1B).

Although valve reflux contributes to the underlying pathophysiology of varicose veins, the cause of primary valve failure is less understood. There is no consensus as to whether primary valve incompetence is the inciting event in varicose veins or rather incompetence results from persistent vein wall dilation. Clearly, there are abnormalities in the vein wall in varicose veins that may be independent of valvular reflux and be related to their development. Secondary valve failure may occur in the setting of direct injury, phlebitis or venous hypertension due to proximal obstruction. In this setting, proximal obstruction may be the result of compression from the May–Thurner syndrome, or deep venous thrombosis. Independent of obstruction, deep venous thrombosis has the potential to cause secondary valve failure by direct damage to the valve or fibrosis of the vein wall, preventing the ability of the valve mechanism to remain competent.[1]

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