Pathology

The precise pathophysiology of venous insufficiency has yet to be elucidated. This describes some of the areas in which research has started to reveal its multifactorial pathogenesis.

Mechanical Abnormalities

Anatomic differences in the location of the superficial veins of the lower extremities may contribute to the pathogenesis. Primary venous insufficiency may involve both the axial veins (great and small saphenouss), either, or neither. Perforating veins may be the sole source of venous pathophysiology, perhaps because the great saphenous vein is supported by a well-developed medial fibromuscular layer and fibrous connective tissue that bind it to the deep fascia. In contrast, tributaries to the small saphenous vein are less supported in the subcutaneous fat and are superficial to the membranous layer of superficial fascia (Fig. 65-4). These tributaries also contain less muscle mass in their walls. Thus, these veins, and not the main trunk, may become selectively varicose.

FIGURE 65-4 Dilation of superficial venous tributaries caused by increased transmission of pressure by the perforating veins.

When these fundamental anatomic peculiarities are recognized, the intrinsic competence or incompetence of the valve system becomes important. For example, failure of a valve protecting a tributary vein from the pressures of the small saphenous vein allows a cluster of varicosities to develop. Furthermore, communicating veins connecting the deep with the superficial compartment may have valve failure. Pressure studies have shown that there are two sources of venous hypertension. The first is gravitational and is a result of venous blood coursing in a distal direction down linear axial venous segments. This is referred to as hydrostatic pressure and is the weight of the blood column from the right atrium. The highest pressure generated by this mechanism is evident at the ankle and foot, where measurements are expressed in centimeters of water or millimeters of mercury. The second source of venous hypertension is dynamic. It is the force of muscular contraction, usually contained within the compartments of the leg. If a perforating vein fails, high pressures (range, 150 to 200 mm Hg) developed within the muscular compartments during exercise are transmitted directly to the superficial venous system. Here, the sudden pressure transmitted causes dilation and lengthening of the superficial veins. Progressive distal valvular incompetence may occur. If proximal valves such as the saphenofemoral valve become incompetent, systolic muscular contraction is supplemented by the weight of the static column of blood from the heart. Furthermore, this static column becomes a barrier. Blood flowing proximally through the femoral vein spills into the saphenous vein and flows distally. As it refluxes distally through progressively incompetent valves, it is returned through perforating veins to the deep veins. Here, it is conveyed once again to the femoral veins, only to be recycled distally.

Molecular Abnormalities

On a molecular level, several abnormalities have been identified in extremities that manifest venous hypertension. Fundamental defects in the strength and characteristics of the venous wall have been identified. Varicose veins demonstrate decreased amounts of elastin and collagen, suggesting a contributing role toward venous pathophysiology.³

Risk Factors

Risk factors for the development of varicose veins include advancing age, female gender, heredity, and history of trauma to the extremity. Venous function is undoubtedly influenced by hormonal changes. In particular, progesterone liberated by the corpus luteum stabilizes the uterus by causing the relaxation of smooth muscle fibers.² This directly influences venous function. The result is passive venous dilation, which in many cases causes valvular dysfunction. Although progesterone is implicated in the first appearance of varicosities in pregnancy, estrogen also has profound effects. It produces the relaxation of smooth muscle and a softening of collagen fibers. Furthermore, the estrogen-to-progesterone ratio influences venous distensibility. This ratio may explain the predominance of venous insufficiency symptoms on the first day of a menstrual period, when a profound shift occurs from the progesterone phase of the menstrual cycle to the estrogen phase. Although heredity is widely acknowledged as a risk factor for varicose vein development, the precise genetic mechanism has yet to be elucidated.

Symptoms

Venous valvular dysfunction causes venous hypertension and, as such, patients’ symptoms are attributed to excess venous pooling. The patient with symptomatic varicose veins commonly reports heaviness, discomfort, and extremity fatigue. The pain is characteristically dull, does not usually occur during recumbency or early in the morning, and is exacerbated in the afternoon, especially after periods of prolonged standing. Swelling is commonly described. The discomforts of aching, heaviness, and/or fatigue are usually relieved by leg elevation or elastic support. Cutaneous burning, termed venous neuropathy, can also occur in patients with advanced venous insufficiency. Pruritus occurs from excess hemosiderin deposition and tends to be located at the distal calf or in areas of phlebitic varicose branch segments.

Physical Examination

A comprehensive examination includes assessment of the arterial circulation. Briefly, palpation of the femoral, popliteal, dorsalis pedis, and posterior tibialis pulses is performed. Nonpalpable pulses necessitate further evaluation. Auscultation of pulse flow is indicated when a thrill or widened pulse is appreciated. Demonstration of decreased hair, dependent rubor, pallor on elevation, and tissue loss are all indicative of advanced arterial ischemia.

The venous examination includes assessment of the patient in the standing and supine positions. Standing increases venous hypertension and dilates veins, thereby facilitating examination. Patients with superficial axial incompetence commonly exhibit palpable great saphenous veins (Fig. 65-5). Palpable cords may be present. Visual inspection is critical. Signs of advanced venous insufficiency include hyperpigmentation in the gaiter distribution, secondary to hemosiderin deposition, and lipodermatosclerosis. Lipodermatosclerosis develops over time, due to prolonged ambulatory venous hypertension and chronic inflammation. Physical examination findings that reflect lipodermatosclerosis are: brawny edema of the distal calf, “champagne bottle leg,” fibrotic, hypertrophic skin, and hyperpigmentation. Advanced lipodermatosclerosis may involve fibrosis of the Achilles tendon, impairing motor function of the extremity. Atrophie blanche is an area of pale hue, visualized around the medial malleolus; it is commonly mistaken for a healed ulcer because of its lighter pigmentation (Fig. 65-6). Corona phlebectica is a term used to describe an accumulation of tiny telangiectasias or venous flare, usually located at the medial malleolus.

FIGURE 65-5 Varicose veins.

FIGURE 65-6 Lipodermatosclerosis, atrophie blanche, and brawny edema.

Venous stasis ulcers exhibit pathognomonic features that distinguish them from their arterial or neuropathic counterparts. Venous ulcers are not generally painful and appear at the medial malleolus, not in the mid to distal foot. Lack of arterial pulses in patients with a venous ulcer isunusual.

Venous stasis dermatitis is visualized at the distal ankle and can mimic eczema or dermatitis of another cause. It is this important attention to supporting features of the physical examination and history, as well as confirmation with duplex reflux examination, that will distinguish advanced venous stasis disease from dermatologic conditions.

Diagnostic Evaluation of Venous Dysfunction

The Perthes test for deep venous occlusion and Brodie-Trendelenburg test of axial reflux have been replaced by in-office use of the continuous wave, hand-held Doppler instrument supplemented by duplex evaluation. The hand-held Doppler instrument can confirm an impression of saphenous reflux, which in turn dictates the operative procedure to be performed in a given patient. A common misconception is the belief that the Doppler instrument is used to locate perforating veins. Instead, it is used in specific locations to determine incompetent valves—for example, the hand-held, continuous wave, 8-MHz flow detector placed over the greater and lesser saphenous veins near their terminations. With distal augmentation of flow and release, normal deep breathing, and performance of a Valsalva maneuver, valve reflux is accurately identified. Formerly, the Doppler examination was supplemented by other objective studies, including photoplethysmography, mercury strain gauge plethysmography, and photorheography. These are no longer in common use.

Another instrument reintroduced to assess physiologic function of the muscle pump and venous valves is air displacement plethysmography.⁴ Its use was discontinued after the 1960s because of its cumbersome nature. Computer technology has now allowed its reintroduction, as championed by Christopoulos and colleagues.⁵ It consists of an air chamber that surrounds the leg from knee to ankle. During calibration, leg veins are emptied by leg elevation and the patient is then asked to stand so that leg venous volume can be quantitated and the time for filling recorded. The filling rate is then expressed in milliliters per second, thus giving readings similar to those obtained with the mercury strain gauge technique.

Duplex technology more precisely defines which veins are refluxing by imaging the superficial and deep veins. The duplex examination is commonly done with the patient supine, but this yields an erroneous evaluation of reflux. In the supine position, even when no flow is present, the valves remain open. Valve closure requires a reversal of flow with a pressure gradient that is higher proximally than distally. Thus, the duplex examination needs to be done with the patient standing or in the markedly trunk-elevated position.^6,7

Imaging is obtained with a 7.5- or 10-MHz probe; the pulsed Doppler consists of a 3.0-MHz probe. The patient stands, with the probe placed longitudinally on the groin. After imaging, sample volumes can be obtained from the femoral and saphenous veins. This flow can be observed during quiet respiration or distal augmentation. Sudden release of augmentation allows the assessment of valvular competence. The small saphenous vein and popliteal veins are similarly examined. Reflux times of 3 seconds or longer is considered significant. Perforator veins can be visualized well with the duplex examination. Demonstration of duplex images of to and fro flow, with the presence of dilated segments, constitutes findings compatible with a refluxing perforator. Additionally, Doppler studies can provide the clinician with information about the deep system. Widespread use of duplex scanning has allowed a comparison of findings between standard clinical examinations and duplex Doppler studies.⁸

Classification Systems

In 1994, the American Venous Forum devised the CEAP classification system, which is a scoring system that stratifies venous disease based on clinical presentation, etiology, anatomy, and pathophysiology (Table 65-3). It is useful in helping the physician assess a limb afflicted with venous insufficiency and then arrive at an appropriate treatment plan. A revised CEAP was introduced that included a venous disability score (VDS) to document a patient’s ability to perform activities of daily living.⁹ Although the CEAP classification is a valuable tool to grade venous disease, assessment of outcomes following intervention cannot be realized. As a result, two additional scoring systems, the venous clinical severity scoring system (VCSS) and venous segmental disease score (VSDS), enhance the CEAP score with the increased ability to plot outcome. These three classification modalities now provide clinical researchers with invaluable tools to study treatment outcomes.¹⁰

Table 65-3 Classification of Chronic Lower Extremity Venous Disease