Epidemiology

Varicose veins (VVs) are tortuous, dilated, bulging, superficial veins typically measuring 4 mm or larger.¹ Varicose veins are the most common manifestation of chronic venous insufficiency (CVI) and affect up to 25% of women and 15% of men.^1,2 In the Framingham Study, which includes men and women between the ages of 30 and 62 from the town of Framingham, Massachusetts, the annual incidence of VVs is 2.6% among women and 1.9% among men.³ Risk factors include female gender, advancing age, family history, pregnancy, prolonged standing, obesity, vascular malformations, and hormone therapy.^1,4 Varicose veins are more common in patients of European ancestry compared to Blacks or Asians.³ Approximately 4% of the women presenting with VVs have pelvic vein reflux as the underlying etiology.⁵ Pregnancy and deep venous reflux are also associated with VV recurrence after treatment.⁴

Other patterns of venous pathology include reticular veins, which are smaller, 1- to 3-mm diameter, flat, blue-green colored, less tortuous veins.¹ Telangiectasias, or spider veins, are 1 mm or less, and blue, black, purple, or reddish in appearance.¹ A cross-sectional study of a random sample of 1566 subjects 18 to 64 years of age from the general population in Scotland found that telangiectasias and reticular veins were each present in approximately 80% of men and 85% of women.⁶

The chronic nature of VVs has a major impact on healthcare resources. It is estimated that venous ulcers cause the loss of approximately 2 million working days annually, generating a cost of more than $3 billion per year in the United States alone.³ Moreover, beyond the purely economical impact of VVs, chronic venous disease is associated with reduced quality of life, with particularly negative impact on pain, physical function, and mobility measures.³ The same is true for patients who develop venous ulcers, with effect on quality of life directly related to severity of disease.³

Anatomy

Broadly, the veins of the lower extremity are divided into three systems confluent in a single network, which ultimately drains into the external iliac vein. This venous network includes the superficial veins, deep venous system, and their mutual connections, as well as the perforators (Fig. 54-1). The deep compartment includes the deep venous system and it is bordered by the fascia muscularis. The superficial compartment is externally bordered by the dermis.⁷ The tissue situated under the dermis is called the tela subcutanea (subcutaneous tissue) and contains the saphenous vein. Within the superficial compartment, a narrow anatomical space called the saphenous compartment can be identified by ultrasound evaluation. Externally bordered by the saphenous fascia, this compartment covers the proper venae saphenae and their beginnings. The term perforating veins or perforators is reserved only for those veins that penetrate the fascia muscularis to connect the superficial system to the deep venous system. Conversely, communicating veins connect veins of the same venous system.

Figure 54-1 Lower-extremity venous anatomy schematics.

GSV, great saphenous vein; SSV, small saphenous vein.

The great saphenous vein (GSV) is the longest vein in the entire human body. It starts at the medial side of the foot and courses proximally along the medial side of the calf as the marginal medial vein together with the saphenous nerve.⁷ The main tributaries are the posterior accessory GSV and the anterior accessory GSV. The vein continues alone on the medial side of the thigh and crosses through the saphenous hiatus into the common femoral vein. The normal caliber of the GSV is 3 to 4 mm, and it has 10 to 20 valves.⁷ The GSV is bifid in about 20% of legs, but two venous trunks of the GSV in the same compartment, constituting a true duplication, occurs in only 1% of cases. The small saphenous vein (SSV) is the second largest vein of the lower limb. It begins on the lateral side of the foot dorsum and runs along the lateral margin of the foot as the lateral marginal vein. It penetrates the popliteal fascia into the popliteal vein. In one third of cases, blood flows via various communicating veins to the system of the great saphenous. In one tenth of cases, it flows via the gastrocnemii veins and perforating veins into the deep venous system. The SSV is usually 3 mm wide and contains 7 to 13 valves. It is accompanied by the small saphenous artery, which must not be confused with the vein during sclerotherapy injection.⁷

Some of the perforating veins are consistently located. The thigh perforators include the medial thigh (formerly Hunter’s perforator), anterior thigh, lateral thigh, and posterior thigh perforating veins, and the pudendal perforating vein. The knee perforators include the medial knee (formerly Boyd’s perforator), suprapatellar, lateral knee, infrapatellar, and popliteal fossa perforating veins. The leg perforators include the paratibial, posterior tibial (formerly Cockett’s perforating vein), anterior leg, lateral leg, and posterior leg (medial and lateral gastrocnemius, intergemellar, para- Achillean) perforating veins. Other groups include the gluteal, ankle, and foot perforating veins. The perforator system does play a key role in calf muscle pump function (Fig. 54-2A).

Figure 54-2 Calf “muscle pump” and varicose veins (VVs).

A, Normal calf muscle pump physiology during relaxation and contraction. B, Deep vein obstruction heralds perforator vein incompetence and associated secondary VV. C, Conversely, deep venous system and perforator system are independent of primary VV. CVI, chronic venous insufficiency.

(Adapted from Sumner DS: venous dynamics–varicosities. Clin Obstet Gynecol 24:743–760, 1981.)

A system of subcutaneous veins spreads on the lateral aspect of the thigh and leg as a developmental remnant of the embryonic lateral marginal vein, which fades out and is replaced with the system of the saphenous veins and may be abnormally developed in patients with Klippel-Trénaunay’s or Parkes-Weber’s syndromes. In relation to the surface, there are three levels of venous plexuses: dermal, hypodermal, and deep. The dermal veins involve the superficial subpapillary venous plexus and the deep dermal venous plexus⁷ (Fig. 54-3).

Figure 54-3 Venous drainage of the lower limb.

(Adapted from Kachlik D, Pechacek V, Baca V, Musil V: The superficial venous system of the lower extremity: new nomenclature. Phlebology 25:113–123, 2010.)

Pathogenesis

Varicose veins are caused by weakness in the vein wall, and according to their underlying etiology can be divided into primary or secondary. Primary VVs result from idiopathic structural or functional defects in the venous system. Secondary VVs result from underlying venous obstruction, most commonly deep vein thrombosis (DVT) or underlying deep venous insufficiency¹ (see Fig. 54-2B-C). Primary valvular incompetence is more frequent. Approximately 8 in 10 individuals with VVs have primary valvular incompetence. Secondary valvular reflux is usually due to trauma or thrombosis. Congenital anomalies only occur in about 2% of cases.³ Secondary chronic venous disease progresses faster than primary.

A key factor in the development of VVs is venous hypertension. Venous pressure is directly proportional to the weight of the column of blood from the right atrium to the foot and is reduced by pressures generated by muscle contractions. When standing, venous pressure is as high as 90 mmHg. It temporarily increases with muscle pumping, but then rapidly decreases as the functioning venous valves guide blood flow toward the heart. A well-functioning calf muscle pumping mechanism decreases the venous pressure to less than 30 mmHg.³ The constant insult of increased venous pressure degenerates in stretching, splitting, tearing, thinning, and adhesion of valves, causing inflammation.³ Adjuvant factors for development of excessive venous hypertension include failure of the calf muscle pump and obesity. Ultimately, prolonged venous hypertension leads to venous valvular incompetence or reflux and venous dilation.¹ Venous defects increase venous hypertension and cause weakened venous walls, abnormal distention of the surrounding connective tissue, and separation of valve cusps.

Elevated venous pressure may also generate edema. Prominent swelling is not a usual feature of VVs, but episodic ankle edema is common.⁸ A small percentage of patients develop complications including dermatitis, superficial thrombophlebitis, or bleeding. Thrombophlebitis may occur spontaneously or result from an injury. Skin changes in chronic venous disease are proportionately related to the severity of venous hypertension. Up to 100% of patients with postexercise venous pressures of more than 90 mmHg develop venous ulcers.³ Patients with CVI and deep vein incompetence are at greatly increased risk of developing ulcers.⁹ Conversely, frequent dorsiflexion of the ankle and an effective calf muscle pump are protective factors (see Fig. 54-2A). Poor prognostic factors favoring progression include the combination of reflux and obstruction, ipsilateral recurrent DVT, and multisegmental involvement.¹⁰

Inflammatory changes also contribute to the genesis of VVs. Blood returning from feet that have been passively dependent for 40 to 60 minutes is depleted of leukocytes, suggesting that leukocytes accumulate and locally participate in the inflammatory cascade.³ Circulating leukocytes and vascular endothelial cells (ECs) express several types of adhesion molecules. Integrin binding promotes firm adhesion of leukocytes, the starting point for their migration out of the vasculature and degranulation. The activated leucocytes shed L-selectin into the plasma and express members of the integrin family.³ This is the backbone of the microvascular leukocyte-trapping hypothesis. Local inflammation associated with intercellular adhesion molecule (ICAM)-1 expression increases monocyte and macrophage adhesion. The valve damage is augmented by disturbed excessive collagen type 1 synthesis, which increases venous rigidity.³ Finally, matrix metalloproteinases (MMPs) and serine proteinases favor the accumulation of extracellular matrix (ECM) material in VVs.^3,11

Clinical Manifestations

Clinical manifestations of VV range from cosmetic problems to severe symptoms, including ulceration. Chronic venous insufficiency can be classified by clinical presentation, etiology, anatomy, and pathophysiology (CEAP Classification)^8,12 (see Chapter 55). Clinically, however, the patterns may be classified as complicated and uncomplicated varices. Uncomplicated VVs may need only cosmetic treatment or reassurance. Patients with complicated VVs may develop heaviness, fatigue, local pain, spontaneous bleeding, and superficial thrombophlebitis. Varicose veins may cause edema, pain, and skin changes such as stasis dermatitis and ulceration. Venous ulcerations can take more than 9 months to heal, with one study reporting that 66% of ulcers last longer than 5 years.¹ All these symptoms impair activities of daily living.¹

Multiple questionnaires and instruments measure the effect of venous disease on quality of life. Most are subjective and completed by the patient. The Chronic Venous Insufficiency Questionnaire (CIVIQ) was validated in a sample of 2001 patients and measures the psychological, social, physical, and pain domains. A revised version of the instrument, the CIVIQ 2, equally weighted the categories across 20 questions to provide a global score. This measure is used to follow quality-of-life (QOL) improvement after therapy for chronic venous insufficiency, including VVs. The Aberdeen Varicose Vein Questionnaire (AVVQ) includes 13 questions on physical symptoms and social issues, including pain, ankle edema, ulcers, compression therapy use, and the effect of VVs on daily activities. The disease- specific index is graded from 0 to 100 (extreme venous symptoms).¹³ This measure has also been validated for patient follow-up after intervention.¹⁴ The Venous Insufficiency Epidemiological and Economic Study (VEINES) instrument consists of 35 items in two categories to generate two summary scores. It includes the VEINES-QOL, with 25 QOL questions, and the VEINES-Sym, with 10 symptom questions.¹⁴ The focus of this measure is on physical symptoms of venous disease, in particular postthrombotic syndrome. It has been validated in patients with DVT. In 2004, Kahn et al. compared the VEINES and the 36-item Short-Form Health Survey (SF-36) with CEAP classification in 1531 patients from four countries to examine the effect of patient-related QOL reporting on interpreting outcomes in venous studies. Higher CEAP class was directly associated with and predictive of the VEINES-QOL.¹⁴ The Charing Cross Venous Ulceration Questionnaire (CXVUQ) was developed for patients with venous ulcers, and its performance is not impaired by the treatment option selected.¹⁴ Finally, the Venous Severity Score (VSS) system was derived from the CEAP classification and has three elements: the venous disability score (VDS), venous segmental disease score (VSDS), and venous clinical severity score (VCSS). The VCSS has been recently revised and includes multiple parameters: pain, VVs, inflammation, edema, skin induration, pigmentation, ulcers (size, number, duration), and compression therapy.¹⁵ The Venous Clinical Severity Score is useful for following changes with treatment.^14,15

Physical Examination

Initial inspection of the leg may reveal edema, prominent VVs, cyanosis, plethora, hyperpigmentation, lipodermatosclerosis, or ulcerations. On inspection, VVs may be observed as tortuous, dilated, bulging, superficial veins measuring 4 mm or larger; the patient is ideally examined in the standing position to allow venous reflux.¹Lipodermatosclerosis is a consequence of localized chronic inflammation and fibrosis of the skin and subcutaneous tissue of the lower part of the leg.¹⁶ The skin changes will often occur at the “gaiter area” above the medial malleolus. Atrophie blanche is a localized circular, whitish, avascular, atrophic skin area surrounded by capillaries and sometimes hyperpigmentation, consistent with severe chronic venous insufficiency. Similarly, a phlebectatic crown (fan-shaped small intradermal veins on medial or lateral aspects of the foot) may herald severe venous insufficiency.

Trendelenburg and Perthes tests may be used during the exam to differentiate superficial from deep venous insufficiency (also see Chapter 55). In the Trendelenburg test, the leg is elevated and a tourniquet applied above the knee. This obstructs the superficial veins, which will promptly fill after standing if the patient has deep vein incompetence (secondary VVs). If after standing, the vein requires more than 20 seconds to refill, but prompt filling follows tourniquet removal, the exam is consistent with primary VVs. In the Perthes test, the leg is elevated and the tourniquet placed at the midthigh or proximal calf. When the patient stands and walks, the VVs will refill owing to incompetent perforators¹⁶ (Figs. 54-4 and 55-5). These maneuvers may be complemented with Brodie Trendelenburg percussion: a finger is placed over the distal area of a VV while the proximal segment of the vein is percussed. A transmitted impulse at the lower end suggests incompetence.

Figure 54-4 Physical examination of varicose veins (VVs).

A, Medial great saphenous vein (GSV) VVs are observed on a right leg. B, Limb is elevated and tourniquet positioned above knee; with tourniquet applied and patient standing, VVs are not evident. This is suggestive of primary venous incompetence.

Figure 54-5 Physical examination of varicose veins (VVs).

A, Leg is elevated so VVs are drained. B, Return of VVs only after tourniquet is removed. C, Findings suggestive of incompetent perforator veins, consistent with secondary varicosities.

Imaging and Physiological Testing

Duplex ultrasonography is useful in the evaluation of VVs (also see Chapter 12). The test is performed with the patient standing or in reverse Trendelenburg position, and is used to detect acute or chronic thrombosis, postthrombotic changes, obstructive flow, and incompetence in the deep veins. Reflux, demonstrated by reversal of flow, is pathological whenever longer than 0.5 seconds.¹⁷ Duplex ultrasonography is not reliable for assessment of the iliac and caval veins, but it is sensitive for evaluation of saphenous vein reflux and useful for identification of incompetent perforator veins.

Impedance plethysmography, strain gauge plethysmography, and air plethysmography may be used to detect venous obstruction and reflux in large veins above the knee. Photoplethysmography, most commonly used with and without a tourniquet, can be employed to evaluate superficial venous insufficiency. A venous refilling time less than 20 seconds without a tourniquet that normalizes to over 20 seconds with a tourniquet is compatible with GSV incompetence.¹⁷

Venography may provide information regarding pelvic vein obstruction in patients with postthrombotic disease.¹⁶ Ascending venography is performed with the patient at 45 degrees, non–weight- bearing, with legs down as contrast is infused. Contrast filling the superficial vein denotes incompetence. Ascending venography is useful to determine vein obstruction, collateralization, and recanalization. Descending venography is more useful to diagnose venous insufficiency. In this scenario, the contrast is injected into the common femoral vein above the saphenofemoral junction. The patient is initially in supine position, and after the contrast dye injection, the table is tilted feet downward. Contrast leakage to the knee or distally is abnormal.¹⁷ Venography is usually indicated in the setting of endovenous intervention, but is difficult in the setting of a swollen leg. There is limited experience with magnetic resonance venography (MRV) or computed tomography (CT) to evaluate venous insufficiency and VVs.

Management

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