Lower extremity venous disease is extremely common, with varicose veins remaining the most frequently encountered venous condition followed by chronic venous insufficiency.^1,2 The two conditions often occur together, but each condition may also be present clinically without the other. Lower extremity venous disease comprises a clinical spectrum ranging from completely asymptomatic telangiectasias to symptomatic varicose veins to debilitating venous ulcers.^1,2 The most frequently encountered symptoms associated with varicose veins include leg swelling, pain, itching, nocturnal cramping, and leg heaviness. Patients with chronic venous insufficiency often present with leg edema, skin hyperpigmentation, stasis dermatitis of the skin involving the ankles, fibrosis of the subcutaneous fat (lipodermatosclerosis), and ulceration.^1,2 Lower extremity venous ulceration remains a significant worldwide health problem resulting in significant morbidity.^1,2

Deep venous thrombosis (DVT) of the lower extremities is another highly prevalent venous condition encountered by health care providers of all disciplines.³ Much has been published regarding venous thromboembolic disease^4,5,6,7,8; therefore, the content of this chapter is limited to the intrinsic venous disorders of the lower extremities.

Prevalence estimates of lower extremity venous disease vary widely by geographic location, with the highest reported rates observed in Western countries. The variability in estimates is likely attributable to population differences in risk factor distribution, methods of measurement, variability in diagnosis, and disease definition.^1,2,9,10 The prevalence of lower extremity varicose veins is estimated to be as high as 56% in men and 73% in women.^9,10 The prevalence of chronic venous insufficiency is estimated to be as high as 17% in men and 40% in women.¹⁰ Lower extremity venous ulceration has been reported to occur in approximately 0.3% to 1% of the adult population worldwide.^9,11

Risk factors associated with the development of lower extremity venous disease are listed in Table 30-1. Family history, female gender, age, and pregnancy have been well established as risk factors for developing varicose veins.^9,10 These risk factors have also been shown to contribute to the development of chronic venous insufficiency.^9,10 Regarding the development of venous ulceration, in addition to the risk factors shown in Table 30-1, history of lower extremity phlebitis, lower extremity trauma, DVT, and congestive heart failure have been shown to be associated with the development of venous ulceration.¹¹

Chronic venous insufficiency with venous ulceration is extremely prevalent in the United States and is also the seventh leading cause of chronic debilitating disease.² Approximately 10% to 35% of the U.S. population has some form of chronic venous insufficiency.^1,2 More than 500,000 men and women experience chronic venous ulcers.^1,2,11 Venous ulcers are associated with significant health care costs and substantial economic effects in terms of days of work lost and diminished quality of life.^2,11 The population-based cost in the United States for treatment of chronic venous insufficiency and venous ulcers has been estimated to be more than $1 billion a year.² In addition, more than 6 million days of work are lost each year because of complications associated with chronic venous ulcers.¹¹ Furthermore, patients’ quality of life is significantly impacted by the loss of workdays and debilitating symptoms.^2,11

The development of the blood vessels occurs between the third and eighth weeks of embryonic gestation.¹² The primitive circulation begins to develop toward the end of the third week after appearance of the newly fused heart. This is followed by rapid changes in the fourth week when extensive remodeling occurs and continues through the final month of the embryonic period.¹² Development at the cephalad end of the embryo proceeds more rapidly than at the caudal end as the arteries and veins change and interact with the growing thoracoabdominal organs, parietes, and extremities.¹²

Primitive vascular channels appear in the limb during the third gestational week, when a capillary network is initially present during the undifferentiated stage.¹³ This is followed by large plexiform structures present during the retiform stage, and finally, large channels, arteries, and veins appear during the maturation stage.^12,13

The earliest veins that develop are the vitelline veins from the yolk sac, the umbilical veins from the chorion, and the cardinal veins from the body proper.¹² Venous developmental changes are more complex than arterial changes and involve additions, deletions, interconnections, positions, and flow changes.¹² The vitelline and umbilical veins eventually become the hepatic sinusoids, hepatic veins, portal vein, superior mesenteric vein, and left umbilical vein.¹² The paired cardinal veins undergo a series of changes leading to the mature venous drainage of the body.^12,13 The left-sided cardinal veins regress, leaving the right-sided veins, which become the superior vena cava (SVC) and inferior vena cava (IVC) (Figure 30-1).^12,13 The distal ends of the post cardinal veins persist after regression and eventually become the iliac veins.

Persistence of the left subcardinal vein results in a double IVC in as many as 2% to 3% of individuals and a single left-sided IVC in 0.2% to 0.5%.^13,14 Renal vein anomalies include a retroaortic left renal vein (2%) with or without a normal anterior left renal vein and a circumaortic renal collar (1%).^13,14

Persistence of embryonic veins after birth results in venous malformations of the pelvis and lower extremities.¹³ The marginal vein, often seen in patients with Klippel-Trenaunay syndrome, is a persistent large, lateral, superficial embryonic vein that contributes to the development of chronic venous insufficiency.¹³ Other developmental anomalies include a persistent sciatic vein, valvular agenesis, venous aneurysms, and primary valvular insufficiency.¹³

The muscle fascia divides the lower extremity soft tissues into a superficial compartment and deep compartment (Figure 30-2). The venous system of the lower extremities include both the deep veins that lie below the muscular fascia and drain blood directly into the IVC and the superficial veins that lie above the muscular fascia and drain the superficial compartment. The saphenous fascia covers the saphenous subcompartment and separates the great saphenous vein and small saphenous vein from other veins in the superficial compartment. Connecting the two venous systems are the perforating veins that traverse the muscular fascia and normally drain blood from the superficial system into the deep venous system (see Figure 30-2).¹⁵ Also present within the superficial compartment is the reticular venous plexus and subpapillary venous plexus. Communicating veins connect veins within the same compartment.¹³ The deep, superficial, and most perforating veins contain bicuspid valves that maintain unidirectional venous flow. The nomenclature of the lower extremities veins has recently been updated (Table 30-2).^13,15

The deep veins comprise the venous component of the neurovascular bundle of the lower extremities. The deep veins are adjacent to the similarly named arteries and often occur as paired structures at the popliteal, calf, and ankle levels (Figure 30-3).^13,15 The major pelvic veins include the common iliac, internal iliac, and external iliac veins, all of which drain directly into the IVC. The overlying right common iliac artery may compress the left common iliac vein, resulting in left iliofemoral vein thrombosis (May-Thurner syndrome), which is often caused by a chronic stenosis or occlusion of the vein.¹³

The superficial veins include the subpapillary venous plexus, the reticular venous plexus, and all of the veins in the superficial compartment (see Figure 30-2). The great saphenous vein and its tributaries comprise the major superficial venous system of the thigh and medial leg (Figure 30-4). The small saphenous vein and its tributaries comprise the major superficial venous system of the lateral leg (see Figure 30-4). The great saphenous vein drains into the common femoral vein at the confluence of the superficial inguinal veins (formerly known as the saphenofemoral junction). The confluence of the superficial inguinal veins is made up of the great saphenous vein, superficial circumflex iliac, superficial epigastric, and external pudendal veins.^13,15 The small saphenous vein originates from the lateral side of the foot and drains into the popliteal vein. Below the level of the gastrocnemius muscle, the small saphenous vein runs adjacent to the sural nerve, which is prone to injury during surgical stripping procedures.

The perforating veins traverse the muscle fascia connecting the superficial venous system to the deep venous system (Figure 30-5). Competent valves within the perforating veins ensure superficial to deep, unidirectional flow in the calf and thigh. Perforating vein valvular incompetence may result in venous congestion, varicosities, and chronic skin changes, including ulceration.^1,2,13,15 The most important perforating veins of the lower extremity are the medial calf perforators.^13,15 There are two main groups of medial calf perforators, the posterior tibial and the more proximal paratibial perforating veins. The posterior tibial perforating veins (Cockett perforators) connect the posterior accessory great saphenous vein with the posterior tibial veins (see Figure 30-5).

The CEAP (clinical, etiology, anatomy, pathophysiology) classification of chronic venous disorders was developed and adopted worldwide to facilitate meaningful communication about chronic venous disorders and to serve as a basis for more scientific analysis of treatment alternatives.^16,17 An international ad hoc committee of the American Venous Forum developed the first CEAP consensus document in 1994.¹⁶ This document was later revised in 2004.¹⁷

The CEAP classification includes a description of the clinical class (C) based on objective findings—the etiology (E); the anatomical (A) distribution of the affected veins in the superficial, deep, and perforating venous systems; and the underlying pathophysiology (P), which is attributable to reflux, obstruction, or both (Table 30-3).¹⁷ Basic CEAP classification designates only the highest clinical (C) classification based on symptoms. Advanced CEAP clinical classification includes all symptoms present and further designates any of 18 involved venous segments with the pathophysiology (P) (Table 30-4).¹⁷ A symptomatic patient presenting with varicose veins, leg pain, leg edema, and lipodermatosclerosis and is found to have reflux of the great saphenous veins above and below the knees bilaterally, with incompetent calf perforating veins, would have a basic CEAP classification of C_4bs, E_p, A_s,p, P_r, and an advanced CEAP classification of C_2,3,4bs, E_p, A_s,p, P_r2,3,18.

Varicose Veins

Lower extremity varicose veins are extremely prevalent. Varicose veins are dilated, palpable, tortuous superficial veins (usually >3 mm in diameter) that are found beneath the dermis (subcutaneous space) and drain into communicating veins, incompetent tributaries, and truncal (saphenous) veins (see Figures 30-2 and 30-6).¹ Dilatation of the varicose vein results in valvular incompetence. In addition to varicose veins, patients often present with telangiectasias (usually <1mm in diameter) that arise from the subpapillary venous plexus and are found in the dermis.^1,18 Commonly known as spider veins, telangiectasias are dilated postcapillary venules demonstrating backflow from incompetent reticular (feeder) veins or directly from incompetent tributary or truncal veins.¹⁸ Telangiectasias associated with venous insufficiency are usually dark red or blue (see Figure 30-6). Larger bluish vessels that are raised above the skin are termed venulectasias.¹⁸ Reticular veins are flat, incompetent, dilated blue and green veins (usually ≤3 mm in diameter) that arise from the reticular venous plexus and are found in the subdermal space (see Figure 30-6).¹ Reticular veins serve as incompetent feeding veins to telangectasias.¹⁸

Primary varicose veins are those that develop in patients without a previous history of an underlying venous condition. In contrast, secondary varicose veins develop as a result of a prior DVT, congenital venous malformation, or arteriovenous malformation.¹⁹ The majority of patients presenting with varicose veins have primary varicose veins. Approximately 25% to 40% of patients with primary varicose veins report symptoms that include aching, itching, heaviness, tiredness, cramping, and swelling.^2,10,19,20 In the Edinburgh Vein Study, a cross-sectional population study, 32% of women and 40% of men had lower extremity varicose veins, and 19% of all patients were found to have valvular incompetence of the great saphenous vein.^9,10,21 In another study of patients with varicose veins, the vast majority (60%–70%) had valvular incompetence of both the saphenofemoral junction and great saphenous vein.²² Furthermore, superficial venous insufficiency is found in up to 80% of women with varicose veins.²³ The likelihood of concomitant superficial venous insufficiency being present in patients with varicose veins increases with the presence of symptoms.^2,10,19,20 Clearly, a significant percentage of patients presenting with lower extremity varicose veins have underlying venous insufficiency. By definition, dilated, tortuous varicose veins demonstrate valvular incompetence. However, not every patient with primary varicose veins presents with venous insufficiency. Therefore, treatment of patients with primary varicose veins without underlying venous insufficiency should be limited to approaches and procedures that are aimed at treating the varicosities. In contrast, treatment of patients with primary varicose veins associated with underlying venous insufficiency requires treatment of both the varicosities and the underlying chronic venous insufficiency.

Diagnosis. A careful history and physical examination is usually sufficient to make a diagnosis of primary and secondary varicose veins. The clinical evaluation should focus on the patient’s symptoms and cosmetic concerns, the extent and distribution of the varicose veins (including reticular veins and telangiectasias), and the severity and location of the stigmata of chronic venous insufficiency (edema, hyperpigmentation, stasis dermatitis, lipodermatosclerosis, ulceration).¹⁹ Patients should be questioned regarding a family history of varicose veins and their history of DVT and superficial thrombophlebitis as well as the time of onset of varicose veins and progression of symptoms and past and anticipated future pregnancies.¹⁹

Patients with primary varicose veins presenting with secondary skin changes associated with chronic venous insufficiency may be indistinguishable from patients with secondary varicose veins. For proper diagnosis, the sequence of varicose vein development and skin changes is important.¹⁹ Patients with primary varicose veins will report the appearance of varicose veins occurring many years before the onset of the secondary skin changes of chronic venous insufficiency. In contrast, patients with secondary varicose veins may not recall a DVT but do describe having normal legs followed by the development of secondary skin changes and the appearance of varicose veins at a later time.¹⁹

Because a significant percent of patients with primary varicose veins have underlying venous insufficiency, venous duplex ultrasound examination is essential for proper diagnosis and treatment planning. Patients with secondary varicose veins also require a venous duplex ultrasound examination for thorough assessment of the superficial, deep, and perforating venous systems. Diagnosis of venous insufficiency via venous duplex ultrasound examination is discussed in the Chronic Venous Insufficiency section.

Complications. The major complications of varicose veins are thrombophlebitis and bleeding in addition to those complications associated with concomitant venous insufficiency (frequently found in patients with primary varicose veins), which include hyperpigmentation, stasis dermatitis, lipodermatosclerosis, and ulceration.^{1,2,19,21,22,24,25}

Varicose Vein Bleeding. Bleeding associated with varicose veins and venous insufficiency is uncommon and usually occurs from a varix in an area where the overlying skin is thin and prone to breakdown because of long-standing venous insufficiency. The true incidence of bleeding is unknown. Fatal hemorrhage from bleeding varicose veins is exceedingly rare, with only a handful of cases reported in the world’s medical literature.²⁵

Superficial Thrombophlebitis. Thrombophlebitis or superficial thrombophlebitis is thrombosis of the superficial veins, which most often occurs in the veins of the lower extremities but may occur in other areas as well. Thrombophlebitis may occur in both varicose veins and nonvaricose veins, with the saphenous veins and their tributaries being the most commonly affected veins.^26,27 The incidence of thrombophlebitis in patients with varicose veins varies widely in published reports from 4% to 59%.²⁶ Thrombophlebitis presents with pain, erythema, and swelling around a superficial vein that becomes firm and on palpation feels like a cord. Varicose tributaries of the great saphenous vein and small saphenous vein are most commonly affected.²⁸ When thrombophlebitis involves the saphenous trunks, the great saphenous vein is involved in 60% to 80% of cases, and the small saphenous vein in 10% to 20% of cases.²⁶ Because of the risk of thrombus propagation into the deep venous system via the saphenofemoral and saphenopopliteal junctions, development of saphenous thrombophlebitis has a higher risk of DVT and pulmonary embolism.^26,27,28 Propagation into the deep venous system has been reported to occur in 2.6% to 15% of cases.²⁶ In addition, all patients with thrombophlebitis should undergo venous duplex ultrasound examination to determine the extent of the superficial thrombosis and to assess the deep venous system. Furthermore, in patients without a history of varicose veins or an underlying venous condition who develop saphenous thrombophlebitis, thrombophilia and malignancy should be suspected and the appropriate workup performed.²⁶

In the majority of patients with thrombophlebitis, the clinical course is benign and self-limiting with resolution of symptoms in 10 to 14 days. Conservative treatment consists of compression stockings, ambulation, warm compresses, and nonsteroidal antiinflammatory drugs. Failure of conservative treatment or propagation of thrombophlebitis is an indication of anticoagulation.²⁶ In cases of saphenous thrombophlebitis in which thrombosis involves the saphenofemoral or saphenopopliteal junction without extension into the deep vein, surgical treatment with saphenous ligation and anticoagulation are equally good treatment options.²⁶ Saphenous thrombophlebitis propagation into the deep venous system requires standard anticoagulation for DVT.

Treatment. Indications for treatment of varicose veins include patient desire for treatment and symptoms associated with varicose veins, namely pain, edema, leg heaviness, and itching. Thrombophlebitis and bleeding are also indications for varicose vein treatment. The majority of patients with primary varicose veins present with superficial venous insufficiency. Patients with clinically significant venous insufficiency (i.e., hyperpigmentation, stasis dermatitis, lipodermatosclerosis, and ulceration) should also be offered treatment.

Treatment of patients with primary varicose veins without underlying venous insufficiency should be limited to approaches and procedures that are aimed at treating the varicosities. In contrast, treatment of patients with primary varicose veins associated with underlying venous insufficiency requires treatment of both the varicosities and the underlying chronic venous insufficiency. In addition, treatment of secondary varicose veins also requires treatment of the underlying cause of the chronic venous insufficiency (i.e., valvular incompetence or venous obstruction). Treatment of patients with chronic venous insufficiency is discussed in the next section.

Compression Therapy. Graduated compression stockings improve both the symptoms and venous hemodynamics in patients with varicose veins.^29,30 Grade II compression (20–30 mm Hg) is recommended and has been shown to confer maximal relief of varicose vein symptoms.^29,30 The benefit of the compression therapy depends on the compliance of the patient.³⁰ Compliance is variable and difficult to assess.²⁴ In addition, compression stockings not only provide symptom relief but may also prevent progression of the venous disease.^29,30 In the Bonn Vein Study, a cross-sectional population study of 3072 randomly recruited residents from Bonn, Germany, 23% received venous disease treatment and 15% wore graduated compression stockings (range, 1% with C0 to 82% with C5/6 CEAP clinical classification). Compliance was high: compression stockings were worn 5 or more days per week by 73% of patients and 8 or more hours a day by 83% of patients. On average, 71% of the participants said that the disease for which the compression stockings were prescribed had improved as a result of the compression therapy.^31,32

Sclerotherapy. Sclerotherapy involves the injection of a liquid or foam sclerosing agent for the targeted elimination of telangiectasias, reticular veins, varicose veins, and perforating veins.³³ Sclerotherapy is considered to be the treatment of choice for small-caliber varicose veins, reticular veins, and telangectasias.³⁴ The various available sclerosing agents produce an endothelial injury of the vein, resulting in transformation into a fibrous cord, a process known as sclerosis.³³ This fibrous cord is eventually absorbed over time (Figure 30-7).