Venous Disease

Chapter 65 Venous Disease

An understanding of venous physiology provides the surgeon with valuable information with which to formulate a diagnostic and treatment plan. Technologic advances have broadened the therapeutic armamentarium. This chapter will provide the reader with a thorough overview of the physiology and pathophysiology of the venous system, followed by an evaluation of available diagnostic modalities and therapeutic interventions and then by a discussion of specific venous disorders.


To determine whether pathophysiology is present, precise knowledge of venous anatomy is essential. After the location and type of venous incompetence have been determined, a therapeutic plan can be constructed. Venous drainage of the legs is the function of two parallel and connected systems, the deep and superficial systems. The nomenclature of the venous system of the lower limb was revised in 2002 and the most relevant changes are addressed here.1 The revised nomenclature is delineated in Tables 65-1 and 65-2.

Table 65-1 Superficial Veins

Greater or long saphenous vein Great saphenous vein
Superficial inguinal veins
External pudendal vein External pudendal vein
Superficial circumflex vein Superficial circumflex iliac vein
Superficial epigastric vein Superficial epigastric vein
Superficial dorsal vein of clitoris or penis Superficial dorsal vein of clitoris or penis
Anterior labial veins Anterior labial veins
Anterior scrotal veins Anterior scrotal veins
Accessory saphenous vein Anterior accessory great saphenous vein
  Posterior accessory great saphenous vein
  Superficial accessory great saphenous vein
Smaller or short saphenous vein Small saphenous veinCranial extension of small saphenous vein
  Superficial accessory small saphenous vein
  Anterior thigh circumflex vein
  Posterior thigh circumflex vein
  Intersaphenous veins
  Lateral venous system
Dorsal venous network of the foot Dorsal venous network of the foot
Dorsal venous arch of the foot Dorsal venous arch of the foot
Dorsal metatarsal veins Superficial metatarsal veins (dorsal and plantar)
Plantar venous network Plantar venous subcutaneous network
Plantar venous arch  
Plantar metatarsal veins Superficial digital veins (dorsal and plantar)
Lateral marginal vein Lateral marginal vein
Medial marginal vein Medial marginal vein

Table 65-2 Deep Veins

Femoral vein Common femoral vein
  Femoral vein
Profunda femoris vein or deep vein of thigh Profunda femoris vein or deep femoral vein
Medial circumflex femoral vein Medial circumflex femoral vein
Lateral circumflex femoral vein Lateral circumflex femoral vein
Perforating veins Deep femoral communicating veins (accompanying veins of perforating arteries)
  Sciatic vein
Popliteal vein Popliteal vein
  Sural veins
  Soleal veins
  Gastrocnemius veins
  Medial gastrocnemius veins
  Lateral gastrocnemius veins
  Intergemellar vein
Genicular veins Genicular venous plexus
Anterior tibial veins Anterior tibial veins
Posterior tibial veins Posterior tibial veins
Fibular or peroneal veins Fibular or peroneal veins
  Medial plantar veins
  Lateral plantar veins
  Deep plantar venous arch
  Deep metatarsal veins (plantar and dorsal)
  Deep digital veins (plantar and dorsal)
  Pedal vein

Superficial Venous System

The superficial veins of the lower extremity form a network that connects the superficial dorsal veins of the foot and deep plantar veins. The dorsal venous arch, into which empty the dorsal metatarsal veins, is continuous with the great saphenous vein medially and the small saphenous vein laterally (Fig. 65-1).

The great saphenous vein, in close proximity to the saphenous nerve, ascends anterior to the medial malleolus, crosses and then medial to the knee (Fig. 65-2). It ascends in the superficial compartment and empties into the common femoral vein after entering the fossa ovalis. Before its entry into the common femoral vein, it receives medial and lateral accessory saphenous veins, as well as small tributaries from the inguinal region, pudendal region, and anterior abdominal wall. The posterior arch vein drains the area around the medial malleolus and, as it ascends up the posterior medial aspect of the calf, it receives medial perforating veins, termed Cockett’s perforators, before joining the great saphenous vein at or below the knee.

The small saphenous vein arises from the dorsal venous arch at the lateral aspect of the foot and ascends posterior to the lateral malleolus, rising cephalad in the midposterior calf. The small saphenous vein continues to ascend, penetrates the superficial fascia of the calf, and then terminates into the popliteal vein. The exact entry of the small saphenous vein into the popliteal vein is variable. The sural nerve lies parallel to the small saphenous vein.

Perforating Venous System

Perforating veins connect the superficial venous system to the deep venous system by penetrating the fascial layers of the lower extremity. These perforators run in a perpendicular fashion to the axial veins previously described. Although the total number of perforator veins is variable, up to 100 have been documented. The perforators enter at various points in the leg—the foot, medial and lateral calf, and mid and distal thigh (Fig. 65-3) Some have been named Cockett’s perforators, which connect the posterior arch and posterior tibial veins, Boyd’s perforators, which connect the great saphenous and gastrocnemius veins, and Hunterian and Dodd’s perforators, which connect the great saphenous and superficial femoral veins. The perforator veins have an important function. Their valve system aids in preventing reflux from the deep to the superficial system, particularly during periods of standing and ambulation.

Normal Venous Histology and Function

The venous wall is composed of three layers, the intima, media, and adventitia. Vein walls have less smooth muscle and elastin than their arterial counterparts. The venous intima has an endothelial cell layer resting on a basement membrane. The media is composed of smooth muscle cells and elastin connective tissue. The adventitia of the venous wall contains adrenergic fibers, particularly in the cutaneous veins. Central sympathetic discharge and brainstem thermoregulatory centers can alter venous tone, as can other stimuli, such as temperature changes, pain, emotional stimuli, and volume changes.

The histologic features of veins vary, depending on the caliber of the veins. The venules, the smallest veins, rangefrom 0.1 to 1 mm and contain mostly smooth muscle cells, whereas the larger extremity veins contain relatively few smooth muscle cells. These larger caliber veins have limited contractile capacity in comparison to the thicker walled great saphenous vein. The venous valves prevent retrograde flow; it is their failure or valvular incompetence that leads to reflux and its associated symptoms. Venous valves are most prevalent in the distal lower extremity, whereas as one proceeds proximally, the number of valves decreases to the point that no valves are present in the superior vena cava and inferior vena cava (IVC),.

Most of the capacitance of the vascular tree is in the venous system. Because veins do not have significant amounts of elastin, veins can withstand large volume shifts with comparatively small changes in pressure. A vein has a normal elliptical configuration until the limit of its capacitance is reached, at which point the vein assumes a round configuration.

The calf muscles augment venous return by functioning as a pump. In the supine state, the resting venous pressure in the foot is the sum of the residual kinetic energy minus the resistance in the arterioles and precapillary sphincters. Thus, a pressure gradient is generated to the right atrium of approximately 10 to 12 mm Hg. In the upright position, the resting venous pressure of the foot is a reflection of the hydrostatic pressure from the upright column of blood extending from the right atrium to the foot.

The return of the blood to the heart from the lower extremity is facilitated by the muscle pump function of the calf, a mechanism whereby the calf muscle, functioning as a bellows during exercise, compresses the gastrocnemius and soleal sinuses and propels the blood toward the heart. The normally functioning valves in the venous system prevent retrograde flow; when one or more of these valves become incompetent, symptoms of venous insufficiency can develop. During calf muscle contraction, the venous pressure of the foot and ankle drop dramatically. The pressures developing in the muscle compartments during exercise range from 150 to 200 mm Hg and, when there is failure of perforating veins, these high pressures are transmitted to the superficial system.

Venous Insufficiency

There are three categories of venous insufficiency—congenital, primary, and secondary. Congenital venous insufficiency is comprised of predominantly anatomic variants that are present at birth. Examples of congenital venous anomalies include venous ectasias, absence of venous valves, and syndromes such as Klippel-Trenaunay syndrome. Primary venous insufficiency is an acquired idiopathic entity. This is the largest clinical category and represents most of the superficial venous insufficiency encountered in the office. Secondary venous insufficiency arises from a post-thrombotic or obstructive state and is caused by a deep vein thrombus or primary chronic obstructive process.

Primary Venous Insufficiency

There are three main anatomic categories of primary venous insufficiency—telangiectasias, reticular veins, and varicose veins. Telangiectasias, reticular varicosities, and varicose veins are similar but exhibit distinct variations in caliber. Telangiectasias are very small intradermal venules that are too diminutive to demonstrate reflux. Reticular veins are vein branches that enter the tributaries of the main axial, perforating, or deep veins. The axial veins, the great or small saphenous veins, represent the largest caliber veins of the superficial venous system.


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.

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.

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.

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.

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

C Clinical signs (grade0-6), supplemented by “A” for asymptomatic and “S” for symptomatic presentation
E Classification by cause (etiology)—congenital, primary, secondary
A Anatomic distribution—superficial, deep, or perforator, alone or in combination
P Pathophysiologic dysfunction—reflux or obstruction, alone or in combination
Clinical Classification (C0-6)
Any limb with possible chronic venous disease is first placed into one of seven clinical classes (C0-6), according to the objective signs of disease.
Clinical Classification of Chronic Lower Extremity Venous Disease*
0 No visible or palpable signs of venous disease
1 Telangiectasia, reticular veins, malleolar flare
2 Varicose veins
3 Edema without skin changes
4 Skin changes ascribed to venous disease (e.g., pigmentation, venous eczema, lipodermatosclerosis)
5 Skin changes as defined above with healed ulceration
6 Skin changes as defined above with active ulceration
*Limbs in higher categories have more severe signs of chronic venous disease and may have some or all of the findings defining a less severe clinical category. Each limb is further characterized as asymptomatic (A)—for example, C0-6,A—or symptomatic (S)—for example, C0-6,S. Symptoms that may be associated with telangiectatic, reticular, or varicose veins include lower extremity aching, pain, and skin irritation. Therapy may alter the clinical category of chronic venous disease. Limbs should therefore be reclassified after any form of medical or surgical treatment.
Classification by Cause (EC, EP, or ES)
Venous dysfunction may be congenital, primary, or secondary. These categories are mutually exclusive. Congenital venous disorders are present at birth but may not be recognized until later. The method of diagnosis of congenital abnormalities must be described. Primary venous dysfunction is defined as venous dysfunction of unknown cause but not of congenital origin. Secondary venous dysfunction denotes an acquired condition resulting in chronic venous disease—for example, deep venous thrombosis.
Classification by Cause of Chronic Lower Extremity Venous Disease
Congenital (EC) Cause of the chronic venous disease present since birth
Primary (EP) Chronic venous disease of undetermined cause
Secondary (ES) Chronic venous disease with an associated known cause (e.g., post-thrombotic, post-traumatic, other)
Anatomic Classification (AS, AD, or AP)
The anatomic site(s) of the venous disease should be described as superficial (AS), deep (AD), or perforating (AP) vein(s). One, two, or three systems may be involved in any combination. For reports requiring greater detail, the involvement of the superficial, deep, and perforating veins may be localized by use of the anatomic segments.
Segmental Localization of Chronic Lower Extremity Venous Disease
Superficial Veins (AS1-5)  
 1 Telangiectasia/reticular veins
  Greater (long) saphenous vein
 2 Above knee
 3 Below knee
 4 Lesser (short) saphenous vein
 5 Nonsaphenous
Deep Veins (AD6-16)  
 6 Inferior vena cava
 7 Common
 8 Internal
 9 External
10 Pelvic: gonadal, broad ligament
11 Common
12 Deep
13 Superficial
14 Popliteal
15 Tibial (anterior, posterior, or peroneal)
16 Muscular (gastrointestinal, soleal, other)
17 Thigh
18 Calf
Pathophysiologic Classification (PR,O)
Clinical signs or symptoms of chronic venous disease result from reflux (PR), obstruction (PO), or both (PR,O).
Pathophysiologic Classification of Chronic Lower Extremity Venous Disease
Reflux (PR)  
Obstruction (PO)  
Reflux and obstruction (PR,O)  
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Aug 1, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Venous Disease

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