Epidemiology and Risk Factors of Chronic Venous Disease
Chronic venous disease (CVD) is a condition that affects the superficial and deep venous systems resulting in venous hypertension and a cascade of biochemical and vessel wall changes that lead to a spectrum of pathologies ranging from telangiectasias to venous stasis ulcerations. Chronic venous insufficiency (CVI) is an advanced form of CVD, generally presenting with lower extremity edema, trophic skin changes, and venous ulcerations. This chronic condition has often been neglected by providers because of its chronic and subtle progression and the lack of emphasis on its clinical presentation and pathophysiology within the general medical education curriculum. Unfortunately, CVI has a major impact on society, negatively affecting the quality of life of patients and consuming large health care dollars and resources.
CVD is highly prevalent in the United States and western Europe but its true prevalence is unknown because of variability in the definition of the disease and methodology of evaluation. An estimated 25 million people in the United States have chronic venous disease, with 2 million to 6 million having CVI, and nearly 500,000 have venous stasis ulceration. In the Edinburgh Vein Study, a cross-sectional study of a random sample of 1566 subjects, the prevalence of telangiectasias and reticular veins was approximately 80% and 85%, varicose veins 40% and 16%, and ankle edema 7% and 16% in men and women, respectively. Various studies have shown that the prevalence of varicose veins ranged from 2% to 56% in men and 1% to 60% in women. This prevalence increases with age. In the Edinburgh study, the overall prevalence of venous reflux by duplex ultrasound was 9.4% of men and 6.6% of women but rose to 21.2% in men and 12.0% in women over the age of 50. Similarly trophic skin changes seem to increase with age with a prevalence of 1.8% in young women 30 years to 39 years of age, and 20.7% in women over the age of 70 years. Finally, venous ulcers occur in approximately 1% of the general population and also increase with age.
The incidence of CVD or its occurrence within a defined period of time has been evaluated in the Framingham Study. Every second year and over a period of 16 years, subjects were examined for the appearance of varicose veins. The 1-year incidence rate of varicose veins was found to be 1.97% for men and 2.6% for women. In the Edinburgh Vein Study the annual incidence rate in developing varicose veins was 1.4%, with incidence rates similar in men and women.
Several studies have suggested that women have a higher incidence of CVD but this has not been shown in more recent studies. Women are likely to be more aware of their varicose veins and therefore are more likely to participate in studies leading to a selection bias. Also, age-adjusted prevalence of CVD in females has not been consistently performed in studies. In addition, pregnancy is a risk factor for CVD and is likely to bias the overall prevalence of CVD against women. Race has also been linked to CVD. In the San Diego Population Study, CVD was less prevalent in Blacks and Asians when compared with subjects of European origin. Another study showed that English women are five times at risk of CVD than Egyptian women. Furthermore, other risk factors have been linked to CVD and they include obesity, standing occupation, pregnancy, heredity, and prior history of limb trauma. In the Edinburgh Vein Study subjects with a family history of venous disease were more likely to develop varicose veins (odds ratio [OR] 1.75). Also, in the same study obesity was associated with an age-adjusted OR of 3.58 with the development of CVI. In another study, multivariate logistic regression analysis showed that female gender (OR 2.2), increasing age (OR 2.2 to 2.8), a reported positive family history for varicose veins (OR 4.9), increasing number of births (OR 1.2 to 2.8), standing posture at work (OR 1.6), and higher weight (OR 1.2) and height (OR 1.4) were independent predictors of varicose veins.
CVI has a significant direct and indirect socioeconomic burden on society. In the United States, venous ulcerations resulted in a loss of 2 million workdays per year. In France and Sweden, 2.24 billion euros and 73 million euros were spent per year for the treatment of CVI, respectively. A study from Germany found that inpatient and outpatient direct costs were 250 million euros and 234 million euros, respectively, loss of working days costs were 270 million euros, and drug costs were 207 million euros. The presence of venous ulcerations also impacted on quality of life substantially with more than 20% of ulcers remained not healed within 2 years follow-up. These ulcers have been responsible for early retirement of 12.5% of workers with this condition.
Venous Anatomy and Physiology
Treatment of chronic venous insufficiency requires a good understanding of normal venous anatomy and physiology. The veins of the lower limbs are divided into the superficial venous system, the deep venous system, and the perforator veins, connecting the superficial and deep veins at various levels from the foot to the gluteal area ( Figure 27-1 ). The superficial venous system is located within the superficial compartment surrounded anteriorly by the hyperechoic saphenous fascia and posteriorly by the muscular fascia. Within the saphenous compartment reside the saphenous veins, accompanying arteries, and saphenous nerves. A saphenous vein exiting the saphenous compartment is better described as a tributary. The superficial veins of the lower limbs are numerous and interconnected in a network that eventually empties into two primary trunks that feed into the deep venous system: the great saphenous vein (GSV), and the small saphenous vein (SSV). These superficial veins connect to the deep system at the level of the common femoral vein for the GSV and quite often the popliteal vein for the SSV. Also, several perforators connect these superficial systems and their tributaries to the deep system. When discussing anatomy of the venous system, it is important to adhere to the current international nomenclature that has been adopted by the Union Internationale de Phlebologie (UIP) and is currently in use. Below is an anatomic description of the venous system of the lower limbs from this consensus meeting.
Superficial Veins of the Lower Limb
Great Saphenous Vein
The great saphenous vein (GSV) is the longest and main superficial vein of the lower limb. It begins at the medial end of the arch as a continuation of the medial marginal vein of the foot. It ascends slightly anteriorly to the medial malleolus and continues anteromedially in the lower leg before it takes a short posterior course behind the medial condyle of the tibia at the level of the knee. In the lower thigh it ascends anterolaterally, then takes a medial course to below the inguinal ligament, passing through the cribriform fascia that covers the fossa ovalis to join the common femoral vein (CFV) at the saphenofemoral junction (SFJ). The GSV is located within the saphenous compartment. The latter has been compared with the “Egyptian eye” when seen on a transverse scan by B-mode ultrasound ( Figure 27-2 ). The superficial fascia is the upper eyelid, the deep fascia is the lower eyelid, and the lumen of the GSV is the iris. Outside the “eye,” the saphenous trunk is called a superficial tributary even though it can still play the role of a main axial superficial vein. There are several anatomic variations to the GSV; it can be a single GSV within the “eye” and no large tributary, rarely two parallel GSV within the same compartment (true duplication), or a single GSV in the proximal thigh, and at various distances exit the “eye” to become a large subcutaneous tributary (present in about 30% of the time). Large tributaries running parallel to the entire length of the GSV outside the saphenous compartment can also be present and enter the GSV at different levels.
There are several valves in the GSV ranging from 8 to 20 in number. They are mostly located at the junctions with other veins. A constant terminal valve in the GSV is located 1 mm to 2 mm distal to the SFJ. Often, a preterminal valve is seen 2 cm distal to the terminal valve and delineates the distal limit of the SFJ area. At the SFJ, a confluence of proximal veins is seen and includes the superficial epigastric vein, superficial circumflex iliac vein, and external pudendal vein ( Figure 27-3 ). Their clinical importance is in their ability to transmit retrograde flow into the GSV despite a competent terminal valve. Also, the GSV receives many tributary veins; some may be large, including the anterior accessory saphenous vein (AASV) (present in 41% of subjects and entering the GSV within 1 cm of the SFJ), and posterior accessory saphenous vein (PASV), often entering the GSV distal to the preterminal valve at variable distance. In addition, the anterior thigh circumflex vein ascends obliquely into the anterior thigh and enters either the GSV or the AASV; the posterior thigh circumflex vein ascends obliquely into the posterior thigh and may originate from the thigh extension of the small saphenous vein (SSV), directly from the SSV, or from the lateral vein plexus, and enters the GSV. The lateral extension of the SSV into the thigh that connects with the posterior circumflex vein is often called the vein of Giacomini ( Figure 27-4 ).
Anterior Accessory Saphenous Vein
The AASV enters laterally the GSV just below the SFJ. Close to the SFJ both AASV and GSV often share the same saphenous compartment. The AASV, however, has its own saphenous eye more distally and can be distinguished from the GSV by the “alignment” sign where it runs anterior and parallel to the GSV and in line with the femoral artery and femoral vein.
Posterior Accessory Saphenous Vein
The PASV ascends parallel and posterior to the GSV within its own fascial compartment. It is not always easily found and it connects at various lengths with the GSV below the SFJ area. The PASV can be present above or below the knee. The below-the-knee segment that connects to the GSV is called Leonardo’s vein, or posterior arch vein, and is present in approximately 27% of subjects.
Small Saphenous Vein (SSV)
The small saphenous vein (SSV) is a continuation of the lateral marginal foot vein and ascends behind the lateral malleolus to the posterior aspect of the calf in between the medial and lateral heads of gastrocnemius muscle. The SSV lies within the interfascial compartment across its length. On transverse duplex ultrasound, the SSV appears within the “eye,” similar to the GSV. Proximally, it is within a triangular compartment outlined by the superficial fascia anteriorly, and the lateral and medial heads of the gastrocnemius muscle laterally and medially, respectively. The SSV generally terminates in the popliteal vein at the saphenopopliteal junction (SPJ) but not always ( Figure 27-5 ). The SPJ is mostly located within 2 cm to 4 cm above the knee crease but this can significantly vary. The SSV continues into the thigh as the thigh extension (TE). TE is present in 95% of subjects and is intrafascial in position within a triangular compartment defined by the superficial fascia anteriorly, the semitendinous muscle medially, and the biceps femoris muscle laterally. The TE may end in the inferior gluteal vein, connected via a sciatic perforator or posterolateral thigh perforator to the femoral vein, or connected to the GSV via the posterior thigh circumflex vein. Both the TE of the SSV together with the posterior thigh circumflex vein that empties into the GSV are described as the vein of Giacomini. The gastrocnemius veins may merge with the SSV to empty into the popliteal vein or they could empty directly into the popliteal vein near the SPJ. Like the GSV, there is a terminal valve in the SSV close to the popliteal vein and a preterminal valve generally located below the TE of the SSV.
Perforators of the Lower Limb
The superficial veins are connected to the deep veins via the perforator veins ( Table 27-1 ) that penetrate the deep fascia. More than 40 perforator veins have been described. The perforators are located at several levels in the lower limb: foot, ankle, lower leg, knee, thigh, and gluteal area ( Figure 27-6 ). From a historic point of view, they have been named after individuals who described them. Descriptive terms to their location are preferred and have been widely adopted, as follows:
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The perforators of the foot (venae perforantes pedis) are described into dorsal, medial, lateral, and plantar foot perforators.
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The ankle perforators (venae perforantis tarsalis) are the medial, anterior, and lateral ankle perforators.
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The perforators of the leg (venae perforantes cruris) are separated into four main groups:
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Medial leg perforators (paratibial and posterior tibial). The paratibial perforators connect the GSV or its tributaries to the posterior tibial vein (PTV) and the posterior tibial perforators connect below the knee PASV to the PTV. These perforators are indicated by their location as upper, middle, and lower.
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Anterior leg perforators connect the anterior tributaries of the GSV to the anterior tibial veins (ATV).
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Lateral leg perforators connect veins of the lateral venous plexus to the peroneal veins.
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Perforators of the posterior leg (medial gastrocnemius perforators, lateral gastrocnemius perforators, intergemellar perforators (connecting the SSV to the soleal veins) and para-Achillean perforators (connecting the SSV to the peroneal veins).
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The perforators of the knee (venae perforantes genus) are designated as medial, lateral, suprapatellar, infrapatellar, and popliteal fossa knee perforators.
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The perforators of the thigh (venae perforantes femoris) are separated into the following:
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Medial thigh (perforators of the femoral canal and inguinal perforators) connecting the GSV or its tributaries to the femoral vein
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Anterior thigh
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Lateral thigh
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Posterior thigh (posteromedial, sciatic perforators, posterolateral) and pudendal perforators
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The perforators of the gluteal muscles (venae perforantes glutealis) are divided in superior, mid, and lower perforators.
| PERFORATOR GROUPS | SUBGROUPS |
|---|---|
| Foot | Dorsal, plantar, lateral, medial |
| Ankle | Anterior, medial, and lateral |
| Leg | Medial (paratibial and posterior tibial) [GSV or tributaries to PTV] Anterior [GSV tributaries to ATV] Lateral [lateral venous plexus to peroneal] Posterior (medial and lateral gastrocnemius, intergemellar [SSV to soleal]) Para-achillean [SSV to peroneal] |
| Knee | Medial, lateral, suprapatellar, infrapatellar, popliteal fossa |
| Thigh | Medial (femoral canal, inguinal), anterior, lateral, posterior (posteromedial, sciatic, posterolateral, pudendal) |
| Gluteal | Superior, mid, lower |
Deep Venous System
The deep venous system is located below the muscular fascia in the deep compartment. It is comprised of axial veins and intramuscular veins. The deep venous system eventually receives all venous flow that empties in the right atrium. The main axial veins are the popliteal vein (PV) that becomes the femoral vein (FV) above the knee when it passes through the adductor canal then the common femoral vein (CFV) as it joins the deep femoral vein (DFV) at the groin level. The CFV leads to the iliac veins, then the inferior vena cava to the right atrium.
Intramuscular venous sinusoids coalesce and form the venous plexi within the soleal and gastrocnemius calf muscles. These gastrocnemius lateral and medial veins connect to form an extramuscular trunk that travels 1 cm to 4 cm into the popliteal fossa and empties directly into the popliteal vein, or into the SSV at the level of the SPJ, or simultaneously into both popliteal and SSV. The soleus veins unite into one or several main trunks and terminate in either the PTV or the peroneal vein. The term sural veins refers to the lateral and medial gastrocnemius veins, soleal vein, and intergemellar vein, which courses deep to the SSV between the heads of the gastrocnemius muscles.
Physiology of the Venous System
The venous system functions as a large reservoir storing about 70% of the blood in a subject. It also serves as a low-flow, low-pressure conduit moving venous blood to the heart. Flow into the venous system travels against gravity and therefore a series of muscle pumps and valves are built in to assist in this flow. Predominantly calf muscle contraction and to a lesser extent foot and thigh muscles increase fascial compartment pressures, compressing the intramuscular veins and venous plexi in the calf and driving venous flow upward against gravity. Negative intrathoracic pressure also assists in the process of forward flow. A series of unidirectional bicuspid valves are present in the lower limb and superficial venous systems that continue to ensure a forward flow of blood to the heart against gravity. Valves are also present at the perforators that prevent flow from the deep system back into the superficial system. The CFV typically has one valve. The inferior vena cava and common iliac veins have no valves. Infrequently, a valve can be seen in the external iliac vein. The infrainguinal veins have several valves located at different levels but most seem to concentrate at the knee level and below.
The resting standing venous pressure is approximately 80 to 90 mm Hg. Following ambulation, the muscle contraction moves the venous flow forward emptying the venous system and dropping the pressure to 15 to 30 mm Hg. When muscle relaxation occurs the venous system refills slowly (more than 20 seconds) from arterial inflow into the superficial and deep veins, distending the veins and allowing the valves ( Figure 27-7 ) to open, creating a single pipe of fluid with a pressure at the ankle equal to the height of the column of blood. In a competent valve system, contraction of the muscle leads to quick emptying of the veins with no refluxing of flow backward, and a quick drop of pressure in the venous system typically more than 50% decrease from the resting standing pressure.
Etiology and Pathophysiology of Chronic Venous Insufficiency
The main pathophysiologic mechanism of CVI is high venous pressure in the lower extremity due to failure in keeping venous upward flow toward the heart. This can result from backward reflux of venous flow through incompetent valves in the deep or superficial venous systems, or the perforators that connect both. Venous obstruction in the deep system can also impede venous flow and contribute to high venous pressure. In addition, muscular dysfunction can also contribute to reducing forward venous flow and along with reflux becomes an important risk factor for venous ulceration. When valve incompetence is present, the backward flow of blood to the lower veins contributes to raising the venous pressure faster to resting level (in less than 10-20 seconds). Also the drop of venous pressure in an incompetent valve system with ambulation is blunted and venous pressure remains higher than 50% its resting value. The constant high venous pressure in the lower limb is ultimately responsible for venous microangiopathy and subsequently the development of signs and symptoms of chronic venous insufficiency.
Valve incompetence in the superficial veins may be due to primary valve failure or weakness in the vessel wall. Secondary causes of valve incompetence can be trauma, hormonal effects, thrombophlebitis, or high pressure. There are several potential sources of reflux from the deep system into the superficial system via incompetent perforators, or incompetent SPJ, or SFJ. Also reflux can be transmitted from the GSV, perineal veins, and thigh perforators to the SSV via the Giacomini vein, or backward from the SPJ to the GSV, or the veins of the posterior aspect of the thigh via the same system. The deep system could also develop significant reflux mostly due to obstruction, partial or complete. This can be related to deep vein thrombosis (DVT), stenosis, or extrinsic compression. Compression of the iliac vessels can produce obstruction to upward venous flow resulting in high venous pressure leading to vein dilation, and reflux. Iliac extrinsic compression is quite often an underestimated cause of CVD and a high index of suspicion is needed to correctly identify this problem. Finally, muscle pump dysfunction is a contributor to venous ulcerations in patients with venous reflux. Reflux in conjunction with muscle pump failure is a significant risk factor for developing venous ulcers. The presence of good muscle pump function lessens the chance of ulcerations in patients with severe reflux, and the presence of poor muscle function can increase the risk of ulceration, even when minimal reflux is present.
Venous microangiopathy is the result of high venous pressure transmitted to the microvasculature of the lower legs. In its mild form, CVI results in an increase in transcapillary diffusion of sodium fluorescein (NaF), a marker of leak in the capillary bed seen early in the disease process and is accompanied by an increase in pericapillary space (halo). As CVI progresses and becomes more severe, capillary thromboses occur, leading to a reduced capillary density and a reduction in transcutaneous oxygen tension (tcpO2), particularly at the ulcer rim. The remaining capillaries become more elongated and tortuous. They become more permeable because of the stretching of their inter-endothelial pores. Larger molecules can exit the capillaries into the extracapillary space, leading to chronic inflammation and edema and eventually skin trophic changes and ulcerations. Also, in the severe stages of CVI, there is a destruction of the lymphatic capillary network and an increase in the permeability of the remaining lymphatic fragments suggesting lymphatic microangiopathy. Dysfunction of local nerve fibers also occurs.
There are several hypotheses on how microangiopathy leads to venous ulcerations. Browse and colleagues proposed the fibrin cuff theory, which centers on the leak of fibrinogen into the pericapillary space. This results in pericapillary fibrin cuffs that were thought to be a barrier for diffusion of oxygen. Fibrin cuffs, however, are not a specific finding for venous ulceration and were found not to impair oxygen diffusion significantly. Another theory is the trapping of leukocytes in the capillaries, or postcapillary venules with subsequent release of their inflammatory mediators and proteolytic enzymes leading to endothelial injury. Finally, trapping of leaked growth factors in the pericapillary space is thought to prevent their ability to participate in the healing of damaged capillary bed.
Evaluation and Classification of the Patient with Chronic Venous Insufficiency
Chronic venous disease (CVD) presents with a spectrum of pathologies ranging from telangiectasia to skin hyperpigmentation to venous ulcers. The term CVI is generally used for patients with an advanced form of CVD generally presenting with symptoms and signs of lower extremity edema, trophic skin changes, and venous ulcerations.
The initial evaluation of a patient with CVI starts with a comprehensive history and physical examination. Symptoms of CVI include heaviness, achiness, tightness, itching, muscle cramps, involuntary movements of the limb, and tingling. These worsen when patients are standing and improve when the feet are elevated at heart level. Patients’ symptoms are worse as the day progresses and generally mild or fewer symptoms are noted in the morning prior to standing out of bed. The interference of symptoms with daily activity and the response to prior treatment such as compression garments should be documented. Risk factors for developing CVD should be identified, such as advanced age, a higher weight and height, standing occupation, heredity, prior injury, surgeries or trauma, history of DVT, multiple pregnancies, and ethnic background. A past history of early childhood varicose veins is important to note as it may be related to some rare congenital blood vessel malformations such as in Klippel–Trénaunay–Weber syndrome. Providers need to keep in mind other sources of pain that may mimic CVI, including tendinitis, arthritis, neuropathy, or arterial insufficiency. Careful history and examination should help in identifying these etiologies.
The physical examination should be performed in a warm, well-lit room and when the patient is standing. The entire leg needs to be checked starting from the inguinal area to the foot, and findings of abnormal veins, skin changes, or ulcerations need to be well documented on a drawing showing the anterior, posterior, medial, and lateral parts of the leg. Palpation over the GSV, SSV, SFJ, and SPJ may reveal additional varicosities, subcutaneous cords, or areas of indurations not visible with inspection only. Palpation of the SFJ with cough can reveal a thrill that indicates reflux at this level (cough impulse test). Also, a tap on the GSV distally while palpating the SFJ area may allow the feeling of a transmitted pulse to the SFJ indicating GSV distention. The opposite is true with a tap on the SFJ, allowing a feeling of transmitted pulse to the distal GSV indicating reflux (the tap test). These tests, however, lack good sensitivity in identifying reflux at the SFJ. The Brodie-Trendelenburg test can help identify perforator reflux into the GSV. The patient’s leg is elevated 45 degrees and blood is massaged up the leg from the foot. A tourniquet is then applied proximally close to the groin area. The patient is then allowed to stand up. If no dilation of the lower leg veins is seen after 20 to 30 seconds, perforator valves are likely to be competent. If after releasing the tourniquet, the veins in the leg distend quickly, this indicates that the superficial venous system is incompetent. This test is highly sensitive but poorly specific in identifying superficial and perforator reflux. Another test that can be performed in the office is the Perthes test. A tourniquet is placed below the knee in a standing position. The patient is asked to raise the heel 10 times. If varicosities empty, this indicates that the perforators of the lower superficial venous system are competent and reflux is likely cranial to the tourniquet. On the other hand, if more distention occurs to the varicosities of the lower leg, this indicates that reflux is present in the deep perforators below the knee. The presence of severe pain in the calf with raising the heel repetitively could indicate the presence of DVT. These physical maneuvers have been widely replaced with duplex ultrasound to the lower leg that has a higher accuracy in identifying the presence and location of the reflux.
Once the examination and history are obtained, disease needs to be classified based on its clinical presentation. The Clinical, Etiologic, Anatomic, and Pathophysiology (CEAP) classification system was developed at the American Venous Forum annual meeting in 1994, and revised in 2004. The physical findings are divided into seven clinical manifestations ranging from no visible findings of CVD to active venous ulcerations. Given the progression of CVD, the classification also reflects the natural clinical progression of this disease. The etiologic, anatomic and pathophysiologic classifications require additional anatomic and functional testing that will be discussed later. The CEAP classification is described in Table 27-2 and clinical manifestations are shown in Figures 27-8 to 27-11 .
| GRADE | DESCRIPTION |
|---|---|
| C 0 | No visible or palpable signs of venous disease |
| C 1 | Superficial telangiectasias (intradermal, less than 1 mm, flat, red vessels) or reticular veins (subdermal, 1-3 mm, flat, bluish) or venulectasias (rise above skin, 1-2 mm, blue) |
| C 2 | Varicose veins (diameter more or equal 3 mm) |
| C 3 | Ankle edema |
| C 4 | Changes in skin and subcutaneous tissue |
| C4a: Pigmentation or eczema | |
| C4b: Lipodermatosclerosis or atrophie blanche | |
| C 5 | Healed venous ulcer |
| C 6 | Active venous ulcer |
The venous clinical severity score (VCSS) ( Table 27-3 ) was designed to complement the CEAP score and to provide a method to serially assess the severity of disease over time, and in response to a treatment. The advantage of the VCSS is that it is dynamic and is able to capture changes in disease severity whereas the CEAP class is descriptive and static, particularly in its advanced classes (IV to VI).
| ATTRIBUTE | ABSENT = 0 | MILD = 1 | MODERATE = 2 | SEVERE = 3 |
|---|---|---|---|---|
| Pain | None | Occasional pain or other discomfort | Daily pain or other discomfort | Daily pain or discomfort, limits most regular daily activities |
| Varicose veins ≥3 mm in diameter | None | Scattered, includes corona phlebectatica | Confined to calf or thigh | Involves calf and thigh |
| Edema | None | Limited to foot and ankle | Extends above ankle but below knee | Extends to knee and above |
| Pigmentation | None or focal | Limited to perimalleolar area | Diffuse over lower third of calf | Above lower third of calf |
| Inflammation | None | Limited to perimalleolar area | Diffuse over lower third of calf | Above lower third of calf |
| Induration | None | Limited to perimalleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
| Number of active ulcers | 0 | 1 | 2 | ≥3 |
| Duration of longest active ulcer | None | <3mo | >3 mo but <1 yr | Not healed for >1 yr |
| Size of largest active ulcer | None | Diameter <2 cm | Diameter 2 to 6 cm | Diameter >6 cm |
| Compression therapy | Not used | Intermittent use of stockings | Wears stockings most days | Full compliance: stockings |
The venous severity score (VSS) is another scoring system that grades disease severity and is sum score of multiple other scoring systems including VCSS, Venous Segmental Disease Score (VSDS), and Venous Disability Score (VDS). Other scoring systems are present and one should adopt a scoring system that complements the CEAP score in order to be able to assess longitudinal changes in patients’ symptoms and signs of CVI either naturally or after intervention.
Anatomic and Physiologic Testing of Chronic Venous Insufficiency
There are several anatomic and physiologic tests that can be utilized to diagnose and understand the etiology of chronic venous insufficiency. The most practical and commonly used test in an office setting is the duplex venous ultrasound (DU) and to a lesser extent plethysmography.
Duplex Venous Ultrasound of the Lower Limb
Duplex venous ultrasound (DU) is likely to be the most widely used technique in the diagnosis of venous disorders, including DVT and superficial venous disease. This section will focus on the use of DU in the diagnosis and management of patients with chronic superficial venous disease. An evaluation of the deep venous system is routinely performed when assessing superficial venous reflux to rule out coexistent DVT, assess for deep venous reflux, and assist in the diagnosis of potential iliac obstructive disease.
Spectral Doppler flow is utilized to determine the degree of reflux in the superficial venous and deep venous systems ( Figure 27-12 ). Reflux in the deep venous system is evaluated in the supine position with the head elevated 10 degrees to 15 degrees. Evaluation of the superficial venous system needs to be performed in the standing position with distal augmentation and with the patient standing with the weight mostly on the contralateral leg. The heel of the leg under examination should be flat on the floor to avoid calf muscle contraction during the test. The cutoff for abnormal retrograde flow is greater than 500 ms in the superficial system and deep calf veins but greater than 1000 ms in the femoropopliteal vein. Reflux in the perforator vein is abnormal if it is more than 350 ms but the cutoff for clinical intervention is more than 500 ms. Reflux is best reported in seconds rather than graded in severity as mild, moderate, or severe as the correlation with the severity of disease is not standardized, and is variable. Initially, the SSV is interrogated, including its relationship to the popliteal vein. The thigh extension of the SSV will also need to be identified along with its termination. Next, the GSV and its tributaries are evaluated. In approximately 2% of the time, there is a duplicate GSV. Reflux and GSV sizes are measured at the level of the SFJ, mid thigh, and above and below the knee. Mapping the AASV and the PASV follows the GSV. Furthermore, tributaries at least 50% the size of the native saphenous veins are mapped. Finally, perforators’ veins are mapped, which is particularly important in patients with healed and nonhealed venous ulcerations. An extensive mapping of perforators is less useful. Perforators large enough to be more than 3.5 mm in diameter and with reflux more than 500 ms are of particular importance in patients with venous ulcerations as these perforators are typically the target for therapeutic intervention. The mapping data are then compiled into a diagram that will be utilized for diagnostic and therapeutic intervention.
