Introduction
History of the Procedure
The description of varicose veins as a clinical entity can be traced back as early as the fifth century BC. Forefathers of medicine including Hippocrates and Galen described the disease and treatment modalities, which are still used today.1 Throughout the centuries, surgical treatments have evolved from large, open surgeries to minimally invasive approaches.
Problem
Varicose veins represent a significant clinical problem and are not just a “cosmetic” issue because of their unsightly nature. The problem arises from the fact that varicose veins actually represent underlying chronic venous insufficiency with ensuing venous hypertension. This venous hypertension leads to a broad spectrum of clinical manifestations, ranging from symptoms to cutaneous findings like varicose veins, reticular veins, telangiectasias, swelling, skin discoloration, and ulcerations (see Image 1-6).

Pathway leading to varicose veins and other
clinical manifestations of venous hypertension.
Varicose veins and even chronic venous insufficiency can be managed conservatively with stockings and compression. More aggressive management can be pursued for cosmesis, worsening cutaneous findings or symptoms despite conservative management, or if the patients prefer surgical management. Most procedures to treat varicose veins can be elective, and emergent treatment and workup is usually reserved for bleeding varicosities or if deep venous thrombosis is suspected.
Frequency
The incidence and prevalence of varicose veins has been studied in a number of cross-sectional studies. In 1973, the United States Tecumseh community health study estimated that about 40 million persons (26 million females) in the US were affected.2 In 1994, a review by Callam found half of the adult population have minor stigmata of venous disease (women 50-55%; men 40-50%) and fewer than half have visible varicose veins (women 20-25%; men 10-15%).3 In 2004, these finding were also seen in a French cross-sectional study that found the odds ratio per year for varicose veins were 1.04 for women and 1.05 for men.4 Age and gender have been the only consistently identified risk factors for varicose veins.2,4
Etiology
The cause of primary varicose veins is incompetent venous valves that result in venous hypertension. Secondary varicose veins result from deep venous thrombosis and its sequelae or congenital anatomic abnormalities. The etiology of these varicose veins can be classified into the following three groups:
- Primary: Valvular insufficiency of the superficial veins, most commonly at the saphenofemoral junction.
- Secondary
- Mainly caused by deep vein thrombosis (DVT) that leads to chronic deep venous obstruction or valvular insufficiency. Long-term clinical sequelae from this have been called the postthrombotic syndrome.
- Catheter-associated DVTs are also included.
- Pregnancy-induced and progesterone-induced venous wall and valve weakness worsened by expanded circulating blood volume and enlarged uterus compresses the inferior vena cava and venous return from the lower extremities.
- Trauma
- Congenital: This includes any venous malformations. A few examples are listed as follows:
- Klippel-Trenaunay variants
- Avalvulia
Pathophysiology
Varicose veins are simply dilated, tortuous veins of the subcutaneous/superficial venous system. However, the pathophysiology behind their formation is complicated and involves the concept of ambulatory venous hypertension. To understand this, the anatomy of the lower extremity venous system must be briefly discussed. Two venous systems are found in the lower extremity, the deep and superficial (see Image 7). The deep system ultimately leads backs to the inferior vena cava, then to the heart. The superficial system is found above the deep fascia of the lower extremity, within the subcutaneous tissue. Many superficial veins exist, but they all drain into the 2 largest, the greater saphenous vein (GSV) and the short saphenous vein (SSV), formerly called the lesser saphenous vein.

Schematic diagram of the deep and superficial
venous systems of the lower extremity: (1) Normal venous
drainage; arrows depict the flow of venous blood. (2) Venous
hypertension bold arrows are pathways of venous
reflux.
The superficial venous system is connected to the deep system at a number of the following locations:
- Perforator veins: These veins transverse the deep fascia of the lower extremity. A number of named perforators are found at the thigh, knee, and leg. See the Anatomy section for more details (see Image 8).

Named perforators along the greater saphenous
distribution.
- Saphenofemoral junction (SFJ): This is located proximally at the groin where the GSV meets the femoral vein (see Images 9 and 10).

Major tributaries of the greater saphenous
system.

Saphenofemoral junction.
- Saphenopopliteal junction (SPJ): This is located behind the knee where the SSV joins with the popliteal vein (see Image 9).
In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg and toward the heart (see Image 7). One-way venous valves are found in both systems and the perforating veins. Incompetence in any of these valves can lead to a disruption in the unidirectional flow of blood toward the heart and result in ambulatory venous hypertension (see Image 7). Furthermore, incompetence in one system can often lead to incompetence in another. In a study by Shami et al, the limbs of 59 patients with venous ulceration were assessed by color duplex ultrasound scanning.
5 In 53% of patients only superficial venous reflux was found, in 15% isolated deep venous reflux was found, and in 32% a combination of deep and superficial venous reflux was found.
Incompetence in the superficial venous system alone usually results from failure at valves located at the SFJ and SPJ. The gravitational weight of the column of blood along the length of the vein creates hydrostatic pressure, which is worse at the more distal aspect of the length of vein (see Image 7, circle A).
6 Incompetence of the perforating veins leads to hydrodynamic pressure. The calf pump mechanism helps to empty the deep venous system, but if perforating vein valves fail, then the pressure generated in the deep venous system by the calf pump mechanism are transmitted into the superficial system via the incompetent perforating veins (see Image 7, circle B).
6 Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious cycle. Pooled blood and venous hypertension leads to venous dilatation, which then causes greater valvular insufficiency. Over time, with more local dilatation, other adjacent valves sequentially fail, and after a series of valves has failed, the entire superficial venous system is incompetent. As mentioned before, this can then cause subsequent perforator and deep venous valvular dysfunction (see Image 1).
The inciting etiology of superficial valvular insufficiency is often difficult to determine because the clinical manifestations of venous hypertension are delayed. The original cause can be classified as primary, secondary, and congenital as previously described.
The clinical finding of varicose veins, reticular veins, and telangiectasias are due to the hypertension in the superficial venous system that spreads to collateral veins and tributary veins, causing dilated tortuous structures. Treatment modalities are geared towards correcting the superficial venous hypertension.
7 At times, the degree or venous hypertension does not correlate to the clinical findings. The presence and size of visible varicosities are not reliable indicators of the volume or pressure of venous reflux. A vein that is confined within fascial planes or is buried beneath subcutaneous tissue can carry massive amounts of high-pressure reflux without being visible at all. Conversely, even a small increase in pressure can eventually produce massive dilatation of an otherwise normal superficial vein that carries very little flow.
In contrast to the superficial veins, the deep veins do not become excessively distended. They can withstand the increased pressure because of their construction and the confining fascia.
Presentation
Subjective symptoms
Patients may have a host of symptoms, but they are usually caused by venous hypertension rather than the varicose veins themselves. Often, symptoms are purely aesthetic, and patients desire treatment of the unsightly nature of the tortuous, dilated varicosities. Complaints of pain, soreness, burning, aching, throbbing, heavy legs, cramping, muscle fatigue, pruritus, night cramps, and "restless legs" are usually secondary to the venous hypertension. Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives).
Also, pain associated with venous hypertension is usually a dull ache that worsens after prolonged standing, and improves by walking or by elevating the legs. This is in contrast to the pain of arterial insufficiency, which is worse with ambulation and elevation. Subjective symptoms are usually more severe early in the progression of disease, less severe in the middle phases, and more severe again with advancing age. Patients who have become acclimatized to their chronic disease may not volunteer information about symptoms. After treatment, patients are often surprised to realize how much chronic discomfort they had accepted as "normal."
Venous history
The venous history should also include the following elements:
- History of venous insufficiency (eg, date of onset of visible abnormal vessels, date of onset of any symptoms, any known prior venous diagnoses, any history of pregnancy-related varices)
- Presence or absence of predisposing factors (eg, heredity, trauma to the legs, occupational prolonged standing, sports participation)
- History of edema (eg, date of onset, predisposing factors, site, intensity, hardness, modification after a night's rest)
- History of any prior evaluation of or treatment for venous disease (eg, medications, injections, surgery, compression)
- History of superficial or deep thrombophlebitis (eg, date of onset, site, predisposing factors, sequelae)
- History of any other vascular disease (eg, peripheral arterial disease, coronary artery disease, lymphedema, lymphangitis)
- Family history of vascular disease of any type
Physical Examination Findings
The physical examination of the venous system is fraught with difficulty. As mentioned earlier, the severity of symptoms does not necessarily correlate with the size or extent of visible varices or with the volume of reflux. Furthermore, most of the deep venous system cannot be directly inspected, palpated, auscultated, or percussed. In most areas of the body, examination of the superficial venous system must serve as an indirect guide to the deep system.
Inspection
Inspection should be performed in an organized manner, usually progressing from distal to proximal and from front to back. The perineal region, pubic region, and abdominal wall must also be inspected. The following items should be noted:
- Surgical scars from prior intervention
- Pigmentations and skin changes (ie, brownish darkening of the skin, resulting from extravasated blood that causes lipodermatosclerosis. This usually occurs in medial ankle region but may extend to leg and foot.)
- Varicose veins – Visible, palpable veins in the subcutaneous skin greater than 3 mm (see Image 4)

Varicose veins.
- Reticular veins (also called blue veins, subdermal varices, and venulectasias) – Visible, dilated bluish subdermal, nonpalpable veins 1-3 mm (see Image 3).

Reticular veins.
- Telangiectases (also called spider veins, hyphen webs, and thread veins) – Dilated intradermal venules greater than 1 mm in diameter (see Image 2).

Telangiectasias.
- Eczema – Erythematous dermatitis, which may progress to blistering, weeping, or scaling eruption of the skin of the leg.
- Atrophie blanche (white atrophy) – Localized, often circular whitish and atrophic skin areas surrounded by dilated capillaries and sometimes hyperpigmentation. (Scars of healed ulceration are excluded from this definition.)
- Corona phlebectatica (also called malleolar flare and ankle flare) – Fan-shaped pattern of numerous small intradermal veins on the medial or lateral aspects of the ankle and foot.
- Ulcers of the medial ankle – Most likely the result of underlying venous insufficiency. (Skin changes or ulcerations that are localized only to the lateral aspect of the ankle are more likely to be related to prior trauma or to arterial insufficiency than to pure venous insufficiency; see Images 5 and 6.)

Lipodermatosclerosis.

Venous stasis ulcer.
Palpation
The entire surface of the skin is palpated lightly with the fingertips because dilated veins may be palpable even where they are not visible. Distal and proximal arterial pulses are also palpated. An ankle-brachial index is useful if arterial insufficiency is suggested.
- The anteromedial surface of the lower limb is the territory of the greater saphenous vein (GSV). The arch of the vein may be palpated in some patients with healthy veins, but this segment of the vein is particularly well appreciated in patients with truncal reflux at the saphenofemoral junction (SFJ). It is best palpated 2 fingerbreadths below the inguinal ligament and just medial to the femoral artery. If reflux is present, a forced coughing maneuver may produce a palpable thrill or sudden expansion at this level.
- The posterior surface of the calf is the territory of the short saphenous vein. This may be palpable in the popliteal fossa in some slender patients. Normal superficial veins above the foot are usually not palpable even after prolonged standing.
- Palpation of an area of leg pain or tenderness may reveal a firm, thickened, thrombosed vein. These palpable thrombosed vessels are superficial veins, but an associated DVT may exist in as many as 40% of patients with superficial phlebitis.
- Varices of recent onset are easily distinguished from chronic varices by palpation. Newly dilated vessels sit on the surface of the muscle or bone; chronic varices erode into underlying muscle or bone, creating deep "boggy" or "spongy" pockets in the calf muscle and deep palpable bony notches, especially over the anterior tibia.
- Palpation often reveals fascial defects in the calf along the course of an abnormal vein at sites where superficial tributaries emerge through openings in the superficial fascia. Incompetent perforating veins may connect the superficial and deep venous systems through these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence.
Percussion
This technique is useful in determining whether 2 venous segments are directly interconnected. With the patient in a standing position, a vein segment is percussed at one position while an examining hand feels for a "pulse wave" at another position. Percussion can be used to trace out the course of veins already detected by palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks. Valsalva or cough with the examiners hand over the medial aspect of the knee can often elicit a palpable pulse wave with florid saphenofemoral junction incompetence.
Indications
Surgical removal or obliteration of varicose veins is often for cosmetic reasons alone. Noncosmetic indications include symptomatic varicosities (eg, pain, fatigability, heaviness, recurrent superficial thrombophlebitis, bleeding), or for the treatment of venous hypertension after skin or subcutaneous tissue changes, such as lipodermatosclerosis, atrophie blanche, ulceration, or hyperpigmentation, have developed.8
Conservative treatment with stockings and external compression is an acceptable alternative to surgery, but worsening cutaneous findings or symptoms despite these measure usually warrant intervention. Nonetheless, a patient's desire for surgical management over conservative treatment or for cosmetic purposes alone are both reasonable relative indications for surgery.
Relevant Anatomy
The greater saphenous vein (GSV) originates on the medial foot as part of the venous arch and receives tributaries from deep veins of the foot as it courses upward along the anterior aspect of the medial malleolus. From the ankle, the GSV continues along the anteromedial aspect of the calf to the knee and into the thigh, where it is found more medially. From the upper calf to the groin, the GSV is usually contained within an envelope of thin fascia. Visualization of this fascial envelope is an important way of identifying the GSV with duplex ultrasound. This fascial envelope often prevents the GSV from becoming significantly dilated, even when large volumes of reflux pass along its entire length. A normal GSV is typically 3-4 mm in diameter in the mid thigh.
Along its course, a variable number of named perforating veins may connect the GSV to the deep system at the femoral, posterior tibial, gastrocnemius, and soleal veins. The Cockett perforators, between the ankle and the knee, are a special group of perforating veins. Rather than directly connecting the superficial to deep venous systems, they connect the subfascial deep system with the posterior arch vein, which then empties into the GSV (see Image 8).

Named perforators along the greater saphenous
distribution.
Besides perforating veins, the GSV has numerous superficial tributaries as it passes through the thigh. The most important of these are the posteromedial and anterolateral thigh veins, found at the level of the mid thigh, and the anterior and posterior accessory saphenous veins at the level of the canal of Hunter in the upper thigh, where a perforating vein often connects the GSV to the femoral vein. Just below the SFJ, the GSV receives several additional important tributary veins. These include the lateral and medial femoral cutaneous branches, the external circumflex iliac vein, the superficial epigastric vein, and the internal pudendal vein (see Image 9). These tributaries are frequently involved in the reflux that leads to the appearance of surface varicose veins on the lower thigh or upper calf.

Major tributaries of the greater saphenous
system.
The termination point of the GSV into the common femoral vein is called the saphenofemoral junction in the English literature but is known as the
crosse (ie, shepherd's crook) in the French medical literature (see Image 9). The terminal valve of the GSV is located within the junction itself. In most cases, at least one additional subterminal valve is present within the first few centimeters of the GSV. Most patients have a single subterminal valve that can be readily identified approximately 1 cm distal to the junctional valve.
Reflux at or near the SFJ does not always come through the terminal valve of the GSV, nor does it always involve the entire trunk of the GSV. Reflux can enter the GSV below the subterminal valve or even immediately below the junction, passing through a failed subterminal valve to mimic true SFJ incompetence. Reflux can also pass directly into any of the other veins that join the GSV at that level, or it may pass a few centimeters along the GSV and then abandon the GSV for another branch vessel (see Image 7).

Schematic diagram of the deep and superficial
venous systems of the lower extremity: (1) Normal venous
drainage; arrows depict the flow of venous blood. (2) Venous
hypertension bold arrows are pathways of venous
reflux.
When a perforating vein is the primary site of reflux, dilatation of the vessel proceeds both proximally and distally. When dilatation reaches the most proximal portion of the vein, the saphenofemoral or saphenopopliteal junction is often recruited as a secondary point of reflux. Although most large varices are tributaries off of an incompetent GSV or SSV, failed perforating veins or connecting veins can also give rise to independent varices in the greater saphenous distribution without involving the saphenous system itself. Identifying the originating point and the primary pathway of reflux in the thigh is often difficult, which is why duplex ultrasound has become so helpful in varicose vein workup.
9,10 Contraindications
- Patients with venous outflow obstruction should not have their varicosities ablated because they are important bypass pathways that allow blood to flow around the obstruction.
- Those patients who cannot remain active enough to reduce the risk of postoperative deep vein thrombosis (DVT) should not undergo surgery.
- Surgery during pregnancy is contraindicated because many varicose veins of pregnancy spontaneously regress after delivery.
Workup
Laboratory Studies
- No currently available lab test is useful in the diagnosis or therapy of varicose veins.
- Patients with varicose veins may have a spuriously positive D-dimer test result because of chronic low-level thrombosis within varices. See the eMedicine topic Deep Venous Thrombosis and Thrombophlebitis for more information.
Diagnostic Procedures
The duplex ultrasound (US) has become the most useful tool for workup and has replaced many of the physical examination maneuvers and physiological tests once used for diagnosis.
Tests used to rule out deep vein thrombosis obstruction as a cause of varicose veins
- Duplex US: This is noninvasive imaging with good sensitivity and selectivity. See the DVT section for more discussion.
- Perthes maneuver/Linton test: This is a physical examination technique in which a tourniquet is placed over the proximal part of the leg to compress any superficial varicose veins while leaving deep veins unaffected. The patient walks or performs toe-stands to activate the calf-muscle pump which normally causes varicose veins to be emptied. However, if obstruction of the deep system exists, then activation of the calf-muscle pump causes a paradoxical congestion of the superficial venous system and engorgement of varicose veins resulting in a positive test. To verify, the patient is then placed supine, and the leg is then elevated (Linton test). If varices distal to the tourniquet fail to drain after a few seconds, again deep venous obstruction must be considered. This test is rarely performed in practice today with the advent of duplex imaging and assessment of the superficial and deep venous systems.
- Maximum venous outflow (MVO): The MVO is a functional test to help detect obstruction to venous outflow. It can help detect more proximal occlusion of the iliac veins and IVC, as well as extrinsic causes of obstruction in addition to DVTs. MVO uses plethysmography (technique to measure volume changes of the leg) to measure the speed at with which blood can flow out of a maximally congested lower leg when an occluding thigh tourniquet is suddenly removed.11
- Magnetic resonance venography (MRV): The most sensitive and most specific test to find causes of anatomic obstruction. MRV is particularly useful because unsuspected nonvascular causes for leg pain and edema may often be seen on the scan image when the clinical presentation erroneously suggests venous insufficiency or venous obstruction. However, this is an expensive test used only as an adjuvant when doubt still exists.11
Tests used to demonstrate reflux
- Duplex US with color-flow imaging (sometimes called triplex ultrasound): This is a special type of 2-dimensional ultrasound that uses Doppler-flow information to add color for blood flow in the image. Vessels in the blood are colored red for flow in one direction and blue for flow in the other, with a graduated color scale to reflect the speed of the flow. Venous valvular reflux is defined as regurgitant flow with Valsalva that lasts great than 2 seconds.
- Trendelenburg test: This physical examination technique distinguish patients with reflux at the SFJ from those with incompetent deep venous valves. The leg is elevated until the congested superficial veins have all collapsed. Direct pressure is used to occlude the GSV just below the SFJ. The patient stands with the occlusion still in place. If the distal superficial varicosities remains empty or fills very slowly, the principal entry point of high pressure into the superficial system is at the SFJ. Rapid filling despite manual occlusion means that some other reflux pathway is involved.
- Doppler auscultation: A Doppler transducer is positioned along the axis of a vein with the probe at an angle of 45° to the skin. When the distal vein is compressed, audible forward flow exists. If the valves are competent, no audible backward flow is heard with the release of compression. If the valves are incompetent, an audible backflow exists. These compression-decompression maneuvers are repeated while gradually ascending the limb to a level at which the reflux can no longer be appreciated.
- Venous refilling time (VRT): This is a physiologic test, again using plethysmography. The VRT is the time necessary for the lower leg to become infused with blood after the calf-muscle pump has emptied the lower leg as thoroughly as possible. In healthy subjects, venous refilling is greater than 120 seconds. In patients with mild and asymptomatic venous insufficiency, VRT is between 40 and 120 seconds. In patients with significant venous insufficiency, VRT is abnormally fast at 20-40 seconds. Such patients often complain of nocturnal leg cramps, restless legs, leg soreness, burning leg pain, and premature leg fatigue. A VRT of less than 20 seconds is markedly abnormal, and is nearly always symptomatic. If the VRT is less than 10 seconds, venous ulcerations are likely.11
- Muscle pump ejection fraction (MPEF): The MPEF test is used to detect failure of the calf muscle pump to expel blood from the lower leg. MPEF results are highly repeatable but require a skilled operator. The patient performs ankle dorsiflexion 10-20 times, and plethysmography is used to record the change in calf blood volume. In healthy patients, the venous systems will drain, but in patients with muscle pump failure, severe proximal obstruction, or severe deep vein insufficiency, the amount of blood remaining within the calf has little or no change.11
Tests used to define anatomy
- Duplex US
- Two-dimensional ultrasound forms an anatomic picture based on the time delay of ultrasonic pulses reflected from deep structures. Structures that absorb, transmit, or scatter ultrasonic waves appear as dark areas; structures that reflect the waves back to the transducer appear as white areas in the image. Vessel walls reflect ultrasound waves; blood flowing in a vessel absorbs and scatters ultrasound waves in all directions. The normal vessel appears as a dark-filled, white-walled structure.
- Duplex ultrasound is a combination of anatomic imaging by 2-dimensional ultrasound and flow detection by Doppler shift. With duplex ultrasound, after the 2-dimensional anatomic image is displayed, a particular spot in the image can be selected for Doppler-shift measurement of flow direction and velocity.
- Structural details that can be observed include the most delicate venous valves, small perforating veins, reticular veins as small as 1 mm in diameter, and (using special 13-MHz probes) even tiny lymphatic channels.
- Direct contrast venogram: An intravenous catheter is placed in a dorsal vein of the foot, and radiographic contrast material is infused into the vein. X-rays are then used to obtain an image of the superficial venous anatomy. If deep vein imaging is desired, a superficial tourniquet is placed around the leg to occlude the superficial veins and contrast is forced into the deep veins. Assessment of reflux can be difficult because it requires passing a catheter from ankle to groin, with selective introduction of contrast material into each vein segment. This is a labor-intensive and invasive venous imaging technique with a 15% chance of developing new venous thrombosis from the procedure itself. It is rarely used, and has been replaced by duplex ultrasound. Its use is reserved for difficult or confusing cases.
Staging
This classification is based on the clinical, etiological, anatomic, pathophysiological (CEAP) classification from the American Venous Forum, last revised 2004.12 It is used to standardize recording of venous disease, as follows:
- Clinical
- C0 - No visible or palpable signs of venous disease
- C1 - Telangiectases or reticular veins
- C2 - Varicose veins
- C3 - Edema
- C4a - Pigmentation or eczema
- C4b - Lipodermatosclerosis or atrophie blanche
- C5 - Healed venous ulcer
- C6 - Active venous ulcer
- S – Symptomatic, includes: ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and other complaints attributable to venous dysfunction
- A - Asymptomatic
- Etiologic classification
- Ec - Congenital
- Ep - Primary
- Es - Secondary (post-thrombotic)
- En - No venous cause identified
- Anatomic classification
- As - Superficial veins
- Ap - Perforator veins
- Ad - Deep veins
- An - No venous location identified
- Pathophysiologic classification
- Basic CEAP
- Pr - Reflux
- Po - Obstruction
- Pr,o – Reflux and obstruction
- Pn - No venous pathophysiology identifiable
- Advanced CEAP: Same as basic CEAP, with addition that any of 18 named venous segments can be used as locators for venous pathology
- Superficial veins: (1) telangiectasias or reticular veins, GSV (2) above knee or (3) below knee, (4) small saphenous vein, or (5) nonsaphenous veins
- Deep veins: (6) Inferior vena cava, (7) common iliac vein, (8) internal iliac vein, (9) external iliac vein, (10) pelvic veins - gonadal, broad ligament veins, other, (11) common femoral vein, (12) deep femoral vein, (13) femoral vein, (14) popliteal vein, (15) crural veins (anterior tibial, posterior tibial, peroneal veins (all paired)), or (16) muscular veins - gastrocnemial, soleal veins, other.
- Perforating veins: (17) Thigh or (18) calf
Example: A patient has painful swelling of the leg, and varicose veins, lipodermatosclerosis, and active ulceration. Duplex scanning on May 17, 2004, showed axial reflux of the great saphenous vein above and below the knee, incompetent calf perforator veins, and axial reflux in the femoral and popliteal veins. No signs of post-thrombotic obstruction are present.
- Classification according to basic CEAP: C6,S, Ep,As,p,d, Pr.
- Classification according to advanced CEAP: C2,3,4b,6,S, Ep,As,p,d, Pr2,3,18,13,14 (2004-05-17, L II).12
Treatment
Surgical Therapy
The surgical treatment of varicose veins have been under development for more than 2000 years, but until the present era, relatively little weight was given to the cosmetic outcome of treatment. Current therapies are becoming less invasive with improved recovery, but long-term outcomes are uncertain. Therapies aim to remove the superficial venous system either through surgery, endovenous ablation, or sclerotherapy ablation.
In 90% of cases where venous hypertension is from superficial and perforator vein reflux, removal or obliteration of the GSV alone can resolve the venous hypertension.7,13 However, in the remaining 10%, additional treatment to the incompetent perforator veins may be needed. Additionally, if severe deep venous incompetence exists, treatment of the GSV alone usually does not resolve the venous hypertension. In both these cases, additional interventions with subfascial endoscopic perforating vein surgery (SEPS), perforator vein ablation, and/or venous reconstruction can be attempted, but these details are not further discussed in this article.
For now, the authors will discuss the procedures to remove or obliterate the superficial venous system, starting from most to least invasive. Historical perspectives, advantages, and disadvantages to each technique will also be addressed. However, prior to any intervention, duplex US should always be used to map all major reflux pathways, and a skin marker should be used to mark all surface vessels to be removed.
Open Techniques
The Rindfleisch-Friedel procedure of the early 1900s involved one incision to the level of the deep fascia that wrapped around the leg 6 times, creating a spiral gutter that brought into view a large number of superficial veins, each one of which was ligated. This wound was left open to heal by granulation. The Linton procedure, introduced in the late 1930s, used a large linear medial leg incision that brought into view all the superficial and perforator veins of the leg. Incompetent superficial veins were removed, and perforating veins were interrupted.
14 Friedrich Trendelenburg, in the late 1800s, introduced a midthigh ligation of the GSV. The outcomes were variable, and this procedure was later modified by Trendelenburg's student Perthes, who advocated a groin incision and a ligation of the GSV at the saphenofemoral junction. Later, even better outcomes were found if saphenectomy (removal of the GSV) with ligation at the SFJ was performed over ligation alone. In a randomized trial, two thirds of patients with ligation without saphenectomy could be expected to need reintervention within 5 years for recurrent reflux, either through recanalization or collateral formation around the ligated GSV.
14,15 GSV saphenectomy
Surgical removal of the GSV has evolved from large open incisions to less invasive stripping. Original methods of stripping used different devices and variations of techniques. The Mayo stripper was an extraluminal ring that cut the tributaries as it was passes along the vein. The Babcock device was an intraluminal stripper with an acorn-shaped head that pleated up the vein as it pulled the vessel loose from its attachments. The Keller device was an internal wire used to pull the vein through itself, as is done today with perforation-invagination (PIN) strippers.
Currently, the technique of PIN stripping begins with a 2- to 3-cm incision made at the groin crease. The femoral vein and SFJ are exposed with dissection and all tributaries of the SFJ must be identified and flush-ligated to minimize the incidence of reflux recurrence.
After ligation and division of the junction, the stripping instrument (usually a stiff but flexible length of wire or plastic) is passed into the GSV at the groin and threaded through the incompetent vein distally to the level of the upper calf. The stripper is brought out through a small incision (5 mm or smaller) approximately 1 cm from the tibial tuberosity at the knee. An inverting head is attached to the stripper at the groin and is secured to the proximal end of the vein. The vessel is then inverted into itself, tearing away from each tributary and perforator as the stripper is pulled downward through the leg and out through the incision in the upper calf (see Image 11). If desired, a long epinephrine-soaked gauze or ligature may be secured to the stripper before invagination, allowing hemostatic packing to be pulled into place after stripping is complete.
An older technique of stripping to the ankle (rather than to just the knee) has fallen into disfavor because of a high incidence of complications, including damage to the saphenous nerve, which is closely associated with the vein below the knee.9
SSV saphenectomy
Removal of the short saphenous vein is complicated by variable local anatomy and risk of injury to the popliteal vein and peroneal nerve. The saphenopopliteal junction must be located by duplex examination before beginning the dissection, and adequate direct visualization of the junction is essential. After ligation and division of the junction, the stripping instrument (often a more rigid stripper that facilitates navigation) is passed downward into the distal calf, where it is brought out through a small incision (2-4 mm). The stripper is secured to the proximal end of the vein, which is invaginated into itself as it is pulled downward from knee to ankle and withdrawn from below.
Stab phlebectomy (or ambulatory phlebectomy)
Performed by Galen as early as the second century, this procedure came back into modern favor during the 1960s and has increased in popularity ever since. This procedure is extremely useful for the treatment of residual vein clusters after saphenectomy and for removal of nontruncal tributaries when the saphenous vein is competent.
A microincision is made over the vessel using a tiny blade or a large needle, a phlebectomy hook is introduced into the microincision, and the vein is delivered through the incision. With traction, as long a segment as possible is pulled out of the body until the vein breaks or cannot be pulled any further. Another microincision is made and the process is begun again and repeated along the entire length of the vein to be extracted. Short segments of veins can be removed through tiny incisions without ligatures, and skin closure is not necessary.9
Endovascular Techniques
Endovenous (EV) laser
A laser fiber produces endoluminal heat that destroys the vascular endothelium. A Seldinger technique is used to advance a long catheter along the entire length of the truncal varicosity (usually the GSV) to be ablated. A bare laser fiber is passed through the catheter until the end protrudes from the tip of the catheter by approximately 2 cm, and the laser fiber tip is positioned at the SFJ just distal to the subterminal valve. The position is confirmed by ultrasound and by use of the laser guide light.
Under ultrasound guidance, tumescent solution with a local anesthetic is injected around the entire length of the vessel, separating it from its fascial sheath. This serves to insulate the heat from damaging adjacent structures, including nerves and skin, as well as pain control.
Firm pressure is applied to collapse the vein around the laser fiber, and the laser is fired generating heat, leading to intraluminal steam bubbles and irreversible endothelial damage and thrombosis. The fiber and catheter are withdrawn approximately 2 mm, and the laser is fired again. This process is repeated along the entire course of the vessel.
16 Radiofrequency (RF) ablation
RF thermal energy is delivered directly to the vessel wall, causing protein denaturation, collagenous contraction, and immediate closure of the vessel. In contrast to laser therapy, the RF catheter actually comes into contact with the lumen walls.
An introducer sheath is inserted into the proposed vein of treatment (again usually the GSV). A special RF ablation catheter is passed through the sheath and along the vein until the active tip is at the SFJ just distal to the subterminal valve. Just like the endovenous laser, tumescent local anesthetic is injected.
Metal fingers at the tip of the RF catheter are deployed until they make contact with the vessel endothelium. RF energy is delivered, both in and around the vessel to be treated. Thermal sensors record the temperature within the vessel and deliver just enough energy to ensure endothelial ablation. The RF catheter is withdrawn a short distance, and the process is repeated all along the length of the vein to be treated.
Minimally Invasive Techniques
Cutaneous electrodesiccation This is an old technique involving electrical cautery for destruction of small vessels that is rarely used today because of the disfiguring cutaneous injury.
Sclerotherapy Chemical sclerosis of varicose veins has waxed and waned in popularity since the late 1800s. Modern sclerosants with an acceptable risk profile became widely available in the 1930s, and, since that time, there use has expanded. Initially, sclerotherapy was used as a surgical adjunct after saphenectomy to treat residual varicosities, reticular veins, or telangiectasias. Now it is being used to treat the GSV and main tributaries.
Under US guidance, a sclerosing substance is injected into abnormal vessels to produce endothelial destruction that is followed by formation of a fibrotic cord and eventual reabsorption of all vascular tissue layers (see Image 12).
Local treatment of the superficial manifestations of venous insufficiency will always fail if the underlying high points of reflux have not been found and treated. Even when the patient appears to have only primary telangiectasias and the initial treatment seems to be successful, recurrences will be seen very quickly if unrecognized reflux exists in larger subsurface vessels.
Caution must be used when using sclerosing agents, inadvertent injection into an arteriovenous malformation or directly into an unrecognized artery can cause extensive tissue loss or loss of the entire limb. Inadvertent injection of concentrated sclerosants into the deep system can cause DVT, pulmonary embolism, and death.
The most commonly used sclerosants today are polidocanol and sodium tetradecyl sulfate. Both are known as detergent sclerosants because they are amphiphilic substances, inactive in dilute solution, but biologically active when they form micelles. These agents are preferred because they have a low incidence of allergic reactions, produce a low incidence of staining and other adverse cutaneous effects, and are relatively forgiving if extravasated. Polidocanol, the most forgiving sclerosing agent, was originally developed as a local anesthetic agent.
Other agents that have fallen out of favor include sodium morrhuate, associated with a relatively high incidence of anaphylaxis. Ethanolamine oleate, a weak detergent, is excessively soluble, decreasing its ability to denature cell surface proteins. Hypertonic saline in a 20% or 23.4% solution can be used as a sclerosing agent, but, because of dilutional effects with injection, it is difficult to achieve adequate sclerosis of large vessels without exceeding a tolerable salt load. If extravasated, it almost invariably causes significant necrosis.
The addition of foam with the sclerosing agents has allowed for decreased amounts of sclerosing agent injection and improved efficacy.
17 Foam pushes blood out of the vein, allowing for less dilution and more contact of the sclerosant with the endothelium. Homemade foam is usually air agitated in saline. This has theoretical risks of air emboli, so commercially available foam consists of mostly carbon dioxide. Varisolve (BTG, West Conshohocken, PA) is one such product using carbon dioxide foam and polidocanol sclerosant (see Image 13).
18 
Varisolve canister and appearance of foam with
polidocanol.
In the US, sodium tetradecyl sulfate, sodium morrhuate, and ethanolamine oleate were all developed prior to the establishment of the FDA. These agents have never been submitted to the FDA for approval, but they are available in the United States as grandfathered agents. No FDA–approved foam/sclerosing agents are available; however, the Varisolve product is currently under clinical trials in the United States after being used extensively in Europe.
18 Postoperative Details
After treatment of large varicose veins by any method, a 30- to 40-mm Hg gradient compression stocking is applied and patients are instructed to maintain or increase their normal activity levels. Most practitioners also recommend the use of gradient compression stockings even after treatment of spider veins and smaller tributary veins.
Ace wraps and other long-stretch bandages should not be used. These elastic bandages fail to maintain adequate compression for more than a few hours. They often slip or are misapplied by patients, with a resulting tourniquet effect that causes distal swelling and increases the risk of DVT.
Activity is particularly important after treatment by any technique because all modalities of treatment for varicose disease have the potential to increase the risk of DVT. Activity is a strong protective factor against venous stasis. Activity is so important that most venous specialists will not treat a patient who is unable to remain active following treatment.
Follow-up
For patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education articles Varicose Veins, Blood Clot in the Legs, and Phlebitis.
Complications
A correct diagnosis of superficial venous insufficiency is essential. Veins should be treated only if they are incompetent and if a normal collateral pathway exits. Removal of a saphenous vein with a competent termination will not aid in the management of nontruncal tributary varices.
In the setting of deep system obstruction, varicosities are hemodynamically helpful because they provide a bypass pathway for venous return. Hemodynamically helpful varices must not be removed or sclerosed. Ablation of these varicosities will cause rapid onset of pain and swelling of the extremity, eventually followed by the development of new varicose bypass pathways.
The most annoying minor complications of any venous surgery are dysesthesias from injury to the sural nerve or the saphenous nerve. Subcutaneous hematoma is a common complication, regardless of treatment technique used. It is easily managed with warm compress, NSAIDS, or aspiration if necessary.
At the saphenofemoral junction, accidental treatment of the femoral vein by inappropriate RF or laser catheter placement, or spread of sclerosant (not visualizing progression with US), or inappropriate surgical ligation can all lead to endothelium damage at the deep vein, causing deep vein thrombosis (DVT) formation with the potential of pulmonary embolism (PE) and even death.16
Other complications, such as postoperative infection and arterial injury, are less common and may be kept to a minimum through strict attention to good technique.
Endovenous treatment techniques (with RF and laser therapy) have the potential of excessive tissue heating, which can lead to skin burns. This problem can be avoided if sufficient volumes of tumescent anesthetic are injected to elevate the skin away from the vein.16
Outcome and Prognosis
With appropriate treatment, the vast majority of patients have a good outcome and the progression of their disease is arrested. Saphenectomy has been the criterion standard to which most therapies are compared.
In a randomized trial comparing radiofrequency (RF) ablation to saphenectomy, 2-year reoccurrence rates were nonsignificantly different at 14% versus 21%, respectively. Quality of life scores were better for RF obliteration versus saphenectomy.19
The long-term results of endovenous (EV) laser compared with saphenectomy have not been as well validated. In a randomized trial, follow-up was only 6 months, and the authors found 0% versus 5.8% recanalization in EV laser versus saphenectomy. Saphenectomy did have higher postoperative pain, but overall quality of life scores remained equal. Other results were similar between the saphenectomy versus EV laser groups; mean time to resume normal physical activity was 7.7 versus 6.9 calendar days, mean time to resume work was 7.6 versus 7.0 calendar days, and total cost of the procedures, including lost wages, were $3948 versus $4347, respectively.20
One randomized trial has compared RF to EV laser ablation of the GSV. This was a single institution, and they found significantly increased closure rate after RF (80%) versus EV laser (66%) treatment at one year follow-up. The DVT, paresthesias, leg edema, and superficial thrombophlebitis complication rates were equal in the 2 groups.21
Foam sclerotherapy has been used in Europe, and phase III randomized clinical trials, with multiple arms, have compared it with saphenectomy and sclerotherapy without foam. At 12 months, GSV closure rates were 87.2% in the saphenectomy versus 68.2% in the Varisolve arm. But in the other arm, sclerotherapy without foam versus Varisolve, closure rates for the Varisolve group were much improved at 93.8%. Although surgery was more efficacious, Varisolve did cause less pain and patients returned to normal more quickly.18 In the 710 patients enrolled, no pulmonary embolus were found, and DVTs were found in 2.5% of Varisolve, none in surgery, and 0.8% in those who received sclerotherapy without foam. In the US clinical trials are underway to assure there is no increased risk of embolic stroke from the use of Varisolve.
Future and Controversies
Management of varicose veins has evolved over the centuries and will continue to do so. Less invasive techniques continue to be refined but long-term efficacy must always be questioned and compared with the criterion standard of surgical saphenectomy.
Multimedia

Media file 1:
Pathway leading to varicose veins and other
clinical manifestations of venous hypertension.

Media file 2:
Telangiectasias.

Media file 3:
Reticular veins.

Media file 4:
Varicose veins.

Media file 5:
Lipodermatosclerosis.

Media file 6:
Venous stasis ulcer.

Media file 7:
Schematic diagram of the deep and superficial
venous systems of the lower extremity: (1) Normal venous
drainage; arrows depict the flow of venous blood. (2) Venous
hypertension bold arrows are pathways of venous
reflux.

Media file 8:
Named perforators along the greater saphenous
distribution.

Media file 9:
Major tributaries of the greater saphenous
system.

Media file 10:
Saphenofemoral junction.

Media file 11:
Perforation-invagination (PIN) stripping
schematic.

Media file 12:
Ultrasound image of the GSV after foam
sclerotherapy treatment. Note the hyperechogenicity within the
vein is from the foam.

Media file 13:
Varisolve canister and appearance of foam with
polidocanol.
References
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Kalra M, Gloviczki P. Surgical treatment of venous ulcers: role of subfascial endoscopic perforator vein ligation. Surg Clin North Am. Jun 2003;83(3):671-705. [Medline].
Caggiati A, Allegra C. Historical Introduction. In: The Vein Book. New York, New York: Elsevier; 2006:1-14.
Dwerryhouse S, Davies B, Harradine K, Earnshaw JJ. Stripping the long saphenous vein reduces the rate of reoperation for recurrent varicose veins: five-year results of a randomized trial. J Vasc Surg. Apr 1999;29(4):589-92. [Medline].
Johnson CM, McLafferty RB. Endovenous laser ablation of varicose veins: review of current technologies and clinical outcome. Vascular. Sep-Oct 2007;15(5):250-4. [Medline].
Rabe E, Otto J, Schliephake D, Pannier F. Efficacy and safety of great saphenous vein sclerotherapy using standardised polidocanol foam (ESAF): a randomised controlled multicentre clinical trial. Eur J Vasc Endovasc Surg. Feb 2008;35(2):238-45. [Medline].
Wright D, Gobin JP, Bradbury AW, et al. Varisolve® polidocanol microfoam compared with surgery or sclerotherapy in the management of varicose veins in the presence of trunk vein incompetence: European randomized controlled trial. Phlebectomy. 2006;21:180-90.
Lurie F, Creton D, Eklof B, Kabnick LS, Kistner RL, Pichot O. Prospective randomised study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. Eur J Vasc Endovasc Surg. Jan 2005;29(1):67-73. [Medline].
Rasmussen LH, Bjoern L, Lawaetz M, Blemings A, Lawaetz B, Eklof B. Randomized trial comparing endovenous laser ablation of the great saphenous vein with high ligation and stripping in patients with varicose veins: short-term results. J Vasc Surg. Aug 2007;46(2):308-15. [Medline].
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Keywords
varicose veins, varicose vein, varicosities, varicosity, telangiectasia, venectasia, spider vein, reticular vein, venous disease, swollen veins, telangiectatic veins, vein disease, venous insufficiency, chronic venous insufficiency
Contributor Information and Disclosures
Author
Wesley K Lew, MD, Resident, Department of General Surgery, University of Southern California
Disclosure: Nothing to disclose.
Coauthor(s)
Fred A Weaver, MD, Professor of Surgery, University of Southern California; Chief, Division of Vascular Surgery, Director of Noninvasive Vascular Laboratory, Program Director of Vascular Surgery, University of Southern California University Hospital;
Fred A Weaver, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Surgery of Trauma, American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Peripheral Vascular Surgery Society, Phi Beta Kappa, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Society of University Surgeons, and Western Surgical Association
Disclosure: CVRx Consulting fee Review panel membership
Craig F Feied, MD, FACEP, FAAEM, FACPh, Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group
Craig F Feied, MD, FACEP, FAAEM, FACPh is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Phlebology, American College of Physicians, American Medical Association, American Medical Informatics Association, American Venous Forum, Medical Society of the District of Columbia, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.
Medical Editor
Richard M Stillman, MD, FACS, Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center
Richard M Stillman, MD, FACS is a member of the following medical societies: American College of Angiology, American College of Surgeons, Association for Academic Surgery, and Society of University Surgeons
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Vincent Lopez Rowe, MD, Assistant Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center
Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, Association for Academic Surgery, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, and Society for Vascular Surgery
Disclosure: Nothing to disclose.
CME Editor
Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.
Chief Editor
William H Pearce, MD, Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University School of Medicine
William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, and Western Surgical Association
Disclosure: Nothing to disclose.