Varicose Vein Surgery

Practice Essentials

The description of varicose veins as a clinical entity can be traced back as early as the fifth century BCE. Hippocrates, Galen, and others described the disease and treatment modalities, which are still used today.^[1]  Throughout the centuries, surgical treatments have evolved from large open procedures to minimally invasive approaches.

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.

Varicose veins and even chronic venous insufficiency can be managed conservatively with stockings and compression. More aggressive management can be pursued if cosmetic improvement is desired, if cutaneous findings or symptoms worsen despite conservative management, or if the patients prefer surgical management. Most procedures to treat varicose veins can be elective, and emergency treatment and workup are usually reserved for bleeding varicosities or cases where deep venous thrombosis (DVT) is suspected.

For patient education resources, see Varicose Veins, Blood Clot in the Legs, and Phlebitis.

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Anatomy

Two venous systems are found in the lower extremity: deep and superficial (see the image below). The deep system ultimately leads backs to the inferior vena cava (IVC), 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 two largest: the great saphenous vein (GSV; also referred to as the greater saphenous vein) and the small saphenous vein (SSV; also referred to as the short, smaller, or lesser saphenous vein).

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Schematic diagram of deep and superficial venous systems of lower extremity: (1) Normal venous drainage; arrows depict flow of venous blood. (2) Veno....

The 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 ultrasonography (DUS). 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 midthigh.

Along its course, a variable number of named perforating veins transverse the deep fascia of the lower extremity and connect the GSV to the deep system at the femoral, posterior tibial, gastrocnemius, and soleal veins (see the image below). The Cockett perforators, between the ankle and the knee, are a special group of perforating veins. Rather than directly connecting the superficial to the deep venous system, they connect the subfascial deep system with the posterior arch vein, which then empties into the GSV.

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Named perforators along great saphenous distribution.

Besides perforating veins, the GSV has numerous superficial tributaries as it passes through the thigh (see the image below). The most important of these are the posteromedial and anterolateral thigh veins, found at the level of the midthigh, 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.

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Major tributaries of great saphenous system.

Just below its junction with the common femoral vein, 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. These tributaries are frequently involved in the reflux that leads to the appearance of surface varicose veins on the lower thigh or upper calf.

The termination point of the GSV into the common femoral vein, located proximally at the groin, is called the saphenofemoral junction (SFJ) in the English literature but is known as the crosse (ie, shepherd's crook) in the French medical literature (see the image below). 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.

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Saphenofemoral junction.

The saphenopopliteal junction (SPJ) is located behind the knee where the SSV joins with the popliteal vein.

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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 process, it is necessary to be familair with the anatomy of the lower-extremity venous system, as outlined above (see Anatomy).

In healthy veins, the flow of venous blood is through the superficial system into the deep system and up the leg and toward the heart (see the image below). 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.

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Schematic diagram of deep and superficial venous systems of lower extremity: (1) Normal venous drainage; arrows depict flow of venous blood. (2) Veno....

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 DUS scanning.^[2] 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 the 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 circle A in the image above).^[3]

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.

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 SFJ or the SPJ 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 GSV 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 DUS has become so helpful in varicose vein workup.^{[4, 5]}

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.^[3]

Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious circle. 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. The inciting etiology of superficial valvular insufficiency is often difficult to determine because the clinical manifestations of venous hypertension are delayed (see Etiology).

The clinical findings 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.^[6]

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.

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Etiology

The etiology of varicose veins can be subdivided into three categories: primary, secondary, and congenital (see the image below).

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Pathway leading to varicose veins and other clinical manifestations of venous hypertension.

The cause of primary varicose veins is valvular insufficiency of the superficial veins, most commonly at the SFV, resulting in venous hypertension.

Secondary varicose veins are mainly caused by DVT that leads to chronic deep venous obstruction or valvular insufficiency. Long-term clinical sequelae from this have been called the postthrombotic syndrome. This category also includes catheter-associated DVT. Pregnancy-induced and progesterone-induced venous wall and valve weakness worsened by expanded circulating blood volume and enlarged uterus can compress the IVC and hinder venous return from the lower extremities. Trauma is another possible cause of secondary varicose veins.

The congenital category includes any venous malformations. Examples include Klippel-Trenaunay variants and avalvulia.

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Epidemiology

The incidence and prevalence of varicose veins has been studied in a number of cross-sectional studies.

In 1973, the US Tecumseh community health study estimated that about 40 million persons (26 million females) in the United States were affected.^[7] In 1994, a review by Callam found that half of the adult population have minor stigmata of venous disease (women, 50-55%; men, 40-50%) and that fewer than half have visible varicose veins (women, 20-25%; men, 10-15%).^[8] In 2004, these findings were also seen in a French cross-sectional study that found the odds ratio per year for varicose veins to be 1.04 for women and 1.05 for men.^[9]

Age and sex have been the only consistently identified risk factors for varicose veins.^{[7, 9]}

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Prognosis

With appropriate treatment, the vast majority of patients have a good outcome and the progression of their disease is arrested. Surgical stripping of the GSV, or saphenectomy, has been the criterion standard to which most therapies are compared.

In a randomized trial entitled the EVOLVeS (EndoVenous radiofrequency ObLiteration Versus ligation and Stripping) study, 68 legs were randomly assigned to undergo radiofrequency ablation (RFA) or surgical stripping of the GSV. Immediate success rates for RFA and stripping on the day of treatment were 95% and 100%, respectively. At 3 weeks, DUS confirmed closure of the GSV in 90.9% of the RFA group.^[10]

In the extended 2-year follow-up, there was a nonsignificant difference of the cumulative rates of recurrent varicose veins: 14% for RFA and 21% for stripping. However global quality-of-life scores were still in favor of RFA.^[11]

In a randomized trial of 137 legs, endovenous laser ablation (EVLA) was compared with saphenectomy. Both methods were equally efficacious at obliterating the GSV, but the saphenectomy group had higher postoperative pain scores. Other similar results between the saphenectomy and EVLA groups included time to resume normal physical activity (7.7 vs 6.9 days), time to resume work (7.6 vs 7 days), and total cost of the procedures ($3948 vs $4347 USD).^[12]

In another trial of 280 patients randomized to EVLA compared with saphenectomy, follow-up was extended to more than 1 year. At 1 year, the authors noted lower rates of clinical recurrence with EVLA versus surgery (4% vs 20.4%). Twelve of 23 surgical recurrences were related to an incompetent below-the-knee GSV and 10 to neovascularization. In the EVLA group, five recurrences were reported; two were related to neoreflux in the groin tributaries and one to recanalization.^[13]

In a subsequent randomized trial of 500 patients and 580 legs, endovenous ablation, RFA, foam sclerotherapy, and surgical stripping were compared. At 1 year, the failure rates were significantly different in each group. The highest failure rates were seen in the foam ablation (16.3%) and endovenous ablation (5.8%) groups. The lowest failure rates were seen in the RFA (4.8%) and stripping groups (4.8%), though these two groups also had the highest postintervention pain scores.^[14]

Foam sclerotherapy has been compared with saphenectomy and sclerotherapy without foam in phase III randomized clinical trials. At 12 months, GSV closure rates were 87.2% for saphenectomy versus 68.2% for Varisolve (BTG, West Conshohocken, PA; now marketed in the United States as Varithena).^[15] However, in the other arm (sclerotherapy without foam vs Varisolve), closure rates for Varisolve were much improved (93.8%). Although surgery was more efficacious, Varisolve caused less pain and allowed patients to return to normal more quickly. No pulmonary embolism (PE) was found, and DVT was found in 2.5% of Varisolve patients, no surgery patients, and 0.8% of those who received sclerotherapy without foam.

A study by Obi et al suggested that the combination of transilluminated powered phlebectomy with RFA may yield better outcomes, as measured by the venous clinical severity score, than the use of RFA alone.^[16]

A study by Rass et al that included 400 patients with GSV incompetence found the rate of same-site occurrence to be higher after EVLA than after high ligation and stripping of the GSV at 5-year follow-up (18% vs 5%).^[17]

In a randomized clinical trial comparing the results of conventional surgery, EVLA, and ultrasonography (US)-guided foam sclerotherapy in patients with varicose GSVs at 5 years, van der Velden et al found that the first two approaches were more effective than the third in obliterating the GSV at the end point of follow-up.^[18]

A 2014 Cochrane review found clinical trial evidence to suggest that US-guided foam sclerotherapy, EVLA, and RFA are at least as effective as surgery in treating GSV varicosities, though this evidence was lacking in robustness.^[19]

A 2016 Cochrane review comparing endovenous ablation (laser or radiofrequency) or foam sclerotherapy with conventional surgical repair for SSV varicosities found that recanalization or persistence of reflux at 6 weeks and recurrence of reflux at 1 year were less frequent with endovenous treatment than with conventional surgery; however, because of low-quality evidence, foam sclerotherapy could not be effectively compared with conventional surgery.^[20]

Wallace et al evaluated long-term (5-year) outcomes of EVLA and conventional surgery for symptomatic varicose veins due to GSV incompetence and found the former to be more effective on preventing clinical recurrence.^[21]  At 5 years, the clinical recurrence rate was 34.3% for surgery and 20.9% for EVLA. Technical success rates as assessed via DUS were 85.4% for surgery and 93.2% for EVLA. Patient-reported outcome measures were similar for the two groups.

In a randomized controlled trial that included 798 patients with primary varicose veins at 11 centers, Brittenden et al compared the 5-year outcomes of EVLA, US-guided foam sclerotherapy, and surgery.^[22]  The primary outcomes were disease-specific quality of life and generic quality of life, as well as cost-effectiveness. Disease-specific quality of life 5 years after treatment was better after EVLA or surgery than after foam sclerotherapy. The majority of the probabilistic cost-effectiveness model iterations favored laser ablation.

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History

Patients with varicose veins may have a host of symptoms, but they are usually caused by venous hypertension rather than by the varicosities 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).

In addition, pain associated with venous hypertension is usually a dull ache that is worsened by prolonged standing and is improved by walking or by elevating the legs. This is in contrast to the pain of arterial insufficiency, which worsens 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."

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

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Physical Examination

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 - Brownish darkening of the skin, resulting from extravasated blood that causes lipodermatosclerosis; this usually occurs in the medial ankle region but may extend to the leg and foot
• Varicose veins – Visible, palpable veins in the subcutaneous skin greater than 3 mm in diameter (see the first image below)
• Reticular veins (also called blue veins, subdermal varices, and venulectasias) – Visible, nonpalpable dilated bluish subdermal veins 1-3 mm in diameter (see the second image below)
• Telangiectases (also called spider veins, hyphen webs, and thread veins) – Dilated intradermal venules greater than 1 mm in diameter (see the third image below)
• 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 the fourth and fifth images below)

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Varicose veins.

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Reticular veins.

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Telangiectasias.

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Lipodermatosclerosis.

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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 (ABI) is useful if arterial insufficiency is suggested.

The anteromedial surface of the lower limb is the territory of the great 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 two 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 small saphenous vein (SSV). 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 deep venous thrombosis (DVT) may exist in as many as 40% of patients with superficial phlebitis.

Varices of recent onset are easily distinguished from chronic varices by means of 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

Percussion is useful in determining whether two 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 relations between the various varicose vein networks. Valsalva maneuver or cough with the examiner's hand over the medial aspect of the knee can often elicit a palpable pulse wave with florid SFJ incompetence.

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Approach Considerations

No currently available laboratory 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. For more information, see Deep Venous Thrombosis.

Duplex ultrasonography (DUS) has become the most useful tool for workup and has replaced many of the physical examination maneuvers and physiologic tests once used for diagnosis (see below).

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Tests for Ruling Out Deep Venous Thrombosis As Cause

Duplex ultrasonography

DUS is a noninvasive imaging modality with good sensitivity and selectivity for ruling out deep venous thrombosis (DVT) in this setting. (See Deep Venous Thrombosis.)

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 paradoxic 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. Currently, with the advent of duplex imaging and assessment of the superficial and deep venous systems, this test is rarely performed in practice.

Maximum venous outflow

Maximum venous outflow (MVO) is a functional test to help detect obstruction of venous outflow. It can help detect more proximal occlusion of the iliac veins and the inferior vena cava (IVC), as well as extrinsic causes of obstruction in addition to DVT. MVO uses plethysmography (a technique for measuring 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.^[23]

Magnetic resonance venography

Magnetic resonance venography (MRV) is the most sensitive and most specific test for finding 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 that is used only as an adjuvant when doubt still exists.^[23]

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Tests for Demonstrating Reflux

Duplex ultrasonography with color-flow imaging

DUS with color-flow imaging (sometimes called triplex ultrasonography [US]) is a special type of two-dimensional (2D) US 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 longer than 2 seconds.

Trendelenburg test

The Trendelenburg test is a physical examination technique that is used to distinguish patients with reflux at the saphenofemoral junction (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 great saphenous vein (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 the limb gradually ascends to a level at which the reflux can no longer be appreciated.

Venous refilling time

The venous refilling time (VRT) is a physiologic test that uses 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, the VRT is longer than 120 s. In patients with mild and asymptomatic venous insufficiency, the VRT is 40-120 s. In patients with significant venous insufficiency, the VRT is abnormally fast, 20-40 s. Such patients often complain of nocturnal leg cramps, restless legs, leg soreness, burning leg pain, and premature leg fatigue. A VRT shorter than 20 s is markedly abnormal and is nearly always symptomatic. If the VRT is shorter than 10 s, venous ulcerations are likely.^[23]

Muscle pump ejection fraction

The muscle pump ejection fraction (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 shows little or no change.^[23]

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Tests for Delineating Anatomy

Duplex ultrasonography

With 2D US, an anatomic picture is generated on the basis of the time delay of ultrasonic pulses reflected from deep structures. Structures that absorb, transmit, or scatter ultrasonic waves appear as dark areas in the image; structures that reflect the waves back to the transducer appear as white areas. 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.

DUS is a combination of anatomic imaging by 2D US and flow detection by Doppler shift. With DUS, after the 2D 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 (with special 13-MHz probes) even tiny lymphatic channels.

Direct-contrast venography

In direct-contrast venography, 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 material 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.

Direct-contrast venography is a labor-intensive and invasive venous imaging technique that carries a 15% risk of new venous thrombosis developing from the procedure itself. It is rarely used in current practice and has largely been supplanted by DUS. Its use is reserved for difficult or confusing cases.

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Staging

The clinical-etiologic-anatomic-pathophysiologic (CEAP) classification formulated by the American Venous Forum, last revised in 2004,^[24] is used to standardize recording of venous disease. Each of the four components of this classification is assessed individually, and the components are combined to determine the CEAP classification.

The clinical component of the CEAP classification is assessed as follows:

• C₀ - No visible or palpable signs of venous disease
• C₁ - Telangiectases or reticular veins
• C₂ - Varicose veins
• C₃ - Edema
• C_4a - Pigmentation or eczema
• C_4b - 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

The etiologic component of the CEAP classification is assessed as follows:

• E_c - Congenital
• E_p - Primary
• E_s - Secondary (postthrombotic)
• E_n - No venous cause identified

The anatomic component of the CEAP classification is assessed as follows:

• A_s - Superficial veins
• A_p - Perforator veins
• A_d - Deep veins
• A_n - No venous location identified

The pathophysiologic component of the CEAP classification is assessed in two ways, basic and advanced. The basic approach to this component includes the following:

• P_r - Reflux
• P_o - Obstruction
• P_r,o – Reflux and obstruction
• P_n - No venous pathophysiology identifiable

The advanced approach is the same as the basic one, with the additional option that any of 18 named superficial, deep, or perforating venous segments can be used as locators for venous pathology. The superficial veins that can be used, with their assigned numbers, are as follows:

• Telangiectasias or reticular veins (1)
• GSV above the knee (2)
• GSV below the knee (3)
• Small saphenous vein (SSV) (4)
• Nonsaphenous veins (5)

The deep veins that can be used, with their assigned numbers, are as follows:

• IVC (6)
• Common iliac vein (7)
• Internal iliac vein (8)
• External iliac vein (9)
• Pelvic veins - Gonadal, broad ligament veins, other (10)
• Common femoral vein (11)
• Deep femoral vein (12)
• Femoral vein (13)
• Popliteal vein (14)
• Crural veins - Anterior tibial, posterior tibial, peroneal veins (all paired) (15)
• Muscular veins - Gastrocnemial, soleal veins, other (16)

The perforating veins that can be used, with their assigned numbers, are as follows

• Thigh (17)
• Calf (18)

The following example illustrates the difference between the two approaches.^[24] A patient has painful swelling of the leg, and varicose veins, lipodermatosclerosis, and active ulceration. DUS on May 17, 2004, shows axial reflux of the GSV above and below the knee, incompetent calf perforator veins, and axial reflux in the femoral and popliteal veins. No signs of postthrombotic obstruction are present. The basic and advanced CEAP classifications for this patient are as follows:

• Basic CEAP - C_6,S, E_p,A_s,p,d, P_r
• Advanced CEAP - C_2,3,4b,6,S, E_p,A_s,p,d, P_{r2,3,18,13,14} (2004-05-17, L II)

• References

Approach Considerations

Surgical removal or obliteration of varicose veins is often for cosmetic reasons alone. Noncosmetic indications include treatment of symptomatic varicosities (eg, pain, fatigability, heaviness, recurrent superficial thrombophlebitis, bleeding) and treatment of venous hypertension after skin or subcutaneous tissue changes (eg, lipodermatosclerosis, atrophie blanche, ulceration, or hyperpigmentation) have developed.^[25]

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.

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.

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.

• References

Surgical Therapy

Surgical treatment of varicose veins has 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 and yielding improved recovery, but long-term outcomes are uncertain. Therapies aim to remove the superficial venous system through either surgery, endovenous ablation, or sclerotherapy.^[26]

In 90% of cases where venous hypertension is from superficial and perforator vein reflux, removal or obliteration of the great saphenous vein (GSV) alone can resolve the venous hypertension.^{[6, 27]} In the remaining 10%, however, 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, proceeding from most invasive to least invasive. Historical perspectives, advantages, and disadvantages to each technique will also be addressed. However, before any intervention, duplex ultrasonography (DUS) 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 six 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.^[28]

In the late 1800s, Trendelenburg 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 (SFJ).

Later, even better outcomes were found if saphenectomy (removal of the GSV) with ligation at the SFJ was performed in place of ligation alone. In a randomized trial, two thirds of patients treated with ligation without saphenectomy could be expected to need reintervention within 5 years for recurrent reflux, either from recanalization or from collateral formation around the ligated GSV.^{[28, 29, 30]}

Excision of GSV

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 passed 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 the 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 (≤5 mm) incision 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 the image below). 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.

View Image

Perforation-invagination (PIN) stripping schematic.

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.^[4]

Excision of SSV

Removal of the small saphenous vein (SSV) is complicated by the variable local anatomy and the risk of injury to the popliteal vein and peroneal nerve. The saphenopopliteal junction (SPJ) must be located by duplex examination before the dissection is begun, and adequate direct visualization of the SPJ is essential.

After ligation and division of the SPJ, 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 (2-4 mm) incision. 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

Performed by Galen as early as the second century, stab phlebectomy (also referred to as ambulatory phlebectomy) 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 with 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.^[4]

Endovascular techniques

Endovenous laser treatment

A laser fiber produces endoluminal heat that destroys the vascular endothelium. In endovenous laser treatment of varicose veins, a Seldinger technique is used to advance a long catheter along the entire length of the truncal varicosity to be ablated (usually the GSV). 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 means of ultrasonography (US) and the use of the laser guide light.

Under US 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 that leads 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.^{[31, 26]}

Radiofrequency ablation

In radiofrequency ablation (RFA) of varicose veins, radiofrequency (RF) thermal energy is delivered directly to the vessel wall, causing protein denaturation, collagenous contraction, and immediate closure of the vessel. Unlike the endovenous laser fiber, 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 catheter is passed through the sheath and along the vein until the active tip is at the SFJ just distal to the subterminal valve. As with 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.

Subramonia and Lees found that in comparison with conventional high ligation and stripping, RFA of GSV varicosities took longer to perform, but patients returned to their normal activities significantly earlier and had significantly less postoperative pain.^[32]

Cyanoacrylate

Endovenous treatment of varicose veins with N-butyl cyanoacrylate is receiving increasing interest and has shown promising midterm results.^{[33, 34]}

Minimally invasive techniques

Cutaneous electrodesiccation

This is an old technique involving electrical cautery for destruction of small vessels. Because of the disfiguring cutaneous injury, it is rarely used today.

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, their use has expanded. Initially, sclerotherapy was used as a surgical adjunct after saphenectomy to treat residual varicosities, reticular veins, or telangiectasias. Currently, 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 the image below).

View Image

Ultrasonogram of great saphenous vein after foam sclerotherapy. Note that hyperechogenicity within vein is from foam.

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 exercised in the use of sclerosing agents. Inadvertent injection into an arteriovenous malformation (AVM) 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 (PE), 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 reduction of the amount of sclerosing agent injected, as well as improved efficacy.^[35] Foam pushes blood out of the vein, decreasing dilution and increasing contact of the sclerosant with the endothelium. Homemade foam is usually air-agitated in saline. Because of the theoretical risks of air embolism, commercially available foam consists mostly of carbon dioxide. Varisolve (known as Varithena in the United States) is one such product, using carbon dioxide foam and polidocanol sclerosant (see the image below).^{[15, 26]}

View Image

Varisolve canister and appearance of foam with polidocanol.

In the US, sodium tetradecyl sulfate, sodium morrhuate, and ethanolamine oleate were all developed before the establishment of the US Food and Drug Administration (FDA). These agents have never been submitted to the FDA for approval, but they are available in the United States as grandfathered agents. In November 2013, Varithena (Biocompatibles, Oxford, CT) was approved by the FDA for clinical use in the United States.^[36]

• References

Postoperative Care

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.

O'Hare et al found that compression bandaging for 24 hours, followed by use of thromboembolus-deterrent stockings for the remainder of 14 days, gave results comparable to compression bandaging for 5 days. In a randomized trial in patients undergoing foam sclerotherapy for primary uncomplicated varicose veins, no significant difference was noted in vein occlusion, phlebitis, skin discoloration, or pain at 2 and 6 weeks with the two techniques.^[37]

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.

Guidelines for the use of compression therapy after invasive treatment of superficial veins of the lower extremities have been published (see Guidelines).

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.

• References

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 the treatment technique used. It is easily managed with warm compress, nonsteroidal anti-inflammatory drugs (NSAIDs), or aspiration if necessary.

At the SFJ, accidental treatment of the femoral vein by inappropriate RF or laser catheter placement, spread of sclerosant (not visualizing progression with US), and inappropriate surgical ligation can all lead to endothelial damage at the deep vein, causing DVT formation with the potential for PE and even death.^[31]

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.^[31]

• References

AVF/SVS/ACP/SVM/IUP Guidelines for Compression After Invasive Treatment of Lower-Extremity Superficial Veins

In 2019, clinical practice guidelines for the use of compression therapy after invasive treatment of superficial veins of the lower extremities were published by the American Venous Forum (AVF), the Society for Vascular Surgery (SVS), the American College of Phlebology (ACP), the Society for Vascular Medicine (SVM), and the International Union of Phlebology (IUP).^[38] Recommendations included the following:

• When possible, compression (elastic stockings or wraps) is suggested after surgical or thermal procedures to eliminate varicose veins. 
• If compression dressings are to be used postprocedurally in patients undergoing ablation or surgical procedures on the saphenous veins, those providing pressures >20 mm Hg together with eccentric pads placed directly over the vein ablated or operated on provide the greatest reduction in postoperative pain.
• In the absence of convincing evidence, best clinical judgment is recommended to determine the duration of compression therapy after treatment. 
• Compression therapy is suggested immediately after treatment of superficial veins with sclerotherapy to improve outcomes of sclerotherapy. 
• In the absence of convincing evidence, best clinical judgment is recommended to determine the duration of compression therapy after sclerotherapy. 
• In a patient with a venous leg ulcer, compression therapy is recommended over no compression therapy to increase venous leg ulcer healing rate and to decrease the risk of ulcer recurrence. 
• In a patient with a venous leg ulcer and underlying arterial disease, it is suggested to limit the use of compression to patients with an ankle-brachial index (ABI) exceeding 0.5 or cases where absolute ankle pressure is >60 mm Hg.

• References