Varicose Vein Surgery 

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.

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, as depicted in the image below.

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]}

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

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, as depicted in the image below. 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.

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, as depicted in the image below. Named perforators along the greater saphenous distribution.
• Saphenofemoral junction (SFJ): This is located proximally at the groin where the GSV meets the femoral vein, as depicted in the images below. 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, as depicted in the image below. Major tributaries of the greater saphenous system.

In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg and toward the heart. 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. 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, as depicted in circle A of the image above.^[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, as depicted in the image below.^[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, as depicted in the image below.

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.

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, as depicted in the image below.Varicose veins.
• Reticular veins (also called blue veins, subdermal varices, and venulectasias) – Visible, dilated bluish subdermal, nonpalpable veins 1-3 mm, as depicted in the image below. Reticular veins.
• Telangiectases (also called spider veins, hyphen webs, and thread veins) – Dilated intradermal venules greater than 1 mm in diameter, as depicted in the image below. 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, as depicted in the images below. 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.

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.

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, as depicted in the image below.

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, as depicted in the image below. 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 is called the saphenofemoral junction in the English literature but is known as the crosse (ie, shepherd's crook) in the French medical literature, as depicted in 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.

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, as depicted in the image below.

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]}

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.