Background

Varicose veins and telangiectasia (spider veins) are the visible surface manifestations of an underlying problem with reverse venous flow, which is also termed venous insufficiency syndrome. Venous insufficiency syndromes describe venous blood deviating from a normal flow path and flow in a retrograde direction so that fluid accumulates, causing a "congested" leg. Mild forms of venous insufficiency are merely uncomfortable, annoying, or cosmetically disfiguring, but severe venous disease can produce serious systemic consequences and can lead to loss of life or limb. Most patients with venous insufficiency have subjective symptoms that may include pain, soreness, burning, aching, throbbing, cramping, muscle fatigue, and restless legs. Over time, chronic venous insufficiency leads to cutaneous and soft tissue breakdown that can be debilitating. Chronic venous insufficiency eventually produces chronic skin and soft tissue changes that begin with mild swelling and then progress to include discoloration, inflammatory dermatitis, recurrent or chronic cellulitis, cutaneous infarction, ulceration, and even malignant degeneration. See the image below.

Patient with large tortuous varicose veins, highvolume venous reflux, and early stasis changes of the medial ankle.

Chronic nonhealing leg ulcers, bleeding from varicose veins, and recurrent phlebitis are serious problems that are caused by venous insufficiency and can be relieved by the correction of venous insufficiency. See the image below.

Typical chronic medial leg ulceration associated with longstanding venous insufficiency. The ulcer had been present for 12 years and was refractory to every treatment approach until treatment of the refluxing superficial varices was performed. Treatment consists of endovenous ablation, foam sclerotherapy, or ambulatory phlebectomy.

Pathophysiology
Varicose veins and spider veins are normal veins that have dilated under the influence of increased venous pressure. In healthy veins, one-way valves direct the flow of venous blood upward and inward. Blood is collected in superficial venous capillaries, flows into larger superficial veins, and eventually passes through valves into the deep veins and then centrally to the heart and lungs. Superficial veins are suprafascial, while deep veins are within the muscle fascia. Perforating veins allow blood to pass from the superficial veins into the deep system. Within muscle compartments, muscular contraction compresses deep veins and causes a pumping action that can produce transient deep venous pressures as high as 5 atmospheres. Deep veins can withstand this pressure because of their construction and because their confining fascia prevents them from becoming excessively distended. In contrast to deep veins, the venous pressure in superficial veins normally is very low. Exposure to high pressures causes superficial veins of any size to become dilated and tortuous. Perfectly normal veins dilate and become tortuous in response to continued high pressure, as is observed in patients with dialysis shunts or with spontaneous arteriovenous malformations. In a subset of patients with hereditary vein wall weakness, even normal venous pressures produce varicose changes and venous insufficiency.

Elevated venous pressure most often is the result of venous insufficiency due to valve incompetence in the deep or superficial veins. Varicose veins are the undesirable pathways by which venous blood refluxes back into the congested extremity. Ablation of the varicose pathways invariably improves overall venous circulation. Chronically increased venous pressure can also be caused by outflow obstruction, either from intravascular thrombosis or from extrinsic compression. In patients with outflow obstruction, varicosities must not be ablated because they are an important bypass pathway allowing blood to flow around the obstruction. Specific diagnostic tests can distinguish between patients who will benefit from ablation of dilated superficial veins and those who will be harmed by the same procedure. Deep vein thrombosis initially produces an obstruction to outflow, but in most cases the thrombosed vessel eventually recanalizes and becomes a valveless channel delivering high pressures from above downward. Most commonly, superficial venous valve failure results from excessive dilatation of a vein from high pressure of reverse flow within the superficial venous system. Valve failure can also result from direct trauma or from thrombotic valve injury. When exposed to high pressure for a long enough period, superficial veins dilate so much that their delicate valve leaflets no longer meet. In the most common scenario, a single venous valve fails and creates a high-pressure leak between the deep and superficial systems. High pressure within the superficial system causes local dilatation, which leads to sequential failure (through overstretching) of other nearby valves in the superficial veins. After a series of valves have failed, the involved veins are no longer capable of directing blood upward and inward. Without functioning valves, venous blood flows in the direction of the pressure gradient: outward and downward into an already congested leg. As increasing numbers of valves fail under the strain, high pressure is communicated into a widening network of dilated

superficial veins in a recruitment phenomenon. Over time, large numbers of incompetent superficial veins acquire the typical dilated and tortuous appearance of varicosities. Varicose veins of pregnancy most often are caused by hormonal changes that render the vein wall and the valves themselves more pliable. The sudden appearance of new dilated varicosities during pregnancy still warrants a full evaluation because of the possibility that these may be new bypass pathways related to acute deep vein thrombosis. The sequelae of venous insufficiency are related to the venous pressure and to the volume of venous blood that is carried in a retrograde direction through incompetent veins. Unfortunately, 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 highpressure 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. International The prevalence of venous disease is higher in Westernized and industrialized countries, most likely due to alterations in lifestyle and activity.
Mortality/Morbidity

Death can occur because of bleeding from friable varicose veins,[1] but the mortality associated with varicose veins is almost entirely due to the association of this condition with venous thromboembolism. When treating a patient with varicose veins, the possibility of associated deep venous thrombosis must always be considered because the mortality rate of unrecognized and untreated thromboembolism is 3060%.

Patients with varicose veins are at increased risk of deep vein thrombosis because venous stasis and injury often cause

superficial phlebitis that can pass through perforating vessels to involve the deep venous system. Varicose veins may arise after an unrecognized episode of deep vein thrombosis that causes damage to venous valves. Such patients have some underlying risk factor for thromboembolism and are at especially high risk for recurrence. Varicose veins may sometimes serve as an important pathway for venous return in a patient with acute blockage of the deep venous system from any cause. This most often occurs after an episode of deep vein thrombosis, but it may also be a response to tumor growth or to impaired portal flow through a cirrhotic liver.
Sex

Because of hormonal factors, varicosities and telangiectasia are more common in women than in men at any age.[2]
Age

Most varicose and spider veins in adults have their genesis in childhood. Serial examinations of children aged 10-12 years and again 4 and 8 years later showed that symptoms are experienced (and venous test results are abnormal) before any abnormal veins are visible at the surface of the skin. When abnormal veins do become visible, reticular veins usually appear first and are followed after several years by incompetent perforators. Smaller telangiectatic webs and large varicose veins usually become visible only in adulthood, many years after the true onset of disease. Although varicosities continue to worsen and to recruit new areas of involvement throughout life, only a small number of new cases appear after the childbearing years.

History
Patients with varicose veins may present with acute varicose complications, including variceal bleeding, new onset of dermatitis, thrombophlebitis, cellulitis, and ulceration. Patients may also consult a physician because of worsening chronic symptoms or for a variety of other reasons. Some are seeking

advice on the medical implications of varicose veins. Others have purely aesthetic concerns.

A careful history exposes the patient's underlying concerns and guides further workup and treatment planning. o Treatment that does not properly address the patient's primary concerns cannot result in a satisfactory overall outcome. o Patients who have become acclimatized to their chronic disease may not volunteer information about symptoms. Common symptoms that should be elicited include leg heaviness, exercise intolerance, pain or tenderness along the course of a vein, pruritus, burning sensations, restless legs, night cramps, edema, skin changes, and paresthesias. o Subjective symptoms usually are more severe early in the progression of disease, less severe in the middle phases, and worse again with advancing age. o Symptoms do not correlate with the size or extent of visible varices or with the volume of reflux. o Not all symptomatic patients are aware of their symptoms because the onset may be extremely gradual. After treatment, patients are often surprised to realize how much chronic discomfort they had accepted as normal. o Common symptoms of telangiectasia include burning, swelling, throbbing, cramping, and leg fatigue. Pain associated with larger varicose veins usually is a dull ache that is worse after prolonged standing. o Pain caused by venous insufficiency is often improved by walking or by elevating the legs in contrast to the pain of arterial insufficiency, which is worse with ambulation and elevation. o Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives). o A small number of women regularly experience pain associated with their varicose veins after sexual intercourse. The venous history should also include the following elements: o History of venous insufficiency (eg, date of onset of visible abnormal vessels, date of onset of any symptoms, any

o o o o

known prior venous diagnoses, any history of pregnancyrelated 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
The physical examination of the venous system is fraught with difficulty. In most areas of the body, the deep venous system cannot be inspected, palpated, ausculted, or percussed. Examination of the superficial venous system must serve as an indirect guide to the deep system. Veins and their connections become gradually better defined through inspection, palpation, percussion, and hand-held Doppler examination to form a venous map that later guides treatment. The courses of all the dilated veins that are identified may be marked along the leg with a pen and later transcribed into the medical record as a map of all known areas of superficial reflux.

Inspection: Inspection is 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. o Inspection may reveal such findings as ulceration, telangiectasias, atrophie blanche, interdigital mycosis, acrocyanosis, eczematous lesions, microulcers, stasis dermatitis, flat angiomata, prominent varicose veins, scars from a prior surgical operation, or evidence of previous sclerosant injections. Measuring and photographing lesions

is recommended because patients undergoing treatment for varicose and spider veins often forget the original appearance of their legs and feet and may report that preexisting lesions were caused by treatment. o Normal veins typically are visibly distended at the foot and ankle and occasionally in the popliteal fossa. For other regions of the leg, visible distension of superficial veins usually implies disease. Translucent skin may allow normal veins to be visible as bluish subdermal reticular pattern, but dilated veins above the ankle usually are evidence of venous pathology. o Discolored skin often is a sign of chronic venous stasis, particularly if it is localized along the medial ankle and the medial aspect of the lower leg. Nonhealing ulcers in this area are most likely due to underlying venous stasis. 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. Palpation: The entire surface of the skin is lightly palpated with the fingertips because dilated veins may be palpable even where they are not readily observed. Palpation helps to locate both normal and abnormal veins. After light palpation to identify superficial vascular abnormalities, deeper palpation helps to elucidate the causes and sources of the superficial problems. o Palpation begins with the anteromedial surface of the lower limb (the territory of the long saphenous vein), proceeds to the lateral surface (collateral varicose veins of large trunks and nonsaphenous varicose veins), and finally focuses on the posterior surface (territory of the short saphenous vein) of both lower limbs. The location, size, shape, and course of all varicosities are noted, and the diameter of the largest vessel is measured as accurately as possible. o Both distal and proximal arterial pulses should be palpated. An ankle-brachial index is useful if any suspicion of arterial insufficiency exists. o The arch of the long saphenous vein may be palpable in some patients who do not have varicose veins, but it is particularly well appreciated in patients with truncal reflux at the saphenofemoral junction. 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. o The short saphenous vein may be palpable in the popliteal fossa in some slender patients. Other normal superficial veins above the foot usually are not palpable even after prolonged standing. o 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 vein thrombosis may exist in up to 40% of patients with superficial phlebitis. When completely thrombosed, the popliteal vein (a continuation of the femoral vein as it passes behind the knee and into the calf) may sometimes be palpated in the popliteal fossa, and the same is true of the common femoral vein at the groin. Palpation for deep thrombosis is not reliable because the vast majority of cases of deep vein thrombosis do not produce any palpable abnormality. o 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. o 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 though these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence. Percussion: Venous percussion is useful to determine whether different venous segments are directly interconnected. Percussion can be used to trace the course of veins already detected on palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks. o 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. The propagation of a palpable pulse wave demonstrates a patent superficial venous segment with open or incompetent valves connecting the 2 positions. The examination findings can be misleading because prolonged standing causes even a normal vein to become distended. If valves have floated open, a pulse wave may be propagated even in a normal vein. The technique is most valuable when a bulging venous cluster in the lower leg has no obvious connection with veins in the upper thigh, yet a palpable pulse wave demonstrates the existence of an unseen connection. o Percussion can be used to elucidate the course of any significant superficial vein. With the patient standing, the lowest portion of the vein is percussed while the opposite hand searches above for a percussion wave. The procedure is repeated along the entire course of the vein and then along every identifiable superficial vein until a clear anatomic picture has been elucidated. Perthes maneuver: The Perthes maneuver is a traditional technique intended to distinguish antegrade flow from retrograde flow in superficial varices. Antegrade flow in a variceal system indicates that the system is a bypass pathway around deep venous obstruction. This is critically important because, if deep veins are not patent, superficial varices are an important pathway for venous return and must not be sclerosed or surgically removed. o To perform the Perthes maneuver, a Penrose tourniquet is placed over the proximal part of the varicose leg in such a way as to compress superficial varicose veins but not the deep veins. The patient walks or performs toe-stands to activate the calf muscle pump. The calf muscle pump normally causes varicose veins to be emptied, but if deep system obstruction exists, then the varicose veins paradoxically become more congested. o If the result of the Perthes maneuver is positive (ie, distal varices have become engorged), then the patient is placed supine with the tourniquet in place and the leg elevated (Linton test). If varices distal to the tourniquet do not drain after a few seconds, deep venous obstruction must be suspected. These maneuvers are not consistently reliable and are of primarily historical interest.

Trendelenburg test: The Trendelenburg test can often be used to distinguish patients with superficial venous reflux from those with incompetent deep venous valves. o The leg is elevated until the congested superficial veins have all collapsed. An examining hand is used to occlude a varicose vein just below the saphenofemoral junction or at another point of suspected reflux from the deep system into the superficial varicosity. The patient stands with the occlusion still in place. o If the distal varicosity remains empty or fills very slowly, the principal entry point of high pressure into the superficial system has been identified. Rapid filling despite manual occlusion of the suspected high point of reflux means that some other reflux pathway is involved. Doppler auscultation: The physical examination as described thus far cannot differentiate dilated veins of normal function from true varicosities that carry venous blood in a retrograde direction. Doppler examination is an adjunct to the physical examination that can directly show whether flow in a suspect vein is antegrade, retrograde, or to-and-fro. o When used as part of the physical examination, a Doppler transducer is positioned along the axis of a vein with the probe at an angle of 45 to the skin. Gentle tapping on the underlying vessel produces a strong Doppler signal and confirms the correct positioning of the transducer. o An augmentation maneuver is performed by compressing and then releasing the underlying veins and muscles below the level of the probe. Compression causes forward flow in the direction of the valves. Release of compression causes backward flow through incompetent valves, but no Doppler signal is noted if the valves are competent and the blood cannot flow backwards. o These compression-decompression maneuvers are repeated while gradually ascending the limb to a level where the reflux can no longer be appreciated. o Each superficially visible or palpable is investigated in this way. If no visible or palpable dilated varices exist, the presence or absence of retrograde flow is documented at the top, middle, and bottom of long and short saphenous veins on each leg.

Doppler flow assessment adds a great deal of information to the physical examination findings, but patients with significant varicosities should also be evaluated by duplex ultrasonography, which combines Doppler flow detection with 2-dimensional ultrasound imaging.

Causes
Intrinsic pathological conditions and extrinsic environmental factors combine to produce a wide spectrum of varicose disease.

Most varicose disease is due to elevated superficial venous pressures, but some people have an inborn weakness of vein walls and can develop varicosities even in the absence of elevated venous pressures. Some patients with varicose veins of the legs also have abnormally distensible veins in the forearm and hand veins. Heredity is important in determining susceptibility to primary valvular failure, but the specific genetic factors responsible for varicosities have not yet been elucidated. o Reflux at the saphenofemoral junction (where the superficial greater saphenous vein joins the deep common femoral vein) is twice as likely when a parent had a similar condition. o Monozygotic twins are concordant with regard to varicose veins in 75% of cases. The prevalence of varicose veins is 43% in female relatives of patients with varicose veins but is only 19% in male relatives. Prolonged standing leads to increased hydrostatic pressures that can cause chronic venous distention and secondary valvular incompetence anywhere within the superficial venous system. o If proximal junctional valves become incompetent, high pressure passes from the deep veins into the superficial veins and the condition rapidly progresses to become irreversible. o Women are particularly susceptible to this type of varicose problem because vein walls and valves periodically become more distensible under the influence of cyclic increases in progesterone. Pregnancy is a common cause of varicosities. o During pregnancy, circulating hormonal factors increase the distensibility of vein walls and soften valve leaflets.

At the same time, the veins must accommodate a greatly expanded circulating blood volume. o Late in pregnancy, the enlarged uterus compresses the inferior vena cava, causing further venous hypertension and secondary distension of leg veins. o Depending on the relative contributions of these mechanisms, varicose veins of pregnancy may or may not spontaneously regress after delivery. o Treatment of existing varicose veins prior to pregnancy has been shown to prevent the progression of disease and reduce the recruitment of other veins during pregnancy. Age is an independent risk factor for varicosities. With advancing age, the elastic lamina of the vein becomes atrophic and the smooth muscle layer begins to degenerate, leaving a weakened vein that is more susceptible to dilatation. Wherever a venous outflow obstruction exists, varicose veins may arise as a bypass pathway. Such veins are an important pathway for venous return and must not be ablated.
o

Imaging Studies

The goal of imaging studies is to identify and map all areas of acute or chronic obstruction and all areas of reflux within the deep and superficial venous systems. Successful imaging of the deep venous system requires a thorough knowledge of venous anatomy and physiology and a meticulous attention to detail. The most useful modalities available for venous imaging are contrast venography, magnetic resonance imaging (MRI), and color-flow duplex ultrasonography. Duplex ultrasonography is the standard imaging modality for diagnosis of varicose insufficiency syndromes and for treatment planning and preoperative mapping. Two-dimensional ultrasonography 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; blood flowing in a vessel absorbs and scatters ultrasound in all directions. The normal vessel appears as a dark-filled white-walled structure.

Duplex ultrasonography is a combination of anatomic imaging by 2-dimensional ultrasound and flow detection by Dopplershift. With duplex ultrasonography, 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. Color-flow imaging (sometimes called triplex ultrasonography) is a special type of 2-dimensional ultrasonography that uses Doppler flow information to colorize areas of the image in which flow has been detected. Vessels in which blood is flowing 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. Modern color-flow duplex ultrasonography equipment can provide flow information in conjunction with surprisingly high-resolution views of both deep and superficial venous systems. 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. Magnetic resonance venography (MRV) is the most sensitive and most specific test for deep and superficial venous disease in the lower legs and in the pelvis, where other modalities cannot reach. MRV is particularly useful because unsuspected nonvascular causes for leg pain and edema may often be observed on the MRV scan when the clinical presentation erroneously suggests venous insufficiency or venous obstruction. Direct contrast venography is the most labor-intensive and invasive imaging technique. In most centers, it has been replaced by duplex ultrasonography for routine evaluation of venous disease, but the technique remains extremely useful for difficult or confusing cases.[3] An intravenous catheter is placed in a dorsal vein of the foot, and radiographic contrast material is infused into the vein. If deep vein imaging is desired, a superficial tourniquet is placed around the leg to occlude the superficial veins and force contrast into the deep veins more quickly. Assessment of reflux by direct contrast venography is a difficult procedure that requires passing a catheter from ankle to groin with selective introduction of contrast material into each vein segment.

Nearly 15% of patients undergoing venography for detection of deep venous thrombosis (DVT) develop new thrombosis after contrast venography. The incidence of contrast-induced DVT in patients who undergo venography for diagnosis and mapping of varicose veins is not known.

Other Tests

Color-flow ultrasound imaging has become accepted as the standard for evaluation of venous anatomy and gross physiology. For many patients, color-flow imaging alone may be sufficient. For complex cases, however, physiologic tests of venous function may reveal more information. Physiologic parameters most often measured are the venous refilling time (VRT), the maximum venous outflow (MVO), and the calf muscle pump ejection fraction (MPEF). The availability of small, relatively inexpensive Duplex ultrasound imaging has reduced the need for physiologic testing. The venous refilling time is the time necessary for the lower leg to become suffused with blood after the calf muscle pump has emptied the lower leg as thoroughly as possible. When perfectly healthy patients are in a sitting position, venous refilling of the lower leg occurs only through arterial inflow and requires at least 2 minutes. In patients with mild and asymptomatic venous insufficiency, some venous refilling occurs by means of reflux across leaky valves. These asymptomatic patients have a VRT that is 40120 seconds. In patients with significant venous insufficiency, venous refilling occurs through high-volume reflux and is fairly rapid. These patients have an abnormally fast VRT of 20-40 seconds, reflecting retrograde venous flow through failed valves in superficial and/or perforating veins. This degree of reflux may or may not be associated with the typical symptoms of venous insufficiency. Such patients often report nocturnal leg cramps, restless legs, leg soreness, burning leg pain, and premature leg fatigue. A venous refilling time of less than 20 seconds is markedly abnormal and is due to high volumes of retrograde venous flow. High-volume reflux may occur via the superficial veins, the large perforators, or the deep veins. This degree of reflux is nearly always symptomatic. If the refilling time is shorter

than 10 seconds, venous ulcerations are so common as to be considered virtually inevitable. The MVO measurement is used to detect obstruction to venous outflow from the lower leg, regardless of cause. It is a measure of the speed with which blood can flow out of a maximally congested lower leg when an occluding thigh tourniquet is suddenly removed. The advantage of MVO testing is that it is a functional test rather than an anatomic one, and it is sensitive to significant intrinsic or extrinsic venous obstruction from any cause at almost any level. It can detect obstructing thrombus in the calf veins, the iliac veins, and the vena cava, where ultrasonography and venography are insensitive. It also detects venous obstruction due to extravascular hematomas, tumors, and other extrinsic disease processes. The disadvantage of the test is that it is sensitive only for significant venous obstruction and does not detect partially obstructing thrombus. It is not useful for detection of venous insufficiency states. A normal MVO absolutely does not rule out deep vein thrombosis. 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 to obtain clean meaningful tracings. The patient is asked to perform 10-20 tiptoes or dorsiflexions at the ankle, and the change in some physical parameter that reflects calf blood volume is recorded as the calf muscle is pumped. In patients without varicose veins, 10-20 tiptoes or ankle dorsiflexions cause the venous capacitance circuit of the calf to be emptied. In patients with muscle pump failure, severe proximal obstruction, or severe deep vein insufficiency, tiptoes or ankle dorsiflexions have little or no effect on the amount of blood remaining within the calf.

Medical Care
Superficial varicosities are the result of high-pressure flow into a normally low-pressure system. Varicosities carrying retrograde flow are hemodynamically harmful because they cause recirculation of oxygen-poor, lactate-laden venous blood back into an already congested extremity. The primary goal of

treatment is the ablation of these reflux pathways with resulting improvement of venous circulation. In the rare 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. This condition is encountered rarely, but when it is, ablation of these varicosities causes rapid onset of pain and swelling of the extremity, eventually followed by the development of new varicose bypass pathways. Sclerotherapy, laser and intense-pulsed-light therapy, radiofrequency (RF) or laser ablation, and ambulatory phlebectomy are the modern techniques used to ablate varicosities. Numerous reports describe success rates of greater than 90% for less invasive techniques, which are associated with fewer complications, with comparable efficacy.[4,
5]

Chemical sclerosis or endovenous chemoablation (sclerotherapy) is the most widely used medical procedure for ablation of varicose veins and spider veins.[6] In this procedure, a sclerosing substance is injected into the abnormal vessels to produce endothelial destruction that is followed by formation of a fibrotic cord and eventually by reabsorption of all vascular tissue layers. For most veins, a detergent sclerosing agent is agitated with air to create a foam similar to shaving foam. A thorough diagnostic evaluation is essential prior to treatment. A high degree of technical skill is necessary for effective sclerotherapy for the following reasons: o Local treatment of the superficial manifestations of venous insufficiency is unsuccessful 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 are observed very quickly if unrecognized reflux exists in larger subsurface vessels. o Missing the diagnosis of superficial truncal incompetence can cause significant complications (especially skin staining and telangiectatic matting) if spider veins and superficial

tributaries are treated while high-pressure feeders remain open. o Delivery of sclerosant to subsurface feeding vessels that are not visible is usually performed under ultrasonographic guidance. o Missing the diagnosis of deep system disease can lead to bad outcomes in several ways. Symptoms become immediately worse if an unrecognized bypass pathway is ablated. Missing the diagnosis of underlying venous thrombosis can lead to fatal embolism. Unrecognized deep venous insufficiency can lead to early or immediate recurrence of treated superficial disease.[7] o Selection of the correct sclerosant and the correct volume and concentration of sclerosant depends on the type and location of disease, internal volume of the vessel to be treated, positioning of the patient, and many other factors. The minimum effective concentration and volume should always be used because sclerosant inevitably passes into the deep venous system, where endothelial injury can lead to disastrous consequences. o Some sclerosants (eg, hypertonic sodium chloride solution) are highly caustic. Extravasation of even a single drop of these agents can lead to skin sloughing and a very poor cosmetic result. o Inadvertent injection into an arteriovenous malformation (or directly into an unrecognized underlying artery) can cause extensive tissue loss or loss of the entire limb. o Inadvertent injection of concentrated sclerosants into the deep system can cause deep vein thrombosis, pulmonary embolism, and death. The proper use of sclerosing agents requires special training and extended study. Specific dosing and technique recommendations for the administration of sclerosants are beyond the scope of this article. o The most commonly used sclerosants today are polidocanol and sodium tetradecyl sulfate, both known as detergent sclerosants because they are amphiphilic substances that are inactive in dilute solution but are 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 cutaneous adverse

effects, and are relatively forgiving if extravasated.[8] These are best delivered as a foam, which is made by agitating the solutions with air to create a frothy substance. Sodium morrhuate is an older detergent sclerosant that is made up of a mixture of saturated and unsaturated fatty acids extracted from cod liver oil. The agent is of variable composition and has been associated with a relatively high incidence of anaphylaxis. The incidence of extravasation necrosis is high with this drug. Ethanolamine oleate, a synthetic preparation of oleic acid and ethanolamine, has weak detergent properties because its attenuated hydrophobic chain lengths make it excessively soluble and decrease its ability to denature cell surface proteins. High concentrations of the drug are necessary for effective sclerosis. Allergic reactions are uncommon, but reports exist of pneumonitis, pleural effusions, and other pulmonary symptoms following the injection of ethanolamine oleate into esophageal varices. The principal disadvantages of the drug are a high viscosity that makes injection difficult, a tendency to cause red cell hemolysis and hemoglobinuria, the occasional production of renal failure at high doses, the possibility of pulmonary complications, and a relative lack of strength compared with other available sclerosants. Hypertonic sodium chloride solution in a 20% or 23.4% solution can be used as a sclerosing agent. The principal advantage of the agent is the fact that it is a naturally occurring bodily substance with no molecular toxicity, but the disadvantages of the agent make it unsuitable except in the hands of highly skilled practitioners. Because of dilutional effects, achieving adequate sclerosis of large vessels without exceeding a tolerable salt load is difficult. It can cause significant pain on injection and significant cramping after a treatment session. If extravasated, it almost invariably causes significant necrosis. Seeing patients with dozens of disfiguring scars at the sites of extravasation of hypertonic sodium chloride solution is not uncommon. Because it causes immediate red blood cell hemolysis and rapidly disrupts vascular endothelial continuity, it may

cause marked hemosiderin staining that is not cosmetically acceptable. o Food and Drug Administration (FDA) approval of drug labeling is an important concern for physicians and patients in the United States. Polidocanol is the most widely used sclerosant in the world, but the agent has not been approved by the FDA. Sotradecol, sodium morrhuate, and ethanolamine oleate all were developed prior to the establishment of the FDA. These agents are available in the United States as grandfathered agents. The newest form of Sotradecol was cleared by the FDA in 2006. It is highly purified with no contaminants. o The safety of sclerosing agents in pregnancy has not been established. Transcutaneous pulsed dye laser and intense-pulsed-light (IPL) therapy has proven effective for the tiniest surface vessels (eg, those found on the face), but this modality is not generally useful as primary therapy for treatment of spider veins of the lower extremity. This is true for several reasons. o Because of the physics of light absorption, delivering an ablative dose of thermal energy to the vessel without damaging the overlying skin is difficult. o The degree of patient-to-patient variability of light absorption in the skin is high. Even an experienced practitioner may inadvertently cause painful skin burns that can lead to permanent hyperpigmentation or hypopigmentation. o For most patients, the laser pulses are significantly more painful than the 30-gauge needles used for microsclerotherapy. o Most spider veins have associated feeding vessels that must be treated by some other means before the tiny surface vessels are amenable to laser or IPL treatment. Dudelzak et al report successful treatment of facial spider veins (telangiectasias) with a 980-nm diode laser. No complications were reported.[9]

Surgical Care
The primary goal of surgical therapy is to improve venous circulation by correcting venous insufficiency through the removal of major reflux pathways. Common surgical approaches to large-vein varicose disease include ligation of the saphenofemoral junction with vein stripping, phlebectomy

performed through microincisions, endovenous radiofrequency thermal ablation, and endovenous laser thermal ablation. The principal surgical approach to small-vein disease is by microincisional phlebectomy followed by sclerotherapy.

Endovenous laser therapy is a thermal ablation technique that uses a laser fiber placed inside the vein.[10] o Seldinger over-the-wire technique is used to place a long catheter along the entire length of the truncal varix to be ablated. A bare laser fiber is passed through the catheter until the end protrudes from the tip of the catheter by about 2 cm and the laser fiber tip is positioned at the saphenofemoral junction just distal to the subterminal valve. The position is confirmed by ultrasonography and by use of the laser guide light. o Under ultrasonographic guidance, very dilute, high volume local tumescent anesthetic is injected around the vessel to be ablated until a halo of tumescence is observed along the entire length of the vessel, separating it from its fascial sheath. o Firm pressure is applied to collapse the vein around the laser fiber, and the laser is fired with settings sufficient to cause irreversible thermal endothelial damage. o The laser may be set for continuous delivery of energy, in which case the fiber and catheter must be withdrawn at a slow and constant rate, or for intermittent pulses, in which case the fiber and catheter are withdrawn about 2 mm after each pulse and the process is repeated along the entire course of the vessel. o One system, using a 1320-nm laser, uses an automatic pullback mechanism. Radiofrequency ablation is a thermal ablation technique that uses a specially developed proprietary RF catheter placed inside the vein. The first version was cleared by the FDA in 1999. The most recent version using a redesigned simpler RF catheter was introduced into the market in 2007. o A cutdown, stab incision with vein exteriorization, or simple needle puncture using a Seldinger over-the-wire technique is used to place an introducer sheath into the truncal varix to be ablated.

A special RF ablation catheter is passed through the sheath and along the vein until the active tip is at the saphenofemoral junction just distal to the subterminal valve. Position of the tip is confirmed by ultrasonography. o Tumescent volumes of local anesthetic are injected in quantities sufficient to separate the vessel from the overlying skin and other delicate tissues along its entire length. o In the old system, metal fingers at the tip of the RF catheter were deployed until they made contact with the vessel endothelium. In the new system, 7 cm of the tip is heated to 120 C using RF energy. Tissue heating occurs both in and around the vessel to be treated. o Thermal sensors record the temperature within the vessel. Energy is delivered until the tissue temperature is just sufficient to ensure endothelial ablation. o The RF catheter is withdrawn every 7 cm and the process is repeated all along the length of the vein to be treated. The stab-avulsion technique (ambulatory phlebectomy) allows removal of short segments of varicose and reticular veins through tiny incisions, using special hooks developed for the purpose. This procedure is extremely useful for treatment of residual clusters after saphenectomy and for removal of nontruncal tributaries when the saphenous vein is competent. o With the patient in a standing position, duplex ultrasonography is used to map the locations of all refluxing vessels to be removed. The vessel locations are marked on the skin using an indelible marker. The position of the veins is confirmed with the patient recumbent using a vein illumination device as the position of the vein relative to the skin may change with positioning of the leg. o The leg is prepped, and the patient is draped for the procedure. o A microincision is made over the vessel using a tiny blade or a large needle. o A phlebectomy hook is introduced into the microincision, and the vein is delivered through the incision. o Using traction on the vein, as long a segment as possible is pulled out of the body, tearing it loose from its tributaries and other attachments. o When the vein breaks or cannot be pulled any further, another microincision is made and the process is begun
o

again and repeated along the entire length of the vein to be extracted. o No ligatures are used in the procedure, and no sutures are used to close the microincisions. Saphenectomy with saphenofemoral ligation is the old approach performed using an internal stripping tool and an invagination technique. This technique has been replaced by endovenous ablation techniques. o A 2- to 3-cm incision is made at the groin crease beginning at the femoral artery and extending medially. The saphenofemoral junction is exposed by dissection. o After ligation and division of the junction and all associated tributaries, the stripping instrument (usually a stiff but flexible length of wire or plastic) is passed into the greater saphenous vein at the groin and is threaded through the incompetent vein distally to the level of the upper calf, where it is brought out through a small incision (5 mm or less) approximately 1 cm from the tibial tuberosity at the knee. o 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. o If desired, a long gauze or ligature may be secured to the stripper before invagination, allowing a hemostatic packing to be pulled into place after stripping is complete.

Activity

Prolonged standing is a risk factor for venous insufficiency syndromes. Activity is a protective factor. 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 deep vein thrombosis. Activity is a strong protective factor against venous stasis. Activity is so important that most specialists will not initiate treatment for a patient who is unable to remain active following each treatment session.

Further Outpatient Care

After treatment of large varicose veins by any method, a 30-40 mm Hg gradient compression stocking is applied and the patient is instructed to maintain or increase his or her normal

activity level. 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 2 techniques.[11] Most practitioners recommend the use of gradient compression stockings after treatment of spider veins as well as after treatment of varicose veins. The value of compression stockings in this setting is theoretical but is as yet unproven. Because of the risk of deep vein thrombosis after treatment, immediate duplex ultrasonographic examination is indicated for any symptoms that extend beyond the immediate site of treatment.

Complications of varicose disease include venous ulcers, variceal bleeding, and venous thromboembolism.