VARICOSE VEINS


INTRODUCTION

Varicose veins and telangiectasia (spider veins) are usually normal veins that have dilated under the influence of increased venous pressure. They are the visible surface manifestation of an underlying syndrome of venous insufficiency. Venous insufficiency syndromes allow venous blood to escape from its normal flow path and flow in a retrograde direction down into an already congested leg.

Mild forms of venous insufficiency are merely uncomfortable, annoying, or cosmetically disfiguring, but severe venous disease can produce severe 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 extremely debilitating.

Chronic venous insufficiency eventually produces chronic skin and soft tissue changes that begin with mild swelling. The syndrome eventually progresses to include discoloration, inflammatory dermatitis, recurrent or chronic cellulitis, cutaneous infarction, ulceration, and even malignant degeneration. Chronic nonhealing leg ulcers, recurrent phlebitis, and variceal bleeding are serious problems that are caused by venous insufficiency and can be relieved by the correction of venous insufficiency.

Death can occur as a result of bleeding from friable varicose veins, but the mortality associated with varicose veins is almost entirely caused by secondary venous thromboembolism. Patients with varicose veins are at increased risk of deep vein thrombosis (DVT) because venous stasis and injury often cause superficial phlebitis that can pass through perforating vessels to involve the deep venous system. When treating a patient with varicose veins, the possibility of associated DVT must always be considered because the mortality rate associated with unrecognized and untreated thromboembolism is 30-60%.

New varicose veins may appear after an unrecognized episode of DVT that causes damage to venous valves. Such patients have some underlying risk factors for thromboembolism and are at especially high risk for recurrence.

Varicose veins may sometimes be an important pathway for venous return, as when they provide a bypass pathway for venous return in patients with acute blockage of the deep venous system from any cause. This most often occurs after an episode of DVT, but it may also be a response to tumor growth or to impaired portal flow through a cirrhotic liver.

History of the Procedure: Methods for the treatment of varicose veins have been under development for more than 2000 years, but until the present era, relatively little weight was given to the cosmetic outcome of treatment. Many historical surgical approaches were unpalatable to patients. The Rindfleisch-Friedel operation of the early 1900s, for example, involved cutting a deep (ie, to the level of the deep fascia) spiral gutter that wrapped around the leg 6 times, bringing 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 (see Image 3), introduced in the late 1930s, also used an open approach for removal of incompetent vessels and subfascial interruption of perforating veins, and this procedure also led to cosmetically undesirable outcomes.

The Trendelenburg procedure, introduced by Friedrich Trendelenburg in the late 1800s, was a method of vein treatment in which the saphenous vein was ligated through a midthigh incision. This procedure was later modified by Trendelenburg's student Perthes, who advocated a groin incision and a saphenofemoral ligature. Although called the Trendelenburg procedure, the midthigh ligation procedure was actually performed as early as the seventh century. Through the ages, the vast majority of patients who have been treated for varicose disease have undergone some variant of this procedure.

Several new approaches to stripping the greater saphenous vein (GSV) were introduced in the first few years of the 20th century. The Mayo stripper is an extraluminal ring that cuts the tributaries as it passes along the vein. The Babcock device is an intraluminal stripper with an acorn-shaped head that pleats up the vein as it pulls the vessel loose from its attachments. The Keller device is an internal wire used to pull the vein through itself, as is done today with perforation-invagination (PIN) strippers.

Chemical sclerosis of varicose veins has waxed and waned in popularity since the late 1800s. Modern sclerosants with an acceptable risk profile first became widely available in the 1930s and have been used since that time both as a surgical adjunct and as primary therapy for varicose veins.

Stab avulsion using phlebectomy hooks was performed by Galen during the second century, and a similar procedure was used by others before him. The procedure came back into modern favor during the 1960s and has increased in popularity ever since.

The newest techniques for vein ablation use thermal energy delivered to the endovenous wall by means of laser or by radiofrequency (RF) heating. These may be the first truly new approaches to vein treatment of the past 2000 years.

Problem: Venous disease is extremely common and increases with age, being present in more than half the population by age 65 years. The most common type is venous insufficiency, and the most visible manifestations are varicose veins and telangiectasias, with other cutaneous and soft tissue abnormalities developing over time. Most patients with venous insufficiency have subjective symptoms that may be very mild or very severe. Treatment aims to correct the underlying defect, removing or closing down points of reflux that can prevent venous blood from returning to the central circulation.

Frequency: The incidence and prevalence of venous insufficiency disease depend on the age and sex of the population. Varicosities and telangiectasia are more common in women than in men at any age. In the Tecumseh community health study, varicosities were observed in 72% of women aged 60-69 years but in only 1% of men aged 20-29 years.

Smaller reticular varicosities occur relatively early in life. Only a small number of new cases develop after the childbearing years. Truncal varicosities and telangiectatic webs are relatively less common in youth and continue to appear throughout life. Serial examinations of approximately 500 children at age 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. Abnormal reticular veins appear first. These reticular veins are followed after several years by incompetent perforators and eventually by truncal varicosities.

The prevalence of venous disease is higher in westernized and industrialized countries than in less-developed countries.

Etiology: Intrinsic pathological conditions and extrinsic environmental factors combine to produce a wide spectrum of varicose disease. Most varicose disease is caused by 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. Such patients also have abnormally distensible veins in the forearm and hand.

Heredity is important in determining susceptibility to primary valvular failure, but the specific genetic factors responsible for varicosities have not yet been elucidated. Reflux at the saphenofemoral junction (SFJ) (where the superficial GSV joins the deep common femoral vein) is twice as likely when a parent had a similar condition. Monozygotic twins are concordant with regard to varicose veins in 75% of cases. The prevalence rate of varicose veins is 43% in female relatives of patients with varicose veins, but 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. 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.

Women are particularly susceptible to varicose disease because vein walls and valves periodically become more distensible under the influence of cyclic increases in progesterone. Pregnancy increases this susceptibility because circulating hormonal factors associated with pregnancy increase the distensibility of vein walls and soften valve leaflets. At the same time, the veins must accommodate a greatly expanded circulating blood volume. Late in pregnancy, the enlarged uterus compresses the inferior vena cava, causing further venous hypertension and secondary distension of leg veins. Depending on the relative contributions of these mechanisms, varicose veins of pregnancy may or may not spontaneously regress after delivery. Treatment of existing varicose veins before pregnancy reduces 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, new varicose veins may appear as a bypass pathway. Such veins are important pathways for venous return and must not be ablated.

Pathophysiology: 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 that are 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 will dilate and become tortuous in response to continued high pressure, as is seen in patients with dialysis shunts or with spontaneous arteriovenous malformations. In a subset of patients with hereditary vein wall weakness, normal venous pressures can produce varicose changes and venous insufficiency.

Elevated venous pressure is most often the result of venous insufficiency with reflux through incompetent valves in the deep or superficial veins. Varicose veins are the undesirable pathways by which venous blood refluxes back into the congested extremity. In patients with venous insufficiency and reflux through varicose veins, 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 obstruction to venous outflow, varicosities must not be ablated because they are important bypass pathways that allow blood to flow around the obstruction.

DVT initially produces an obstruction to outflow, but most thrombosed large vessels eventually recanalize to become valveless channels that deliver high pressures from above.

Superficial venous valve failure may result from direct trauma or from thrombotic valve injury, but valve failure most commonly is due to the effects of high pressure within the superficial venous system. When exposed to high pressure for a long time, 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 of other nearby valves in the superficial veins. After a series of valves has 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, ie, outward and downward into an already congested leg.

As more and more 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 vein walls and the valves themselves more pliable, but 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 DVT.

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 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.

Clinical: 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. Treatment that does not address the patient's primary concerns will not result in a satisfactory overall outcome.

Subjective symptoms are usually more severe early in the progression of disease, less severe in the middle phases, and worse 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." 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.

The severity of symptoms does not correlate with the size or extent of visible varices or with the volume of reflux. Common symptoms of telangiectasia include burning, swelling, throbbing, cramping, and leg fatigue. Pain associated with larger varicose veins is usually a dull ache that is worse after prolonged standing

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. Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives). 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:

• 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 because most of the deep venous system cannot be directly inspected, palpated, ausculted, or percussed. In most areas of the body, examination of the superficial venous system must serve as an indirect guide to the deep system.

Veins and their connections gradually become better defined through inspection, palpation, percussion, and hand-held Doppler examination, all of which help form a venous map that will inform and guide any 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 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 also must be inspected. Inspection may reveal such findings as cutaneous ulceration, telangiectasias, acrocyanosis, eczema, brown spots, ochre dermatitis, flat angiomata, prominent varicose veins, scars from a prior surgical operation, or evidence of previous sclerosant injections. Inspection should also detect interdigital mycosis, plantar callus, tiny ulcers on the edges of an area of atrophie blanche, and other small problems. Any visible lesions should be measured and photographed.

Healthy veins typically are visibly distended only at the foot and ankle. Visible distension of superficial veins in other regions of the leg usually implies disease. Translucent skin may allow normal veins to be visible as a bluish subdermal reticular pattern, but dilated veins above the ankle are usually evidence of venous pathology.

Darkened, discolored, stained skin is often 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 most likely are 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.

Palpation is an important part of the venous examination. The entire surface of the skin is palpated lightly with the fingertips because dilated veins may be palpable even where they are not visible. 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.

Palpation begins over the anteromedial surface of the lower limb along the territory of the long saphenous vein. Palpation then proceeds to the lateral surface, where collateral varicose veins of the saphenous trunk may be found along with nonsaphenous varicose veins. Finally, the posterior surface is palpated in the territory of the short saphenous vein. The location, size, shape, and course of all varicosities are noted, and the diameter of the largest vessel is measured as accurately as possible. Distal and proximal arterial pulses are also palpated. An ankle-brachial index is useful if arterial insufficiency is suggested.

The arch of the long saphenous vein may be palpated in some patients with normal veins, but this segment of the vein is particularly well appreciated in patients with truncal reflux at the 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 short saphenous vein may be palpable in the popliteal fossa in some slender patients. Other 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. 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. 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 DVT do not produce any palpable abnormality.

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.

After palpation, venous percussion is useful to determine whether 2 venous segments are directly interconnected. 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.

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 healthy vein to become distended, and if valves have floated open, a pulse wave may be propagated in any 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.

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 anatomical picture has been brought into focus.

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 a 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.

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 any superficial varicose veins while leaving deep veins unaffected. 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 activating the calf-muscle pump causes paradoxical congestion of the superficial venous system and engorgement of varicose veins.

If the Perthes maneuver is positive and the distal varices have become engorged, the patient is placed supine with the tourniquet in place and the leg is elevated (Linton test). If varices distal to the tourniquet fail to drain after a few seconds, deep venous obstruction must be considered. These maneuvers are not consistently reliable.

Trendelenburg test

The Trendelenburg test can often distinguish patients with superficial venous reflux 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 a varicose vein just below the SFJ or at another point of possible reflux from the deep system into the superficial varicosity. The patient stands with the occlusion still in place.

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 possible 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 show directly whether flow in a suspect vein is antegrade, retrograde, or to-and-fro.

• 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.

• An augmentation maneuver is performed by compressing and then releasing the underlying veins and muscles below the level of the probe. Compression causes audible forward flow in the direction of the valves. Release of compression causes audible backward flow through incompetent valves. If the valves are competent, blood will not flow backward when compression is released, thus no Doppler signal will be heard.

• These compression-decompression maneuvers are repeated while gradually ascending the limb to a level at which the reflux can no longer be appreciated.

• Each superficially visible or palpable vein 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, but patients with significant varicosities should also be evaluated using duplex ultrasound, which combines Doppler flow detection with 2-dimensional ultrasound imaging.

Lab Studies:

• No currently available lab test is useful in the diagnosis or therapy of varicose veins.

• Patients with varicose veins may have a spuriously positive D-Dimer test result because of chronic low-level thrombosis within varices. See Deep Venous Thrombosis and Thrombophlebitis for more information.

Imaging Studies:

• The goal of imaging 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 ultrasound.

• Duplex ultrasound is the standard imaging modality used for the diagnosis of varicose insufficiency syndromes and for treatment planning and preoperative mapping.

• Two-dimensional ultrasound forms an anatomic picture based on the time delay of ultrasonic pulses reflected from deep structures. Structures that absorb, transmit, or scatter ultrasonic waves appear as dark areas; structures that reflect the waves back to the transducer appear as white areas in the image. Vessel walls reflect ultrasound waves; blood flowing in a vessel absorbs and scatters ultrasound waves in all directions. The normal vessel appears as a dark-filled white-walled structure.

• Duplex ultrasound is a combination of anatomic imaging by 2-dimensional ultrasound and flow detection by Doppler-shift. With duplex ultrasound, after the 2-dimensional anatomic image is displayed, a particular spot in the image can be selected for Doppler-shift measurement of flow direction and velocity.

• Color-flow imaging (sometimes called triplex ultrasound) is a special type of 2-dimensional ultrasound 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 ultrasound 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 seen on the scan image when the clinical presentation erroneously suggests venous insufficiency or venous obstruction.

• The direct contrast venogram is the most labor-intensive and invasive venous imaging technique.

• Venography has been replaced by duplex ultrasound for the routine evaluation of venous disease, but the technique remains extremely useful for difficult or confusing cases.

• 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 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:

• Physiologic tests of venous function are important adjuncts to anatomic imaging of venous disease. The physiologic parameters most often measured are the venous refilling time (VRT), the maximum venous outflow (MVO), and the calf muscle pump ejection fraction (MPEF).

• Venous refilling time

• The VRT 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 a patient with perfectly normal veins and arteries is in a sitting position, venous refilling of an empty 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 between 40 and 120 seconds.

• In patients with significant venous insufficiency, venous refilling occurs rapidly through high-volume reflux. 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 complain of nocturnal leg cramps, restless legs, leg soreness, burning leg pain, and premature leg fatigue.

• A VRT of less than 20 seconds is markedly abnormal and implies 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 less than 10 seconds, venous ulcerations are so common as to be virtually inevitable.

• Maximum venous outflow

• The MVO test helps detect obstruction to venous outflow from the lower leg, no matter what the 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 test. It is sensitive to significant intrinsic or extrinsic venous obstruction from any cause at almost any level. It can help detect obstructing thrombus in the calf veins, the iliac veins, and the vena cava, where ultrasound and venography are insensitive. It also helps detect venous obstruction from extravascular hematomas, tumors, and other extrinsic disease processes.

• The disadvantage of the test is that it is sensitive only for significant venous obstruction and usually does not detect partially obstructing thrombi. It is not useful for detection of venous insufficiency states. A normal MVO result absolutely does not rule out DVT.

• Muscle pump ejection fraction

• 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 and meaningful tracings. The patient performs 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 with normal veins and normal muscle pump function, 10-20 tiptoes or ankle dorsiflexions will empty the venous capacitance circuit of the calf.

• 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 therapy: 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.

In the absence of deep system obstruction, superficial varicosities are nothing more than the inevitable 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 and the improvement of venous circulation.

Sclerotherapy, laser ablation, RF ablation, and surgical extirpation are the modern techniques used to ablate varicosities. Cutaneous electrodesiccation is an older technique for destruction of small vessels. Electrodesiccation is rarely used by experts because it usually leads to disfiguring cutaneous injury with no real improvement in venous disease.

Chemical sclerosis, often called sclerotherapy, is the most widely used medical procedure for ablation of varicose veins and spider veins. In this procedure, a sclerosing substance is injected into abnormal vessels to produce endothelial destruction that is followed by formation of a fibrotic cord and eventually by reabsorption of all vascular tissue layers. A thorough diagnostic evaluation is essential before treatment. The following caveats must be observed:

• 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.

• Missing the diagnosis of superficial truncal incompetence can cause significant complications (especially skin staining and telangiectatic matting) if tributary varices and spider veins are treated while high-pressure feeders remain open.

• Missing the diagnosis of deep system disease can lead to poor outcomes in several ways. Symptoms will become immediately worse if an unrecognized bypass pathway is ablated. Missing the diagnosis of underlying venous thrombosis can lead to fatal embolism. Unrecognized insufficiency of the deep venous system can lead to early or immediate recurrence of treated superficial disease.

• In all but the smallest vessels, injected sclerosant is diluted by intravascular blood before it reaches the vascular endothelium. The injected concentration and volume must be selected to deliver the minimum effective sclerosing concentration at the vessel wall. Too high a concentration risks collateral damage to adjacent structures, and too low a concentration causes insufficient injury and leads to recanalization of the abnormal vessel.

• 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.

• Delivery of an effective concentration of sclerosant to the endothelial wall of proximal truncal varices may require placement of long endovenous catheters and infusion under ultrasound guidance.

• Delivery of sclerosant to subsurface feeding vessels that are not visible is usually performed under ultrasound guidance.

• Some sclerosants (eg, hypertonic saline) are highly caustic. Extravasation of even a single drop of these agents can lead to skin sloughing and a very poor cosmetic result.

• Inadvertent injection into an arteriovenous malformation (or directly into an unrecognized underlying artery) can cause extensive tissue loss or loss of the entire limb.

• Inadvertent injection of concentrated sclerosants into the deep system can cause DVT, pulmonary embolism, and death.

The most commonly used sclerosants today are Polidocanol and sodium tetradecyl sulfate. Both are known as detergent sclerosants because they are amphiphilic substances 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 adverse cutaneous effects, and are relatively forgiving if extravasated. Polidocanol, the most forgiving sclerosing agent, was originally developed as a local anesthetic agent. Unlike other sclerosants, Polidocanol may be injected into the tissues in large volumes without causing local tissue necrosis.

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. Extravasation of the drug causes severe and extensive necrosis.

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 injection of ethanolamine oleate into esophageal varices may cause pneumonitis, pleural effusions, and other pulmonary symptoms. The principal disadvantages of the drug for sclerosis of peripheral veins 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. Extravasation necrosis can occur with this agent.

Hypertonic saline in a 20% or 23.4% solution can be used as a sclerosing agent. Saline 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, it is difficult to achieve adequate sclerosis of large vessels without exceeding a tolerable salt load. It can cause significant pain upon injection and significant cramping after a treatment session. If extravasated, it almost invariably causes significant necrosis; it is not uncommon to see patients with dozens of disfiguring scars at the sites of extravasation of hypertonic saline. 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.

Approval of drug labeling by the US Food and Drug Administration (FDA) is an important concern for physicians and patients in the United States. Polidocanol is the most widely used sclerosant in most countries, including the United States, 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 have never been submitted to the FDA for approval, but they are available in the United States as grandfathered agents. Hypertonic saline is not approved for use as a sclerosant but is available as an abortifacient.

The safety of sclerosing agents in pregnancy has not been established.

Surgical therapy: 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 varicose disease include vein stripping with flush ligation of the SFJ and all tributaries, avulsion phlebectomy performed through microincisions, endovenous RF thermal ablation, and endovenous laser thermal ablation. Smaller veins are surgically treated by microincisional phlebectomy, and residual telangiectasias are managed by sclerotherapy.

Preoperative details: A careful history and physical examination, including continuous-wave Doppler, are essential to developing an appropriate diagnosis and treatment plan. All major reflux pathways are mapped using color-flow duplex ultrasound, and surface vessels to be removed are indicated with a skin marker.

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.

Intraoperative details: Stripping and ambulatory phlebectomy are traditional approaches to the ablation of venous reflux, but several recently introduced techniques, including endovenous laser therapy and RF ablation therapy, offer a potentially less-invasive approach as compared to saphenofemoral ligation and stripping or phlebectomy. The procedures are very similar technically but use different types of equipment to deliver thermal energy to the vessel.

Endovenous laser

• Endovenous laser therapy is a thermal ablation technique that uses a laser fiber placed inside the vein to destroy the vascular endothelium.

• 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 approximately 2 cm, and the laser fiber tip is positioned at the SFJ just distal to the subterminal valve. The position is confirmed by ultrasound and by use of the laser guide light.

• Under ultrasound guidance, dilute local anesthetic is injected around the vessel to be ablated until a halo of tumescence is seen along the entire length of the vessel, separating it from its fascial sheath.

• 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.

• 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.

Radiofrequency ablation

• RF ablation is a thermal ablation technique that uses a specially developed proprietary RF catheter placed inside the vein to heat the vessel wall and surrounding tissues. This tissue heating causes protein denaturation, collagenous contraction, and immediate closure of the vessel.

• A formal cutdown, simple stab incision with vein exteriorization by hook, or 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 SFJ just distal to the subterminal valve. The position of the tip is confirmed by ultrasound.

• 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.

• Metal fingers at the tip of the RF catheter are deployed until they make contact with the vessel endothelium. RF energy is delivered through the metal catheter fingers and passes through the surrounding tissues; tissue heating occurs both in and around the vessel to be treated.

• Thermal sensors record the temperature within the vessel. Energy is delivered until the tissue temperature is just sufficient 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.

Ambulatory phlebectomy

• 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 the treatment of residual clusters after saphenectomy and for removal of nontruncal tributaries when the saphenous vein is competent.

• With the patient in a standing position, duplex ultrasound 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 leg is prepped and the patient is draped for the procedure.

• A microincision is made over the vessel using a tiny blade or a large needle.

• A phlebectomy hook is introduced into the microincision, and the vein is delivered through the incision.

• 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.

• When 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.

• No ligatures are used in the procedure, and skin closure is not necessary.

Saphenectomy

High ligation without saphenectomy has a high rate of early recurrent reflux through the same incompetent vein, but saphenectomy guarantees the elimination of axial reflux through the vein that has been removed. Saphenous veins that have been removed do not grow back, but accessory veins, collateral veins, and tributary veins can dilate rapidly under the influence of high pressure and can appear in the same distribution as the vein that has been removed.

The most popular technique for saphenectomy today uses an internal stripping tool and an invagination technique to invert the vessel and pull it through itself using endovenous traction, reducing the likelihood of injury to adjacent structures (see Images 5-6). For removal of the GSV, a 2- to 3-cm incision is made at the groin crease beginning at the femoral artery and extending medially, and the SFJ is exposed by dissection.

Before stripping the GSV, all tributaries of the SFJ must be identified and flush-ligated to minimize the incidence of early recurrence. After ligation and division of the junction, the stripping instrument (usually a stiff but flexible length of wire or plastic) is passed into the GSV at the groin and threaded through the incompetent vein distally to the level of the upper calf. The stripper is brought out through a small incision (5 mm or smaller) approximately 1 cm from the tibial tuberosity at the knee. An inverting head is attached to the stripper at the groin and is secured to the proximal end of the vein. The vessel is then inverted into itself, tearing away from each tributary and perforator as the stripper is pulled downward through the leg and out through the incision in the upper calf. If desired, a long epinephrine-soaked gauze or ligature may be secured to the stripper before invagination, allowing hemostatic packing to be pulled into place after stripping is complete.

An older technique of stripping to the ankle 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.

Removal of the lesser saphenous vein is complicated by variable local anatomy and risk of injury to the popliteal vein and peroneal nerve. The saphenopopliteal junction must be located by duplex examination before beginning the dissection, and adequate direct visualization of the junction is essential. After ligation and division of the junction, the stripping instrument (often a more rigid stripper that facilitates navigation) is passed downward into the distal calf, where it is brought out through a small incision (2- to 4-mm). The stripper is secured to the proximal end of the vein, which is invaginated into itself as it is pulled downward from knee to ankle and withdrawn from below.

Postoperative details: After treatment of large varicose veins by any method, a 30- to 40-mm Hg gradient compression stocking is applied and patients are instructed to maintain or increase their normal activity levels. Most practitioners recommend the use of gradient compression stockings after treatment of spider veins and after treatment of varicose veins. The value of compression stockings in this setting is widely accepted, but unproved.

Ace wraps and other long-stretch bandages should not be used. These elastic bandages fail to maintain adequate compression for more than a few hours. They often slip or are misapplied by patients, with a resulting tourniquet effect that causes distal swelling and increases the risk of DVT.

Activity is particularly important after treatment by any technique because all modalities of treatment for varicose disease have the potential to increase the risk of DVT. Activity is a strong protective factor against venous stasis. Activity is so important that most venous specialists will not treat a patient who is unable to remain active following treatment.

Caption: Picture 2. Varicose veins. Named perforators along the greater saphenous distribution.

Caption: Picture 3. Varicose veins. The Linton procedure for subfascial interruption of incompetent perforators.

Caption: Picture 4. Varicose veins. Saphenofemoral ligation (ie, "crossectomy").

Caption: Picture 6. Varicose veins. Perforation-invagination (PIN) stripping schematic close-up.

REFERENCES

• Coon WW, Willis PW 3rd, Keller JB: Venous thromboembolism and other venous disease in the Tecumseh community health study. Circulation 1973 Oct; 48(4): 839-46
• Diehm C, Allenberg JR: Color Atlas of Vascular Diseases. 1st ed. New York, NY: Springer Publishing; 1999: 1-396.
• Feied CF: Deep vein thrombosis: the risks of sclerotherapy in hypercoagulable states. Semin Dermatol 1993 Jun; 12(2): 135-49
• Goldman MP, Weiss RA, Bergan JJ: Varicose Veins and Telangiectasias: Diagnosis and Treatment. 2nd ed. St. Louis, Mo: Quality Medical Publishing; 1999: 1-562.
• Tretbar LL: Venous Disorders of the Legs. 1st ed. New York, NY: Springer Publishing; 1998: 1-138.
• Weiss RA, Feied CF, Weiss MA: Vein Diagnosis & Treatment: A Comprehensive Approach. 1st ed. New York, NY: McGraw-Hill; 2001: 1-304.
• Zimmet SE: Venous leg ulcers: modern evaluation and management. Dermatol Surg 1999 Mar; 25(3): 236-41