Chapter 249. Treatment for Varicose and Telangiectatic Leg Veins

Bulging varicose veins and unsightly “roadmap” telangiectatic webs affect millions of patients around the world. The incidence is highest in Caucasian patients in which telangiectasias comprise the most common of all cosmetic complaints. This is borne out by epidemiologic surveys in which leg telangiectasia are reported in 70% of women.1 These same 24 city studies of thousands of patients indicate that 53% of the population over 50 years of age show some venous reverse flow.1 Women are at least 4 times more likely than men to develop telangiectasia, while males have double the risk of developing large varicose veins.2 Women aged over 50 years are five times more likely than women aged 29 or less to develop large varicose veins. Pregnancy increases the risk of varicose vein development by a factor of 1.5× to 3× and is associated with higher risks following three pregnancies.1,3,4 Increased body mass index correlates with a higher risk of reverse flow or reflux which leads to pain, swelling and abnormalities of the saphenous system.5,6 A positive familial history of disease is well known to increase the risk for varicose veins. Varicose veins may cause significant morbidity including chronic stasis dermatitis, ankle edema, spontaneous bleeding, superficial thrombophlebitis, recurrent cellulitis, lipodermatosclerosis and skin ulceration on the ankle and foot.

The incidence of varicose veins increases with each decade of life. Increased incidence has led to increased demand for treatment of varicose and telangiectatic veins as the average age of the US population grows. While 41% of women in the fifth decade have varicose veins, this number rises to 72% in the seventh decade.7 Statistics for men are similar with 24% incidence in the fourth decade, increasing to 43% by the seventh decade. Six million workdays per year may be lost in the United States due to complications of varicose veins, although this number is being affected by endovenous ablation techniques.8 Treatment is now much less complicated as an outpatient procedure avoiding dreaded stripping. As such noninvasive treatments are more frequently utilized so that lost workdays may actually be decreasing, although these statistics do not exist.

The main techniques employed in the dermatologist's office for treatment of cosmetic spider veins are sclerotherapy and lasers. For larger varicose veins, dermatologic surgeons employ sclerotherapy (with or without Duplex ultrasound guidance), ambulatory phlebectomy, and endovenous ablation by radiofrequency or laser. Sclerotherapy, which is defined as the intravascular introduction of a sclerosing substance, is the most frequently utilized procedure. We recommend that the term be changed to “endovascular chemoablation” which more accurately describes the procedure, although sclerotherapy is so entrenched that this will be unlikely to occur.

Sclerotherapy gained acceptance in the United States as a highly effective treatment during the early 1990s as it can be utilized for veins of all sizes.9 With the addition of foaming the sclerosant, utility has been expanded further.10 Sclerotherapy is also an important adjunctive therapy to surgical techniques such as ambulatory phlebectomy for saphenous tributaries11,12 and endovenous ablation of refluxing saphenous veins.13,14 Knowledge of venous anatomy and physiology, principles of venous insufficiency, methods of diagnosing venous abnormality, uses and actions of sclerosing solutions and proper use of compression are essential elements of successful venous therapy.

Primitive stripping and cauterization were practiced by Celsus, while ligation was mentioned by Antillus (30 ad). In the second century ad, Galen proposed tearing out the veins with hooks, a precursor to the modern day technique of ambulatory phlebectomy originated by Swiss dermatologist Robert Muller in the late 1960s.

A crude concept of sclerotherapy appeared in 1682, as Zollikofer described injection of acid into a vein to create a thrombus. By the late 1700s, the critical role of saphenofemoral reflux in the pathogenesis of varicose veins had been recognized by a Swiss surgeon, Rima. Reports of use of absolute alcohol as a sclerosing agent appeared from 1835–1840. In 1851, Pravaz attempted sclerotherapy with ferric chloride using his new invention, the hypodermic syringe.

The foundation of modern sclerotherapy can be traced to World War I when Linser and Sicard both noticed the sclerosing effect of intravenous injections used to treat syphilis which often resulted in vein sclerosis. Tournay greatly refined the sclerotherapy technique in Europe. It was not until 1946, when a safe sclerosant, Sotradecol (sodium tetradecyl sulfate) had been tested and described that sclerotherapy began to be seriously studied in the United states.15

Another key to success and acceptance of the treatment of varicose veins by sclerotherapy was the addition of compression. Sigg and Orbach in the 1950s and Fegan in the 1960s emphasized the importance of combining external compression immediately following injections. Starting in the 1980s, Duffy promoted the technique among dermatologists and advocated the use of polidocanol (POL) and hypertonic saline as safe and effective sclerosing solutions.16 In March 1999, the first endovenous obliteration technique utilizing radiofrequency was cleared by the US Food and Drugs Administration (FDA). Dermatologic surgeons were instrumental in developing this technique.14,17,18 Goldman's first American textbook of sclerotherapy integrated the world's phlebology literature, introduced new sclerosing solutions and validated dermatology's claim to expertise in vein treatment.19 Several additional textbooks by dermatologic surgeons have firmly established phlebology within the domain of dermatology.20,21 The newest development in sclerotherapy has been the FDA approval of polidocanol (Asclera, Merz Aesthetics/Bioform, San Mateo, CA) in late spring of 2010. The advantages of this solution are discussed later.

The venous system is comprised of a primary deep venous compartment and superficial compartment with thousands of small veins (perforating veins) connecting the two systems. The deep compartment, “the muscle pump,” normally acts as a conduit for 85%–90% of venous return from the leg. During contraction of the calf muscles, the valves of the perforating veins and associated superficial veins close, allowing blood to flow only proximally at high pressures through the deep system. This generates primary propulsive force returning venous blood to the heart (Fig. 249-1).

The superficial venous system consists of three primary territories: (1) great saphenous vein (GSV) (2) small saphenous vein (SSV) and (3) subdermic lateral venous system (LVS) (Fig. 249-2). Comprising the three major patterns are multiple collateral veins (accessory) and multiple tributary veins emptying into all 3 major superficial systems of the GSV, SSV and LVS. The points of connection (perforating veins) between the superficial and the deep system play important roles as these are sites through which reflux or reverse flow often develops (Fig. 249-3). Due to gravitational hydrostatic pressure, sequential retrograde breakdown of venous valve function often follows a leak at one point leading to propagation of a varicosity. Increased diameter between valve leaflets with failure to oppose properly caused by genetically weak venous wall or venous valve structure may initiate these events. Calf muscle pump pressure plus gravitational hydrostatic forces are transmitted directly via the incompetent perforating vein or communicating veins to the surface veins. Venous hypertension may reach levels higher than systolic arterial blood pressure in the cutaneous venules with the patient erect. Transmission of pressure may result in venular dilatation over a wide area of skin including the formation of telangiectatic webs and more serious consequences such as ulceration.22 This leads to a number of symptoms with heaviness, fatigue, and aching of the legs.23

When present in significant quantity, the volume of blood sequestered and stagnant in reticular veins and associated telangiectatic webs (particularly of the lateral venous system) may cause enough distention to produce symptoms.24 Symptoms are relieved by the wearing of support hose or with rest and elevation of the legs. Prolonged standing or sitting without calf muscle contraction worsens symptoms. The size of the vessels causing moderately severe symptoms may be as small as 1–2 mm in diameter. Sclerotherapy has been reported to yield an 85% reduction in these symptoms as well as superb cosmetic results.24

Contraindications to Treatment of Spider Veins

(Table 249-1)

Vein treatment and, in particular, foam sclerotherapy may be performed safely and effectively in virtually all types of veins, except when reflux exists at the saphenofemoral junction. Since the goal of sclerotherapy is to eliminate reflux at its origin, the goal of noninvasive diagnostic evaluation is to uncover primary sources of high reverse flow pressure. A high rate of recurrence for sclerotherapy is commonly seen when reflux originates at the major saphenous junctions. The techniques of endovenous ablation by radiofrequency or laser are the means by which reflux occurring at the termination point of the saphenous veins is now treated. Five-year data indicates that these techniques are as effective as the old surgical techniques of ligation and stripping to eliminate saphenous veins.25 Our experience at ten years show that these techniques are superior to older surgical techniques. Recent studies show high recurrence rates (30%–50%) following ligation and stripping.26 Archaic and invasive stripping techniques are no longer recommended for primary treatment of saphenous reflux. Endovenous ablation techniques have been embraced due to the high degree of safety and efficacy, without morbidity and downtime of general anesthesia and invasive technique required by stripping.27

Venous treatment is contraindicated in a bedridden patient since ambulation is important for minimizing risks of thrombosis. Similarly, patients under general anesthesia for nonrelated procedures should not undergo simultaneous sclerotherapy. Severely restricted arterial flow to the legs necessitates postponement of vein treatment. A history of deep venous thrombosis (DVT) or previous trauma to the leg (e.g., auto accident) should preclude sclerotherapy until adequately evaluated by Duplex ultrasound. Previous urticaria or suspected allergy to a sclerosing agent should serve as a relative contraindication to use of that particular sclerosing agent.

Pregnancy should be considered a contraindication during the first and second trimester, although extremely painful or bleeding, varices may be treated in the last trimester by endovenous ablation techniques. Treatment is typically postponed since varicosities and telangiectasias may resolve spontaneously 1–6 months postpartum.

Obesity should be considered a relative contraindication since maintaining adequate external compression is difficult. Sclerotherapy of larger varicosities should be postponed until weight reduction is achieved. During hot summer months, heat-induced vasodilatation and inability to comply with wearing of compression hose may also require postponement of treatment.

Pretreatment Evaluation

Physical examination is performed by viewing the patient's legs in a 360° rotation. Palpation is performed along the saphenous vein distributions to rule out early large axial varicosities which cannot be seen. Based on the history and physical examination, noninvasive diagnostic vascular tests are performed as necessary.28 Those patients with a family history of large varicose veins are more likely to have early axial (saphenous) reflux even when presenting with telangiectasias alone.11 Previous venous surgery warrants further testing before treatment.

Once the patient is judged to be a candidate for vein treatment, informed consent is obtained. Any veins visible or palpable suggestive of saphenous system involvement should be minimally evaluated by handheld Doppler ultrasound, which is equivalent to using an enhanced “stethoscope” to hear vein flow. It is generally recommended to supplement Doppler with Duplex ultrasound as this method of visualization of venous anatomy is more reliable and more prevalent. For Doppler to generate or augment an audible signal of flow, a maneuver such as manual compression of the calf must be performed by the examiner. When compression is released, gravitational hydrostatic pressure causes reverse flow to cease within 0.5–1 second when valves are competent, but a long flow sound is audible when valves are incompetent.

The most essential part of the Doppler examination is the examination of the saphenofemoral junction below the inguinal fold just medial to the femoral arterial signal. During a Valsalva maneuver, a continuous and pronounced reflux signal is a reliable sign of valvular insufficiency. An equivocal result may require a duplex ultrasound examination for a definitive answer. Methods of complete Doppler examination are detailed in other texts.11

The gold standard of noninvasive examination of the venous system is duplex ultrasound. This allows direct visualization of the veins and identification of flow through venous valves. An image is created by an array of Doppler transducers, which are switched on and off sequentially. The Duplex examination is often used to uncover hidden sources of reflux prior to beginning any method of treatment or delineate reflux sources when patients experience poor results from sclerotherapy. The declining price and increasing portability of Duplex ultrasound is rapidly making this examination the standard and reducing Doppler ultrasound to a relic of the past.

Sclerotherapy or Endovenous Chemoablation Solutions

Sclerosing solutions have been classified into groups based on chemical structure and effect: hyperosmotic, detergent, and corrosive agents (chemical toxins—salts, alcohols, and acid or alkaline solutions). Commonly employed sclerosing solutions are summarized in Table 249-2.

Hypertonic Saline

Although approved by the FDA only for use as an abortifacient, it is still commonly used in the United States in spite of its shortcomings. Used at a concentration of 23.4% (HS), a theoretical advantage of HS is its total lack of allergenicity when unadulterated. HS has been commonly used in various concentrations from 10% to 30%, with occasional addition of heparin, procaine, or lidocaine. Additional agents typically provide no benefit. Therefore, HS is used either unadulterated or diluted to 11.7% with sterile water for smaller telangiectasias.29

With hypertonic solutions, damage of tissue adjacent to injection sites may easily occur. Skin necrosis may be produced by extravasation at the injection site, particularly when injecting very close to the skin surface. Injection of hyaluronidase into sites of extravasation may significantly reduce the risks of skin necrosis with HS.30 The pain of injection with risks of ulceration of this solution, makes it highly undesirable for modern vein treatment. We strongly recommend against the use of HS, especially with newer safer and less painful sclerosing agents approved by the US FDA.

Hypertonic Saline and Dextrose

(HSD) (Sclerodex, Omega Laboratories Ltd, Montreal, Canada)

HSD is a viscous mixture of dextrose 250 mg/mL, sodium chloride 100 mg/mL, propylene glycol 100 mg/mL, and phenethyl alcohol 8 mg/mL. HSD is a relatively weak sclerosant for local treatment of small vessels, with a total volume of injection not to exceed 10 mL per visit with 0.1–1.0 mL per injection site. HSD is marketed predominately in Canada. Although a slight burning sensation occurs, pain is far less than with HS.

Polidocanol

(Asclera™, Merz Aesthetics, Bioform, San Mateo, CA/Aethoxysklerol, Kreussler & Co, Wiesbaden-Biebrich, West Germany)

The detergent-based POL, a urethane compound, was originally developed as an anesthetic, but was found to have the property of sclerosing small diameter vessels after intradermal injection. POL contains hydroxypolyethoxydodecane dissolved in distilled water with 5% ethanol as a stabilizer. First used as a sclerosing agent in the late 1960s in Germany, POL is popular worldwide for smaller vessels due to painless injection and lowest incidence of cutaneous necrosis with intradermal injection. Lower concentrations of POL were initially suspected to have a lower incidence of hyperpigmentation than HS or STS, but recent clinical trials indicate a significant percentage of hyperpigmentation occurs.31 Asclera was recently approved by the FDA and now represents a safe, virtually painless sclerosing solution available to US dermatologists. The European data indicates safe utilization for over 30 years with recent studies adding to the safety and efficacy data.32,33

Sodium Tetradecyl Sulfate

Sodium tetradecyl sulfate (STS) (Sotradecol™, Bioniche Pharmaceutical, Bioniche Pharma USA LLC, Lake Forest, IL; Fibrovein, S.T.D. Pharmaceuticals, United Kingdom) is an anionic surfactant which occurs as a white, waxy solid which must be carefully purified for sterile injection. It is a highly effective sclerosing agent used worldwide. Approved for use in the United States since 1946, it has been popular with vascular surgeons since the 1960s and first described for use in telangiectasias in the 1970s. A relatively high incidence of postsclerosis pigmentation was reported at inappropriately high doses (1% STS). More appropriate concentrations for superficial telangiectasias are 0.1%–0.2%. Other concentrations are 0.2%–0.5% in reticular veins or small varicosities (1–3 mm diameter), and 0.5% to 3% in larger varicosities related to major sites of valvular reflux. When foamed, this is used in half the concentrations listed above. In repeated studies, both POL and STS are found to be roughly equivalent.34 More data will be available as widespread use of POL becomes routine in the United States with the official approval of polidocanol as Asclera.

Sodium Morrhuate

(Scleromate™, Palisades Pharmaceuticals, Inc., Tenafly, NJ, USA)

Sodium morrhuate is a 5% solution of the salts of saturated and unsaturated fatty acids in cod liver oil. Approximately 10% of its fatty acid composition is unknown and use is limited by reports of fatalities secondary to anaphylaxis.19 Although sodium morrhuate is approved by the FDA for the sclerosis of varicose veins, use in treatment of telangiectasias is not common due to the caustic qualities with potential for cutaneous necrosis and higher risks of allergy. This agent is reserved primarily for sclerosis of esophageal varices. We recommend not using this agent for leg veins.

Chemical Irritants

The chemical irritants include polyiodinated iodine (very caustic) and chromated glycerine (very weak) and are believed to have a direct toxic effect on the endothelium. After injection of polyiodinated iodine salt, the endothelium near the site of injection is destroyed within seconds. The corrosive action is limited due to rapid inactivation by blood proteins. At the sites of endothelial destruction, the chemical can penetrate further and diffuse into deeper layers of the vessel wall causing further destruction. These agents are not cleared by the US FDA.

Recently glycerine (nonchromated) has been rediscovered a valuable sclerosant for telangiectasias. Glycerine (50%–72%) has a low incidence of side effects and minimizes telangiectatic matting and pigmentation. At lower concentration, glycerine may share properties with hypertonic agents rather than having a pure toxic effect. The exact mechanism of action is still being investigated.

A basic principle of treatment is to begin at the largest (reflux sources) and progress to the smallest varicosities and then finally to telangiectasias. When present without larger varicosities, telangiectasias are approached by combined injection of visibly connected reticular veins, venulectases, and telangiectatic webs or networks. Reticular veins are treated only after all sources of reflux from major varicosities have been treated by sclerotherapy and/or surgery. When no clear feeder vessel is seen or identified by Doppler, transillumination (Veinlite, 3Gen, Dana Point, CA, USA) is another method, which may be used to identify the “feeding” reticular vein. (Fig. 249-4). When unable to locate an associated reticular vein, then the point at which the telangiectasias begin to branch out is the site at which to begin injection. Injection of telangiectasias is simultaneously performed with injection of reticular veins in the hopes of decreasing the number of treatments.35

The injection method for telangiectasia is basically as previously described by Goldman, Weiss, and Duffy.16,20,36 The sclerotherapy tray is prepared with the necessary equipment (Table 249-3). A 30-gauge needle, bent to an angle of 10°–30° with the bevel up, is placed on the skin so that the needle is parallel to the skin surface. A 3-cc syringe filled with 1.5–2 cc of solution is held between the index and middle fingers while the fourth and fifth finger support the syringe against the leg in a fixed position facilitating accurate penetration of the vessel. The nondominant hand is used to stretch the skin around the needle and may offer additional support for the syringe (Fig. 249-5). Magnifying lenses or operating loops on the order of 1.5× to 3× may help cannulation of the smallest telangiectasias.

The initial treatment of telangiectatic webs begins with lowest possible concentration that will cause a telangiectasia to sclerose over a period of 1–6 months postinjection. This typically is 0.1% sodium tetradecyl sulfate or 0.2% polidocanol. The approval of polidocanol has increased our use of this solution in addition to use of 50% to 72% glycerine in water. Both of these solutions have seen increasing use in our practice of sclerotherapy. When ineffective sclerosis occurs judged at a subsequent visit, the concentration but not the volume per site of sclerosing solution is increased. Post-treatment compression consists of graduated 20–30 mm Hg or 30–40 mm Hg support hose for 2 weeks for larger veins and OTC 15 mm Hg compression for smaller veins. Treatment intervals vary but allowing 4–8 weeks between treatments helps minimize the number of necessary sessions. Typical results are shown in Fig. 249-6.

Foam Sclerotherapy

Foam sclerotherapy has become a standard of treatment for veins larger than 1 mm as foam completely fills and displaces the blood in the vein. The microbubbles of foam allow maximal contact with the highest concentration of the sclerosant thereby resulting in maximal endothelial cell injury and subsequent fibrosis of the vein wall. This results in more effective sclerotherapy which leads to less treatment sessions. Less total amount of solution is required with foam. This has the additional benefit of decreasing systemic toxicity. An additional advantage of foam is that Duplex-guided sclerotherapy becomes more precise as the foam is very echogenic and easily visualized on ultrasound.

The most utilized technique for foam sclerotherapy is the Tessari technique.37 A luer to luer connector is utilized. One syringe is filled with air and one syringe is filled with a detergent type of sclerosant. The optimal ratio of solution to air is 1:4. The contents of the syringes are shifted back and forth quickly approximately 10–20 times and the turbulent flow generates the foam. (Fig. 249-7) The foamed solution should be used immediately since it degrades within 60–90 seconds. The nature of the foam allows for the same therapeutic effect with approximately half the concentration of sclerosant. For instance, one can substitute 0.1% STS foam for 0.2% STS liquid or 0.25% polidocanol foam for 0.5% liquid. Lower concentrations are used for all size veins. Foamed solution should only be used for varicosities, perforating veins, reticular veins, and larger telangiectasias (1.0–2 mm). Smaller telangiectasia run the risk of increased pigmentation and matting as more inflammation occurs with the relatively increased concentration interacting with the vein wall.38 Liquid sclerosants such as 0.5% POL are recommended for telangiectasias.

Side Effects and Complications of Sclerotherapy

Postsclerotherapy Hyperpigmentation

Postsclerosis pigmentation is defined as the appearance of increased visible pigmentation along the course of a treated vein of any size. Initially, perivascular hemosiderin deposition, and not increased melanin production, causes this appearance39; however, over time, the hemosiderin is replaced by melanin. The incidence of pigmentation is related to dilution and type of sclerosing agent as well as diameter of treated vessel.40 Pigmentation incidence ranges from 11%–30% using HS,24 11%–30% with POL16,41 and up to 30% with STS. The incidence of pigmentation may be reduced in varicose veins by expressing the dark, viscous blood thought to be a liquefied coagulum or intravascular hematoma, which may accumulate 1–4 weeks following sclerotherapy.

Pigmentation clears in 70% within 6 months but rarely persists for greater than a year.40 Attempts to hasten resolution of pigmentation have been mostly unsuccessful as the pigment is dermal hemosiderin and not epidermal melanin. Bleaching agents, exfoliants such as trichloroacetic acid or phenol, cryotherapy, various lasers and intense pulsed light have achieved limited success.42,43 The Q-switched ruby laser has been found to be the most consistently effective for treatment of postsclerosis pigmentation.44

Telangiectatic Matting

Telangiectatic matting is defined as the appearance of groups of new, fine (<0.2 mm diameter) telangiectasias surrounding or replacing a previously treated area in a blush-like manner. A retrospective analysis of over 2,000 patients reports an incidence of 16% in patients treated with HS and POL.45 Resolution usually occurs spontaneously within a 3–12 month period with 70%–80% spontaneous resolution within the first 6 months.46

Matting may also occur as a result of trauma to the leg, in association with pregnancy or hormonal therapy or in scars around previous sites of surgical stripping. Predisposing factors include predilection for certain areas of the leg, such as the medial lower thigh, obesity, hormonal therapy with estrogen, family history, and a longer history of telangiectasias.45 The relative risk factor for development of telangiectatic matting is 3.17 times greater for female patients taking hormonal supplements.47 Successful treatment of matting can be performed with long pulsed dye laser (LPDL) using pulse durations of 6–20 msec.48 The use of enhanced visualization with a cross-polarized light source (Syris Scientific, LLC, Grey, MA) has been found to assist injection of sclerosing solution into telangiectatic matting. Treatment is often not required since matting will resolve spontaneously except when sustained by a source of reflux superiorly.

Cutaneous Necrosis/Ulceration

Cutaneous ulceration may occur with all sclerosing solutions in spite of the most skilled technique. Unavoidably, a tiny amount of sclerosing solution may be left along the needle tract as the needle is withdrawn. Sclerosing solution may also leak out into the skin through the small puncture sites of vessel cannulation. The varicose vein may have a fragile, thin wall, with the injection causing rapid injury leading to sudden unexpected rupture with perivascular accumulation of sclerosant. Additionally, injection may inadvertently occur into a small arteriole associated with telangiectatic varicosities with resultant necrosis and ulceration.

When the dermatologic surgeon recognizes that extravasation has occurred, the risk for necrosis can be minimized by injecting normal saline in a ratio of 10:1 over sclerosant into the extravasation site. Extensive massage of small subcutaneous blebs to spread the trapped sclerosing agent as quickly as possible will minimize prolonged blanching of the area. We have found that application of topical 2% nitroglycerine paste applied immediately to the suspected extravasation site greatly reduces the risks of necrosis but will not always prevent it.

Superficial Thrombophlebitis

This complication is most commonly mistaken for the normal nodular fibrosis (endosclerosis) that occurs with proper sclerotherapy. After sclerotherapy, a nontender, nonpigmented, nonerythematous fibrotic cord may normally be palpable along the course of a treated 4- to 8-mm vein. This frequent finding is due to a liquefied intravascular hematoma with surrounding vein wall sclerosis and is not a thrombosis. In contrast, superficial thrombophlebitis is characterized clinically by a very tender, indurated, linear erythematous swelling. Incidence of superficial thrombophlebitis is quite variable estimated at 1%–0.01% following sclerotherapy,49 although a recent report indicates that the incidence is higher than previously suspected.50 Treatment consists of leg elevation and/or compression and regular administration of aspirin or other nonsteroidal anti-inflammatory drugs. Extension of superficial thrombophlebitis into the deep system is extremely rare.

Pulmonary Embolism

Pulmonary emboli probably occur from extension of a superficial thrombus into the deep venous system. Evidence of extension from superficial thrombus to deep thrombophlebitis should be treated promptly by anticoagulation. The incidence of pulmonary embolism has been associated with injection of large quantities of sclerosant at a single site. The incidence is extremely low with less than 1 case in 50,000.

Arterial Injection

This dreaded medical emergency is fortunately extremely rare. Classic warning signs include immediate intense pain far beyond the normal discomfort at the initiation of injection, although leakage of sclerosant into the arterial circulation may present in an atypical fashion. Continuous intense burning pain with immediate bone white cutaneous blanching over an area of several square centimeters is the usual initial sign. Progression to a sharply demarcated cyanosis within minutes is typical for arterial injection. Emergency treatment involves immediate application of ice, attempts to flush the inadvertently injected artery with normal saline and/or heparin, injection of 3% procaine to inactivate STS and vascular surgery consultation for intravenous anticoagulation. Rarely arterial injection may not be accompanied by any pain or cutaneous signs. This is not widely known. Atypical or nonclassic cases of arterial injection in which signs or symptoms are not seen for up to 24 hours are suspected to arise from A-V malformations.51 Arterial injection may lead to wide areas of skin necrosis and damage to subcutaneous tissue and muscle, which take months to heal. Typically a malpractice lawsuit will be initiated, although the cause can rarely be pinpointed and is often not a result of negligent injection.

Endovenous Ablation/Occlusion Techniques

Endovenous ablation techniques were first developed by dermatologic surgeons.14,13 When it has been determined by ultrasound that the originating point of reverse flow or reflux is the great saphenous vein (GSV) or small saphenous vein (SSV), endovenous radiofrequency or laser techniques are utilized. Ligation and stripping are antiquated techniques that should no longer be utilized. When saphenous system reflux is present, the endovenous occlusion techniques must be performed prior to treatment of visible and associated varicosities, reticular veins, or telangiectasias. Without elimination of reflux, a patient will be doomed to recurrence after recurrence following local treatment.

Radiofrequency

The efficacy for radiofrequency (RF) elimination of reflux is 90% at 2 years and 80% at 5 years.17,25 Our unpublished experience is presently 90% at 10 years with supplemental foam sclerotherapy at follow-up visits. RF endovenous ablation involves the placement of an RF catheter within the varicose vein through a small puncture or incision. The catheter is threaded up to the saphenofemoral junction typically under duplex ultrasound guidance. Critical to the safety and success of the technique is placement of tumescent local anesthesia, which involves first infiltrating the tissue under the skin including thigh muscles to push the saphenous vein further away from the skin and then creating a space between the fascia and the saphenous vein so as to hydro-dissect the vein away from structures such as nerves and arteries. Tumescent anesthesia was developed and perfected by dermatologic surgeons. Once a hydrodissection has been performed with high volume, low concentration of local anesthetic (0.1% lidocaine), or tumescent anesthesia, energy is applied as the catheter is slowly withdrawn. This results in heat directly applied to the vein wall via a computer controlled thermocouple feedback loop. This results in a collagen shrinkage accompanied by complete vein wall occlusion. The newest system is designated ClosureFast and can seal the vein in under 5 minutes.

Laser (Hemoglobin Predominant Absorption—810, 940, and 980 nm)

Endovenous laser treatment is similar to RF in that energy which ultimately releases heat in order to produce endothelial and vein wall shrinkage with subsequent fibrosis. The target for lasers with 810-, 940-, and 980-nm wavelengths is intravascular red blood cell absorption of laser energy. These techniques are highly dependent on correct placement of tumescent local anesthesia so as to protect surrounding nerves from injury. Direct thermal effects on the vein wall without the presence of blood probably do not occur. The extent of thermal injury to tissue is very much dependent on the amount and duration of heat to which the tissue is exposed, which for these lasers is dependent on multiple factors including the presence of blood in the lumen, rate of pullback, and amount of tumescent anesthesia placed around the vein. One in-vitro study model showed that thermal gas production by laser heating of blood in a 6-mm tube results in 6 mm of thermal damage.52,53 Histologic examination of one excised vein demonstrated thermal damage along the entire treated vein with evidence of perforations at the point of laser application described as “explosive-like” photodisruption of the vein wall. This produced the homogeneous thrombotic occlusion of the vessel. Formation of bubbling blood is the proposed mechanism of action for heating surrounding tissue.53 We have found superheating of blood during these procedures to a maximum of approximately 1,200°C.18

These endovenous lasers have short-term efficacy of 90% occlusion over the first year, but the rate decreases with time.54,55 In addition, most patients experience major degrees of postoperative ecchymosis and discomfort. Saphenous nerve injury, skin burns, and deep venous thrombosis have occurred due to the high temperatures of blood heating from these wavelengths, although the overall safety and efficacy record is better than for stripping.56–58

Laser (Water Predominant Absorption—1,320, 1,440, and 1,470 nm)

A variation of the endovenous laser, 1,320 nm, was developed by dermatologic surgeons in 2003 in an attempt to bypass the problems associated with laser wavelength absorption of hemoglobin. Tissue water is the target and the presence or absence of red blood cells within the vessels is unimportant. For more controlled release of laser energy, it is coupled with an automatic pull-back device variable from 0.5–1 mm/s. The penetration of the 1.32-μm wavelength is unique with far less heat and risks than with the hemoglobin absorbing wavelengths.

Endovenous ablation appears best accomplished not by hemoglobin heating but by heating water within collagen in the vein wall as a target. Proebstle et al demonstrated a statistically reduced rate of postoperative pain accompanied by a higher initial success rate using 1,320 nm versus 940 nm.59 Our own experience reflects this, with a reduction in pain and bruising of 80% when switching from 810 nm endovenous to 1,320 nm endovenous. Having treated over 500 greater saphenous veins with 1,320 nm, our incidence of mild pain is 5%. No significant pain interfering with walking has been observed as observed with 50% of 810-nm treatment. A clinical example of varicose veins resulting from reflux at the saphenofemoral junction is shown in Fig. 249-8. Recent data indicates that the 1,440-nm or 1,470-nm wavelengths may also be effective.60 but data is preliminary and there is no comparison data on efficacy between the different water predominant wavelengths.

Ambulatory Phlebectomy

This technique, originally described by Robert Muller and further refined by another Swiss dermatologist (Albert-Adrien Ramelet) involves the use of tiny incisions through which the varicose vein is removed by a small hook.61,62 This safe, outpatient local anesthesia technique allows removal of almost any varicose vein except the saphenofemoral or saphenopopliteal junction, which are treated initially by endovenous ablation techniques. Areas or veins that are resistant to foam sclerotherapy are particularly indicated for ambulatory phlebectomy (Fig. 249-9). Risks minimized compared with sclerotherapy are deep venous thrombosis, postsclerotherapy pigmentation, skin necrosis, and superficial phlebitis. In many cases larger varicose veins coexist with smaller reticular veins and associated telangiectatic webs. It is reasonable to treat larger varicose veins by various surgical techniques and follow up with sclerotherapy of the remaining reticular networks.

Lasers and Light Sources

New trends for improved results with lasers and light sources for spider veins include longer wavelengths, larger spot sizes and cooling to protect the skin (Fig. 249-10). The first report of 1,064-nm Nd:YAG laser indicated that 75% improvement was possible after a single treatment at 3 months.63 These findings were confirmed and mechanism of action explained as heat-induced vessel damage and subsequent fibrosis.64 Recent reports also indicate effectiveness of 940-nm diode laser.65 Shorter wavelengths used in the past, like pulsed dye laser, have limited utility on leg veins although many devices are now being adapted to longer pulse durations up to 40-ms. In our practice, the vast majority of laser treatments are performed using 1,064-nm Nd:YAG in the millisecond domain on isolated telangiectasias, sclerotherapy-resistant telangiectasias, ankle telangiectasias and suspected A-V malformations. Even associated reticular veins with telangiectasias can be treated with 1,064 nm, however, the larger the vein, the more painful the treatment due to increased absorption of infrared energy.66