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Varicose Veins and Spider Veins Treatment & Management

  • Author: Robert Weiss, MD; Chief Editor: William D James, MD  more...
 
Updated: Dec 08, 2015
 

Medical Care

Superficial varicosities are the result of high-pressure flow into a normally low-pressure system. Varicosities carrying retrograde flow are hemodynamically harmful because they cause recirculation of oxygen-poor, lactate-laden venous blood back into an already congested extremity. The primary goal of treatment is the ablation of these reflux pathways with resulting improvement of venous circulation.

In the rare setting of deep system obstruction, varicosities are hemodynamically helpful because they provide a bypass pathway for venous return. Hemodynamically helpful varices must not be removed or sclerosed. This condition is encountered rarely, but when it is, ablation of these varicosities causes rapid onset of pain and swelling of the extremity, eventually followed by the development of new varicose bypass pathways.

Sclerotherapy, laser and intense-pulsed-light therapy, radiofrequency (RF) or laser ablation,[6] and ambulatory phlebectomy are the modern techniques used to ablate varicosities. Numerous reports describe success rates of greater than 90% for less invasive techniques, which are associated with fewer complications, with comparable efficacy.[7, 8]

Chemical sclerosis or endovenous chemoablation

Chemical sclerosis or endovenous chemoablation (sclerotherapy) is the most widely used medical procedure for ablation of varicose veins and spider veins.[1] In this procedure, a sclerosing substance is injected into the abnormal vessels to produce endothelial destruction that is followed by formation of a fibrotic cord and eventually by reabsorption of all vascular tissue layers. For most veins, a detergent sclerosing agent is agitated with air to create a foam similar to shaving foam. A thorough diagnostic evaluation is essential prior to treatment. A high degree of technical skill is necessary for effective sclerotherapy many reasons.

Local treatment of the superficial manifestations of venous insufficiency is unsuccessful if the underlying high points of reflux have not been found and treated. Even when the patient appears to have only primary telangiectasias and the initial treatment seems to be successful, recurrences are observed very quickly if unrecognized reflux exists in larger subsurface vessels.

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

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

Missing the diagnosis of deep system disease can lead to bad outcomes in several ways. Symptoms become immediately worse if an unrecognized bypass pathway is ablated. Missing the diagnosis of underlying venous thrombosis can lead to fatal embolism.[9] Unrecognized deep venous insufficiency can lead to early or immediate recurrence of treated superficial disease.[10]

Selection of the correct sclerosant and the correct volume and concentration of sclerosant depends on the type and location of disease, internal volume of the vessel to be treated, positioning of the patient, and many other factors. The minimum effective concentration and volume should always be used because sclerosant inevitably passes into the deep venous system, where endothelial injury can lead to disastrous consequences.

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

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 deep vein thrombosis, pulmonary embolism, and death.

The proper use of sclerosing agents requires special training and extended study. Specific dosing and technique recommendations for the administration of sclerosants are beyond the scope of this article.

The most commonly used sclerosants today are polidocanol and sodium tetradecyl sulfate, both known as detergent sclerosants because they are amphiphilic substances that are inactive in dilute solution but are biologically active when they form micelles. These agents are preferred because they have a low incidence of allergic reactions, produce a low incidence of staining and other cutaneous adverse effects, and are relatively forgiving if extravasated.[11] These are best delivered as a foam, which is made by agitating the solutions with air to create a frothy substance.

Sodium morrhuate is an older detergent sclerosant that is made up of a mixture of saturated and unsaturated fatty acids extracted from cod liver oil. The agent is of variable composition and has been associated with a relatively high incidence of anaphylaxis. The incidence of extravasation necrosis is high with this drug.

Ethanolamine oleate, a synthetic preparation of oleic acid and ethanolamine, has weak detergent properties because its attenuated hydrophobic chain lengths make it excessively soluble and decrease its ability to denature cell surface proteins. High concentrations of the drug are necessary for effective sclerosis. Allergic reactions are uncommon, but reports exist of pneumonitis, pleural effusions, and other pulmonary symptoms following the injection of ethanolamine oleate into esophageal varices. The principal disadvantages of the drug are a high viscosity that makes injection difficult, a tendency to cause red cell hemolysis and hemoglobinuria, the occasional production of renal failure at high doses, the possibility of pulmonary complications, and a relative lack of strength compared with other available sclerosants.

Hypertonic sodium chloride solution in a 20% or 23.4% solution can be used as a sclerosing agent. The principal advantage of the agent is the fact that it is a naturally occurring bodily substance with no molecular toxicity, but the disadvantages of the agent make it unsuitable except in the hands of highly skilled practitioners. Because of dilutional effects, achieving adequate sclerosis of large vessels without exceeding a tolerable salt load is difficult. It can cause significant pain on injection and significant cramping after a treatment session. If extravasated, it almost invariably causes significant necrosis. Seeing patients with dozens of disfiguring scars at the sites of extravasation of hypertonic sodium chloride solution is not uncommon. Because it causes immediate red blood cell hemolysis and rapidly disrupts vascular endothelial continuity, it may cause marked hemosiderin staining that is not cosmetically acceptable.

Food and Drug Administration (FDA) approval of drug labeling is an important concern for physicians and patients in the United States. Polidocanol is approved by the FDA. Sotradecol, sodium morrhuate, and ethanolamine oleate all were developed prior to the establishment of the FDA. These agents are available in the United States as grandfathered agents. The newest form of Sotradecol was cleared by the FDA in 2006. It is highly purified with no contaminants.

In November 2013, the FDA approved polidocanol injectable foam (Varithena), a pharmaceutical-grade, low-nitrogen polidocanol foam dispensed from a proprietary canister device, for the treatment of incompetent veins and visible varicosities of the great saphenous vein system. Approval was based on 2 placebo-controlled studies, in which most of the treated patients experienced clinically meaningful improvement of the symptoms of superficial venous incompetence and the appearance of visible varicosities.[12]

According the National Institute for Health and Care Excellence (NICE) guidelines, foam sclerotherapy is considered second-therapy after endovenous ablation.[13]

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

Laser therapy

Transcutaneous pulsed dye laser and intense-pulsed-light (IPL) therapy has proven effective for the tiniest surface vessels (eg, those found on the face), but this modality is not generally useful as primary therapy for treatment of spider veins of the lower extremity. This is true for several reasons.

Because of the physics of light absorption, delivering an ablative dose of thermal energy to the vessel without damaging the overlying skin is difficult. The degree of patient-to-patient variability of light absorption in the skin is high. Even an experienced practitioner may inadvertently cause painful skin burns that can lead to permanent hyperpigmentation or hypopigmentation.

For most patients, the laser pulses are significantly more painful than the 30-gauge needles used for microsclerotherapy.

Most spider veins have associated feeding vessels that must be treated by some other means before the tiny surface vessels are amenable to laser or IPL treatment.

Dudelzak et al report successful treatment of facial spider veins (telangiectasias) with a 980-nm diode laser. No complications were reported.[14]

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Surgical Care

The primary goal of surgical therapy is to improve venous circulation by correcting venous insufficiency through the removal of major reflux pathways. Common surgical approaches to large-vein varicose disease include ligation of the saphenofemoral junction with vein stripping, phlebectomy performed through microincisions, endovenous radiofrequency thermal ablation, and endovenous laser thermal ablation. The principal surgical approach to small-vein disease is by microincisional phlebectomy followed by sclerotherapy.

Endovenous laser therapy

Endovenous laser therapy is a thermal ablation technique that uses a laser fiber placed inside the vein.[15]

Seldinger over-the-wire technique is used to place a long catheter along the entire length of the truncal varix to be ablated. A bare laser fiber is passed through the catheter until the end protrudes from the tip of the catheter by about 2 cm and the laser fiber tip is positioned at the saphenofemoral junction just distal to the subterminal valve. The position is confirmed by ultrasonography and by use of the laser guide light.

Under ultrasonographic guidance, very dilute, high volume local tumescent anesthetic is injected around the vessel to be ablated until a halo of tumescence is observed along the entire length of the vessel, separating it from its fascial sheath.

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 laser may be set for continuous delivery of energy, in which case the fiber and catheter must be withdrawn at a slow and constant rate, or for intermittent pulses, in which case the fiber and catheter are withdrawn about 2 mm after each pulse and the process is repeated along the entire course of the vessel.

One system, using a 1320-nm laser, uses an automatic pullback mechanism.

Radiofrequency ablation

Radiofrequency ablation is a thermal ablation technique that uses a specially developed proprietary RF catheter placed inside the vein. The first version was cleared by the FDA in 1999. The most recent version using a redesigned simpler RF catheter was introduced into the market in 2007.

A cutdown, stab incision with vein exteriorization, or simple needle puncture using a Seldinger over-the-wire technique is used to place an introducer sheath into the truncal varix to be ablated.

A special RF ablation catheter is passed through the sheath and along the vein until the active tip is at the saphenofemoral junction just distal to the subterminal valve. Position of the tip is confirmed by ultrasonography.

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.

In the old system, metal fingers at the tip of the RF catheter were deployed until they made contact with the vessel endothelium. In the new system, 7 cm of the tip is heated to 120 º C using RF energy. 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 every 7 cm and the process is repeated all along the length of the vein to be treated.

While widely accepted, there remains a lack of long-term, high-quality trials and class 1A evidence comparing RF ablation efficacy with open surgery.[16]

Stab-avulsion technique

The stab-avulsion technique (ambulatory phlebectomy) allows removal of short segments of varicose and reticular veins through tiny incisions, using special hooks developed for the purpose. This procedure is extremely useful for treatment of residual clusters after saphenectomy and for removal of nontruncal tributaries when the saphenous vein is competent.

With the patient in a standing position, duplex ultrasonography is used to map the locations of all refluxing vessels to be removed. The vessel locations are marked on the skin using an indelible marker. The position of the veins is confirmed with the patient recumbent using a vein illumination device as the position of the vein relative to the skin may change with positioning of the leg.

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 no sutures are used to close the microincisions.

Saphenectomy

Saphenectomy with saphenofemoral ligation is the old approach performed using an internal stripping tool and an invagination technique. This technique has been replaced by endovenous ablation techniques.

A 2- to 3-cm incision is made at the groin crease beginning at the femoral artery and extending medially. The saphenofemoral junction is exposed by dissection.

After ligation and division of the junction and all associated tributaries, the stripping instrument (usually a stiff but flexible length of wire or plastic) is passed into the greater saphenous vein at the groin and is threaded through the incompetent vein distally to the level of the upper calf, where it is brought out through a small incision (5 mm or less) approximately 1 cm from the tibial tuberosity at the knee.

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 gauze or ligature may be secured to the stripper before invagination, allowing a hemostatic packing to be pulled into place after stripping is complete.

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Consultations

If ultrasound imaging demonstrates isolated spider veins without underlying reflux, the problem may be treated in the office without difficulty.

Patients with identifiable underlying reflux or other signs of significant venous disease must be referred for consultation with a phlebologist (a physician or surgeon with a special interest and special training in venous diagnosis and therapeutics).

The American College of Phlebology and the American Venous Forum are national medical specialty societies that can refer patients to a nearby specialist.

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Activity

Prolonged standing is a risk factor for venous insufficiency syndromes. Activity is a protective factor.

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

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Contributor Information and Disclosures
Author

Robert Weiss, MD Associate Professor, Department of Dermatology, Johns Hopkins University School of Medicine

Robert Weiss, MD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American College of Phlebology, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, MedChi The Maryland State Medical Society

Disclosure: Received honoraria from Angiodynamics for speaking and teaching; Received intellectual property rights from CoolTouch Corp for consulting; Received grant/research funds from Cynosure for independent contractor; Received grant/research funds from Palomar for independent contractor.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

John G Albertini, MD Private Practice, The Skin Surgery Center; Clinical Associate Professor (Volunteer), Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine; President-Elect, American College of Mohs Surgery

John G Albertini, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery

Disclosure: Received grant/research funds from Genentech for investigator.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Kelly M Cordoro, MD Assistant Professor of Clinical Dermatology and Pediatrics, Department of Dermatology, University of California, San Francisco School of Medicine

Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Medical Society of Virginia, Society for Pediatric Dermatology, Women's Dermatologic Society, Association of Professors of Dermatology, National Psoriasis Foundation, Dermatology Foundation

Disclosure: Nothing to disclose.

Acknowledgements

Craig F Feied, MD, FACEP, FAAEM, FACPh Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group

Craig F Feied, MD, FACEP, FAAEM, FACPh is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Phlebology, American College of Physicians, American Medical Association, American Medical Informatics Association, American Venous Forum, Medical Society of the District of Columbia, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

References
  1. Goldman MP, Guex JJ, Weiss RA. Sclerotherapy: Treatment of Varicose and Telangiectatic Leg Veins. 5th ed. Philadelphia: Saunders; 2011. 1-416.

  2. Piazza G. Varicose veins. Circulation. 2014 Aug 12. 130 (7):582-7. [Medline].

  3. Chiesa R, Marone EM, Limoni C, Volonte M, Schaefer E, Petrini O. Chronic venous insufficiency in Italy: the 24-cities cohort study. Eur J Vasc Endovasc Surg. 2005 Oct. 30(4):422-9. [Medline].

  4. Racette S, Sauvageau A. Unusual sudden death: two case reports of hemorrhage by rupture of varicose veins. Am J Forensic Med Pathol. 2005 Sep. 26(3):294-6. [Medline].

  5. Cho ES, Kim JH, Kim S, et al. Computed tomographic venography for varicose veins of the lower extremities: prospective comparison of 80-kVp and conventional 120-kVp protocols. J Comput Assist Tomogr. 2012 Sep. 36(5):583-90. [Medline].

  6. Carradice D, Leung C, Chetter I. Laser; best practice techniques and evidence. Phlebology. 2015 Nov. 30 (2 Suppl):36-41. [Medline].

  7. Nael R, Rathbun S. Treatment of varicose veins. Curr Treat Options Cardiovasc Med. 2009 Apr. 11(2):91-103. [Medline].

  8. Nijsten T, van den Bos RR, Goldman MP, et al. Minimally invasive techniques in the treatment of saphenous varicose veins. J Am Acad Dermatol. 2009 Jan. 60(1):110-9. [Medline].

  9. Bruijninckx CM. Fatal pulmonary embolism following ultrasound-guided foam sclerotherapy combined with multiple microphlebectomies. Phlebology. 2015 Sep 2. [Medline].

  10. Muller-Buhl U, Leutgeb R, Engeser P, Achankeng EN, Szecsenyi J, Laux G. Varicose veins are a risk factor for deep venous thrombosis in general practice patients. Vasa. 2012 Sep. 41(5):360-5. [Medline].

  11. Rao J, Wildemore JK, Goldman MP. Double-blind prospective comparative trial between foamed and liquid polidocanol and sodium tetradecyl sulfate in the treatment of varicose and telangiectatic leg veins. Dermatol Surg. 2005 Jun. 31(6):631-5; discussion 635. [Medline].

  12. Brooks M. FDA OKs New Minimally Invasive Treatment for Varicose Veins. Available at http://www.medscape.com/viewarticle/815039. Accessed: December 3, 2013.

  13. Alder G, Lees T. Foam sclerotherapy. Phlebology. 2015 Nov. 30 (2 Suppl):18-23. [Medline].

  14. Dudelzak J, Hussain M, Goldberg DJ. Vascular-specific laser wavelength for the treatment of facial telangiectasias. J Drugs Dermatol. 2009 Mar. 8(3):227-9. [Medline].

  15. Mao J, Zhang C, Wang Z, Gan S, Li K. A retrospective study comparing endovenous laser ablation and microwave ablation for great saphenous varicose veins. Eur Rev Med Pharmacol Sci. 2012 Jul. 16(7):873-7. [Medline].

  16. Goodyear SJ, Nyamekye IK. Radiofrequency ablation of varicose veins: Best practice techniques and evidence. Phlebology. 2015 Nov. 30 (2 Suppl):9-17. [Medline].

  17. O'Hare JL, Stephens J, Parkin D, Earnshaw JJ. Randomized clinical trial of different bandage regimens after foam sclerotherapy for varicose veins. Br J Surg. 2010 May. 97(5):650-6. [Medline].

  18. Cesarone MR, Belcaro G, Ricci A, et al. Prevention of edema and flight microangiopathy with Venoruton (HR), (0-[beta-hydroxyethyl]-rutosides) in patients with varicose veins. Angiology. 2005 May-Jun. 56(3):289-93. [Medline].

  19. Weiss RA, Feied CF, Weiss MA. Vein Diagnosis & Treatment: A Comprehensive Approach. 1st ed. New York, NY: McGraw-Hill; 2001. 1-304.

 
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Patient with large tortuous varicose veins, high-volume venous reflux, and early stasis changes of the medial ankle.
Typical chronic medial leg ulceration associated with long-standing venous insufficiency. The ulcer had been present for 12 years and was refractory to every treatment approach until treatment of the refluxing superficial varices was performed. Treatment consists of endovenous ablation, foam sclerotherapy, or ambulatory phlebectomy.
 
 
 
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