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Patients living with painful swelling from venous reflux disease, or varicose veins, know all too well that the condition is more than just a cosmetic issue. Varicose veins can lead to swelling of the lower limbs, skin inflammations and leg ulcers. Venous reflux symptoms are progressive and will worsen over time, if left untreated. Unfortunately, many health insurers….
Featured ProcedureEndo Laser Closure
Laser energy and radiofrequency energy sources are the modern tools of the venous surgeon which are the basis for remarkable transition away from traditional open surgical “Stripping and Ligation” and Trivex surgeries to the state of the art minimally invasive catheter based procedures. These new methods can now be done in the doctor’s office because the procedures are so precise there is no significant blood loss and no need to “strip” out the vein.
information aboutCardiovascular wellness
The AHA (American Heart Association) recently estimated that the annual rate of new heart attacks in United States is 785,000, another 470,000 will have a recurrent heart attack and another 195,000 will have a silent heart attack. Early intervention is crucial. By the time the disease is apparent it has already damaged and overcome your body’s natural protective immune and stress defense mechanisms. This leads to a cascade of further disability and hopelessness.
Why Choose Advanced Laser Vein Care?
We are not a med spa, we are not here to scare you about your ugly veins. We are here to take care of you. Dr. Bressman is a Diplomate of the American Board of Phlebology and has dedicated his practice to taking care of patients with the full spectrum of venous disorders. Your treatment will be based upon a complete consultation, a full venous duplex ultrasound examination, and tailored to meet your unique needs. We employ both Laser and Vnus Coviden Radiofrequency endovenous ablation therapy, ultrasound guided foam sclerotherapy and Microphlebectomy and will utilize your PPO or Medicare Insurance benefits whenever possible. Most importantly you are placing your problems in hands of a master surgeon with lifetime of experience and a dedication to the art and science of your problem.
Nearly 26% of all women and 13% of all men will develop some form of chronic venous disorder in their lifetime. Until recently, the removal of varicose veins required the actual stripping out of the vein: a surgical procedure that can require a hospital stay because of the painful recovery. The surgical procedure often includes several “stab phlebectomy” incisions which can leave multiple scars and runs the risk of post-operative infections and nerve damage. Today endovenous luminal ablation (EVLA or EndoVascular Laser Therapy) therapy with lasers (Dornier 940 nm) and/or radiofrequency energy (VNUS Covidien) have replaced the need for this type of surgery ...(read more)
Nearly 30 million American men and women will develop some form of venous disorder in their lifetime. The prevalence of visible varicose veins in women increases with age from 22% at age 40 to 72% by age 60. Men also develop varicose veins but are less likely to seek treatment until symptoms worsen. The genetic prevalence for developing varicose veins has been reported as high as 50 % if your mother has them; 70% if your father has them; and over 90% if both parents have varicose veins.
Varicose veins are typically tortuous blue veins greater than 4 mm in diameter that can cause pain, fatigue, heaviness and swelling in their early stages ( CEAP 2 - CEAP 3). It is vitally important for the public to understand that varicose veins are a health concern worthy of medical diagnosis and treatment. If this condition is allowed to progress it can cause even more serious complications termed Chronic Venous Insufficiency (CVI) which affects the skin near the ankles. Untreated CVI leads to discoloration (hyper pigmentation) and more serious disturbances of skin texture (venous stasis dermatitis, lipodermatosclerosis and atrophie blanche) and can progress in its later stages to venous ulceration at the ankle level (CEAP 4 – CEAP 6).
Abnormal Venous Flow, Valve incompetence and Venous Insufficiency
All of the veins in the legs have a series of one way valves that serves to direct venous blood flow to the heart. In the upright position the weight of the column of blood in the veins normally causes the valve leaflets to close (valve competence). If the vein walls enlarge or the valve leaflets have become damaged the venous blood will leak back through the valve (valve incompetence) and will not be efficiently returned to the heart. This can lead to an accumulation of stagnant venous blood in the legs with bulging of the surface veins, edema (swelling of the feet and ankles) and deterioration of the skin. Failure of venous system to clear the normal products of muscle metabolism such as lactic acid, carbon dioxide and oxygen-poor blood causes irritation and leads to symptoms of aching, burning, itching pain, fatigue, tenderness, heaviness, warmth, restless legs and nocturnal leg cramps. If left untreated CVI causes damage at the intracellular levels leading to and increased production of inflammatory cells, increased oxygen free radical production, venous hypertension and impairment of normal capillary flow. If this is allowed to progress it will cause death of the surrounding fat and skin layers and chronic venous ulcer formation. By eliminating these damaged veins (vein ablation procedures) the venous blood will redirect itself through normal vein segments to once again connect with the deep venous system. This restores competence to the musculovenous pump so that the venous blood can be efficiently returned to the heart and then pumped to the lungs and liver in order to refill its oxygen content, remove the accumulated carbon dioxide, neutralize lactic acid and replenish its glucose and other vital nutrients
Deep Venous System and the Musculovenous Pump
Venous blood from the legs has to be actively pumped by the leg muscles so that it will be able to return the blood up to the level of the heart. The largest veins in the legs are the deep veins which are completely surrounded by the muscle compartments in the calf and thigh. The deep vein at the top of the calf is called the Popliteal Vein and it drains all the venous blood from the calf muscles. This vein continues up through the thigh where it drains all of venous blood from the thigh muscles and is called the Femoral Vein. When we walk, or simply cross our legs, or even make minor unconscious changes in the position of our feet, the respective muscles in the calf and thigh exert pressure on the deep veins forcing the venous blood upwards to the heart. These deep veins are the “heart” of the musculovenous pump system. Above the groin area the Femoral Vein courses into the pelvis to form the Iliac Vein. The right and left Iliac Veins join to form the Inferior Vena Cava which returns venous blood into the heart through the Right Atrium. There are no muscles surrounding the deep veins in the pelvis and abdomen to aid in pumping the blood up to the chest. The diaphragm muscle used for breathing creates negative pressure in the chest and this helps to pull the blood up to the level of the heart.
The superficial veins lie under the skin and in the subcutaneous fatty tissue. Superficial veins are not fully surrounded by muscles and not capable of generating the force necessary to return blood to the heart in the upright position. The superficial veins are under the influence of the nervous system and function primarily to maintain body temperature by dilating to allow increased heat loss or contracting to prevent heat loss. When the valves in the superficial veins become incompetent the veins may enlarge and appear raised above the level of this skin and look like twisted bulging chords. The largest superficial vein is the Great Saphenous vein which runs from the inner part of the ankle all the way up to the inner thigh and empties at the groin level into the Femoral Vein through the Saphenofemoral Junction (SFJ). The Small Saphenous Vein runs along the outer part of the ankle and empties into the Popliteal Vein through the Saphenopopliteal junction which is located behind the knee. Other important superficial veins are the Anterior Accessory Saphenous Veins which run along the course of the thigh and empty into the Great Saphenous Vein just below the level of the SFJ. The Lateral Subdermic Complex runs along the outer surface of the calf and thigh and connects with the deep veins in the pelvis and upper thigh.
Connecting the low pressure superficial veins to the high pressure deep veins are a series of perforating veins whose valves are oriented to only permit flow from the superficial venous system to the deep venous system. When the perforator valves fail to close properly, the high pressure created by the musculovenous pump can force the blood in the deep venous system back out to the skin level. This can be identified as a “blown out vein” and causes a palpable defect in the covering of the muscle layer (fascial defect) to enlarge and feel like a hole in the muscle surface. There are several important Perforator Veins in the inner (medial side) of the ankle and calf called Posterior Tibial Perforators (Crockett’s perforators) which connect to the Posterior Arch Vein and the deep veins in the calf. At the top of the inner portion of the calf there are Paratibial Perforator veins (Boyd’s Perforator) . The Dodd’s perforators are located at the lower inner thigh level and the Hunter’s Perforators are located in the upper inner thigh level. Collectively the perforators in the thigh are called the Perforators of the Femoral Canal. Another important connection is the Posterior Thigh Extension Vein (Intersaphenous Vein or Vein of Giacomini) which runs from the Popliteal Vein behind the knee and joins the Great Saphenous Vein just below the SFJ. This intricate system of interconnections allows the venous return of the leg to seek alternative routes around a blood clot in the deep vein of the leg and return venous blood to the groin through the superficial venous system. Failure to detect malfunction of the perforator system (venous reflux from incompetent valves) by an inexperienced practitioner is one of the chief causes for failure and ultimate patient dissatisfaction after venous ablation procedures.
Spider Veins and Reticular Veins (feeding veins):
Spider Veins commonly affect millions of women and cause negative self image and may be associated with symptoms such as alterations in skin texture, discoloration and itching. Unlike varicose veins they rarely bulge above the level of the skin and do not pose a medical risk. However in very rare cases, if they are irritated, they can rupture and cause bleeding. In the great majority of cases they are asymptomatic and are considered a cosmetic blemish and are universally not covered by commercial health insurance plans. The medical term for Spider Veins is Telangiectasias: small, 0.2 to 1.0 mm, red or blue or purple veins located within the dermis layer and lie just below the skin. They are actually a confluence of dilated incompetent intra-dermal venules that, on the outside of the thighs and calves, are part of an extensive network of the Lateral Subdermic Venous System; a system that is separate from the Saphenous system. The Reticular Veins, commonly called “Feeder Veins,” they are 1 to 3 mm wide blue veins that can be seen running in a curvilinear fashion under the skin surrounding the spider complexes. These reticular veins also have incompetent valves allowing venous blood to run out toward the skin instead of draining the venous blood in the normal direction. Spider veins are often associated with a family history of varicose veins and may form as result of local skin injury or sun damage, and are more commonly seen with obesity, advancing age, and thinning of the skin. They are especially sensitive to female hormonal influence and commonly develop in females during their reproductive years. They are usually found on the thighs, calves, ankles, and the nose and tend to be progressive. Spider veins may also result from abnormal micro connections between small subcutaneous arteries and veins (arteriovenous anastomosis) which bypass the normal microscopic capillary network and enlarge to the point that they appear like a spider. These dermal and subcutaneous veins (unlike muscular veins) are innervated by the sympathetic nervous system and they will dilate and contract in response to local and central nervous stimuli such as warming and cooling, stress, and circulating vasoconstrictor peptides such as Endothelin.
Spider vein complexes are commonly seen in two typical distribution patterns: horizontal and vertical arrays. The horizontal pattern runs parallel to the skin and cause a wide fan shaped linear array of telangiectasias. This pattern is very common on the outer thigh and is often seen in close association with reticular feeding veins which are connected to the superficial veins of the skin which are in turn connected to the deeper veins.
In the vertical pattern, the feeding vessel may be a small arteriole or venule which runs perpendicular to the skin and is typically seen as the central core in a spreading blush or arborization pattern. These small arteriovenous or arteriolar spider complexes are connected to the arterial system. Caution must be used when introducing medications into these vessels to prevent skin ulcers and systemic complications. This vertical pattern can be easily appreciated by placing a pencil eraser in the center of the spider, compressing the area to make it disappear and then quickly releasing pressure and watching the spider spread out in a circular pattern.
Spider veins and varicose veins can co-exist and it is important to obtain a proper diagnosis to determine the best means of treatment effectively clear the spider veins and prevent complications from varicose veins. Fortunately spider veins and their reticular feeding veins can be easily treated with a combination of direct injections (sclerotherapy) and topical laser utilizing the Dornier 940 nm wavelength system.
Variability of Varicose Vein Symptoms:
Some people appear to have minimal symptoms because their busy life style does not give them the time to recognize this condition and after a while they accept these symptoms as part of growing old. Some simply have higher pain tolerances but may note that at the end of the day, or after a long airplane trip, their feet are swollen and it just feels better to elevate their legs when they get home. Any activity or occupations associated with prolonged periods of standing aggravates the hereditary condition causing abnormal vein wall expansion and valve leaflet weakness leading to varicose vein progression. This risk is further aggravated if their condition is associated with increased venous pressure from heavy lifting, pregnancy, excess weight gain or simply being tall. Finally their venous insufficiency causes deterioration in the local nerve supply which accounts for the fact that venous skin ulcers are often painless (terminal disease process CEAP 5 - CEAP 6). The size of the incompetent veins, their location, and factors such as the menstrual cycle, constitutional differences in stress levels also accounts for the variability of symptoms.
Superficial Phlebitis, Superficial Venous Thrombosis (SVT), Deep Vein Thrombophlebitis (DVT,) Venous Thromboembolism (VTE) and Post Phlebitic Syndrome
Venous thrombosis (a blood clot in the veins) is the condition where the vein becomes obstructed by a clot which prevents the normal return of blood from the legs to the heart. This causes swelling, pain and inflammation in the vein and in severe cases can comprise the viability of the skin and the deep muscle compartment causing phlegmasia cereula dolens (painful blue leg), or even progress to venous gangrene known as phlegmasia alba dolens (painful white leg). Fortunately these complications are quite rare and can be treated by interventional specialist with mechanical and enzymatic clot dissolution systems. If a clot in the deep venous system extends or breaks free (Venous Thromboembolism) and it is carried up to the heart it will be pumped into the lungs. This is known as a pulmonary embolus (PE) and is a potentially life threatening event. Fortunately this condition, like DVT, can be dealt with by hospital based interventional specialists.
Traditionally venous phlebitis has been classified as Superficial Vein Phlebitis and Deep Vein Thrombophlebitis but it is becoming clear that the two are clearly related.
Superficial Venous Phlebitis often starts out as a tender, red, warm and firm segment in the superficial veins and can be appreciated as a palpable tender cord like segment of vein just below the skin. This occurs most often in an incompetent segment of the Great Saphenous Vein and is associated with pregnancy, obesity, smoking, and the use of oral contraceptives. It can remain relatively isolated in the calf or thigh, or travel towards the deep veins of the calf or thigh. If the inflammation and clot in the superficial veins extends into the Deep Venous System it becomes a Deep Vein Thrombosis (DVT). Superficial Venous Thrombosis (SVT) within 2 cm of the Saphenofemoral Junction or the Saphenopopliteal Junction is clinically considered to be a like a DVT. The conservative standard of care is to treat SVT with warm compresses, elevation, anti-inflammatory pain medications (NSAIDs like Feldene, Mobic, Naprosyn, Naproxen and Celebrex) and compression stockings. This standard is being replaced by a newer proactive approach which initially employs outpatient anticoagulant injections such as Lovenox or Enoxaprin, then continuing the patients on oral Coumadin (generic Warfarin). Anticoagulants control the risk of SVT becoming a DVT and allow the body to more quickly dissolve these initial clots and relieve the associated pain and swelling. A limited drainage procedure under local analgesia will also give dramatic pain relief if clinically indicated.
DVT, Virchow’s Triad, and Pulmonary Emboli
Over 150 years ago Dr. Rudolph Virchow’s recognized 3 factors that lead to an increase in DVT. Injury to the inner (endothelial) wall of the veins is the initial stimulus that activates the clotting cascade under normal conditions. Conditions such as trauma, crush injury, or surgeries such as hip and knee replacements can cause an increased release of the normal factors that trigger this clotting response.
Alterations in blood flow leading to stagnant flow (stasis) can trigger increased clotting tendencies. This can be caused by inefficient venous return which occurs in veins with incompetent valves or in areas of saccular or aneurismal dilation. Other causes of stagnant flow occur during periods of relative inactivity of the musculovenous pump paralysis during cramped seating conditions (economy class syndrome), in paralyzed patients or in patients confined to bed for long periods. Dehydration is another factor in changing blood flow characteristics and this is why we encourage people to hydrate well and routinely get up and walk around the cabin or do foot exercises during long airplane or car trips.
Hypercoagulable states are conditions where there is a surplus, deficit or imbalance of the normal clotting factors which can accelerate the clotting cascade. This can develop as the result of metabolic influence from certain cancers (Trousseau’s Syndrome), oral contraceptives, hormone replacement therapies, autoimmune diseases (Antiphospholipid antibodies , Lupus Anticoagulant, and Anticoardiolipin antibody) and inflammatory conditions such as Inflammatory Bowel Disease and Nephrotic syndrome. Thrombophilias are another cause of the Hypercoagulable state and are inherited genetic conditions that result from an abnormal concentration or activity of a clotting factor or from a decrease in the activity of normal factors which are responsible for controlling coagulation. Examples of Thrombophilia states are AntiThrombin III deficiency, Protein S deficiency, Protein C Deficiency, Factor V Leiden mutation and Protein C resistance, Prothrombin 20210A mutation, and Factor VIII elevation These conditions are quite rare, however in patients who have had a DVT their frequency can approach 25%. Like all genetic conditions if the abnormal defect is passed on by both parents (homozygous) then even a minor tendency in each of the parents can lead to serious consequences in their children.
The end stage result of the inflammatory process caused by clot formation in the deep vein is the permanent destruction of the integrity of the vein and is guardian valves. The body has the capability to dissolve some of the clot but this often leaves the vein wall narrowed and renders the valves incompetent. In more severe cases, or cases where there is an unrecognized chronic clotting condition (coagulopathy) the deep vein pathway is completely closed and this will cause permanent swelling of the leg and lead to severe skin changes (lipodermatosclerosis, atrophie blanche) and venous ulceration. The venous blood will try to form new ways to get around the blocked deep vein using the superficial venous system. This can lead to the formation of large varicose veins or the process may be more diffuse and hidden deep inside the thickened skin of the swollen leg. Traditional therapy advocates rapid anticoagulation with heparin, administered in a hospital setting, until outpatient transition can be made to a Vitamin K antagonist such as Coumadin or Warfarin . To minimize the long term disabilities that can result, anticoagulants are recommended for a period of 6 to 12 months as well as lifelong use of graduated elastic compression stockings. Today the standard of care in severe cases is rapidly moving toward a more proactive treatment model utilizing the skill of the interventional therapist to remove as much of the clot as possible with enzymatic and mechanical devices such as TPA infusion, Angiojet, Trellis device, angioplasty and stents. This still needs to be followed by oral anticoagulation and stockings. Less severe cases are now being treated on an outpatient basis with self administered dosing of newer agents such as Lovenox, Enoxaprin and Fondaparinux.. These medicines are prepackaged, simple to use and similar to the concept diabetics giving themselves their own insulin injection. The patient still needs to transition to oral agents and we recommend thigh high, open toed graduated elastic compression stockings: Carolan, Jobst, Juzo, Medi, Sigvaris, and Venosan on a life time basis. Contrary to the popular belief that removing varicose veins associated with post phlebitis syndrome would aggravate venous drainage, Professor Peter Gloviczki, MD of the Mayo Clinic and others have proved that ablating the incompetent superficial veins and perforator will improve the patient’s condition as long as they continue to wear graduated elastic compression stockings.
Venous Ulcers (CEAP 5, CEAP 6)
The most severe gradation of the CEAP scale C5 and C6 states refer to the problems of chronic venous ulceration which tends to be an ongoing and recurring problem for patients with severe venous insufficiency. This usually results from Postphlebitic Syndrome or from a combination of Superficial Vein Insufficiency and/or Perforator Vein insufficiency. These will appear as shallow irregular ulcers that occur just above the ankle on either the inner or outer side of leg and are surrounded by brown stained skin (lipodermatosclerosis, hyper pigmentation) and frequently associated with varicose veins or blown out perforators. They can be distinguished from arterial insufficiency ulcers (dry gangrene) because the heel and rest of the foot are spared. Traditional therapy has been chronic compression stockings or a non stretch Unna Boot, local wound care and leg elevation. However the recurrence rate with these measures alone is notoriously high. Adjunctive therapy with hyperbaric oxygen, skin grafting, and medications to address alterations in the collagen metabolism, blood viscosity and metalloproteinase alterations has not proved to be significantly beneficial. The most promising methods of treatment are directly aimed at controlling the perforator and primary superficial venous reflux with laser or radiofrequency ablation and/or ultrasound guided foam sclerotherapy. In severe cases relieving ambulatory venous hypertension by means of enzymatic or mechanical thrombolysis, angioplasty or stents will give a better result. One of the most promising new developments has been popularized by Dr. Ronald Bush of the Midwest Vein and Laser Center who has recognized that surrounding these ulcers are a network of incompetent reticular varices which are under a lot of pressure. Dr. Bush realized if we can achieve a Terminal Interruption at the Reflux Source (TIRS) the ulcers will heal much faster. The TIRS technique involves ultrasound guided foam sclerotherapy around the ulcer in addition to ablation closure of the superficial and larger perforator veins. This is also my preferred method of treatment and this approach has shortened venous ulcer healing from a couple of months to just a few weeks and has eliminated the need for questionable adjunctive therapies. Venous ulceration is a reflection of chronic end stage damage to the venous system therefore it is important to realize that lifelong follow up care and control of venous hypertension with stockings or a non compression device like CircAid is still necessary.
Rare forms of Venous Diseases: May Thurner Syndrome, Pelvic Congestion Syndrome and Klippel Trenaunay Syndrome.
May Thurner Syndrome is an infrequent condition where the internal iliac artery crosses over the iliac vein and compresses the soft vein causing a partial blockage with an increased resistance to normal outflow resulting in venous hypertension and ultimately thrombosis of the iliac vein. For anatomic reasons this more frequently involves the left leg in women but it can also occur in men and sometimes it will affect the right leg. The compression of the vein is at the level of the pelvic vessels and this may make it difficult to appreciate on conventional duplex ultrasound examination. This condition can lead to chronic swelling, varicose veins and non healing ulcers. Now interventional specialists have a variety of enzymatic and mechanical devices (angioplasty and stents) to clear out clot and open the damaged vein to relieve symptoms.
Pelvic Congestion Syndrome (PCS):
PCS is related to valvular incompetence in the ovarian veins which leads to venous hypertension and engorgement of the venous drainage of the vagina, uterus and ovaries and their supporting ligaments. This can cause symptoms of heaviness, fullness, pain, pressure in the lower abdominal and pelvic regions, back aches, discomfort in the vulva, vagina, and inner thighs, pain during intercourse (dyspareunia) and uncomfortable menses with prolonged bleeding. There are other causes for these symptoms such as endometriosis, pelvic adhesions from chronic infections (PID, pelvic inflammatory disease) and uterine fibroid tumors. Consultation with a gynecologist is a mandatory first step to pursuing this diagnosis. The presence of varicose veins in the vulva, vagina and inner thighs with or without varicose vein in the legs, history of multiple pregnancies and weight gain of more than 40 pounds with each pregnancy are important clues in establishing this diagnosis. The diagnosis may be suggested by the findings of dilated ovarian or pelvic veins on diagnostic laparoscopy, or CT scan but the best confirmation of the diagnosis is from selective pelvic venography or MRI contrast examination. Once the diagnosis is confirmed treatment with embolization (mechanical or chemical agents) can be used to occlude the refluxing veins and reduce the venous hypertension. The subsequent treatment of the residual external varices in the genital area and upper thighs can then be treated in our office with ultrasound guided foam sclerotherapy or Microphlebectomy procedures.
Klippel Trenaunay Syndrome (KTS).
KTS is a very congenital condition in which the deep venous system in the leg(s) failed to properly develop leaving only the superficial system as a means of returning blood up to the level of the pelvis. It can occur in discrete or skipped areas or involve the whole leg. These results in a massive enlargement of the superficial and reticular venous system with tell tale large dark blue and red venous splotchy varicosities which increase as the child grows older and results in bone overgrowth and a swollen and deformed and elongated leg. This is a very complex condition which requires referral to a specialty hospital or university center.
Lymphedema is the result of the congenital absence, subsequent blockage or invasion, or delayed deterioration of the fluid collecting channels that drain the tissue fluid back to the heart. These very fine lymph channels (lymphatics) run parallel to the veins and like the veins they also contain one way flow valves and have a similar muscular-lymphatic pumping system. Lymphedema may present early in life in the congenital form or may develop in the late teens or early 30’s as a result of deterioration of the lymphatic channels.. These patterns often run in families. Lymphedema may also result from damage to the lymphatics from injury, surgery, radiation therapy, or from tumor invasion resulting in swelling of the arm or leg. Lymphedema is not a venous disorder but may occur in patients with varicose veins. Lymphedema will result in lifelong swelling of the legs which is amendable to massage and compression therapy but at the present time there is no definitive cure. Left untreated Lymphedema will lead to chronic infections (lymphangitis) and skin problems and can be quite disabling. Newer devices for controlling leg swelling such as CircAid and Lympha Press have also made it easier for patients to help take care of themselves.
CEAP Classification System:
This is the benchmark system used to describe the C (clinical), E (etiology), A (anatomic) and P (physiological) findings in patients with different states of venous insufficiency. Basic CEAP is an abbreviated system for following clinically significant stages.
|C0||no signs of venous disease|
|C1||telangiectasias, spider veins, reticular veins|
|C3||edema as a result of venous insufficiency|
|C4||changes in the skin and subcutaneous tissue as a result of venous insufficiency|
|C5||healed venous ulcer|
|C6||active venous ulcer|
Gloviczki, P., Comerota, A., Dalsing, M., Eklor, B., Gillepsie, M., Gloviczki M., Wakefiled, T., The care of patients with varicose veins and associated chronic venous diseases: Clinical practice guidelines of the Society of Vascular Surgery and the American Venous Forum, J Vasc Surg. 2011 May, 54(5 Suppl:: 2S-48 S.
“Age and sex composition: 2010” In 2010 United States of American Census (c2010br-032010 http://www.census.gov/prod/cen2010br-03.pdf “Chronic venous insufficiency.” Vascular Web. Society for Vascular Surgery, Jan.2011.Web. http://www.vascualrweb.org/vascularhealth/Pages/chronic-venous -sinsufficiency.aspx
Criqui MH et al. Epidemiology of chronic peripheral venous disease; JJ Bergan Editor, The Vein book, Elsevier Academic Press (2007): 30. “Varicose Veins and Spider Veins.” Department of Health and human Services, June 2010. Web. http://www.womenshealth.gov/publications/our-publications/fact-sheet/varciose-spider-veins.pdf.
Almeida JI, Kaufman J, Goeckeritz O, et al. Radiofrequency Endovenous ClosureFAST versus Laser Ablation for the Treatment of Great Saphenous Reflux: A multicenter, Single-Blinded, Randomized Study(Recovery Study). JVIR; June 2009
“Sclerotherapy: varicose and spider vein treatment.” VeinDirectory.org. Oct.2009.Web. http://www.veindirectory.org/content/scherotherapy.asp Primary Chronic Venous Disorders, Journal of Vascular Surgery, Meissner et al., Vol 46, pp 54 S- 66 S. December Supplement 2007
Venous Insufficiency, Seminars In Interventional Radiology, C. Fan and T. Andrews, Vol 22(3) pp 157-161C September 20005
New Technique to Heal Venous Ulcers: Terminal Interruption of the Reflux Source (TIRS) Perspectives in Vascular Surgery and Endovascular Therapy 22(3): 194-199, 2010
The Vein Book, Edited by John J. Bergan, 2007, p. 133. Handbook of Venous Disorders, 3rd Edition, Guidelines of the American Venous Form, 2009, p 105. Sclerotherapy Treatment of Varicose and Telangietctatic Leg Veins, Mitchel P. Goldman & John J. Bergan, Third Edition, p 26 -28; 118-121; 126-128.