No, although many patients may have multiple areas of venous reflux involving multiple viens, once a single vein is treated the efficacy of that treatment is over 95%. In other words, once a vein is ablated, that vein will stay closed permanently. Ablation is a very durable solution. Other veins, may, however require additional treatments including ablation or other therapeutic modalities such as sclerotherapy or phlebectomy depending on the size and location of the offending veins.
If I am sending a patient to you who has an ulcer, should I also send him or her to a wound center as well?”January 28th, 2013 | Posted by in vein-center - (0 Comments)
No, foot ulcers can have various etiologies, several of which have to do with the circulatory system in general, such as – arterial insufficiency, diabetes, venous insufficiency and/or a combination of any or all of the above. At Center for Vein Restoration, we can evaluate the patient and his or her specific wound at any of our centers. Those ulcers that are from a source such as diabetes and/or arterial insufficiency can be cared for at our sister practice “The Center for Vascular Medicine,” which specializes in these types of patient care issues. Wounds that are from a venous etiology can be cared for and definitively treated at a CVR office.
Center for Vein Restoration is excited to announce we’re expanding to the New York market; we’ll soon be opening our first clinic in Westchester County, NY. Helping us lead this expansion is our newest team member, Gautam V. Shrikhande, MD. Dr. Shrikhande is a talented, vascular surgeon and Assistant Professor of Surgery and Director of the Vascular Laboratory, Columbia University Medical Center. He is Board Certified in General and Vascular Surgery and is a Registered Physician in Vascular Interpretation (RPVI). He recently joined Center for Vein Restoration – the largest physician-led vein treatment practice in the country — to lead its expansion into the New York market; CVR already serves patients in more than 20 clinical locations in the Mid Atlantic and East Coast, with corporate headquarters near Washington D.C.
While a skilled clinician, Dr. Shrikhande also is known as a talented researcher and prolific writer. His published papers have appeared in many top medical journals, including the Journal of Vascular Surgery, the World Journal
of Surgery, Blood, Hepatology, Vascular and Endovascular Surgery and the Journal of Endovascular Therapy, He also recently co-edited a book – Diabetes and Peripheral Vascular Disease: Diagnosis and Management (Humana Press) – a guide for physicians, which is available on Amazon.com (http://tinyurl.com/c89zsku). He also is in the process of patenting a specialized filter to be used in vascular surgery.
Dr. Shrikhande studied at Trinity College in Hartford, Conn., and earned his MD at the University of Connecticut Medical School. He later trained in general surgery at Beth Israel Deaconess Medical Center, Harvard Medical School. He completed his vascular surgery fellowship at New York Presbyterian, the University Hospitals of Cornell and Columbia. He resides in the Carnegie Hill neighborhood of Manhattan with his wife, Dr. Allyson Shrikhande, and their daughter, and is a member of the Guggenheim.
by Robert C. Kiser, DO, MSPH
As animals, humans are classified as members of the Domain Eukaryota, kingdom Animalia, Phylum Chordata, class Mammalia, Order Primates, Family Hominidae, Genus Homo, and Species Homo sapiens. Physicians with degrees such as MD, DO, and DPM specialize in the diagnosis and treatment of humans. All other species are diagnosed and treated by physicians with designations such as Doctors of Veterinary Medicine. Traditionally there has been relatively little communication between human physicians and those who specialize in other species. The “zoobiquity” movement in medicine recognizes that ailments and diseases are ubiquitous across many animal species.1
The zoobiquity movement has spearheaded the attempt to increase communication between physicians who tend to human patients and those that tend to other species. The purpose of zoobiquity is to allow important discoveries in all of animal and human science to be shared by all the medical and scientific disciplines involved in the care of any species. An excellent and interesting book on Zoobiquity is “Zoobiquity: What Animals Can Teach Us About Health and the Science of Healing” by cardiologist Barbara Natterson-Horowitz and Kathryn Bowers. The book gives many examples of how human and animal medical fields pursue parallel courses, and often can provide important information for each other.
Humans are unique among animals in their manifestation of chronic venous insufficiency of the lower extremities. This is largely because humans are bipedal, long-limbed and do not have the inelastic leg skin of birds. However, humans are not unique in getting varicose veins or at least distended and irregular veins; there are relatively few species that are known to be afflicted with them. Those that are do not manifest the same skin changes that humans experience.
Domestic cows can often be seen to have varicose veins on their distended udders. In one of the closest analogies to human venous disease, a Pandharpuri buffalo (in India) was found to have a varicose sacral (tail) vein, leading to venous ulcer and signs such as hair loss of the tail and skin changes. In the case of the buffalo, however the cause was venous hypertension secondary to an arteriovenous fistula which is an unusual cause of varicose veins in humans.2 Horses can get venous insufficiency and varicose veins of their legs, including enlarged leg veins known as “blood spavins.” Neither of these forms of enlarged vein routinely cause the type of skin changes or ulcerations that occur in humans with long-standing varicose veins. Horses also can manifest vulvar and vaginal varicosities, which can cause prolonged spontaneous bleeding. 3
In addition to animals that show similar disease patterns to humans, zoobiquity looks for animals that one would expect to have certain conditions but do not. Giraffes are evolutionarily and zoobiquitously interesting animals for several reasons. The giraffe’s extraordinarily long neck and height has required numerous adaptations as well as manifesting interesting vestigial anatomy that is peculiarly inefficient. The giraffe is often cited as an example of an animal exhibiting the tendency for a successful or selectively neutral design to remain in the gene pool despite its apparent inefficiency. In particular, the recurrent laryngeal nerve becomes tremendously inefficient in the giraffe; it originates as a branch of the vagus nerve and courses around thoracic arterial structures and then returns to the laryngeal area. This is a short and direct course in, say a fish where the analogous nerve takes a direct path to the gills. In the giraffe it takes the same embryological-anatomical route, requiring a descent from the head, down the long neck and into the thoracic cavity where it does not connect, but rather wraps around arteries and then winds its way back up the to the larynx. This is the case with other vertebrates as well, but the length of the giraffe neck provides an extreme example of how evolution has kept this nerve in a working but extravagantly inefficient anatomical course.
Similarly the length of the neck requires the arterial supply to the head to have several adaptations, including thick arterial walls to allow the blood pressure requirements for perfusion of the brain. The average arterial pressure for the giraffe is 185±41.6 mmHg (systolic 211.1±37.6 mmHg; diastolic 151.4±32.6 mmHg).5 Certainly one would expect that giraffes, of all animals, would frequently develop venous insufficiency and varicose veins. However, this is not the case. The immunity of giraffes to varicose veins fascinated the inventor Frank Shaw, whose beloved wife Hertha suffered from intractable lymphedema. His discovery was that giraffes, despite having venous pressures of 250mmHg at their ankles, are immune from varicose veins because their skin is inelastic and their veins, being compressed by the tight and inelastic skin, cannot become distended. He used this observation to fashion the “Circ-Aid” device, which is a series of inelastic straps that wrap around the leg and provide relief from venous insufficiency and varicose veins while active and upright.6
Animal models for human disease can be essential for scientific hypothesis testing, although animal models of venous insufficiency have been very challenging to create. Most mammals being quadrupeds, attempts at creating increased venous pressure usually require the creation of an arterial-venous fistula. A canine model using greyhounds walking on their hind limbs allowed for measurement of increased venous pressures with upright posture, but no varicose veins or stasis changes were seen.7 A porcine model for venous hypertension that produces varicose veins has been created using a saphenous arterial-venous fistula. This approach has demonstrated the development of varicose veins of the hind limbs, with valve failure and macro and microscopic changes that are consistent with those found in humans. Due to the relative thickness of the pigs’ skin and the youth of the subjects at date, however, no stasis skin changes have been seen.8
Conclusion and Preview
Humans are fairly unique in the presentation of the cluster of signs and symptoms known as venous insufficiency, varicose veins and venous stasis skin changes. In next quarter’s newsletter, we will look at the evolutionary causes of the human predisposition to varicose veins.
Update on New Practice Guidelines
by Arun Chowla, MD, FACS
LM, a 78 year old female was seen in the emergency room with leg pain and localized swelling in the calf. Patient had no significant past medical history except for varicose veins. No history of prior leg clots or family history of clotting disorders. Physical exam showed a tender, reddened, indurated area over the lower thigh and medial calf. Patient was sent home with NSAIDS and supportive measures. Ultrasound of the left leg showed superficial thrombophlebitis involving the superficial calf veins and the great saphenous vein.
Patient presented for further evaluation and her pain and redness had improved with mild residual induration. Ultrasound in the office showed extension of great saphenous venous thrombus into the common femoral vein.
Treatment with Lovenox was started and continued on coumadin for 3 months. Follow up ultrasound in 3 months showed reflux in the great saphenous vein and resolution of the deep venous thrombosis. Patient underwent Radiofrequency Closure of the great saphenous vein as an outpatient procedure without complications. Coumadin was stopped after the follow up.
Superficial Thrombophlebitis: Clinical Guidelines
Superficial Thrombophlebitis (SVT) refers to a clot in a superficial vein associated with surrounding inflammation. The usual clinical presentation is pain. tenderness, induration or erythema along a superficial vein. It is usually treated with NSAIDS (Ibuprofen, etc), compression stockings and warm compresses.
SVT is associated with varicose veins, malignancy, pregnancy, estrogen therapy, travel and history of prior leg clots.
Although SVT is less studied than deep venous thrombosis (DVT), it is seen more commonly in the general population. Incidence of SVT is about 3-11%, compared to DVT which is about 1%. It may involve the great saphenous vein in 2/3 of the patients.
It is generally considered a benign, self limited disorder; but it may be complicated by extension of thrombus in the deep venous system. A recent prospective study of 844 patients with SVT > 5cm, 4% had symptomatic PE and ultrasound found proximal DVT in 10% and distal DVT in an exam was recommended in these patients with SVT above the knee.
The aim of treatment is not only to relieve
local symptoms but also to prevent thromboembolic complications.
But the role of anticoagulation is controversial. Most studies have been small and have shown benefit over placebo, but the evidence was of low quality. The CALISTO Study (Comparison of Arixtra in Lower Limb Superficial Thrombophlebitis with Placebo) was recently published which showed benefit of Fondaparinux(Arixtra 2.5mg/d for 45 days) over placebo in 3,000 patients with lower limb SVT > 5cm, with lowered incidence of venous thromboembolism, recurrent SVT, and extension of SVT.
Based on these studies, the American College of Chest Physicians have also issued new guidelines in February 2012 and have recommended anticoagulation for patients with SVT who are at increased risk for venous thromboembolism (SVT>5cm, proximity to deep veins <5cm, positive medical risk factors). Positive medical risk factors include prior clots, cancer, surgery, thrombophilia, estrogen therapy or prolonged travel. Fondaparinux 2.5mg daily or enoxaparin 40 mg daily for a period of 4 weeks is recommended. If DVT is present, patient should be fully anticoagulated.
Ligation of great or small saphenous vein may be considered in patients in whom anticoagulation is contraindicated. Otherwise surgery for SVT was found to be associated with a higher risk for thromboembolism. Patient with isolated SVT and no associated risk factors may be diagnosed by physical exam and treated with NSAIDS, compression stockings and ambulation. Repeat physical exam should be done in 7-10 days to evaluate for extension or resolution.
Duplex Ultrasound should be done in patients with SVT >5cm, involvement of GSV or SSV, presence of phlebitis above the knee, or extension of phlebitis on serial exam. In summary, new data from recent studies and guidelines from ACCP have clarified the role of anticoagulation in SVT. SVT should not be regarded as a benign disorder and further evaluation and anticoagulation should be considered in patients high risk for thromboembolism. SVT may also be a marker for thrombophilia or other conditions like malignancy and therefore recurrent SVT should prompt further detailed assessment and evaluation.
When you think of the Olympics you probably think of elite athletes, exciting competitions and emotional medal ceremonies. Varicose veins probably don’t factor in. Or do they?
Well believe it or not, even the world’s best athletes can and do get varicose veins. Just ask Summer Sanders, a gold-medal winning Olympic swimmer turned sports commentator and reporter, TV show host and actress. This year Summer is sharing her story as the spokesperson of a campaign called “Rethink Varicose Veins,” which aims to educate the public about this common condition and help to dispel some myths.
“Like many moms, my lifestyle requires me to be on my feet constantly. I noticed my legs were heavy and achy after a long day, but I assumed these symptoms were just something I had to deal with,” says Summer. “My doctor and I decided the best path for me was a minimally-invasive treatment. The procedure was quick and I was back to my regular activities within a short period of time. Now my legs feel great!”
Summer’s experience helps shed light on the real story of varicose veins – that people from all walks of life and of all shapes and sizes get varicose veins. In fact, the single biggest determining factor is heredity. Other major risk factors include standing or sitting for long periods of time, being pregnant, being overweight, getting older or having a history of DVTs.
“My own mother suffered from varicose veins most of her life,” says Summer. “She was often on her feet due to her work as a flight attendant and would find herself in pain during long trips. She began to notice her varicose veins when she was pregnant with me and always joked that varicose veins are hereditary; according to my mom, you get them from your kids! It soon hit me that, even though I was active, I was starting to get my mother’s legs.
“Now my legs feel awesome again. Varicose veins are not just a cosmetic issue; you don’t have to live with them anymore.”
Learn more about Summer’s story by visiting the campaign website at www.rethinkvaricoseveins.com And enjoy the Olympics!
by Robert C. Kiser, DO, MSPH
Human skin is messy. Epidermis, from microscopic cells to macroscopic flakes are constantly being shed and replenished from lower layers. Furthermore, if epidermis is injured by trauma it must replenish itself to provide the protective, semi-permeable barrier against the environment that it maintains. This process requires a dynamic balance between building up of skin and shedding or breaking down skin. If the building up of skin is too exuberant, conditions such as psoriasis and Ichthyosis occur in which the skin becomes thick and scaly. When skin does not replenish and heal fast enough, or when conditions favor break- down of skin more than growth of new skin, ulcers develop.
Types of Ulcers: Mechanical Pressure
Ulcers may be caused by many different factors, or several factors acting in concert. Pressure ulcers, decubitus ulcers, or “bed sores” occur when constant pressure and/or sheer forces are exerted on tissue, usually overlying a bony prominence, over a prolonged period of time. Curiously, although decubitus ulcers have been known of for thousands of years, the exact pathophysiology has not been elucidated. It is believed that the mechanical forces change interstitial pressures and pressure gradients, reduce capillary exchange, and create an environment in which tissue necrosis is favored over tissue healing.
Skin cancer can manifest as erosive non- healing ulcers
Numerous systemic diseases are associated with cutaneous ulcers, including diabetes, renal disease, lupus and inflammatory bowel diseases.
Ulcers of Venous Insufficiency or Venous Stasis Ulcers
Venous stasis ulcers will be the topic of the rest of this article. Ulcers are the end- stage of venous insufficiency. The region most commonly affected is the “gaiter region” – the area just above the ankle, most commonly the medial, but sometimes the lateral malleolus. Venous insufficiency occurs when the valves within the veins no longer function properly. Valves within veins assist venous blood to go up the leg against gravity. When these valves no longer function properly, blood flows back down the lower extremity and creates a gravity-dependent, gradient pressure within the venous system. This leads to elevated pressures within the veins, all the way back to the capillary networks where oxygen from arterial blood is exchanged with tissues, and deoxygenated venous blood full of metabolic byproducts of cellular respiration is collected. These “dammed-back” capillaries undergo changes such as fibrin cuffing, which further diminish nutrient exchange. The befouled environment leads to changes in the surrounding tissues including the deposition of collagen in the skin and adipose tissue.
The point prevalence of venous stasis ulceration western nations is estimated to be from 0.02 to 1 percent.1 Risk factors include age, obesity, history of leg injury and history of venous thromboembolism (VTE). Venous stasis ulcers were responsible for 2 million work days lost in 2002.
Symptoms and Presentation
Venous stasis ulcers present with areas of poorly healing skin wounds, generally of the medial malleolus, red-based or exudative, with local skin necrosis and irregular borders. Frequently the surrounding tissue has other signs of venous insufficiency, such as hyperpigmentation, pitting or woody edema, excess collagen deposition and fibrosis. The patient will frequently complain of factors that limit quality of life, including pain, odor, exudation, spontaneous bleeding and alteration of lifestyle (such as no longer being able to swim or wear shorts). Without proper treatment, venous stasis ulcers can take many months to heal. Patients may suffer with their ulcers for months or even many years without bringing the condition to the attention of their physician. Often there is some provoking trauma such as a scrape or bump, and barring such trauma patients will often complain that that they have been bitten by a “spider.” Frequently the patient self-diagnoses the ulcer as a “brown-recluse bite,” even in areas that brown recluse spiders are extremely uncommon. Like proteolytic spider bites, ulcers take a long time to heal and heal with scarring. Unlike such bites, ulcers tend to recur after healing if appropriate measures are not taken to treat the underlying venous insufficiency causing the ulcer.
The mainstay of treatment for venous stasis ulcers is compression. Compression can be provided by dressings, single or multilayered bandaging, graduated compression stockings, or Velcro-strap devices. Compression may be elastic or inelastic. The most common form of single-layer bandage is the zinc-paste bandage created by Paul Gerson Unna (1850-1929). Unna’s boots have numerous formulations, but the principle components are a cotton bandage impregnated with zinc paste, glycerin and sometimes calamine. Gelatin and other chemicals sometimes are used to emulsify and spread the zinc paste. The application of the boot requires hands- on training to perform effectively. Principles include starting at the metatarsal bases and wrapping to the tibial tubercle and applying with sufficient firmness in an even, contour-forming pressure to avoid gauging the skin. The boot is left in place for 7-10 days and then changed – although earlier changes can be necessary for very exudative wounds or if there is sufficient edema that the bandage becomes loose. Unna’s boot has many advantages, including being an inelastic compression that provides compression during ambulation, but is non-compressive when the patient is recumbent and not ambulating.
Multilayer bandages may include layers of sponge-foam, cotton- wool, crepe, elastic-stretch bandages, and Coban-type self-adherent bandages. The advantages of the multilayer bandages include the ability to absorb moisture and exudate, the increased circumference the wadding or foam layer provides allows for decreased point pressure while maintaining adequate circumferential pressure to the limb, the ability to apply granulation favoring or antimicrobial dressings directly to the wound. The disadvantages of the multi- layer dressings include cost and the bulk of the dressing.
Another aspect of wound care that is important is debridement. Debridement of necrotic debris should be provided to encourage growth of granulation tissue. Debridement can be mechanical (sharp or blunt) or chemical. Several products are available for chemical debridement, including balsam of Peru-castor oil mixes (such as Granulex) and collagenase (Santyl). One of the most effective and safe chemical debridement creams, in the author’s opinion and experience, was papain-urea cream (Accuzyme). Unfortunately, the Food and Drug Administration took Accuzyme off the market several years ago.3
Antibiotics are seldom useful in the treatment of venous stasis ulcers unless signs of infection are present. These signs include increase in pain beyond the baseline, increasing erythema of the skin surrounding the ulcer, and lymphangitis, a rapid increase in the size of the ulcer.4 Antibiotics are frequently overprescribed for venous stasis ulcers on the basis of necrosis and exudate. Unfortunately, the necrosis of ulcerating skin is generally not due to bacteria, but due to autolysis of the skin cells, and therefore antimicrobials do not improve the situation, and may increase the potential for super- infection with resistant organisms.5
The underlying cause of venous stasis ulceration is venous stasis. Using modern techniques such as radiofrequency ablation, endovenous laser ablation, and ultrasound-guided sclerotherapy the root cause of the imbalance in healing and breaking down skin tissue can be corrected, and balance restored. By addressing and correcting the increased pressure in the superficial system, but ablating refluxing axial veins or perforating veins, the phlebologist not only can help to heal the venous stasis ulcer, but can prevent chronic recurrence. Older techniques such as vein stripping and ligation and the Linton procedure for perforator closure were sometimes avoided while the ulcer was open, as these techniques utilized incisions through or near already compromised skin. With more modern, minimally invasive techniques, the points of high superficial venous pressure can be addressed with 2mm or smaller incisions, and the balance of healing versus lysis of skin restored. By addressing the underlying cause of the ulcer, the phlebologist, working with the primary physician and/or wound healing center, can help to provide long-term wound healing for the venous stasis ulcer.
by Nicos Labropoulos, PhD, DIC, RVT, Professor of Surgery and Radiology, Stony Brook Universtiy Medical Center. and Antonios P. Gasparis, MD, Associate Professor of Surgery, Director, Stony Brook Vein Center
Chronic venous disease (CVD) is the most prevalent form of vascular disease, affecting about a third of adult Americans. Most patients present with varicose veins but swelling and skin damage are common as well. The signs and symptoms of CVD are result of venous hypertension that develops from reflux, obstruction or a combination of both. In patients with CVD, around 70-80% will have superficial reflux with or without perforator vein incompetence and 10% isolated deep reflux. Combined superficial and deep vein disease has been reported to occur in about 10-20%. Congenital CVD and chronic venous obstruction are rare (Figure 1). While treatment of the isolated superficial venous system in patients with CVD is expected and has been shown to have good outcomes, the role, efficacy and complications of superficial intervention in patients with combined disease has been controversial. In patients with mixed pathology, deep venous obstruction occurs in a small number of limbs, which is either primary or secondary. The majority though, will have underlying reflux which will be segmental and is likely to occur due to volume overload from the recirculating reflux blood in the superficial veins. However, axial vein reflux, which is most often a result of previous thrombosis, also is seen, as about two thirds of patients with proximal vein thrombosis will develop reflux at one year. Patients with a previous episode of thrombosis may have vein segments without or with partial recanalization leading to obstruction or to a combination of reflux and obstruction.
Segmental deep-vein reflux due to superficial vein incompetence is most often seen at the saphenofemoral (SFJ) and saphenopopliteal junctions (SPJ). It also can be due to reflux in the gastrocnemius veins (almost always the medial) and perforator veins (Figure 2). The reflux in the perforator veins is not isolated but it occurs only in the presence of reflux in superficial veins that are connected with the affected perforators. Longstanding reflux in the superficial and perforator veins may lead to reflux development in the deep veins that are connected with the affected perforators. This is the same phenomenon as in the case of SFJ, SPJ and gastrocnemial veins. Deep vein reflux which is induced by the superficial vein incompetence is easily eliminated in >95% of patients after treating the superficial veins. This has been demonstrated in different studies and it does concur with our experience as well. It has to be noted that many patients may have deep vein reflux due to previous thrombosis. In such occasions the deep vein reflux may improve in some cases after elimination of the superficial reflux, but it does not disappear. The latter is more prevalent in the presence of axial reflux, such as when there is reflux in continuity from the common femoral vein to popliteal or more distal (Figure 3).
Traditional advice has been against saphenous ablation in the presence of deep venous obstruction. This was felt because of the thought that secondary saphenous varices result from deep venous obstruction and function as collaterals. Therefore, it was feared that obstructive disease may be made functionally more severe by removing the saphenous vein that may be functioning as important collateral. When testing venous outflow function in patients with previous deep vein thrombosis, Labropoulos et al. demonstrated that only 9.6% of limbs had their venous outflow reduced by occlusion of the superficial veins. The deep collaterals seem to be more important than the superficial venous system in bypassing the obstruction. Raju et al.,when comparing patients with and without deep obstruction who underwent saphenectomy, found similar outcomes in the two groups with no clinical deterioration in those with obstruction. In addition, the risk of DVT following saphenous ablation does not seem to be increased in patients with previous thrombotic events as shown by Puggioni et al. Therefore, the saphenous vein plays an insignificant role as a collateral pathway in patients with deep venous obstruction and can be safely treated to correct underlying hemodynamic pathology.
In patients with advanced CVD (C4-6) and superficial reflux, interrogation of the deep venous system for proximal obstruction, even in the absence of previous DVT, is warranted. Marston et al. found that as many as 30% of patients with chronic venous insufficiency have iliac vein obstruction on CT scan. When obstruction is in the iliac veins, consideration for its significance and intervention should be considered. The presence of such combined disease (superficial reflux and iliac vein obstruction) may warrant treatment of both levels of disease, as it is impossible to identify the pivotal diseased segment that contributes to the clinical presentation. In fact, we are presently unable to quantify segmental reflux or obstruction or describe how they interact. It is, therefore, reasonable to treat the superficial reflux and the proximal obstruction with iliac vein stenting. This can be done in a staged or combined fashion. Neglen et al. reported combined saphenous ablation and iliac vein stenting in 99 limbs with significantly improved hemodynamic parameters, improved clinical symptoms (pain and swelling) and significant improvement in all quality-of-life categories after treatment. This was achieved with good 4-year patency (>90%) and low complication rate.
Patients with mixed superficial and deep pathology and significant clinical symptoms (especially C4-6) should be offered not only treatment of their superficial system but also evaluation and therapy of any underlying iliac vein obstruction with excellent clinical outcomes. When evaluating the superficial veins in patients with deep vein obstruction it is necessary to demonstrate significant reflux in the superficial veins prior to intervening. This is very important as superficial veins can be dilated in order to compensate for the deep vein obstruction. In such patients the diameter change should not be compared with the studies on patients with primary superficial vein reflux. Therefore, superficial veins with large diameter should not be removed unless there is significant reflux that may contribute to the patients’ signs and symptoms. Patients with deep vein obstruction are evaluated in the supine position. However, when these patients are tested for reflux, this must be done in the standing position. This is paramount as reflux should be evaluated in the standing position in all patients. We overemphasized this for the patients with venous obstruction as many centers still examine reflux in the supine position in such patients.
By Robert Kiser, DO, MSPH
Vulvar varicosities are a source of embarrassment and pain for many women but they are often reluctant to discuss their condition or symptoms with their doctors. These varicosities can easily be missed in casual examination, as they are less obvious in the supine position and may not be seen until the patient stands or assumes an upright sitting or squatting position.
When evaluating lower extremity varicose veins, varicosities in the proximal inner thigh should prompt the physician to consider a pudendal origin. The question, ―Do you have any varicose veins of the vulva or labia? should be asked as well as questions about pelvic congestion symptoms. There are a variety of treatments that can help to improve or eliminate these symptoms.
Background and Epidemiology
Vulvar varicosities occur in an estimated 4% of women1 and 15.8-23% of those with lower extremity varicose veins. Most occur during pregnancy and resolve within a few months. When they do not resolve they may cause symptoms of pain, itching, burning, dysparunia, and are perceived by some women as a cosmetic nuisance.
Vulvar varicosities may occur as isolated tributary varicosities or may be a sign of underlying pelvic venous insufficiency. They can also be associated with Pelvic Congestion Syndrome (PCS). PCS results from venous insufficiency (reflux) of the ovarian veins. This important but under-diagnosed condition is associated with symptoms of dysparunia, chronic pelvic pain, feeling of pelvic fullness and discomfort
When signs or symptoms of PCS are reported, a diagnostic transvaginal ultrasound both supine and standing, with and without Valsalva may be ordered to quantify pelvic vein reflux. Magnetic resonance venography is also extremely sensitive to finding dilated gonadal veins and provides an abundance of anatomic information5. Consultation with an interventional radiologist or vascular surgeon for venography and possible coil embolization or fluoroscopy-guided sclerotherapy is warranted when found.
Any patient with symptomatic vulvar varicosities (pregnant or not) should be encouraged to try compression therapy. The company, Prenatal Cradle, makes the V-2 Supporter for the pregnant or non-pregnant woman with vulvar varicosities. This device is similar in appearance to a male athletic supporter, but is contoured to provide compressive support for the vulva, thus preventing the pooling of blood in the labial veins.
Non-surgical and Minimally Invasive Techniques
For vulvar varicosities in the non-pregnant patient, remarkable improvement can be achieved with sclerotherapy. The visible varicosities are injected with a quantity of liquid or foam sclerosant, and the area is then compressed with a pad and the V-2 supporter or similar compression garment7. A few treatments can provide lasting relief and cosmetic improvement in vulvar varicosities. To minimize the risk of complications, the injecting physician should have extensive experience with vein sclerosis and a strong working anatomy of the pelvic venous system.
Persistent Pelvic Congestion Syndrome
For some patients, treatment of vulvar varicosities with a V-2 compression trial followed by compression sclerotherapy affords symptomatic improvement8. Patients with PCS who are not responding to compression should be evaluated by an interventional radiologist or vascular surgeon for possible coil embolization. Under fluoroscopy guidance, the refluxing ovarian veins can be embolized by endovenous insertion of a metallic coil.
After the pelvic venous insufficiency has been treated, if not previously addressed, the vulvar varicosities may be re-evaluated by a phlebologist who practices sclerotherapy to determine whether the varicosities and their associated symptoms have adequately resolved. If not, sclerotherapy of the visible varicosities may be provided if the patient wishes.
Help is available for your patients suffering with Pelvic Venous Syndromes. For more information, call 1-800-FIX-LEGS.
The term Chronic Venous Insufficiency (CVI) describes a condition that affects the venous system of the lower extremities with venous hypertension causing various pathologies including pain, swelling, edema, skin changes, and ulcerations.
Although the term CVI is often used to exclude uncomplicated varicose veins, varicose veins have incompetent valves with increased venous pressure leading to progressive dilation and twisting. We use the term CVI to represent the full spectrum of manifestations of chronic venous disease.
The Venous Ultrasound Exam
At the Center for Vein Restoration, the diagnosis of Chronic Venous Insufficiency is made via patient history and a physical examination with the assistance of noninvasive testing. A portion of the physical exam entails inspection and palpation of the surface of the skin to detect irregularities or bulges. The calf muscle is consistently assessed and measured for indications of fullness or increased girth due to long-standing edema.
Palpation may also reveal tenderness of the dilated veins. Active or healed ulcers are seen with more advanced disease.
There is a broad differential for the common presenting complaint with CVI. As a result, noninvasive ultrasound imaging plays an important role in diagnosing and guiding CVI treatment. Ultrasound imaging, also called ultrasound scanning or sonography, involves exposing part of a patient’s body to high-frequency sound waves to produce pictures of the inside of the body. Unlike x-rays, ultrasound exams do not use ionizing radiation.
Ultrasound imaging helps us to diagnose and treat medical conditions because they can show the structure and movement of the body’s internal organs, as well as blood flowing through blood vessels. A venous ultrasound provides us with pictures of the veins throughout the body that carry blood back to the heart.
This painless noninvasive exam measures the function of the vein valves that are critical to venous function, and can also identify vein blockages. In fact, compared to venography, which requires injecting contrast material into a vein, venous ultrasound is nearly as accurate for detecting blood clots in the calf and almost fully as accurate in finding clots in veins of the thigh.
A Doppler ultrasound may also be part of a venous ultrasound examination. This special ultrasound technique evaluates blood as it flows through a blood vessel, including the major arteries and veins, and the images can help us to see and evaluate blockages to blood flow, such as clots, or the narrowing of blood vessels.
While many patients present with large, clinically obvious bulging varicose veins, other individuals may have significant “silent” reflux (abnormal direction of blood flow) in diseased veins, which can only be detected by Doppler vein mapping a more detailed ultrasound evaluation of the abnormal veins of the legs which illustrates the path of the blood flowing through the abnormal veins and where the trouble begins.
Careful mapping of the lower extremity venous system aids us in determining the optimal treatment plan to meet each patient’s specific needs.