Endovenous treatments for varicose veins

Keywords:treatment, medical, fiber,  Time:11-11-2015

Introduction

Endovenous treatment is currently one of the most frequently used methods for treating varicose veins in the Netherlands. Varicose veins are tortuous and enlarged veins due to weakening in the vein’s wall or valves. They are manifestations of chronic venous disease (CVD), which may lead to serious complications.
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Pathophysiology

CVD can be divided into primary chronic venous disorders, and secondary, mostly due to postthrombotic syndrome and congenital malformations. They all share similar clinical symptoms, but their etiology differs. Varicose veins are more distensible than control veins, suggesting a primary systemic basis for the anomaly.14 The pre-varicose vein wall is less resistant to the pressure that is generated in the upright position. The pressure in the dorsal foot vein is approximately 80-100 mm Hg in the upright position, in supine position only 5-10 mm Hg and normal ambulatory venous pressure should ideally be < 25 mm Hg.

The valves that are present in the veins are unable to perform optimally in the upright position. The insufficiency of valve functioning in the saphenofemoral or saphenopopliteal junction causes descending varicose veins. Insufficient tributaries and perforating veins, on the other hand, can cause saphenous insufficiency without incompetence of the junction. Pittaluga studied the effect of phlebectomies on saphenous vein hemodynamics. After phlebectomy, saphenous reflux duration was significantly decreased, and phlebectomy led to a significant reduction in saphenous vein diameter.15-16 These studies support the hypothesis of an ascending development of varicose veins.
In contrast to primary varicose veins, secondary varicose veins are caused by venous hypertension, which is in most cases the result of damage to the valves and recanalization (reflux type) or residual obstruction (obstructive type) after deep vein thrombosis. Deep vein reflux is mainly due to previous thrombosis that leads to destruction of valves but can also be idiopathic, due to primary deep valvular insufficiency. In the latter case reflux is the result of floppy valve cups, valvular agenesis or aplasia.17-19 Dysfunction of the venous macrocirculation that is not fully compensated by the calf muscle pump action leads to changes in the venous microcirculation.

In patients with CVI due to primary or secondary varicose veins there is always high capillary pressure in the skin microcirculation .20 The resulting skin changes, from hyperpigmentation to leg ulcer, are all caused by the disturbances of the microcirculation. These changes are caused by at least two important phenomena:

Clinical characteristics

Classic symptoms associated with CVD are discomfort, heaviness, aching, muscle cramps and itching. Clinical characteristics of CVD are varicose veins, edema, hyperpigmentation, eczema, induration, lipodermatosclerosis, white atrophy, nail changes, pachyderma, subcutaneous calcification and venous ulcers. (Figure 1). Clinical characteristics of CVD appear when the compensating mechanism of insufficient venous return fails. The progression of

Figure 1. Clinical characteristics of chronic venous insufficiency. A. Telangiectases. B. Varicose veins. C. Varicose veins and hyperpigmentation. Note that the varicose vein reduces the hyperpigmentation of the skin by its own pressure. D. Lipodermatosclerosis. E. Leg ulcer. F. Leg ulcer CVD is characterized by signs and symptoms that increase almost linearly in time. Classically, progression of CVD is divided into three stages: from the adaptation stage to a compensation stage to a decompensation stage, finally leading to symptoms and signs, and later to complications. Venous ulcers are considered to be the end stage complication of CVD and have a lifetime prevalence of 1-2%

Chronic venous disease may have substantial impact on patient’s Health Related Quality of Life (HRQOL), which is comparable to other chronic diseases and is associated with considerable health care costs.2 Several studies confirmed that treatment of venous disease improved HRQOL.24-25 Generic HRQOL instruments can be used in patients with CVD, but disease-specific tests provide more information about the impact of CVD and varicose veins on patients’ everyday lives. The two most commonly used disease specific HRQOL tools for varicose veins and more advanced stages of CVD are respectively the Aberdeen Varicose Vein Questionnaire (AVVQ)26 and the Chronic Venous Insufficiency Quality of Life Questionnaire (CIVIQ).

Diagnosis

The gold standard of diagnosing varicose veins is ultrasound examination.29 Clinical and ultrasound examination are ideally performed in upright position for optimal visualization of anatomy and hemodynamics. Diameter of the veins as well as reflux time can be measured accurately. In two recently published consensus documents of the UIP (Union Internationale de Phlébologie) a detailed methodology for complete duplex ultrasound assessment of the anatomy of the veins of the lower limbs in CVD has been described.29-30 Using standardized investigation methods should improve the quality of duplex investigation. In some exceptional cases (e.g., venous malformations, unusual presentation of recurrent varicose veins) the anatomy can be very challenging to visualize and additional phlebography or CT-venography can be valuable. Ambulatory venous pressure measurements or plethysmography can be added as diagnostic and prognostic tools.31-33 These two investigating methods can be used for assessing and understanding complex hemodynamic problems, causing venous hypertension or when clinical signs are not corresponding with duplex ultrasound findings.

Treatment


There are three main reasons to treat varicose veins. First of all, treatment should prevent occurrence of complications, such as bleeding, edema, eczema, lipodermatosclerosis, and leg ulcers. Especially the treatment of leg ulcers is intensive and very expensive, and leg ulcers.have a major impact on patients’ HRQOL. Therefore, treatment of superficial varicose veins is recommended by many experts in the field to prevent complications. Secondly, treatment also relieves complaints caused by varicose veins, such as heaviness, tired legs, and cramps. Thirdly, cosmetics play an important role and many patients find their way to a phlebologic clinic only because their varicose veins are cosmetically disturbing, and this may affect patients’ HRQOL.The treatment of varicose veins can roughly be divided into four groups: compression therapy, surgical treatment, sclerotherapy and endovenous thermal ablation.

Compression

Compression therapy plays a role since ancient time and can be used as a unique conservative treatment, or additional to other types of treatment.35-36 Compression therapy still plays an important role in modern phlebology.

Surgical treatment

The second type of treatment is surgery and mainly consists of ambulatory phlebectomies, high ligation and stripping. The ancient Greek already recognized the implications of varicose veins and were able to treat them with ambulatory phlebectomies. The first illustration of a varicose vein, discovered at the foot of the Acropolis (Athens) dates from the fourth century BC. It is a tablet that shows a massive leg with a tortuous dilated vein on its medial side, which has all the characteristics of a varicose vein (Figure 2).
In more recent times, the surgical treatment of saphenous varicose veins is one of the very few treatments that barely changed since its invention more than a hundred years ago. In 1884 the German surgeon Madelung invented a radical operation to extirpate the great saphenous vein (GSV) and its perforators through one long skin incision from groin to ankle. In 1905 the American surgeon William Keller introduced the stripping technique using a wire and multiple small incisions.37 Since then, the long skin incision has been abandoned.

William Babcock, also an American surgeon, invented the tools that formed the basis for the current vein stripper.38 The last major revision was the introduction of the high ligation at the saphenofemoral junction (SFJ) that was added to the standard procedure in 1916 by John Homans.39 Similar to this, the small saphenous vein (SSV) was ligated at the saphenopopliteal junction (SPJ). Several variations of the initial method have been made, such as the use of different types of strippers, invaginated stripping and cryostripping, without changing the basic principles of treatment. For decades, the treatment of saphenous varicose veins consisted of ligation at the SFJ or SPJ and short stripping (from the groin to the knee for the GSV and from the popliteal fossa to mid-calf for the SSV). For treating SSV incompetence many surgeons, in particular in the Netherlands, often limited the operation to ligation of the SPJ without stripping the SSV, because of the risk for injuring the sural nerve during the stripping manoeuvre.40 However, results of the latter technique are inferior to that of ligation and stripping the SSV to mid-calf. A recently published study showed that additional stripping of the SSV significantly reduced the rate of recurrent SPJ incompetence after one year, without increasing the rate of complications compared to SPJ ligation alone.41
An important disadvantage of surgery for varicose veins is the well known high recurrence rate (up to 30-60% at long-term).42-43 The main causes for recurrence of varicose veins after surgery are insufficient understanding of venous hemodynamics, inadequate preoperative assessment, incorrect or incomplete surgery, progression of underlying venous disease and neovascularization at and around the ligated junction.44 Improving the quality of preoperative assessment routinely performing duplex ultrasound seems to be very important to reduce recurrence. According to a randomized controlled trial, systematical use of duplex ultrasound significantly lowered the incidence of duplex detected recurrence at the SFJ or SPJ and reduced the number of reinterventions within 2 years after surgery.45
The last years new attention has been drawn to the surgical treatment of tributaries. Ambulatory conservative haemodynamic management of varicose veins (CHIVA), mainly performed in Italy and France, proved to give better results than stripping when considering recurrence rate.46-47 The basic concept is that treatment of varicose veins should recover the venous hemodynamic situation. The newest idea, which is more or less related to the principles of CHIVA, is that tributaries have great impact on the problem of varicose veins. Looking at the outcome of treating only varicose tributaries helps to differentiate between ascending and descending varicose veins. The idea is that treating superficial varicose veins can be divided into two different strategies based on two pathofysiologic concepts. First, treating insufficient tributaries of the insufficient saphenous vein may lead to abolition of the saphenous reflux, so the saphenous vein need not be treated any further (this underlines the concept of ascending varicose veins). Treatment of the saphenous vein alone or in combination with tributaries is based on the descending theory. The effect on the reflux of the saphenous vein by treating insufficient tributaries will be further investigated by our study group. Promising results after performing phlebectomies without treating GSV trunk incompetence have already been reported by Pittaluga.

Sclerotherapy

The third main treatment type is sclerotherapy. Sclerotherapy was known in medicine even before stripping; i.e. since the 19th century. Chassaignac was the first to inject varicose veins with ferrochloride (1855). Since 1911 teleangiectasias and reticular veins have been injected with sodium carbonate and sodium salicylate. Later also quinine, sodium chloride and urethane were used as sclerosants. Fegan added compression to sclerotherapy in 1965 and since then sclerotherapy has always been combined with compression therapy to obtain better results.48-49 Nowadays liquid and foam sclerotherapy are commonly used with detergent sclerosant solutions such as polidocanol and sodium tetradecyl sulfate. Ultrasound guided foam sclerotherapy (UGFS) will be discussed in detail in chapters 2 and 3. Briefly, in UGFS liquid detergent sclerosant solution is mixed with air or a physiological gas to create foam. The sclerosant reacts with the endothelial cells of the vascular wall and in this way induces contraction, thrombus (‘sclerus’) formation and eventually fibrosis of the vein.50-51 Foam is four times more effective than liquid sclerotherapy because of increased contact time with the venous wall, increased surface area of the venous wall, and venous spasm.