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Chronic venous insufficiency. An update
(Portuguese PDF version)

Luís Henrique Gil França¹, Viviane Tavares²

1. Vascular surgeon, Santa Casa de Misericórdia de Curitiba. Post-graduate in Surgical Clinic, Universidade Federal do Paraná.
2. Physical therapist. Specialist in Trauma Orthopedics and Pilate Methods.

Correspondence:
Dr. Luís Henrique Gil França
Rua Coronel Dulcídio, 1189/1801
CEP 80250-100 - Curitiba - PR
Brazil
Phone: +55 (41) 343.0963
E-mail: luishgf@hotmail.com

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ABSTRACT

Chronic venous insufficiency is an extremely relevant disease, attacking people of different ages, and it is associated with socio-economical problems like absence from work and even the early retirement of young people still in a productive phase of life. This disease has an elevated incidence and prevalence, including its association with varicose veins, ulcers and trophic lesions. The diagnosis is clinical, and when necessary, additional tests are used such as photoplethysmography, duplex-scan and phlebogram. Treatment involves bandages or elastic stockings, specific dressings and surgical procedures. The purpose of this article is to create a current review of the evaluation and management of chronic venous insufficiency.

Key words: venous disease, chronic venous insufficiency, venous ulcer.
Palavras-chave: insuficiência venosa, úlcera venosa, diagnóstico.

J Vasc Br 2003;2(4):318-28

Chronic venous insufficiency is a common disease in clinical practice, and its complications, principally venous stasis ulcer, cause significant morbidity. The ulceration affects work productivity, causing retirement due to disability in addition to restricting daily life and leisure activities. For many patients, venous disease causes pain, loss of functional mobility and a decreased quality of life.

In Brazil, the social importance of chronic vein insufficiency (CVI) has come to the attention of the government only during recent years, creating an increased interest in gaining scientific knowledge of the questions related to this disease.¹

DEFINITION

Chronic venous insufficiency is defined as the functional abnormality of the venous system caused by valvular incompetence that may or may not be associated with the obstruction of the venous flow. It can affect the surface venous system, the deep venous system, or both. In addition, venous dysfunction can be the result of a congenital disorder or may be acquired.²

EPIDEMIOLOGY

The prevalence of CVI in the population increases with age. In Europe, 5 to 15% of adults between the ages of 30 and 70 present this disease, being that 1% present a varicose ulcer. In the United States, approximately 7 million people suffer from CVI, which causes 70 to 90% of all lower limb ulcers.^3,4 In an epidemiological study on lower limb venous alterations among the population of Botucatu, São Paulo, Maffei et al.,⁵ estimated a 35.5% prevalence of varicose veins and serious cases of CVI with an open or healed ulcer in 1.5% of these cases.

Silva, ⁶ who studied the socio-economic repercussions of CVI, analyzed the 1984 study published by the Social Security Minister that described the incidence, in descending order of frequency, of the 50 principal causes of diseases that provoked temporary work leave of individuals covered by the Brazilian nationalized social security system as well as the benefits paid as a consequence. The year of reference was 1983, when CVI occupied 14th place. In spite of its high incidence, the author concluded that these numbers do not entirely reflect the Brazilian reality, as more data would be necessary for a concrete conclusion of the problem and its cost for the economy of the nation.⁶

On his study on the risk factors, Scott et al. ⁷ demonstrated that 50% of patients had a history of trauma in the lower affected limb (2.4% risk of CVI development). In addition, he discovered that 45% of patients presented a history of thrombophlebitis (25.7% risk of CVI development) and that a family history of varicose or CVI (suggesting a genetic component), is also associated with an increase of incidence.

PATHOPHYSIOLOGY

The venous system is a capacitating system that functions as a blood reservoir and that has the function of carrying deoxygenated blood back to the heart. The calf veins, in association with the surrounding tissues, form a functional unit known as the muscular pump of the peripheral heart, which actively works to drain venous blood during excercise.⁸

Traditionally, CVI has been grouped into four clinical forms: primary or essential varicose veins, postthrombotic syndrome (PTS), varicose veins due to congenital angioplasties (Klippel-Trenaunay Syndrome, Parkes-Weber Syndrome, Bockenheimer Syndrome) and varicose veins due to acquired arterial-venous fistulas. It is recognized today that varicose veins caused by pregnancy also constitute a separate group, with its own etiopathogenic and pathophysiological characteristics.¹

There are two mechanisms for venous hypertension. The first is hydrostatic pressure, related to the pressure of the blood column of the right atrium. In normal situations, the venous flow travels from the surface to deep venous system through communicating veins with competent valves that impede the blood from returning to the surface veins. The incompetence of deep venous system and communicating valves and the resulting reflux is the cause of venous hypertension.⁸

Venous obstruction in patients that had deep venous thrombosis tends to recanalize in a period of three to six months. After this process, a lesion is caused by venous valve cusp from the thrombotic process, consequently causing venous reflux. With the presence of the reflux at the beginning of the condition, the calf musculature tries to compensate the volume of the insufficient veins, injecting a higher volume of blood. With the aggravation of the reflux, the pump becomes insufficient, causing a cyclical reduction of pressure from 100 mmHg to levels of between 0 and 30 mmHg. Such a process causes the onset of permanent chronic venous hypertension, initiating the symptoms of CVI.⁸

The second mechanism is dynamic and is related to the calf musculature that exercises an important role in venous return. This muscular pump, when it functions perfectly, compresses the deep veins of the calf when it contracts (the largest reservoirs of this system are sinusoidal capillaries of gastrocnemius and soleus muscles). The distal valve of the deep vein and the valves of the perforating veins close and blood is ejected toward the heart. During calf relaxation, a huge reduction of pressure occurs in the deep veins and negative pressures can build, thus resulting in the closure of the proximal valve of the deep axis. In this way, the venous pressure of the superficial network is more elevated than of the deep axes, and the blood is deeply aspirated through the perforating veins. Through an aspirating and compressive action, the hydrostatic venous pressure of an individual is reduced from 100 mmHg to 0-30 mmHg during walking. The muscle pump in healthy individuals ejects blood in such an effective way that is reduces intravascular venous pressure to values close to zero. It may also raise this pressure to values above 200 mmHg. To make this muscle pump work properly the following are necessary: good draining pervious veins with competent valves, eutonic and eutrophic musculature, neural integrity and free joints. The dysfunction of the calf muscle, whether or not it is associated with valvular dysfunction, is also responsible for venous hypertension, carrying an excessive accumulation of liquid and fibrinogen in the subcutaneous tissue, resulting in edema, lipodermatosclerosis and finally, ulceration.⁸

Venous pressure remains elevated in the lower limbs during walking, when in normal conditions it should decrease. In this way, the adjacent tissues are continuously exposed to an elevated venous pressure while the patient remains with his/her legs downward. There is still no explanation for why this elevated pressure leads to the formation of ulcers in the lower limbs. Edema secondary to hypertension could be one of the factors. Still, patients with cardiac insufficiency and/or hepatic congestion with edema of the lower limbs do not develop the skin alterations and ulcers characteristic of patients with chronic venous insufficiency.⁹

Two theories attempt to explain these changes that occur in patients with CVI. The first explains that elevated venous pressure leads to an increase capillary bed size and the enlargement of interstitial pores, permitting excess drainage of the fibrinogen through the pores, which then polymerizes in fibrin. The deposit of fibrin leads to the formation of sleeves that interfere with the diffusion of oxygen and nutrients, predisposing patients to the formation of ulcers.^10,11

The second theory affirms that the leukocytes are kidnapped at the endothelial wall of the capillary bed exposed to elevated venous pressure. The leukocytes then enter into contact with intracellular adhesion molecules in the capillary wall. The cells are activated, and cytokines and free radicals are liberated into the venous bed, causing an inflammatory reaction with a lesion of venous valves and of the adjacent tissue, thus predisposing the individual to ulceration.

DIAGNOSIS

The diagnosis of chronic venous insufficiency is imminently clinical through anamnesis and physical examination. The items to be considered in the anamnesis are the complaint and duration of symptoms, including: the history of current illness; the characterization of previous diseases (especially venous thrombosis); previous traumatisms of the limbs and the existence of varicose disease. The symptoms include a sensation of weightiness and pain in the lower limbs, principally in the evenings, and some patients complain of associated itching. In the physical examination, the following should be observed: hyperpigmentation (the hemoglobin that is found in the interior tissue is transformed into hemosiderin, which causes brown spots on the skin), lipodermatosclerosis (alteration due to the progressive substitution of the skin and subcutaneous tissue by fibrosis), pitting edema (greater in the symptomatic leg), the presence of varicose veins, the presence of nevi, the increase in length of the limb and the atypically located varicose veins. The examination should always be performed under good lighting, with the patient in a standing position after a few minutes of orthostatism.^14,15

The chronic venous stasis ulcer begins spontaneously or traumatically, can have a variable size and depth and cures and reoccurrences are frequent. For primary varicose veins, the ulcer only causes pain when infected. In the after-effect of venous thrombosis, the lesion is usually more painful. Stasis ulcers generally appear on the medial face of the leg, near the medial anklebone. These ulcers have the following characteristics: irregular, flat borders with a red base and serohematic or seropurulent exudate and pigmentation around the outside edge. They are generally not painful, except for when infected.^14,16

CVI evaluation presents a greater degree of complexity than the arterial disease evaluation. The different diagnostic methods for venous disease are dependent examinations and require specific clinical skill.¹⁶

CLASSIFICATION

Widmer proposed the first CVI classification.¹⁷ However, it did not specify the nature of stage I, nor did it specify the differentiation between the trophic alterations in stage II. The classification was as follows:

" Class I - edema, lateral phlebectasia of the feet (corona phlebectatica paraplantaris).

" Class II - trophic alterations (hyperpigmentation and lipodermatosclerosis).

" Class III - open or healed ulcer.

Later, Porter's classification arose, with the following categories:

" Class 0 - Asymptomatic.

" Class 1 - Mild CVI. Moderate edema, discrete pain and local or generalized dilatation of subcutaneous veins.

" Class 2 - Moderate CVI. Moderate to severe edema, varicose veins, strong pain, hyperpigmentation and lipodermatosclerosis.

" Class 3 - Severe CVI. Severe edema, large-caliber varicose veins, accentuated trophic abnormalities and ulcer.

Due to the necessity for more specificity and uniformity in the evaluation of venous disease, the CEAP (clinical; etiology; anatomic; pathophysiology) classification was created. This classification is the one used currently.^2,18

Clinical classification (C):

" Class 0 - Without visible or palpable signs of venous disease.

" Class 1 - Telangiectasias and/or reticular veins.

" Class 2 - Varicose veins.

" Class 3 - Edema.

" Class 4 - Alterations of the skin (hyperpigmentation, lipodermatosclerosis).

" Class 5 - Class 4 with healed ulcer.

" Class 6 - Class 4 with active ulcer.

Etiological classification (E):

" Congenital - EC.

" Primary- EP.

" Secondary - ES: post-thrombotic, post-traumatic and others.

Anatomic classification (A):

" Superficial veins - AS.

" Deep veins - AD.

" Perforating veins - AP.

Pathophysiological classification (P):

" Reflux - PR.

" Obstruction - PO.

" Reflux and obstruction - PR, O.

DIFFERENTIAL DIAGNOSIS

Venous edema, and occasionally cardiac insufficiency, produces hyperpigmentation due to the fragmenting of overflowing erythrocytes. However only venous edema progresses into subcutaneous fibrosis and cutaneous atrophy in response to the erythrocytes and plasmatic overflowing erythrocytes. The pitting edema is typically produced by cardiac insufficiency, but it is also present when the edema is produced by severe hypoproteinemia.¹⁷ Edema due to cardiac insufficiency, similar to venous edema, can be relieved by elevating the extremity, and it is known to disappear at night. However, in the first case, liquid mobilization can produce orthopnea, nocturnal paroxysmal dyspnea and nocturia. Cardiac edema and other orthostatic edemas can also be evidence that the feet are being attacked, and such a symptom never occurs with venous edema. Congestive cardiac insufficiency frequently causes bilateral edema instead of venous edema or lymphedema. However, it is also asymmetrical and is commonly worse on the left side.¹⁷ Lymphedema typically attacks the toes, feet, and ankles in an ascending fashion. In the late stages of lymphedema, pigmentation can occur. However, the skin becomes hypertrophic and the subcutaneous tissue is continuously filled as the lymph accumulate with variable dimensions.^1,17 Patients with chronic lymphedema usually develop painless swelling of the extremity. A pitting edema is not produced or the edema is only partially depressive. It attacks the ankle, and in the majority of patients, the foot. The instep edema is similar to a humpback, and is characteristic in patients with lymphedema. The squared toes, caused by the high amount of protein in the excessive tissue liquid, also represent a characteristic aspect. Although chronic eczematous dermatitis and skin excoriation occur from long-term lymphedema, similarly to hyperkeratosis and lichenification (peau d`órange), frank ulcerations are rare.^1,17 A long-term edema rich in proteins is typically the center of the infection, principally for gram-positive germs, in general beta-hemolytic streptococcus that penetrates the skin through various excoriations, wounds, insect bites, etc., leading to infection of the skin, of the subcutaneous cellular tissue (cellulite) and of the vast subcutaneous lymphatic network (erysipelas). It can spread across great extensions of the leg, with an intense pain and hyperemia of the inflammatory process, and it is generally accompanied by general symptoms and high fever. These cellulite and erysipelas crises frequently worsen the clinical picture due to the increase in lymphatic obstruction.¹ The endocrine causes of edema should also be studied. The most common of these is the edema that appears in thyroid insufficiency and is characterized by myxedema. In addition to the edema, other characteristics of hyperthyroidism should also be studied, such as the full moon face, dry skin, bradylalia, hypohidrosis, hair thinning and bradycardia.¹⁷

The cyclical edema of women is related to pre and intra-menstrual phases, and it is caused by a defect in the renal elimination of sodium. The lipoedema attacks the feminine sex and corresponds to an abnormal deposit of fat in the two legs in a symmetrical fashion.¹⁷ There is not anamnesis, passed from erysipelas and/or cellulite. There is not a thickening of the skin, ulcerations and hyperpigmentation alteration. Other causes should be evaluated, including: gravitational; idiopathic; hypokalemic edema; edema related to medicines; edema due to extrinsic compression (Baker cyst, inguinal hernia, solear syndrome, gastrocnemius veins, venous stenosis, lymphadenopathy, mole tissue tumors and pregnancy); paraneoplasic edema.¹⁷

COMPLEMENTARY EXAMINATION

The continuous wave Doppler is the principal evaluation method after clinical examination, as it can detect reflux in the saphenous-femoral or saphenous-popliteal junction. The venous duplex scan determines the location and morphology of the alterations, principally of the reflux involving the territory of the greater/lesser saphenous vein; the location of the incompetent perforating veins; diagnostic explanation of edema without other signs of CVI; the evaluation of cases of recurring varicose veins and vascular anomalies, the investigation of previous deep venous thrombosis, valvular insufficiency and deep venous system reflux.¹⁵

Ambulatory venous pressure (AVP) refers to the pressure measured in a distal vein (usually a vein from the instep) after an exercise using the calf muscles. It is defined as venous pressure in the superficial veins of the foot after 10 exercises with the tips of the toes in an erect position. In normal limbs with functional valves, the venous pressure of the foot is reduced to 20 mmHg or less due to the exercise. Afterwards, the pressure slowly returns during a period of 20 seconds or more as the calf veins are once again filled with the capillary influx. A high level of correlation has been established between the increasingly higher levels of AVP and the incidence of ulceration of the leg in patients with CVI. The AVP is elevated in the majority of patients with CVI that originates in either the superficial or deep venous systems. Patients with isolated varicose veins and competent communicating veins present a slight elevation in the AVP, whereas the patients with deep valvular incompetence, including the popliteal and perforating vein, tend to have higher levels of AVP. The presence of concomitant proximal deep venous obstruction can increase levels of AVP even further. Ambulatory venous pressure reflects the global effects of valvular incompetence, of anterograde venous flow obstruction and of the failure of the calf muscles. However, measuring AVP does not allow the physician to separate the individual effect of each component that contributes to the presence of CVI. The AVP cannot separate the different components that contribute to the presence of CVI and continue to be within the normal limits in a significant number of patients that develop cutaneous ulceration due to venous stasis.¹⁹

The venous plethysmography can be used in evaluating how much the venous function (obstruction and reflux) has been affected, estimating the proportion of damage to the superficial and deep venous system and in this way predict the results of superficial venous system surgery in the cases that present damage to the superficial and deep systems. It should be considered as a complementary quantitative test.¹⁵

The air plethysmography (APG) is a non-invasive method that quantifies the variation of the volume of the leg as a result of the filling or emptying of the veins due to a change of posture or exercise. For the air plethysmography, a small sleeve is used to cover the entire extension of the leg. The examination is interpreted on a graphic that registers volume and time. The hemodynamic of the calf muscular pump is currently being studied through the APG using the ejection fraction (EF) parameter and the residual volume fraction (RVF). For the air plethysmography, the most important parameter is the venous filling index, which is also used to evaluated the results of surgical treatment.²⁰ The incidence of ulceration is related to the EF and the venous filling index (VFI). EF < than 40% and VFI between 5 and 2 ml/s correspond to an ulceration index of 32%, whereas an EF between 40 and 60% and a VFI with the same values corresponds to an ulceration index of 2%.²¹

The photoplethysmography was first used by Barnes in 1973. With specific dorsiflexion maneuvers of the foot, the capillary network is emptied and the photoplethysmography determines the time necessary for its refilling. A value of less than 20 seconds is compatible with venous hypertension. The degree of insufficiency is classified as: normal (> 20 seconds); mild (15 to 20 seconds); moderate (5 to 15 seconds) and severe (> 5 seconds).^2,14

The phlebography is indicated when the non-invasive methods described above were not decisive enough to provide a clear diagnostic reading and/or orientation of treatment in venous angiodysplasias and the possibility of deep venous system surgery. The ascending phlebography defines the obstruction with precision, while the descending phlebography identifies areas of valvular incompetence. Arteriography is indicated in cases where arteriovenous fistulas are suspected.^8,15

If it is impossible to perform confirming examinations, clinical diagnosis is sufficient for the initiation of clinical treatment.

TREATMENT

Isolated symptoms that need treatment present clinical improvements with the use of venoactive medicines and or elastic compression. The different types of venoactive medicines have diverse effects on the varying symptoms. Diosmin, calcium dobesilate, rutin, rutosides and Indian nut extract provide objective reductions in the rates of edema, and can be used as a complementary therapy.²² These drugs should not substitute elastic compression treatment or the daily habits that improve venous stasis, nor should they replace surgical therapy when correctly indicated.¹⁵

Various studies have demonstrated the effective utilization of venoactive drugs as an auxiliary treatment for CVI. Pittler and Ernst demonstrated clinical improvements for CVI symptoms in patients that used a natural product called Escin (horse-chestnut extract).²³ Laurent et al. ²⁴ performed a prospective, double-blind study on 200 patients to evaluate the efficiency of micronized diosmin. The improvement of the symptoms related to CVI was statistically significant. Widmer ²⁵ demonstrated a significant improvement of edema and of the symptoms related to CVI in patients that received calcium dobesilate in comparison to the control group.

Diuretics are rarely indicated. These drugs cause a rapid mobilization of interstitial liquid to reduce the edema. However, this effect only occurs in cases for which the drainage does not have any influence on the cause of the edema. These drugs cause hemoconcentration and consequently hypercoagulability, and they are contraindicated in cases of post-thrombotic syndrome or lymphedema.¹⁷

In patients with eczema of the lower limbs that have an intense allergic reaction, the use of topical corticosteroids is indicated.²⁶

In the telangiectasias and reticular veins, the treatment of choice is sclerotherapy, with the option of surgical treatment through mini-incisions to remove the reticular veins. Its indication is principally esthetic, and should be evaluated by comparing the improvements with the risks associated with the procedure. The use of different types of lasers has been proposed, however more studies are needed to demonstrate its real effectiveness. The use of venoactive drugs and/or graduated elastic compression stockings is indicated when associated symptoms are present.¹⁵

Surgery is indicated for the presence of reflux in the saphenous-femoral or the saphenous popliteal junction, and given that these trunks do not represent a channel of higher importance in venous emptying. Medicinal methods of compression above 40 mmHg that are compatible with the diameters and the anatomical formation of the leg and inelastic bandages are effective in the postoperative phase and can provide a reduced incidence of relapse.

In patients with edema associated with varicose veins (CEAP3), graduated elastic compression above 35 mmHg is effective. Elastic and inelastic bandages can also be used provided they are properly applied.¹⁵

ELASTIC COMPRESSION

Elastic compression functions by decreasing the diameter of the vessel, pulling together the leaflet of the valves, suppressing or reducing the reflux, decreasing venous pressure, increasing the velocity of venous flow (resulting in the decongestion of the tissues and the aspiration of the capillary bed blood) and by providing the action of a venous pump. The increase of fibrinolytic activity is debatable.¹⁷

The types of elastic compression are divided in four classes according to the European and American classification (Table 1).¹⁷

Table 1- Classification of elastic compression

Classification	Indication
Class I
(light compression- 18-25 mmHg / 15-21 mmHg)	Indicated for the prevention of deep venous thrombosis and for small varicose veins with mild symptoms.
Class II
(medium compression - 26-34 mmHg / 23-32 mmHg)	Indicated for cases of moderate CVI, after surgical treatment of varicose veins, thrombophlebitis, varicose ulcers and for the prevention of deep venous thrombosis in high risk patients.
Class III
(heavy compression - 37-49 mmHg / 34-46 mmHg)	Advanced CVI with reversible edema
Class IV
(very heavy compression - >50 mmHg / >49 mmHg)	Very advanced CVI with irreversible edema.

 

Knee-high stockings are sufficient for treatment. The elastic stockings higher than the knee can obstruct knee flexion.^8,26 In addition, some patients do not tolerate stockings that cover the entire lower limb. Contraindications for the use of elastic stockings are: the presence of chronic obstructive arterial disease of the lower limbs, patients with decompensated cardiac insufficiency and in the presence of abscesses, exudative dermatitis, ulcer of the lower limbs and allergy to some component of the treatment.¹⁷

In the presence of trophic alterations, the use of elastic compression stockings above 35 mmHg can be beneficial. Bandages that are correctly applied can also act favorably.¹⁵

SURGICAL TREATMENT

There is still not sufficient evidence to demonstrate the value of surgical treatment. However, the correction of superficial venous insufficiency with the subsequent functional improvement can promote the improvement of trophic alterations. Surgical reflux correction in the saphenous-femoral or saphenous-popliteal junction can be beneficial, relieving the overload of the deep venous system. The observation that the correction of superficial reflux frequently corrected deep reflux suggests that deep reflux in patients with primary superficial venous insufficiency could be do to superficial reflux. Patients with edema and a past history of deep venous thrombosis should be evaluated more rigorously before they are submitted to surgical treatment.²⁷

In patients with a healed ulcer, compression above 35 mmHg appears to be effective in the prevention of varicose ulcer reoccurrence. Patients that suffer from superficial venous insufficiency presented a healed ulcer should be submitted to surgical treatment.

Patients that present isolated insufficiency of the perforating vein connected to the ulcer should be submitted to ligature or the flow of the perforating vein should be interrupted. The presence of incompetent perforating veins in patients with advanced CVI (CEAP 4-6) and an inadequate response to clinical therapy are indications for the interruption of perforating veins.²⁶ The identification of the mechanisms involved in the appearance of incompetent perforating veins is important, whether these be incidental, causative, or collateral drainage channels. There are four types of perforating vein incompetence: incompetent perforating veins responsible for reflux, leading to the development of primary varicose veins in the superficial venous system; perforating veins that act as a compensating mechanism through the collateral veins to cause venous obstruction; perforating vein enlargement due to superficial venous incompetence and congenital valvular deficiency associated with a defect of the peripheral muscular pump.²⁸

In 1988, Cockett ²⁹ studied the indications for perforating vein ligature. He divided patients into three groups. The first group consisted of patients with superficial venous insufficiency, with our without previous deep venous thrombosis. These patients benefited from the removal of the insufficient veins and the ligature of the perforating veins when necessary. The second group consisted of patients with a previous history of deep venous thrombosis of the calf veins that currently present perforating vein insufficiency but that display no evidence of deep venous system obstruction or reflux. These patients benefit from the ligature of incompetent perforating veins. The third group consisted of patients with severe reflux of the deep venous system. In this case, ligature surgery of the perforating veins was controversial.^28,29

Linton initially proposed the subfascial ligature of the incompetent perforating veins for the treatment of venous ulcers in the lower limbs.³⁰ A surgical incision was made in the medial face of the leg allowing for access to the perforating veins, including the locations below the fascia of the deep posterior compartment. This surgery has some disadvantages, such as: the complications of the postoperative wound and the need for a longer hospital stay. There are some variations of this technique that were developed to diminish the postoperative complications, such as the use of small transversal or longitudinal incisions or the blind divulsion of the perforating veins in the subfascial space.³¹

In 1976, Edwards descried the use of a phlebotomy introduced through the subfascial channel, by means of an incision that was made immediately below the knee and that continued until the level of the medial malleolus to interrupt the perforating. This technique minimized the incision and also made it in an area that was separated from the disease, even though a blind entry was undertaken.³¹ In 1985, Hauer (Germany) described an endoscopic technique to visualize and divide the incompetent perforating veins. His contribution gave rise to Subfascial Endoscopic Perforator Surgery (SEPS).³² The endoscopic technique for perforating veins interruption presents a lower number of complications from the wounds than the open technique and constitutes the preferred methods for the ablation of medial perforating veins. This procedure, accompanied by the ablation of the superficial reflux, if present, effectively reduces the symptoms of CVI and induces the rapid healing of the ulcers. The reoccurrence of ulcers after correction of the perforating veins and of the superficial reflux in patients with post-thrombotic syndrome is much higher than in those patients with primary valvular incompetence. Despite the promising results, a prospective randomized study is necessary to define the long-term benefits of the interruption of incompetent perforating veins in all patients with advanced disease and also to determine which patients with post-thrombotic syndrome should be submitted to an interruption of the perforating veins.³²

A clean, open ulcer in the granulation phase does not constitute a contraindication for SEPS. The contraindications include associated chronic occlusive arterial disease, an infected ulcer, morbid obesity and high-risk patients or patients that are unable to walk. Diabetes, renal insufficiency or ulcers in patients with rheumatoid arthritis or scleroderma are relative contraindications. Patients with previous interruption of the perforating veins or those with extensive cutaneous alterations, large circumferential ulcers or voluminous legs may not be eligible for the procedure. Those with lateral ulcerations should be treated, if appropriate, for open interruption of the lateral or posterior perforating veins.³²

The surgical treatment of the deep venous system is reserved for patients that suffer from a severe form of the disease, when conservative treatment has not been effective. Candidate patients for the treatment generally represent venous claudication (during walking, due to the increase in venous pressure, the patient reports pain of the affected limb that decreases slowly after a prolonged period of rest).³³ The restoration of patency is a rare surgical indication and the presence of iliac vein obstruction, through image examinations, does not constitute an unique indication for surgical treatment. In the absence of claudication, it is important that physiological studies are performed to confirm whether the obstruction is hemodynamically significant, as when collateral veins are well developed, the compensation is sufficient. This step not only establishes the need for surgery, but also determines the probability for therapeutic success.³⁴

Among the surgical options for iliac vein obstruction are: crossed femorofemoral derivations with the contra-lateral saphenous vein (Palma-Dale surgery) or with the right femoroiliac vein with PTFE annular prosthesis.³⁴

Initially described by Palma (Uruguay) and popularized by Dale in the United States, the suprapubic crossed venous bypass is a useful venous reconstruction technique for patients with proximal obstruction. This surgery requires a normal iliofemoral contra-lateral venous system. The results are improved when the affected limb does not experience infrainguinal obstruction or incompetence of the deep venous system. This surgery is especially indicated in young women with chronic iliac vein occlusion followed by left iliofemoral venous thrombosis due to the May-Thurner syndrome. The results vary between 63% and 89% in the clinical improvement. The patency varies between 70% and 85%. Husni et al., report improved results with the use of a temporary distal arterial-venous fistula.³⁵ Endovascular surgical techniques through the use of thrombolysis, angioplasty and stent placement have been recently utilized with solid short-term results.³⁶ Femoral-popliteal derivation with the saphenous vein in situ is used for obstructions of the superficial femoral vein.³⁴

Once the flux obstruction of the exit can be treated through recanalization of the obstructed venous segment or venous derivation, valvular incompetence requires the creation of one or more functional valves to avoid reflux. The restoration of valvular competence should be planned according to the disease etiology. In primary valvular disease, with preserved anatomy and significant hemodynamic reflux (at least level two in the Kistner classification), valvuloplasty is indicated. The precise etiology of this disturbance is unknown, however if the valvular cusp is redundant, it can result in precarious coaptation and reflux. The Kistner valvuloplasty technique uses the direct exposure of the redundant and refluent valvular cusp to place sutures at the base of the cusp, which open the free edges of the valve and makes it competent.³³ The results are satisfactory with a 63% treatment success rate of the ulcer after a period of seven years.³⁷

In cases of valvular lesions, such as in postthrombotic syndrome for example, transplants or valve transpositions are favored. In the selection of patients it is important that reflux is present in the axial veins and that it does not involve the collateral veins. Under this circumstance, interposition of one competent valve can relieve the symptoms. A procedure that is commonly used is the transposition of the axillary vein. The duplex scan should be used to identify a segment of an axillary vein with the right size and with a competent valvular segment. The basilic vein becomes the axillary vein when it crosses the edge of the larger pectoral muscle and can be an acceptable donation source. One of the disadvantages of using the axillary vein is the high percentage of valves that are incompetent. When transferred to the lower limb, they have a propensity for dilation and reflux. A synthetic material covering can by applied around the transferred valve in an attempt to reduce the chances of this complication.³³ The results vary and some studies refer to success rates of between 80% and 90% during four years of follow-up, while there are also success rates of between 35% and 45%.^37,38

ULCER TREATMENT

Ulcer healing occurs in three histologic stages, described as inflammatory, proliferative and scar remodeling. The majority of lesions caused by wounds will close in 30 days when they relate to etiopathogenesis and complications such as simple compressive dressings, and provided they were treated with careful hygiene. In some cases, despite these basic therapeutics, the lesion may evolve chronically, sometimes dragging on for over a year. The closed dressing maintains a humid environment, which avoids the scab formation and increases the speed of epithelial cell migration, of collagen synthesis and of the formation of granulation tissue and angiogenesis. In addition, these dressings maintain a wound exudate that is rich in growth factors that accelerate healing processes.^14,39

Elastic and inelastic bandages are effective. In 1885, German dermatologist Paul Unna introduced the use of a zinc oxide paste associated with elastic compression for the treatment of varicose ulcers that is used even today. The mechanism for action of Unna's boot is through elastic compression that permits the patient to walk, similar to a topical action.^40,41

Many dressings have been launched over recent years, including everything from the modification of traditional dressings closed with Unna paste, gauze and sponges and absorbents filled with medicine, to new products with hydrochloride, alginate fiber agglomerates or activated carbon base. In addition to maintaining the environment of the lesion, these dressings control the moisture, absorb the excess secretion and avoid the softening of the wound edges. Currently, there are the so-called bioactive dressings, created through genetic engineering, that function during on one or more phases of healing. Also in use are equivalents of human flesh formed by a prosthetic bovine mold and filled with keratinocytes and human fibroblasts.^14,42

Pentoxifylline, a hemorrheologic agent, prevents the activation of the leucocytes while liberating free radical, increasing the supply of oxygen to the tissues. Colgan et al., performed a prospective double-blind study on 80 patients with stasis ulcers. After months of treatment with 1200 mg/day of pentoxifylline, 23 of the 38 patients experienced the complete healing of their ulcer. Of the patients that received the placebo, only 12 of 42 experienced the healing of the ulcer. This difference was statistically significant. This drug should be used as an auxiliary treatment in association with elastic compression.^42,43

In patients with an active ulcer, evidence of the medication's efficiency is still limited. Bacteriologic analysis and the routine use of antibiotics are not recommended as they do not influence the diagnosis, treatment and prognosis. Antibiotics should only be used in cases of infections with systemic manifestations. The value of using diverse types of local treatment has not yet been proven, and the use of topical antibiotics is contraindicated.^15,39

Patients that suffer from active venous ulcers and reflux in saphenous-femoral or saphenous- popliteal junction are benefited by surgical treatment.¹⁵

Although non-adhesion to clinical treatment is the most common cause of ulcer healing, other causes should be excluded, principally arterial insufficiency. Fungal and bacterial infections should be properly treatment, and in some cases, a biopsy should be performed to exclude the possibility of basal cell carcinoma or squamous.⁴⁴

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