Venous Insufficiency 

Updated: Oct 22, 2018
Author: Robert Weiss, MD; Chief Editor: William D James, MD 

Overview

Background

In venous insufficiency states, venous blood escapes from its normal antegrade path of flow and refluxes backward down the veins into an already congested leg. Venous insufficiency syndromes are most commonly caused by valvular incompetence in the low-pressure superficial venous system (see the image below) but may also be caused by valvular incompetence in the high-pressure deep venous system (or, rarely, both). In addition, they may result from the congenital absence of venous valves.

Superficial venous insufficiency with skin changes Superficial venous insufficiency with skin changes.

See Superficial Venous Insufficiency: Varicose Veins and Venous Ulcers, a Critical Images slideshow, to help identify the common risk factors and features of this condition and its management options.

Untreated venous insufficiency in the deep or superficial system causes a progressive syndrome (chronic venous insufficiency [CVI]). Historically, CVI was known as postphlebitic syndrome and postthrombotic syndrome, terms referring to the conditions that cause most cases. However, these terms have been largely abandoned because they do not include another common cause of the disease, the congenital absence of venous valves.

In addition to poor cosmesis, CVI can lead to chronic life-threatening infections of the lower extremities. Pain, especially after ambulation, is a hallmark of the disease. CVI causes characteristic changes, called lipodermatosclerosis, to the skin of the lower extremities, which lead to eventual skin ulceration.[1]  

Venous insufficiency is neither uncommon nor benign. Treatment is aimed at ameliorating the symptoms and, whenever possible, at correcting the underlying abnormality. Graduated compression is the cornerstone of modern therapy. Deep system disease is often refractory to treatment, but superficial system disease can usually be treated by ablating the refluxing vessels. Refluxing superficial vessels can safely be removed or ablated without sequelae.

Anatomy

The venous network in the lower extremities commonly affected by CVI is divided into the following three systems (see the images below):

  • Superficial veins (including the great saphenous vein [GSV], the small saphenous vein [SSV], and their tributaries)

  • Deep veins (including the anterior tibial, posterior tibial, peroneal, popliteal, deep femoral, superficial femoral, and iliac veins)

  • Perforating or communicating veins

    Lower-leg venous anatomy. Lower-leg venous anatomy.
    Perforating veins of lower leg. Perforating veins of lower leg.

When the venous network is functioning correctly, every movement of the leg causes blood to be pumped inward and upward past a series of valves (see the image below). During ambulation, the normal pressure in the venous system of the lower leg is nearly zero. Immediately after ambulation, the early standing pressure in the normal leg remains low. Arterial inflow fills the leg veins slowly, and the only source of venous pressure is the hydrostatic pressure of a column of blood as high as the nearest competent valve.

Venous valve. Thrombosis can begin as blood flow b Venous valve. Thrombosis can begin as blood flow becomes turbulent, permitting platelets to remain in valve sinus. This forms nidus of thrombus.

In venous insufficiency, after prolonged standing, the veins are completely filled, and all the venous valves float open. At this time, high hydrostatic venous pressure results from the unbroken column of fluid that extends from the head to the foot. Failed valves cause the column of standing blood in the vein to remain high even during ambulation. The hydrostatic pressure increases during and immediately after ambulation, which cause venous congestion.

Pathophysiology

Various mechanisms are associated with failure of superficial venous valves. Most commonly, congenitally weak vein walls dilate under normal pressures to cause secondary valve failure. Direct injury or superficial phlebitis may cause primary valve failure. Congenitally abnormal valves can also be incompetent at normal superficial venous pressures. Normal veins and normal valves may become excessively distensible under the influence of hormones (as in pregnancy).

High venous pressure is directly responsible for many aspects of venous insufficiency syndrome. Under normal conditions, two major mechanisms in the body operate to prevent venous hypertension. First, bicuspid valves in the veins prevent backflow and venous pooling. Deep venous thrombosis (DVT) commonly occurs at these valves, causing irreversible damage to the valve.

Second, during normal ambulation, calf muscles decrease venous pressures by approximately 70% in the lower extremities (see the image below). With rest, pressures return to normal in approximately 30 seconds. In diseased veins, ambulation decreases venous pressures by only 20%. When ambulation is stopped, pressure in the vein lumen increases slowly, returning to normal over a period of minutes.

Hemodynamic charting of (a) healthy patients, (b) Hemodynamic charting of (a) healthy patients, (b) patients with only varicose veins, (c) patients with incompetent perforator veins, and (d) patients with deep and perforator incompetence.

Venous hypertension in diseased veins is thought to cause CVI through the following sequence of events[2] :

  • Increased venous pressure transcends the venules to the capillaries, impeding flow

  • Low-flow states within the capillaries cause leukocyte trapping

  • Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes

  • Plasma proteins (eg, fibrinogen) leak into the surrounding tissues, forming a fibrin cuff

  • Interstitial fibrin and resultant edema decrease oxygen delivery to the tissues, resulting in local hypoxia

  • Inflammation and tissue loss result

Most cases of superficial vein valve failure occur after primary points of high-pressure leakage develop between the deep system and the superficial system. High pressure leads to secondary valve failure when otherwise normal superficial veins become so widely dilated that the thin flaps of the venous valves can no longer make contact in the lumen of the vessel. Over time, these incompetent superficial veins become visibly dilated and tortuous, at which point they are recognized as varicose veins.

High pressure can enter the superficial veins as a result of the failure of key valves at any point of communication between the deep system and the superficial system. High-pressure leakage from the deep veins to the superficial system has 2 major sources, as follows:

  • Junctional valve failure

  • Perforator valve failure

Junctional high-pressure disease most often results from failure of the primary valve at the junction between the GSV and the common femoral vein at the groin (saphenofemoral junction). Vein incompetence then proceeds distally from the groin, and patients perceive that a large vein is growing down their leg. A less common form of junctional reflux results from failure of the primary valve at the junction between the SSV and the popliteal vein at the knee (saphenopopliteal junction).

Perforator high-pressure disease results from failure of the valves of any perforating vein. The most common sites of primary perforator valve failure are in the midproximal thigh (Hunterian perforator) and in the proximal calf (Boyd perforators). When the primary high-pressure entry point is distal, large clusters of veins are first noticed in the lower leg, with large veins eventually growing up the leg toward the groin.

Not all of the sequelae of venous insufficiency are related to venous hypertension, and not all patients with venous hypertension develop ulceration. Some patients with venous ulceration do not have marked venous hypertension.

Poor clearance of lactate, carbon dioxide, and other products of cellular respiration also contributes to the development of the syndrome. A defect in the clearance of extraneous substances can be quantified: If albumin labeled with a radioactive tracer is injected into the foot tissues, the clearance rate is markedly slowed by deep venous obstruction or by deep or superficial venous incompetence.

Although this effect is referred to as venous stasis, the reduced clearance of cellular metabolites is not always due to true venous stasis. In many cases, the venous blood is moving at a normal speed, but a local recirculation of this venous blood upward through normal veins and downward through varicosities prolongs the average time required for the blood to pass from the heart and lungs through the legs and back to the central circulation.

The time required for an aliquot of radiolabeled blood to pass from the femoral artery through the leg and back to the central circulation is highly correlated with the development of leg ulcers. The aliquot transit time and the clearance time for an extremity are closely related to the volume of retrograde flow through refluxing veins. Superficial varicosities always produce venous recirculation and can result in prolonged clearance that may be localized or affect the whole leg.

Experimental evidence shows that if the peak retrograde flows in the GSV, SSV, and popliteal vein add up to less than 10 mL/s, progressive visible stasis dermatitis and ulceration do not occur. If they add up to more than 15 mL/s, the incidence of ulceration is high. In some cases, purely superficial local reflux with a pressure of more than 7 mL/s can cause local ulceration.

In the San Diego Population Study, levels of circulating P-selectin were found to be correlated with the severity of CVI, though not with the incidence of CVI in general.[3] The study findings suggest that the pathogenesis of CVI may include activation of platelets and endothelial cells.

Etiology

CVI can be caused by congenital absence of or damage to venous valves in the superficial and communicating systems. It can also be caused by venous incompetence due to thrombus formation as favored by the Virchow triad (venous stasis, hypercoagulability, and endothelial trauma[4] ). Varicose veins rarely are associated with the development of CVI. Most cases of venous insufficiency are related to reflux through the superficial veins.

Chronic nonhealing wounds of the lower extremity have many different potential causes, but most chronic lower-extremity ulcers are of venous etiology. The majority of venous ulcers are caused by venous reflux that is purely or largely confined to the superficial venous system; only a minority are caused by chronic DVT or by valvular insufficiency in the deep veins.

Superficial venous insufficiency

In superficial venous insufficiency, the deep veins are normal, but venous blood escapes from a normal deep system and flows backwards through dilated superficial veins in which the valves have failed. More than 80% of varicose veins seen on the leg are caused by venous insufficiency or a leaky valve in the GSV, which terminates near the inguinal ligament as it joins the common femoral vein.

The initial valve failure may occur at any level between the groin and the ankle, but the saphenofemoral junction is the high point of reflux in most patients with severe superficial venous insufficiency. Valve failure can be spontaneous in patients with congenitally weak valves. Congenitally normal valves can fail as a consequence of direct trauma, thrombosis, hormonal changes, or chronic environmental insult (eg, prolonged standing).

Deep venous insufficiency

Deep venous insufficiency can be due to congenital valve or vessel abnormalities, but it most commonly occurs when the valves of the deep veins are damaged as a result of DVT. With no valves to prevent deep system reflux, the hydrostatic venous pressure in the lower extremity increases dramatically.

Klippel-Trénaunay-Weber syndrome

A less common cause of venous insufficiency is Klippel-Trénaunay-Weber (KTW) syndrome, which involves port-wine stains, varicose veins, and bony or soft-tissue hypertrophy. Patients with pure Klippel-Trénaunay syndrome have only venous involvement, whereas those with the Parkes Weber variant also have arteriovenous malformations.

The capillary hemangiomas (port-wine stains) of KTW syndrome, like those of other forms of venous insufficiency, can lead to local skin breakdown and ulceration, bleeding, and secondary infection. This can occur in any organ system of the body.

The sciatic vein is a large superficial vessel that is present during fetal development but usually does not persist. In patients with KTW syndrome, this vein may be noticed at birth, or it may become apparent later in life. The vein extends along the posterolateral aspect of the leg from the foot to the gluteal region. When present, it is invariably a reflux pathway rather than a pathway for antegrade flow.

Patients with KTW syndrome may have atresia of the deep veins, as well as many abnormal venous pathways involving the deep and superficial venous systems. KTW syndrome can produce such severe venous insufficiency that the otherwise normal lymphatic system becomes overwhelmed by the amount of lymph production, which leads to secondary lymphedema.

Surgical attempts to treat the abnormal refluxing veins in KTW syndrome are fraught with peril because postoperative worsening of venous abnormalities is common.

Risk factors

The incidence of CVI rises substantially with age. A history of DVT, which renders venous valves incompetent and thereby causes backflow and increased venous pressure, is a risk factor.

A sedentary lifestyle minimizes the pump action of calf muscles on venous return, causing higher venous pressure. CVI occurs more frequently in women who are obese. Vocations that involve standing for long periods predispose individuals to increased venous pressure in dependent lower extremities. A higher incidence of CVI is observed in men who smoke. Pregnancy is an important causative factor in the development of peripheral venous insufficiency. Contraceptive medication use, hypertension, previous leg injuries, and low intake of cellulose fibbers have also been considered.[5]

Epidemiology

United States statistics

CVI is a significant public health problem in the United States. It has been estimated that 2-5% of all Americans have some changes associated with CVI. Published estimates of the prevalence of varicosities range from 7% to 60% in the adult population, with most studies demonstrating clinical varicose reflux in about 40% of the population.[6] Venous stasis ulcers affect approximately 500,000 people. The mean incidence of hospital admission for CVI is 92 per 100,000 admissions.

International statistics

The frequency of venous insufficiency is believed to be higher in Westernized and industrialized nations than in developing nations, most likely because of differences in lifestyle and activity.

It has been estimated that approximately 1-2% of the adult population presents with lower-limb ulceration, from which 70-90% of these ulcers are attributed to CVI.[5, 7]

Age-related demographics

The prevalence of venous insufficiency increases with age. Peak incidence occurs in women aged 40-49 years and in men aged 70-79 years.

Reticular veins usually appear or are first noticed in adolescence and young adulthood, with only a small number of new cases developing after the childbearing years. Truncal varicosities and telangiectatic webs, on the other hand, are relatively less common in youth and can appear throughout life.

The Bochum study, which assessed a large number of children aged 10-12 years at one point (Bochum I) and again 4 years later (Bochum II), revealed that symptoms and abnormal venous test results occur before any abnormal veins are visible at the surface. Abnormal reticular veins appear first and are followed by incompetent perforatoring veins and truncal varicosities, which appear several years later.[8]

Although active venous ulceration affects less than 1% of the population, its prevalence slightly increases to 3% in individuals older than 65 years.[9]

Sex-related demographics

The incidence and prevalence of deep and superficial venous disease depend on the age and sex of the population, but at any age, such disease is more common in women than in men. In younger men, the incidence is lower than 10%, compared with 30% in similarly aged women. In men older than 50 years, the incidence is 20%, compared with 50% in similarly aged women.[10]

Prognosis

The syndromes of venous hypertension and reduced venous clearance are important causes of morbidity and disability in patients with varicose venous disease (see also Complications).

Without correction of the underlying cause, venous insufficiency is inexorably progressive. Subjective symptoms usually worsen over time.

In many patients, the skin eventually breaks down and nonhealing ulcers develop. A study by Abbade et al determined that longstanding and large ulcers and recurrences are the primary complications encountered by patients who have venous ulcers.[11] Risk factors for these complications include severe lipodermatosclerosis, a previous history of ulcers, and time since first ulcer episode of 2 years or longer.

Chronic nonhealing leg ulceration can be debilitating. Approximately 1 million Americans have an ulceration due to superficial venous disease, and approximately 100,000 are disabled because of their condition. Reflux need not be entirely eliminated for the ulceration to resolve. Ulcers will heal if the net volume and pressure of reflux are reduced below a threshold level. Tissue atrophy and staining are usually not reversible.

Patients have an increased lifetime risk of DVT and pulmonary embolism. Tsai et al, examining the National Inpatient Sample from 1988-2000, found that DVT affected 1.3% of patients and that amputation was necessary in 1.2%, with an overall mortality of 1.6%.[12]

As many as 50% of patients with untreated varicose veins develop superficial thrombophlebitis at some time. This is of grave concern, because unrecognized DVT is present in as many as 45% of patients with what appears to be purely superficial phlebitis. The risk of DVT is 3 times higher in patients with superficial varicosities than in the general population.

Bed rest and intercurrent illness place patients with venous insufficiency at higher risk for DVT. Phlebitis develops in 60% of hospitalized patients with clinically evident superficial venous insufficiency, and in nearly one half of cases, the condition progresses to DVT. Approximately one half of patients with DVT have detectable pulmonary embolism, and the death rate in this group exceeds 1 in 3.

Venous insufficiency syndromes can also lead to death from hemorrhage. Bleeding from lower-extremity varicosities can be fatal[13] ; 23 such fatalities were reported in England and Wales in 1973,[14] and, although there is no central registry to tabulate the frequency with which it occurs, such cases are not unusual in the United States. Bleeding is not a rare problem, but it is often managed incorrectly.

Outcomes for different therapies have varied. Clot lysis (eg, with tissue plasminogen activator or urokinase) and thrombectomy have been tried but have largely been abandoned because of the extremely high recurrence rates.

Saphenous vein crossover grafting for iliofemoral disease has a relatively high failure rate (20%), and thus, ringed polytetrafluoroethylene (PTFE) grafts are now being used. Long-term patency rates have not been determined. The Husni bypass for superficial femoral vein occlusion has an even higher failure rate (approximately 40%) and thus is now performed infrequently.

Surgery for CVI resulting from deep vein incompetence includes valvuloplasty and allograft or cadaveric vein transplant. Valvuloplasty for patients with congenital absence of functional valves, when combined with ligation of perforating veins, yields a superior outcome in 80% of cases after 5 years. Allograft or cadaveric vein transplants are undergoing further evaluation, with long-term results pending.

Patient Education

Patients with venous insufficiency syndromes should be instructed to wear compression stockings as much as they can, unless they also have arterial insufficiency or unless they cannot tolerate the stockings for some other reason.

Patients should also be instructed to avoid prolonged standing or sitting and to perform walking or calf-muscle exercises at regular intervals.

For patient education resources, see Blood Clot in the Legs, Varicose Veins, and Phlebitis.

 

Presentation

History

Patients with venous insufficiency often report subjective symptoms that are typically bothersome early in the disease, become less severe in the middle phases, and then worsen again with advancing age.

Even small telangiectasias are often symptomatic. More than one half of patients who present with telangiectasias smaller than 1 mm in diameter report symptoms that abate after treatment. Common symptoms include the following:

  • Burning

  • Swelling

  • Throbbing

  • Cramping

  • Aching

  • Heaviness

  • Restless legs

  • Leg fatigue

Subjective complaints are also common in patients with truncal varices: 18% of patients with varicosities report frequent or continuous symptoms, whereas almost 50% complain of episodic symptoms.

In addition to poor cosmesis, varicose veins serve as indicators of venous hypertension, the most common reason for patient complaints regarding chronic venous insufficiency (CVI).[15] Venous hypertension in muscles and fascial compartments of the lower leg from exercise and prolonged standing results in the characteristic ache of CVI. The discomfort is described as pain, pressure, burning, itching, dull ache, or heaviness in affected calves or legs.

Episodic pain and other symptoms associated with superficial venous disease may be temporally related to hormonal changes, both physiologic and pharmacologic. One half of all pregnant women with varicose veins complain of pain, and 17% are unable to remain upright for more than 1-2 hours at a time because of the severity of the pain.

Patients with deep system insufficiency are nearly always symptomatic. Leg aching, heaviness, and soreness are the most common subjective symptoms.

Pain caused by venous insufficiency often is improved by walking or by elevating the legs. Warmth tends to aggravate the symptoms of venous insufficiency, and cold tends to relieve them. Compression stockings usually ameliorate or prevent the pain of venous insufficiency.

In many ways, the behavior of the pain caused by venous insufficiency is the opposite of that of the pain caused by arterial insufficiency. The pain of arterial insufficiency usually is worse with walking and worse when the legs are elevated. Cold tends to aggravate the symptoms of arterial insufficiency, whereas warmth tends to relieve them. Compression stockings usually aggravate the pain of arterial insufficiency.

The pain of venous obstruction is worse with walking or warmth but better with elevation of the legs. Compression stockings usually improve the pain of venous obstruction.

Nonhealing ulcers are often noted around the medial malleolus, where venous pressure is maximal because of the presence of large perforating veins.[1] Leg edema, resulting from damage done to capillary basement membranes by white blood cells (WBCs), may be reported.

The characteristic skin changes of lipodermatosclerosis in the lower extremities include capillary proliferation, fat necrosis, and fibrosis of skin and subcutaneous tissues. Skin becomes reddish or brown because of the deposition of hemosiderin from red blood cells.[16]

Physical Examination

The most common physical signs of venous insufficiency are those attributed to the progressive syndromes of chronic venous stasis and chronic venous hypertension. These signs include the following:

  • Edema

  • Hyperpigmentation

  • Venous dermatitis

  • Chronic cellulitis

  • Cutaneous infarction (atrophie blanche)

  • Ulceration

Swelling may result from acute venous obstruction (as in deep venous thrombosis [DVT]) or deep or superficial venous reflux. Alternatively, swelling may be completely unrelated to the venous system. Lower-extremity pitting edema is common in patients with venous insufficiency. Hepatic insufficiency, renal failure, cardiac decompensation, infection, trauma, and environmental effects can also cause lower-extremity pitting edema that may be indistinguishable from edema due to venous obstruction or venous insufficiency.

Lymphatic edema may be a sign of primary lymphatic outflow obstruction, or it may be secondary to the overproduction of lymph as a result of severe venous hypertension (a so-called venolymphatic syndrome).

Darkened, discolored, and stained skin may be a sign of venous stasis, arterial insufficiency, chronic infection, prior injury, or various other conditions (see the image below). Such discoloration is particularly likely to be a sign of chronic venous stasis if it is localized along the medial part of the ankle or the medial aspect of the lower leg; these areas are especially prone to venous hypertension because their drainage largely depends on the competence and patency of the entire great saphenous vein (GSV) and all the attached perforating veins.

Superficial venous insufficiency with skin changes Superficial venous insufficiency with skin changes.

Normal veins are visibly distended at the foot and ankle and, occasionally, in the popliteal fossa; they usually are not visibly distended in the rest of the leg. Translucent skin may cause the normal veins to become visible in a bluish subdermal reticular pattern. A dilated vein above the ankle is usually evidence of venous pathology (see the image below).

Perforator vein bulging into subcutaneous tissue. Perforator vein bulging into subcutaneous tissue.

Nonhealing ulcerations may be due to deep or superficial venous insufficiency (see the images below); other causes include arterial insufficiency, rheumatologic disorders, local trophic effects, unrecognized cancer, and various more exotic conditions. Nonhealing ulcers on the medial part of the ankle are most likely due to underlying venous stasis. Skin changes or ulcerations that are localized to the lateral aspect of the ankle are more likely to be related to prior trauma or arterial insufficiency than to pure venous insufficiency.

Ulcer due to venous insufficiency. Ulcer due to venous insufficiency.
Chronic venous stasis ulcer. Chronic venous stasis ulcer.
Venous stasis ulcer and surrounding dystrophic tis Venous stasis ulcer and surrounding dystrophic tissue.

A long-standing venous ulcer rarely converts to a basal cell carcinoma or squamous cell carcinoma. The venous ulcer may develop collision lesions (eg, basal cell carcinoma and stasis ulceration) at the same site.

The visual appearance of the lower extremities is a useful but not always reliable guide to the peripheral venous condition.[17] Clinical findings in venous disease are also common to many other entities that affect the lower extremities.[18] Physical examination alone is not a reliable means of assessing the venous system. Diagnostic testing nearly always is necessary to rule out deep venous obstruction, to assess the paths of reflux, and to guide treatment planning.

Trendelenburg test

The Trendelenburg test is a traditional part of the physical examination that may help in distinguishing distal venous congestion caused by superficial venous reflux from that caused by incompetence of the valves in the deep venous system.

To perform this test, elevate the patient’s leg until all of the congested superficial veins collapse. Apply direct pressure to occlude the superficial veins below the point of suspected reflux from the deep system into the superficial varicosity. Most often, the GSV is manually occluded just below the saphenofemoral junction at the groin.

With the occlusion still in place, have the patient stand. If the distal varicosity remains empty or fills slowly, quickly remove the occluding hand or tourniquet. If the slow filling observed with occlusion is followed by rapid filling after the occlusion is removed, the principal high-pressure entry point into the superficial system is correctly identified.

Immediate refilling of the varicosity despite manual occlusion indicates that the principal entry point has not yet been identified or that more than 1 reflux pathway is involved. Extremely rapid refilling despite occlusion of the superficial reflux pathways suggests that the valves in the deep veins may be incompetent between the groin and the level at which the reflux escapes the deep system. The result is rapid filling of the superficial system.

If deep venous insufficiency is confirmed with results from further evaluations, the treatment options for the patient may be severely limited.

Complications

The local tissue sequelae of venous insufficiency are due to a combination of high venous pressures and reduced clearance of cellular metabolites from the lower extremity. Complications of untreated venous insufficiency include the following:

  • Recruitment of veins – High venous pressures may cause the recruitment of adjacent normal veins into refluxing circuits

  • DVT

  • Pulmonary embolism (PE)

  • Venous ulceration

  • Secondary lymphedema

Chronic pain, swelling, recurrent cellulitis, and chronic nonhealing leg ulcers (ulcer cruris) are the most common sequelae of venous insufficiency, but they are not the most severe.

 

DDx

Diagnostic Considerations

Misdiagnosing venous disease often is lethal when venous thrombosis is involved, but it is rarely disastrous when the disease is caused by other conditions, because nonthrombotic venous disease is slowly progressive. Although morbidity results in a decreased quality of life and an inability to work, death is rare.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include hepatic insufficiency and lymphedema.

Differential Diagnoses

 

Workup

Laboratory Studies

Many patients with venous insufficiency have clinically unrecognized chronic recurrent varicose thrombosis due to stasis in areas with abnormal veins. Such patients may have elevated levels of D-dimer. This finding reduces the usefulness of that test for the evaluation of patients with suspected acute venous thromboembolic disease.

Laboratory tests may be helpful in patients with venous insufficiency due to Klippel-Trénaunay-Weber (KTW) syndrome because such patients can develop consumptive thrombocytopenia.

Ultrasonography

Duplex ultrasonography is the study of choice for the evaluation of venous insufficiency syndromes. Color-flow duplex imaging uses the Doppler information to color code the 2-dimensional sonogram. On the image, red indicates flow in one direction (relative to the transducer), and blue indicates flow in the other direction.[19] On newer machines, the shade of the color may reflect the flow velocity (in the Doppler mode) or the flow volume (in the power Doppler mode).

When used to evaluate patterns of venous reflux, ultrasonography is both sensitive and specific. Ultrasonographic reflux mapping is essential for the evaluation of peripheral venous insufficiency syndromes.

A study from the United Kingdom compared 27 consecutive patients seen at a varicose vein clinic with 23 normal ambulatory volunteers and found evidence to suggest that the presence of pulsatile flow in the GSV might be a marker of severe chronic insufficiency of the superficial veins.[20]

In the diagnosis of deep venous thrombosis (DVT), ultrasonography has been shown to be superior to contrast venography, and it has now replaced venography in this setting. Duplex ultrasonography is the initial diagnostic imaging modality of choice in patients with suspected DVT.

Intravascular ultrasonography has been gaining acceptance in the management of venous disease. This test uses a catheter-based ultrasound probe to visualize periluminal vascular anatomy in order to assess for obstructive or stenotic disease of the venous system.[21]

Venography

Magnetic resonance venography (MRV) is the most sensitive and specific test for the assessment of deep and superficial venous disease in the lower legs and pelvis, areas not accessible by means of other modalities. MRV is particularly useful because it can help detect previously unsuspected nonvascular causes of leg pain and edema when the clinical presentation erroneously suggests venous insufficiency or venous obstruction.

Current advances in technology have allowed the inclusion of computed tomography and/or MRV in the evaluation of venous disease; however, their use requires intravenous contrast material and appropriate timing in order to obtain a venogram. In other words, a proper technique that would allow the proper visualization to assess for obstructive disease, varicose veins, perforating veins, and other venous abnormalities is required.[21]

Direct contrast venography (see the image below) is a labor-intensive and invasive imaging technique. In most centers, it has been replaced by duplex sonography for the routine evaluation of venous disease. However, the technique remains useful in difficult or confusing cases.

Venogram demonstrating incompetent perforating vei Venogram demonstrating incompetent perforating veins.

An intravenous (IV) catheter is placed in a dorsal vein of the foot, and radiographic contrast material is infused into the vein. A superficial tourniquet is placed around the leg to occlude the superficial veins and force the contrast material into the deep veins.

The assessment of reflux by means of direct contrast venography requires the passage of a catheter from the ankle to the groin with the selective introduction of contrast material into each segment of the vein.

In nearly 15% of patients undergoing venography for detection of DVT, a new thrombosis is detected shortly after a contrast venogram shows negative results. The incidence of contrast-induced DVT in patients who undergo venography for the assessment of venous insufficiency is not known.

Venous Plethysmography

Air plethysmography (APG) is a noninvasive test that has the ability to measure some pathophysiologic mechanisms of CVI, which includes reflux, obstruction, and muscle pump dysfunction. This test facilitates evaluation of venous filling through the venous filling index. It may be useful when venous duplex ultrasound does not provide conclusive information.[21]

Photoplethysmography uses infrared light to assess capillary filling during exercise. Increased capillary filling is indicative of venous reflux and, consequently, of incompetent veins.

Outflow plethysmography involves placing and subsequently releasing a tourniquet on the lower extremity; the veins should quickly return to baseline pressures. Failure to do so indicates reflux.

Physiologic Venous Function Tests

Physiologic tests of venous function are important in assessing the cause and severity of venous insufficiency. The physiologic parameters most often measured are the venous refilling time (VRT), the maximum venous outflow (MVO), and the calf muscle pump ejection fraction (MPEF).

Venous refilling time

The VRT is the time necessary for the lower leg to become suffused with blood after the calf muscle pump has emptied the lower leg as thoroughly as possible. When patients with healthy veins are in a sitting position, venous refilling of the lower leg occurs only by means of arterial inflow and requires at least 2 minutes.

In patients with mild and asymptomatic venous insufficiency, some venous refilling occurs by means of reflux across leaky valves. These asymptomatic patients have a VRT of 40-120 seconds.

In patients with significant venous insufficiency, venous refilling occurs through high-volume reflux and is fairly rapid. An abnormally fast VRT of 20-40 seconds is recorded, reflecting retrograde venous flow through failed valves in superficial or perforating veins. This degree of reflux may be associated with the typical symptoms of venous insufficiency. Patients often complain of nocturnal leg cramps, restless legs, leg soreness, burning leg pain, and premature leg fatigue.

A VRT shorter than 20 seconds is markedly abnormal and is attributable to high volumes of retrograde venous flow. High-volume reflux may occur via the superficial veins, the large perforators, or the deep veins. Patients with this degree of reflux are nearly always symptomatic. When the VRT is shorter than 10 seconds, venous ulcerations are so common as to be considered virtually inevitable.

Maximum venous outflow

MVO testing is performed to detect an obstruction to venous outflow from the lower leg, no matter what the cause. Its results are a measure of the speed with which blood can flow out of a maximally congested lower leg when an occluding thigh tourniquet is suddenly removed.

A major advantage of MVO testing is that as a functional rather than anatomic test, it is sensitive to significant intrinsic or extrinsic venous obstruction due to any cause at almost any level. It can be used to detect obstructing thrombus in the calf veins, the iliac veins, and the vena cava, areas where ultrasonography and venography are insensitive. It can also be used to detect venous obstruction due to extravascular hematomas, tumors, and other extrinsic disease processes.

The main disadvantage of MVO testing is that it is sensitive only for significant venous obstruction and not for partial obstruction. It is not useful for the detection of reflux-induced venous insufficiency. A normal MVO result does not absolutely rule out DVT.

Muscle pump ejection fraction

The MPEF test is used to detect failure of the calf muscle pump to expel blood from the lower leg. Its results are highly repeatable, but a skilled operator is required to obtain clean, meaningful tracings.

The patient is asked to stand on his or her tiptoes 10-20 times or to dorsiflex his or her ankle. The change in a physical parameter that reflects the blood volume in the calf is recorded as the calf muscle is pumped.

In patients with normal veins and a normal calf muscle pump, 10-20 tiptoe motions or ankle dorsiflexions empties the venous capacitance circuit of the calf. In patients with muscle pump failure, severe proximal obstruction, or severe deep venous insufficiency, tiptoe motions or ankle dorsiflexions have little or no effect on the amount of blood remaining in the calf. Venous insufficiency due to this cause is difficult to treat

Ambulatory Venous Pressure Monitoring

Ambulatory venous pressure (AVP) monitoring is the criterion standard in assessing the hemodynamics of CVI. This test involves the insertion of a needle connected to a pressure transducer into the dorsal foot vein. It has been shown to be valuable in assessing the severity and clinical outcomes of CVI. Its use is limited given its invasive nature, possible limitations, and potential alternate diagnostic modalities.[21]

 

Treatment

Approach Considerations

Venous insufficiency is neither uncommon nor benign.[22] Treatment is aimed at ameliorating the symptoms and, whenever possible, at correcting the underlying abnormality.

No oral medication has yet been proven useful for the treatment of venous disease. Graduated compression is the cornerstone of the modern treatment of venous insufficiency. Surgical or endovenous therapy is commonly reserved for those with discomfort or ulcers refractory to medical management. The primary goal of such therapy is to improve the venous circulation by correcting venous insufficiency by removing the major reflux pathways.

As yet, no treatment for deep venous insufficiency has been proved to be both safe and effective. Valvuloplasty is occasionally successful, but the incidence of postoperative deep venous thrombosis (DVT) is high. Venous bypass is successful in select patients. External vein valve banding devices and thermally induced collagen shrinkage procedures are being investigated in clinical trials. Restoration of valvular function to incompetent deep veins remains an important focus of research for vascular physicians.

Although deep system disease is often refractory to treatment, superficial system disease can usually be treated by ablating the refluxing vessels. Refluxing superficial vessels can safely be removed or ablated without sequelae; an incompetent vessel has already proved itself unnecessary because it is carrying venous blood in a retrograde direction. Antibiotics rarely are useful in patients with venous ulcerations.

Consultation with a phlebologist (a physician or vascular surgeon specializing in venous diseases) often yields new options for patients with chronic and seemingly refractory disease. Venous insufficiency syndromes can be diagnosed and treated by means of a variety of specialized techniques with which a generalist may not be familiar. Guidelines have been established by the American Venous Forum and Society for Vascular Surgery,[23] and these guidelines are discussed in a review of modern management of venous insufficiency and varicose veins.[24]

Graduated Compression and Other Physical Modalities

The standard approach has been to use gradient compression stockings that provide 30-40 or 40-50 mm Hg of compression at the ankle, with gradually decreasing compression at more proximal levels of the leg.[25] This amount of graduated compression is sufficient to restore normal venous flow patterns in many or most patients with superficial venous reflux and to improve venous flow, even in patients with severe deep venous incompetence.

The compression gradient is extremely important because nongradient stockings or high-stretch elastic bandages (eg, ACE wraps) may cause a tourniquet effect that can exacerbate the venous insufficiency. The so-called antiembolic stockings that are commonly available in American hospitals do not provide sufficient compression to improve the venous return from the legs, and they are not particularly effective in preventing venous thromboembolism.

No patient with symptoms due to venous insufficiency should be without gradient compression hose, which can be prescribed by any physician. The prescription should specify 1 pair of calf-high (or thigh-high with waist attachment or panty-hose style) compression hose providing a pressure gradient of 30-40 mm Hg, with refills as needed.

A different approach to graduated compression was assessed in a 2012 study of 401 ambulatory patients with CVI, in which standard “degressive” compression stockings were compared with “progressive” compression stockings that applied maximal pressure over the calf.[26] The investigators concluded that the progressive compressive stockings were superior with respect to improvement of pain and lower leg symptoms in patients with CVI, as well as being easier to apply.

Additional physical measures may also be helpful. Leg elevation causes venous flow to be augmented by gravity, lowering venous pressures and ameliorating edema. In a sitting position, the patient’s legs should be above the thighs; supine, they should be above the level of the heart. The Unna boot, first described in 1854, is now a mainstay of treatment for people with venous ulcers. Unna boots are rolled bandages that contain a combination of calamine lotion, glycerin, zinc oxide, and gelatin.

Venous insufficiency is an especially common problem among postmenopausal women. In a randomized, controlled trial involving 65 postmenopausal women with venous insufficiency, the use of myofascial release therapy in combination with kinesiotherapy over a 10-week treatment period was found to yield significant improvements in basal metabolism, intracellular water, diastolic blood pressure, venous blood flow velocity, pain, and emotional role.[27]

Venoablation

Venoablation is reserved for those with discomfort or ulcers refractory to medical management. The primary goal of surgical and endovenous approaches is to correct venous insufficiency by removing the major reflux pathways. Techniques for venoablation include the following:

  • Ligation with stripping

  • Simple ligation and division

  • Sclerotherapy (with or without ligation)

  • Stab evulsion (with or without ligation)

  • Radiofrequency ablation (RFA)[28]

  • Endovenous laser therapy (EVLT)[28]

All methods of venoablation are effective (although there is some disagreement between the medical and the surgical literature as to the prevalence and timing of varicose recurrences). Once the overall volume of venous reflux is reduced below a critical threshold by any mechanism, venous ulcerations heal, and patient symptoms are resolved.[29, 30]

In general, vein ligation is reserved for cases of chronic venous insufficiency (CVI) involving reflux in the saphenous system that causes severe symptoms.[31] Thus, a diagnosis of reflux must be established preoperatively, usually with photoplethysmography or duplex imaging. [#Contraindications]In patients with symptomatic varicosities of the great saphenous vein (GSV), deep occlusion must be ruled out; it is an absolute contraindication to vein ligation. Venography of the deep venous system before superficial vein ligation is imperative.

Sclerotherapy is performed by injecting or infusing a sclerosing substance into the refluxing vessel to produce endothelial destruction and fibrosis of the treated vessel. Injection of a sclerosing agent directly into veins usually is reserved for telangiectatic lesions rather than CVI. Phlebotonics have not been proven to be beneficial for CVI.[32]

EVLT is performed by passing a laser fiber from the knee to the groin and then delivering laser energy along the entire course of the vein. Destruction of the vascular wall is followed by fibrosis of the treated vessel. It has been shown to yield excellent long-term (>5 years) results and a low rate of complications, which vary with the laser wavelength used.

RFA is performed by passing a special radiofrequency (RF) catheter from the knee to the groin and then carrying out controlled and preset heating of the targeted vessel until thermal injury causes shrinkage. The process is repeated every 7 cm along the course of the vein. Initial thermal injury is followed by fibrosis of the treated vessel. RFA has been shown to be effective, with a low rate of complications. It has produced excellent results that have been confirmed with up to 10 years of follow-up.

Subfascial endoscopic perforator surgery (SEPS) has also been employed to treat CVI. Endoscopic techniques are used to find and ligate perforating veins. Preliminary reports showed that after SEPS, the average healing time for ulcers was 42 days, with a recurrence rate of 3%, and that ulcers treated with SEPS healed 4 times faster than ulcers treated conventionally. In addition, the morbidity of SEPS was significantly lower than that of traditional operations.

Overall, approximately 8% of patients require surgical intervention for CVI. Different options are suitable for different conditions (see below). Careful monitoring of a patient’s cardiac status and vital signs is extremely important. In addition, periodic monitoring of hemoglobin and hematocrit levels yields essential intraoperative data.

Varicose bleeding

Patients with varicose bleeding usually present to an emergency department (ED), where the traditional management is to oversew the involved vessel. Patients who have had significant blood loss may be admitted to the hospital, particularly if the bleeding varicosity is large and if the overlying tissue is friable. Oversewing a vessel almost always results in short-term control, but it can also cause short-term recurrence of hemorrhage because the procedure does nothing to ablate the dilated, superficial, thin-walled vessel that has ruptured.

Variceal hemorrhage is best managed by means of primary sclerotherapy with sodium tetradecyl sulfate. Tretbar reported a series of cases that were successfully treated by means of primary compression sclerotherapy over a 3-year period.[33]

Superficial venous insufficiency

For superficial vein treatment, primary surgery offers a lower rate of early recurrence, whereas sclerotherapy produces fewer complications and offers higher rates of patient satisfaction both early and at follow-up. The lower likelihood of early recurrence after surgical treatment offsets the greater risk of complications.[34, 35]

Vein stripping with ligation of the saphenofemoral junction has long been the most commonly adopted surgical approach in cases of superficial venous insufficiency. At present, it is increasingly being replaced by endovenous ablation techniques such as RFA and EVLT.

The original approach to vein ligation for superficial vein disorders involved removal of the entire GSV system; this approach has largely been supplanted by the stab evulsion technique. In stab evulsion, several 2- to 3-mm incisions are made overlying the GSV at various levels. The vein is dissected from the underlying tissues, and any perforators are ligated. A small hook or blunt needle is used to extract as much of the vein as possible.

Typically, stab evulsion is limited to areas above the knee in the GSV system to avoid damage to the saphenous nerve or sural nerve. This technique is reserved for CVI in which reflux in the saphenous system occurs and causes severe symptoms. For this reason, it is mandatory to establish a diagnosis of reflux preoperatively.

Simple ligation and division of the incompetent vessels is not an effective way of treating failed perforating vessels, because this procedure is associated with a high incidence of early recurrence of reflux when it is applied to the GSV.

Skin grafts do not survive for very long unless the venous insufficiency has been treated, and after the venous insufficiency is ablated, the ulcer usually heals quickly, even without grafting.

Deep venous insufficiency

The decision to operate on a patient with venous obstruction in the deep veins should be made only after a careful assessment of symptom severity and direct measurement of both arm and foot venous pressures. Venography alone is not sufficient, because many patients with occlusive disease have extensive collateral circulation, which renders them less symptomatic. Clot lysis (eg, with tissue plasminogen activator [TPA] or urokinase) and thrombectomy have been tried but have largely been abandoned because of extremely high recurrence rates.

For iliofemoral disease, the operation of choice is a saphenous vein crossover graft. In this procedure, the contralateral saphenous vein is mobilized and divided at its distal end, then tunneled suprapubically and anastomosed to the femoral vein on the diseased side (see the image below). The result is diversion of venous blood through the graft and into the intact contralateral venous system. Because of a relatively high failure rate (20%), ringed polytetrafluoroethylene (PTFE) grafts are used. Long-term patency has not been determined.

Venous insufficiency iliofemoral obstruction (Palm Venous insufficiency iliofemoral obstruction (Palma operation). Saphenous vein from contralateral leg tunneled subcutaneously to femoral vein of affected limb; cumulative patency of 75% at 5 years. Procedure relieves venous claudication but may not heal ulcers or relieve swelling.

For occlusion of the superficial femoral vein, the Husni bypass, described by Warren in 1954 and Husni in 1983,[36] may be considered. In this procedure, the ipsilateral GSV is harvested and used as an in-situ popliteal-femoral vein bypass. Because of its high failure rate (approximately 40%), the Husni bypass is performed infrequently. A minimally invasive technique using stents has been described.[37]

Valvuloplasty is reserved for patients with a congenital absence of functional valves. A phlebotomy is performed, and the valve cusps are plicated. To ensure an adequate result, plicating 20-25% of each cusp is recommended. Addition of a PTFE sleeve around the operating site to maintain valve integrity is routine. When combined with ligation of perforating veins, valvuloplasty yields a superior outcome in 80% of cases after 5 years.

With vein segment transposition, a normally functioning vein that is in close proximity to the diseased vessel is identified. The incompetent vein is then dissected, mobilized, and transposed onto the normal vein distal to a functional valve.

With vein valve transplantation, a valve-containing segment of a competent axillary or brachial vein is mobilized and inserted into either the popliteal or the femoral system. The incompetent segment of the leg vein is excised and replaced with the transplant segment. Allograft or cadaveric vein transplants are being evaluated, with long-term results pending.

Complications

Potential complications of surgical ablation of refluxing veins include the following:

  • Infection

  • Nerve injury (eg, to sural or saphenous nerves)

  • Arterial injury

  • Undesirable cosmetic outcomes

Potential complications of sclerotherapy include the following:

  • Allergic reactions to sclerosants

  • Cutaneous necrosis due to extravasation

  • Inadvertent arterial injection (may cause loss of a limb)

Potential complications of RFA and EVLT include the following:

  • Skin burns

  • Thermal injury to adjacent tissues

  • Inadvertent injury to deep veins

Postprocedural care

Anticoagulation with heparin (or low-molecular-weight heparin) in the immediate postoperative period and long-term prophylaxis with warfarin are recommended.

Observe patients frequently for wound infection after discharge, beginning 1 week postoperatively. Sutures or staples typically stay in 2-4 weeks, depending on the health of the skin at the operative site.

Increased pain or swelling is an indication for repeat duplex ultrasonography to rule out DVT.

Activity

Regular activity is an important ameliorating factor in patients with early or mild venous insufficiency syndrome. Prolonged standing or sitting can aggravate the symptoms of venous insufficiency. Patients with advanced disease do not tolerate activity well.

Walking or running, bicycling, and swimming are excellent activities for patients with an intact and functioning calf muscle pump. Patients with obstructed venous outflow usually experience increased pain and swelling with activity. Patients with muscle pump failure usually have a markedly reduced exercise tolerance because of early leg fatigue.

Prevention

In general, patients with venous insufficiency should avoid prolonged standing or sitting. Correction of the underlying problem prevents progression of the disease.

In patients with early venous insufficiency, progression to overt signs of disease (eg, stasis dermatitis, skin breakdown, and ulceration) can virtually always be prevented with the use of compression hose that provide a pressure gradient of 30-40 mm Hg between foot and knee.

Implications

The importance of addressing CVI resides in the fact that over 2.5 million individuals have this disorder, from which around 20% percent present with venous ulcers as a complication.[21] Therefore, a reduction in the quality of life, exposure to financial constraints, and disability are frequently seen in this type of patient. The estimated annual expenditures dedicated to the management of venous ulcer disease exceeds $1 billion; hence, it is important to reduce the risk factors and increase the therapeutic options that could prevent disease and disability from complications of CVI.

 

Guidelines

Guidelines Summary

The Clinical, Etiology, Anatomic, Pathophysiology (CEAP) classification was developed by an international consensus conference to provide uniformity in the reporting, diagnosing, and treating  CVI.[21]

Clinical classification is as follows:

  • C0 - No visible signs of venous disease
  • C1 - Telangiectases or reticular veins
  • C2 - Varicose veins
  • C3 - Edema without skin changes
  • C4 - Changes in skin and subcutaneous tissue: A = Pigmentation or eczema; B = Lipodermatosclerosis or atrophie blanche
  • C5 - Healed ulcer
  • C6 - Active ulcer

Etiologic classification is as follows:

  • Congenital (ie, Klippel-Trenaunay syndrome)
  • Primary
  • Secondary (ie, postthrombotic syndrome, trauma)
  • No venous cause identified

Anatomic classification is as follows:

  • Superficial
  • Deep
  • Perforator
  • No venous location identified

Pathophysiologic classification is as follows:

  • Reflux
  • Obstruction, thrombosis
  • Reflux and obstruction
  • No venous pathophysiology identified in advanced stages
 

Medication

Medication Summary

No oral medication has yet been proven useful for the treatment of venous disease. Findings of prospective studies have not supported some manufacturers’ claims about the effectiveness of their herbal products and nutritional supplements.

Sclerosing agents that are used to ablate refluxing veins and other anatomic structures can be grouped into several categories, including fatty alcohols (detergents), osmotic agents, and caustic agents. The safest and most widely used sclerosing agents are detergents.

Sclerosing Agents

Class Summary

Sclerosing agents are used for the primary sclerosis of reflux pathways and for the ablation of friable thin-walled veins judged to be at high risk for rupture and hemorrhage.

Sodium tetradecyl sulfate (Sotradecol)

Primary sclerotherapy is the treatment of choice for ablation of refluxing superficial venous circuits in the absence of saphenofemoral junctional reflux. It is also the treatment of choice for ablation of venous bleeding sites and friable thin-walled varices. In general, a 1% concentration is most useful; in larger varicosities, a 3% concentration may be used as a liquid. Foam may be made by agitating a 1:4 mixture of solution and air. When a foamed solution is used, a concentration of 0.25-0.5% is sufficient.

 

Questions & Answers

Overview

What is venous insufficiency?

What is the disease course of untreated venous insufficiency?

What is the goal of treatment for venous insufficiency?

Which three venous systems are affected by chronic venous insufficiency (CVI)?

What is the anatomy of the venous network?

How is the venous anatomy affected by venous insufficiency?

What is the pathogenesis of venous insufficiency?

What is the role of high venous pressures in the pathogenesis of venous insufficiency?

What is the role of ambulation in the pathogenesis of venous insufficiency?

What is the role of venous hypertension in the pathogenesis of chronic venous insufficiency (CVI)?

What is the association between high pressures and vein valve failure in the pathogenesis of venous insufficiency?

What are the sources of high-pressure leakage that cause venous insufficiency?

What is junctional high-pressure disease in venous insufficiency?

What is perforator high-pressure disease in venous insufficiency?

What is important to note about the presentation of venous hypertension and venous insufficiency?

What is the role of poor metabolic clearance in the pathogenesis of venous insufficiency?

How do leg ulcers develop during the development of venous insufficiency?

What factors predict the severity of venous insufficiency?

What causes chronic venous insufficiency (CVI)?

What causes the lower-extremity ulcers associated with venous insufficiency?

What is the etiology of superficial venous insufficiency?

What is the etiology of deep venous insufficiency?

What is Klippel-Trénaunay-Weber (KTW) syndrome and how does it cause venous insufficiency?

What are the signs and symptoms of venous insufficiency in Klippel-Trénaunay-Weber (KTW) syndrome?

Why is surgical treatment of venous insufficiency challenging in patients with Klippel-Trénaunay-Weber (KTW) syndrome?

What are the risk factors of chronic venous insufficiency (CVI)?

What is the prevalence of chronic venous insufficiency (CVI) in the US?

What is the global prevalence of venous insufficiency?

How does the prevalence of venous insufficiency vary by age?

How does the prevalence of venous insufficiency vary by sex?

What are the morbidities associated with venous insufficiency?

What increases the risk of deep venous thrombosis (DVT) due to venous insufficiency?

What is the cause of death in venous insufficiency?

What is the prognosis of venous insufficiency?

What information about venous insufficiency should be given to patients?

Presentation

What are symptoms of venous insufficiency?

What is the significance of varicose veins in the evaluation of venous insufficiency?

How do hormonal changes affect the presentation of superficial venous insufficiency?

What are symptoms of deep venous insufficiency?

How can pain caused by venous insufficiency be relieved?

How can venous insufficiency and arterial insufficiency be differentiated?

What worsens the pain of venous insufficiency?

Where do nonhealing ulcers typically occur in venous insufficiency?

What are the dermatologic manifestations of venous insufficiency?

What are the most common physical signs of venous insufficiency?

What is the significance of swelling in the physical exam of venous insufficiency?

What changes in skin tone and texture are characteristic of venous insufficiency?

What is the appearance of veins in venous insufficiency?

How does venous insufficiency cause nonhealing ulcers?

What are characteristics of ulcers due to venous insufficiency?

What are the limitations of physical exam in the diagnosis of venous insufficiency?

What is the role of the Trendelenburg test in the physical exam for venous insufficiency?

How is the Trendelenburg test performed to assess venous insufficiency?

What does the Trendelenburg test reveal about suspected venous insufficiency?

What are complications of untreated venous insufficiency?

What are the most common sequelae of venous insufficiency?

DDX

What conditions should be included in the differential diagnosis of venous insufficiency?

What are the differential diagnoses for Venous Insufficiency?

Workup

What is the role of lab studies in the diagnosis of venous insufficiency?

What is the role of ultrasonography in the diagnosis of venous insufficiency?

What is the role of ultrasonographic reflux mapping in the evaluation of venous insufficiency?

Which ultrasonography finding suggests severe chronic venous insufficiency (CVI) of the superficial veins?

How is ultrasonography used to diagnose deep venous thrombosis (DVT) caused by venous insufficiency?

What is the role of intravascular ultrasonography in the diagnosis of venous insufficiency?

What is the role of magnetic resonance venography (MRV) in the diagnosis of venous insufficiency?

What is the role of direct contrast venography in the diagnosis of venous insufficiency?

How is direct contrast venography performed to assess reflux in venous insufficiency?

What is the incidence of contrast-induced deep vein thrombosis (DVT) in patients treated for venous insufficiency?

What is the role of air plethysmography in the diagnosis of venous insufficiency?

What is the role of photoplethysmography in the diagnosis of venous insufficiency?

What is the role of outflow plethysmography in the diagnosis of venous insufficiency?

What is the role of physiologic venous function testing in the assessment of venous insufficiency?

What is the venous refilling time (VRT) reference range?

What venous refilling time (VRT) suggests mild and asymptomatic venous insufficiency?

What venous refilling time (VRT) suggests significant venous insufficiency?

What does a finding of venous refilling time (VRT) shorter than 20 seconds indicate in venous insufficiency?

What is the role of maximum venous outflow (MVO) testing in the evaluation of venous insufficiency?

What are the advantages of maximum venous outflow (MVO) testing to assess venous insufficiency?

What is the disadvantage of maximum venous outflow (MVO) testing to assess venous insufficiency?

What is the role of the muscle pump ejection fraction (MPEF) test in the evaluation of venous insufficiency?

How is the muscle pump ejection fraction (MPEF) test performed in the evaluation of venous insufficiency?

What is the significance of muscle pump failure during the evaluation of venous insufficiency?

What is the role of ambulatory venous pressure (AVP) monitoring in the evaluation of venous insufficiency?

Treatment

What are the goals of treatment for venous insufficiency?

What are the treatment options for venous insufficiency?

What are the treatment options for deep venous insufficiency?

What are the treatment options for superficial venous insufficiency?

Which specialist consultations are needed for the treatment of venous insufficiency?

What is the standard approach to treatment of venous insufficiency?

What is the significance of the compression gradient in the treatment of venous insufficiency?

What is the benefit of progressive compression stockings for the treatment of venous insufficiency?

What is the physical therapy approach to venous insufficiency?

Which combination therapy may be effective in the treatment of venous insufficiency?

What is the role of venoablation in the treatment of venous insufficiency?

Which venoablation technique is most effective in the treatment of venous insufficiency?

When is vein ligation indicated for the treatment of venous insufficiency?

When is sclerotherapy indicated for the treatment of venous insufficiency?

How is endovenous laser therapy (EVLT) used to treat venous insufficiency?

How is radiofrequency ablation (RFA) used to treat venous insufficiency?

What are the benefits of subfascial endoscopic perforator surgery (SEPS) for the treatment of venous insufficiency?

What is the basis for selection of surgical intervention in the treatment of venous insufficiency?

How is varicose bleeding treated in venous insufficiency?

What are the surgical options for the treatment of superficial venous insufficiency?

What is the most common surgical intervention for superficial venous insufficiency?

How is vein ligation performed in the treatment of superficial venous insufficiency?

When is ligation contraindicated for the treatment of venous insufficiency?

When is surgery indicated for the treatment of deep venous insufficiency?

What is the treatment of choice for iliofemoral disease in venous insufficiency?

What is the role of Husni bypass in the treatment of venous insufficiency?

What is the role of valvuloplasty in the treatment of venous insufficiency?

How is vein segment transposition used in the treatment of venous insufficiency?

How is vein valve transplantation used in the treatment of venous insufficiency?

What are potential complications of surgical ablation of refluxing veins in venous insufficiency?

What are potential complications of sclerotherapy for the treatment of venous insufficiency?

What are potential complications of radiofrequency ablation (RFA) and endovenous laser therapy (EVLT) for the treatment of venous insufficiency?

What is included in postprocedural care for venous insufficiency?

What activity modifications are needed following treatment for venous insufficiency?

How is venous insufficiency prevented?

What are the implications of risk factor reduction and improved treatment for venous insufficiency?

Guidelines

What is the purpose of the CEAP classification system for chronic venous insufficiency (CVI)?

What are the CEAP clinical classifications of chronic venous insufficiency (CVI)?

What are the CEAP etiologic classifications of chronic venous insufficiency (CVI)?

What are the CEAP anatomic classifications of chronic venous insufficiency (CVI)?

What are the CEAP pathophysiologic classifications of chronic venous insufficiency (CVI)?

Medications

Which medications are used for the treatment of venous insufficiency?

Which medications in the drug class Sclerosing Agents are used in the treatment of Venous Insufficiency?