AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 caused by valvular incompetence in the high-pressure deep venous system, low-pressure superficial venous system, or both. Untreated venous insufficiency in the deep or superficial system causes a progressive syndrome involving pain, swelling, skin changes, and eventual tissue breakdown.

Deep venous insufficiency occurs when the valves of the deep veins are damaged as a result of deep venous thrombosis (DVT). With no valves to prevent deep system reflux, the hydrostatic venous pressure in the lower extremity increases dramatically. This condition is often referred to as a postphlebitic syndrome.

Superficial venous incompetence is the most common form of venous disease. 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.

The valves in superficial veins can fail for a variety of reasons. Direct injury or superficial phlebitis may cause primary valve failure. Congenitally weak vein walls may dilate under normal pressures to cause secondary 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).

Most cases of superficial vein valve failure occur after a single point of high-pressure leakage develops between the deep system and the superficial system. High pressure causes 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. The 2 major sources of high-pressure leakage from the deep veins to the superficial system are junctional valve failure and perforator valve failure.

Junctional high-pressure disease most often results from failure of the primary valve at the junction between the greater saphenous vein 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 short saphenous vein 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.

Pathophysiology

When venous valves are working correctly, every movement of the leg causes blood to be pumped inward and upward past a series of valves. 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. 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 when during ambulation. The hydrostatic pressure increased during and immediately after ambulation.

High venous pressure is directly responsible for many aspects of venous insufficiency syndrome, including edema, tissue protein deposition, perivascular fibrin cuffing, red cell extravasation, impaired arterial inflow, and other locally mediated disturbances.

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.

The poor clearance of lactate, carbon dioxide, and other products of cellular respiration also contribute 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 transit time 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 greater and short saphenous veins and popliteal vein add to less than 10 mL/s, progressive visible stasis dermatitis and ulceration do not occur. If the sum is greater 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.

Chronic nonhealing wounds of the lower extremity have many different potential causes, but most chronic lower-extremity ulcers are of venous etiology. Most 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.

Frequency

United States

Published estimates of the prevalence of varicosities range from 7-60% in the adult population, with most studies demonstrating clinical varicose reflux in about 40% of the population.

International

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

Mortality/Morbidity

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).

• 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.
• 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 mortality rate in this group exceeds 1 in 3.
• Bleeding from lower-extremity varicosities can be fatal. Twenty-three such fatalities were reported in England and Wales in 1971, 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 often is managed incorrectly (see Medical Care).

Sex

• The incidence and prevalence of deep and superficial venous disease depend on the age and sex of the population, but the prevalence in women exceeds that of men at any age.
• In younger men, the incidence is less than 10%, compared with 30% in similarly aged women. In older men, the incidence is 20%, compared with 50% in similarly aged women

Age

The prevalence of venous insufficiency increases with age.

• 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 Basle III study included a large number of children aged 10-12 years at one point and again 4 years later. The study 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 perforators and truncal varicosities, which appear several years later.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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, while almost 50% complain of episodic symptoms.
• Patients with deep system insufficiency nearly always are symptomatic. Leg aching, heaviness, and soreness are the most common subjective symptoms.
• 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 its severity.
• 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 arterial insufficiency is the opposite to the behavior of the pain caused by venous insufficiency.
• • The pain of arterial insufficiency usually is worse with walking and worse when the legs are elevated.
  • Cold tends to aggravate the symptoms, 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.

Physical

The visual appearance of the lower extremities is a useful but not always reliable guide to the peripheral venous condition. Clinical findings in venous disease are also common to many other entities that affect the lower extremities. 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. The Trendelenburg test is traditionally part of the physical examination and may be helpful in making the differential diagnosis (see Procedures).

• Swelling may result from acute venous obstruction (as in 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 the 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 due to severe venous hypertension (a so-called venolymphatic syndrome).
• Skin discoloration may be a sign of venous stasis, arterial insufficiency, chronic infection, prior injury, or a host of other conditions (see Image 1).
• Nonhealing ulcerations (see Image 2) may be due to deep or superficial venous insufficiency. Other causes include arterial insufficiency, rheumatologic disorders, local trophic effects, unrecognized cancer, or other more exotic causes.
• 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
• 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.
• Normal veins are visibly distended at the foot and ankle and, occasionally, in the popliteal fossa.
• • Normal veins are usually 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.
• Darkened, discolored, and stained skin is often a sign of chronic venous stasis, particularly 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 length of the greater saphenous vein and all of the perforating veins attached to it.
  • 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.

Causes

The sequelae of venous insufficiency are caused by reflux through superficial or deep veins or by venous outflow obstruction. Most cases of venous insufficiency are related to reflux through the superficial veins.

• Superficial venous insufficiency is most often caused by the failure of a valve in a perforating vein that connects the superficial venous system to the deep venous system.
• • 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 due to direct trauma, thrombosis, hormonal changes, or chronic environmental insult (eg, prolonged standing).
• Deep venous insufficiency can be due to congenital valve or vessel abnormalities, but DVT is the most common cause of deep system valve injury.
• A less common cause of venous insufficiency is Klippel-Trenaunay-Weber (KTW) syndrome, which involves port-wine stains, varicose veins, and bony or soft-tissue hypertrophy. Patients with pure Klippel-Trenaunay syndrome have only venous involvement, whereas those with the Parkes Weber variant also have arteriovenous malformations.
• • Like those of other forms of venous insufficiency, the capillary hemangiomas (port-wine stains) of KTW syndrome can lead to local skin breakdown and ulceration, bleeding, and secondary infection. This can occur in any organ system of the body.
  • The KT, or sciatic vein, is a large superficial vessel that is present during fetal development, but it 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.
  • Surgical attempts to treat the abnormal refluxing veins in KTW syndrome are fraught with peril because postoperative worsening of venous abnormalities is common.
  • 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.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Hepatic insufficiency
Lymphedema

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab 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 the 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 KTW disease because they can develop consumptive thrombocytopenia.

Imaging Studies

• Duplex ultrasonography is the study of choice for the evaluation of venous insufficiency syndromes. A duplex sonogram is the name given to a real-time B-mode (2-dimensional) sonographic image to which continuous-wave (CW) Doppler information is added. With this addition, the investigator can see a plot of flow velocity over time and also listen to the sound of the flow in the area of interest.
• • 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. With the latest-generation machines, the shade of the color may reflect the flow velocity (in the Doppler mode) or the flow volume (in the power Doppler mode).
  • Color-flow systems are easier to use than gray-scale systems, but the addition of color-coded Doppler information has not been shown to increase the sensitivity or specificity of the B-mode scan in the hands of a truly skilled examiner.
  • 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.
  • When used to diagnose DVT, ultrasonography is not as sensitive or specific as contrast venography. Ultrasonography may fail to depict venous thromboembolism in as many as 40% of cases, especially that in the iliac veins, the pelvic veins, the transition zone between the lower thigh and the knee, and the deep veins below the knee. Nonetheless, duplex ultrasonography is the initial diagnostic imaging modality of choice in patients with suspected DVT.
• 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 with other modalities. MRV is particularly useful because it can help in the detection of previously unsuspected nonvascular causes of leg pain and edema when the clinical presentation erroneously suggests venous insufficiency or venous obstruction.
• Direct contrast venography is a labor-intensive and invasive imaging technique. In most centers, duplex sonography has replaced this direct contrast venography in the routine evaluation of venous disease. However, the technique remains useful in difficult or confusing cases.
• • An intravenous 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.

Other 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).
• 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. Patients have an abnormally fast VRT of 20-40 seconds, which reflects retrograde venous flow through failed valves in superficial and/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 venous refilling time of less than 20 seconds is markedly abnormal and due 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. If the refilling time is less than 10 seconds, venous ulcerations are so common that they are considered virtually inevitable.
• The MVO test is used 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.
• • The advantages of MVO testing are that it is a functional test rather than an anatomic test, and it is sensitive to significant intrinsic or extrinsic venous obstruction due to any cause at almost any level.
  • MVO can be used to detect obstructing thrombus in the calf veins, the iliac veins, and the vena cava, where ultrasonography and venography are insensitive.
  • MVO can also be used to detect venous obstruction due to extravascular hematomas, tumors, and other extrinsic disease processes.
  • The disadvantage of the test 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.
• The MPEF test is used to detect failure of the calf muscle pump to expel blood from the lower leg.
• • MPEF 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.

Procedures

• The Trendelenburg test is a traditional physical examination maneuver 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 the Trendelenburg 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 greater saphenous vein is manually occluded just below the saphenofemoral junction at the groin.
  • The patient stands with the occlusion still in place. 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.

TREATMENT

Section 6 of 11  

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• Medication
• Follow-up
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Medical Care

Venous insufficiency is neither uncommon nor benign. Treatment is aimed at ameliorating the symptoms and, whenever possible, at correcting the underlying abnormality. 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; an incompetent vessel has already proved itself unnecessary because it is carrying venous blood in a retrograde direction.

Graduated compression is the cornerstone of the modern treatment of venous insufficiency. Properly fitted gradient compression stockings provide 30-40 or 40-50 mm Hg of compression at the ankle, with gradually decreasing compression at more proximal levels of the leg. This amount of gradient 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, with worsening of 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 one pair of gradient compression hose with a 30-40-mm Hg gradient that is calf-high (or thigh-high with waist attachment or panty hose style), with refills as needed.

All methods of venoablation are effective. Once the overall volume of venous reflux is reduced below a critical threshold by any mechanism, venous ulcerations heal, and patient symptoms are resolved.

• Deep vein valvular incompetence is difficult to treat. Valvuloplasty is occasionally successful, but the incidence of postoperative DVT is high. Venous bypass is successful in select patients. External vein valve banding devices (eg, Venocuff device) and thermally induced collagen shrinkage procedures (eg, Closure procedure) are being investigated in clinical trials. At this time, the restoration of valvular function to incompetent deep veins remains an important focus of research for vascular physicians.
• Patients with varicose bleeding usually present to an emergency department, 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 the 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 Sotradecol. Tretbar reported a series of cases that were successfully treated by means of primary compression sclerotherapy over a 3-year period. Sclerotherapy is performed by injecting or infusing a sclerosing substance into the refluxing vessel to produce endothelial destruction and fibrosis of the treated vessel.
• Endovenous laser therapy (EVLT) is a newer procedure with excellent early (4-y) results and an extremely low rate of complications, but the duration of follow-up is not yet long enough to provide information about mid-term and long-term results. 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.
• Radiofrequency ablation (RFA) is a relatively new procedure that has a low rate of complications. It has produced excellent results that have been confirmed after several years of follow-up. RFA is performed by passing a special radiofrequency (RF) catheter from the knee to the groin and by heating the vessel until thermal injury causes shrinkage. The process is repeated every few centimeters along the course of the vein. Initial thermal injury is followed by fibrosis of the treated vessel.
• Antibiotics rarely are useful in patients with venous ulcerations.

Surgical Care

The primary goal of surgical therapy is to improve the venous circulation by correcting venous insufficiency by removing the major reflux pathways.

Traditional mechanisms of venoablation include ligation with stripping, simple ligation and division, sclerotherapy (with or without ligation), and stab avulsion (with or without ligation). These techniques offer roughly equivalent rates of technical success (although some disagreement exists between the medical and the surgical literature as to the prevalence and timing of varicose recurrences). Two newer methods of venoablation include RFA and EVLT.

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 relatively higher incidence of complications associated with surgery is offset by the relatively lower likelihood of early recurrence. As yet, no treatment for deep venous insufficiency has been proven both safe and effective. All current surgical procedures are experimental, or they have a low success rate and a high complication rate.

• Vein stripping with ligation of the saphenofemoral junction is the most common surgical approach in cases of superficial venous insufficiency.
• Saphenofemoral ligation may be performed in combination with sclerotherapy or with microincision phlebectomy.
• Simple ligation and division of the incompetent vessels is an effective way to treat failed perforating vessels, but this procedure is associated with a high incidence of the early recurrence of reflux when it is applied to the greater saphenous vein.
• Skin grafts do not survive long unless the venous insufficiency has been treated, and after the venous insufficiency is ablated, the ulcer usually heals quickly, even without grafting.

Consultations

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.

Activity

Regular activity is an important ameliorating factor in patients with early or mild venous insufficiency syndrome. Patients with advanced disease do not tolerate activity well.

• Prolonged standing or sitting can aggravate the symptoms of venous insufficiency.
• 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.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Drug Category: Sclerosing agents

These 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.

FOLLOW-UP

Section 8 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Patients who have had significant blood loss from a ruptured varicosity may be admitted to the hospital, particularly if the bleeding varicosity is large and if the overlying tissue is friable.

Further Outpatient Care

• Patients with venous insufficiency syndromes should wear compression stockings unless they also have arterial insufficiency or unless they cannot tolerate the stockings for some other reason.
• Increased pain or swelling is an indication for repeat duplex ultrasonography to rule out DVT.

Deterrence/Prevention

• Patients 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 such as stasis dermatitis, skin breakdown, and ulceration can virtually always be prevented with the use of gradient compression hose with a 30- to 40-mm Hg gradient between foot and knee.

Complications

• Common sequelae of venous insufficiency include pain and paresthesias, stasis dermatitis, nonhealing venous ulcers, hemorrhage, recurrent cellulitis, deep and superficial thrombophlebitis, pulmonary embolism, and death. 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. Chronic pain, swelling, recurrent cellulitis, and chronic nonhealing leg ulcers (ulcer cruris) are the most common sequelae, but they are not the most severe.
• Complications of untreated venous insufficiency
• • Recruitment of veins (High venous pressures may cause the recruitment of adjacent normal veins into refluxing circuits.)
  • Deep venous thrombosis
  • Pulmonary embolism
  • Venous ulceration
  • Secondary lymphedema
• Potential complications of surgical ablation of refluxing veins
• • Infection
  • Nerve injury
  • Arterial injury
  • Undesirable cosmetic outcomes
• Potential complications of RFA and EVLT
• • Skin burns
  • Thermal injury to adjacent tissues
  • Inadvertent injury to deep veins
• Potential complications of sclerotherapy
• • Allergic reactions to sclerosants
  • Cutaneous necrosis due to extravasation
  • Inadvertent arterial injection (may cause loss of a limb)

Prognosis

• 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.
  • Patients have an increased lifetime risk of DVT and pulmonary embolism.
• 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.
• Venous insufficiency syndromes can also lead to death from thromboembolism or hemorrhage.

Patient Education

• Patients should be instructed to wear compression hose as much as tolerated.
• Patients should avoid prolonged standing or sitting. Walking or calf-muscle exercises should be performed at regular intervals.
• For patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education articles Blood Clot in the Legs, Varicose Veins, and Phlebitis.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Missing the diagnosis of DVT
• Missing the diagnosis of superficial venous thrombosis
• The misdiagnosis of stasis dermatitis as contact dermatitis
• The misdiagnosis of venous insufficiency as arterial insufficiency
• Misdiagnosing venous disease often is lethal when venous thrombosis is involved, but other errors are rarely disastrous because nonthrombotic venous disease is slowly progressive: morbidity results in a decreased quality of life and an inability to work, but death is rare.

Special Concerns

• Pregnancy is an important causative factor in the development of peripheral venous insufficiency.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Superficial venous insufficiency with skin changes.
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Media type:  Photo

Media file 2:  Ulcer due to venous insufficiency.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Bonnetblanc JM. Leg ulcerations: a clinical appraisal. Eur J Dermatol. May-Jun 2005;15(3):127-32. [Medline].
• Chiesa R, Marone EM, Limoni C, et al. Chronic Venous Insufficiency in Italy: The 24-cities Cohort Study. Eur J Vasc Endovasc Surg. Jul 8 2005;[Medline].
• Coon WW, Willis PW 3rd, Keller JB. Venous thromboembolism and other venous disease in the Tecumseh community health study. Circulation. Oct 1973;48(4):839-46. [Medline].
• Diehm C, Allenberg JR. Color Atlas of Vascular Diseases. New York, NY: Springer Publishing;1999:1-396.
• Feied CF. Peripheral venous disease. In: Rosen and Barkin, eds, Emergency Medicine Principles and Practice. Vol 3. 4th ed. St. Louis, Mo: Mosby; 1998:. Chap 107.
• Feied CF. Deep vein thrombosis: the risks of sclerotherapy in hypercoagulable states. Semin Dermatol. Jun 1993;12(2):135-49. [Medline].
• Goldman MP. Sclerotherapy: Treatment of Varicose and Telangiectatic Leg Veins. 2nd ed. St. Louis, Mo: Mosby; 1995:. 1-519.
• Racette S, Sauvageau A. Unusual sudden death: two case reports of hemorrhage by rupture of varicose veins. Am J Forensic Med Pathol. Sep 2005;26(3):294-6. [Medline].
• Weiss RA, Feied CF, Weiss MA. Vein Diagnosis & Treatment: A Comprehensive Approach. New York, NY: McGraw-Hill; 2001:. 1-304.
• Zimmet SE. Venous leg ulcers: modern evaluation and management. Dermatol Surg. Mar 1999;25(3):236-41. [Medline].

Article Last Updated: Sep 14, 2005