Chronic Venous Insufficiency

INTRODUCTION

Venous Insufficiency

Robert Weiss, MD; Chief Editor: William D James, MD

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 but may result from valvular incompetence in the high-pressure deep venous system or rarely 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. Most commonly, congenitally weak vein walls may 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).

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 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. 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 when during ambulation. The hydrostatic pressure increases during and immediately after ambulation, which cause venous congestion.

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.

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.2 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.

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 men over 50 years of age, the incidence is 20%, compared with 50% in similarly aged women.3

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 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.4 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

Superficial venous insufficiency with skin changes.

Nonhealing ulcerations 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 the superficial venous system. Greater than 80% of varicose veins seen on the leg are caused by venous insufficiency or a leaky valve in the great saphenous vein, 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 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.

emedicine.medscape.com/article/1085412 Sep 25, 2020

Peripheral Vascular Disease

What is peripheral vascular disease (PVD)?

Peripheral vascular disease (PVD) is a slow and progressive circulation disorder. It may involve disease in any of the blood vessels outside of the heart and diseases of the lymph vessels - the arteries, veins, or lymphatic vessels. Organs supplied by these vessels such as the brain, heart, and legs, may not receive adequate blood flow for ordinary function. However, the legs and feet are most commonly affected, thus the name peripheral vascular disease.

Conditions associated with PVD that affect the veins include deep vein thrombosis (DVT), varicose veins, and chronic venous insufficiency. Lymphedema is an example of PVD that affects the lymphatic vessels.

When PVD occurs in the arteries outside the heart, it may be referred to as peripheral arterial disease (PAD). However, the terms peripheral vascular disease and peripheral arterial disease are often used interchangeably. In the US, 10 million people have peripheral artery disease. PAD occurs in 5 percent of adults older than 50 and in 20 percent of adults older than 70. It is frequently found in people with coronary artery disease, because atherosclerosis, which causes coronary artery disease, is a widespread disease of the arteries.

Conditions associated with PAD may be occlusive (occurs because the artery becomes blocked in some manner) or functional (the artery either constricts due to a spasm or expands). Examples of occlusive PAD include peripheral arterial occlusion and Buerger's disease (thromboangiitis obliterans). Examples of functional PAD include Raynaud's disease and phenomenon and acrocyanosis.

What causes peripheral vascular disease?

PVD is often characterized by a narrowing of the vessels that carry blood to the leg and arm muscles. The most common cause is atherosclerosis (the buildup of plaque inside the artery wall). Plaque reduces the amount of blood flow to the limbs and decreases the oxygen and nutrients available to the tissue. Clots may form on the artery walls, further decreasing the inner size of the vessel and potentially blocking off major arteries.

Other causes of peripheral vascular disease may include trauma to the arms or legs, irregular anatomy of muscles or ligaments, or infection. Persons with coronary artery (arteries that supply blood to the heart muscle) disease are frequently found to also have peripheral vascular disease.

What are conditions associated with peripheral vascular disease?

The term peripheral vascular disease encompasses several different conditions. Some of these conditions include, but are not limited to, the following: atherosclerosis - the build-up of plaque inside the artery wall. Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin. The artery wall then becomes thickened and loses its elasticity.

Symptoms may develop gradually, and may be few, as the plaque builds up in the artery. However, when a major artery is blocked, a heart attack, stroke, aneurysm, or blood clot may occur, depending on where the blockage occurs.

Buerger's disease (thromboangiitis obliterans) - a chronic inflammatory disease in the peripheral arteries of the extremities leading to the development of clots in the small- and medium-sized arteries of the arms or legs and eventual blockage of the arteries. Buerger's disease most commonly occurs in men between the ages of 20 and 40 who smoke cigarettes. Symptoms include pain in the legs or feet, clammy cool skin, and a diminished sense of heat and cold.

Chronic venous insufficiency

A prolonged condition in which one or more veins do not adequately return blood from the lower extremities back to the heart due to damaged venous valves. Symptoms include discoloration of the skin and ankles, swelling of the legs, and feelings of dull aching pain, heaviness, or cramping in the extremities. Deep vein thrombosis (DVT) - a clot that occurs in a deep vein, and has the potential to dislodge, travel to the lungs, occlude a lung artery (pulmonary embolism), and cause a potentially life-threatening event. It is found most commonly in those who have undergone extended periods of inactivity, such as from sitting while traveling or prolonged bed rest after surgery. Symptoms may be absent or subtle, but include swelling and tenderness in the affected extremity, pain at rest and with compression, and raised vein pattern. Raynaud’s phenomenon - a condition in which the smallest arteries that bring blood to the fingers or toes constrict (go into spasm) when exposed to cold or as the result of emotional upset. Raynaud's most commonly occurs in women between the ages of 18 and 30. Symptoms include coldness, pain, and pallor (paleness) of the fingertips or toes. Thrombophlebitis - a blood clot in an inflamed vein, most commonly in the legs, but it can also occur in the arms. The clot can either be close to the skin (superficial thrombophlebitis) or deep within a muscle (deep vein thrombosis). It may result from pooling of blood, venous wall injury, and altered blood coagulation. Symptoms in the affected extremity include swelling, pain, tenderness, redness, and warmth. Varicose veins - dilated, twisted veins caused by incompetent valves (valves that allow backward flow of blood) allowing blood to pool. It is most commonly found in the legs or lower trunk. Symptoms include bruising and sensations of burning or aching. Pregnancy, obesity, and extended periods of standing intensify the symptoms.

What are the risk factors for peripheral vascular disease?

A risk factor is anything that may increase a person's chance of developing a disease. It may be an activity, diet, family history, or many other things. Risk factors for peripheral vascular disease include factors which can be changed or treated and factors that cannot be changed.

Risk factors that cannot be changed include the following:

•  Age (especially older than 50)

•  History of heart disease

•  Male gender

•  Diabetes mellitus (type 1 diabetes)

•  Postmenopausal women

•  Family history of dyslipidemia (elevated lipids in the blood, such as cholesterol), hypertension, or peripheral vascular disease

Risk factors that may be changed or treated include:

•  Coronary artery disease

•  Impaired glucose tolerance

•  Dyslipidemia

•  Hypertension (high blood pressure)

•  Obesity

•  Physical inactivity

•  Smoking or use of tobacco products

Those who smoke or have diabetes mellitus have the highest risk of complications from peripheral vascular disease because these risk factors also cause impaired blood flow.

What are the symptoms of peripheral vascular disease?

Approximately half the people diagnosed with peripheral vascular disease are symptom free. For those experiencing symptoms, the most common first symptom is intermittent claudication in the calf (leg discomfort described as painful cramping that occurs with exercise and is relieved by rest). During rest, the muscles need less blood flow, so the pain disappears. It may occur in one or both legs depending on the location of the clogged or narrowed artery.

Other symptoms of peripheral vascular disease may include:

•  Changes in the skin, including decreased skin temperature, or thin, brittle shiny skin on the legs and feet

•  Diminished pulses in the legs and the feet

•  Gangrene (dead tissue due to lack of blood flow)

•  Hair loss on the legs

•  Impotence

•  Non-healing wounds over pressure points, such as heels or ankles

•  Numbness, weakness, or heaviness in muscles

•  Pain (described as burning or aching) at rest, commonly in the toes and at night while lying flat

•  Pallor (paleness) when the legs are elevated

•  Reddish-blue discoloration of the extremities

•  Restricted mobility

•  Severe pain

•  Thickened, opaque toenails

The symptoms of peripheral vascular disease may resemble other conditions. Consult your physician for a diagnosis.

How is peripheral vascular disease diagnosed?

In addition to a complete medical history and physical examination, diagnostic procedures for peripheral vascular disease may include any, or a combination, of the following:

Angiogram - an x-ray of the arteries and veins to detect blockage or narrowing of the vessels. This procedure involves inserting a thin, flexible tube into an artery in the leg and injecting a contrast dye. The contrast dye makes the arteries and veins visible on the x-ray.

Ankle-brachial index (ABI) - a comparison of the blood pressure in the ankle