Venous Insufficiency

Updated: Oct 22, 2018

 Author: 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 (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.

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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.
 View Media Gallery

Perforating veins of
lower leg.

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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
becomes turbulent, permitting platelets to remain in valve sinus. This forms nidus of
thrombus.

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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) patients with only varicose veins, (c) patients with incompetent
perforator veins, and (d) patients with deep and perforator incompetence.

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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.

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.

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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.

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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.

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 Chronic venous stasis ulcer.

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Venous stasis ulcer and surrounding dystrophic

tissue.

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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.

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

 Allergic Contact Dermatitis

 Basal Cell Carcinoma

 Cellulitis

 Cutaneous Squamous Cell Carcinoma

 Dermatologic Manifestations of Cardiac Disease

 Dermatologic Manifestations of Renal Disease

 Erysipelas

 Generalized Essential Telangiectasia

 Genetics of Klippel-Trenaunay-Weber Syndrome

 Stasis Dermatitis

 Traumatic Ulcers

 Varicose Veins and Spider Veins

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 veins.

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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]

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 (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.

View Media Gallery

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 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 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)

 View full drug information

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.

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