there existed an underestimation of the importance and prevalence of occlusive disease in the

pathophysiology of CVI.152–154 The hemodynamic result is elevated IV pressure noted clinically as pain

especially after exercise.152 If the deep system is primarily involved, the increased pressure generated

with each calf compression may impact the perforating veins resulting in valvular malfunction and lead

to venous hypertension in the superficial system and its capillary network. Asymptomatic primary iliac

venous compression is quite common with intraluminal (27 ± 5%) and varying degrees of external

compression (66% to 88%) observed in the general population.155–160 Left common iliac vein

compression by the right common iliac artery, as well as external iliac vein compression from the

internal iliac artery on either side, and variations thereof have been described.159,161 It has been

suggested that the nonthrombotic iliac stenosis is a “permissive lesion” not clinically significant until

other components of the lower extremity venous circulation fail.162 The good results of iliac vein

stenting in patients with CVI, even in the presence of untreated reflux, demonstrate the impact that

eliminating proximal obstruction has on improving overall venous hemodynamics. In one of the largest

experiences treating ileofemoral venous occlusive disease involving nearly 1,000 patients, compression

of the common iliac vein was seen in 36%, external iliac vein in 18%, and both sites in 46% of limbs.162

Of these patients, 53% of limbs had nonthrombotic compressive lesions (absent history of DVT, no

venographic or ultrasound findings indicating previous DVT); 40% had postthrombotic obstruction; and

7% had a combined etiology. Furthermore, 20% of the patients were men and 25% of the symptomatic

lower limbs were on the right side. Intraluminal webs from repetitive trauma have been reported in

14% to 30% of symptomatic cases of May–Thurner syndrome.161 Extrinsic compression of the iliac and

pelvic veins may also be caused by tumor, fibrosis, or infection. Contents of a femoral hernia can crush

the femoral vein, as can soft tissue tumors of the thigh. Arterial aneurysms can impinge on the femoral

vein. The popliteal vein can be obstructed by a popliteal aneurysm or Baker cyst.125 Aplasia of the vein

or tumors of the vein wall have been described.125,163 DVT is associated with inflammation and

thrombus resolution resulting in external vein wall scarring with stiffening and thickening, as well as

intraluminal recannulation with webs and bands. The venous valves are generally incorporated in the

scarring process leading to even more occlusive debri within the lumen. It is a common cause of venous

occlusive disease due to its rather high prevalence and can involve any part of the venous system.

Valvular insufficiency occurs throughout the lower extremity venous systems. It has been estimated to

account for 85% of symptomatic CVD cases with a 70% incidence of primarily superficial and 30%

primarily deep venous insufficiency, but these observations were likely influenced by the lack of

recognizing associated occlusive disease as a contributing or sole factor in the symptoms noted.153,154

Duplex imaging studies suggest that patients with minimal symptoms tend to have isolated superficial

reflux while those with edema, skin changes, and past or present ulcers have an increasing presence of

perforator and deep disease. In those with more advanced venous disease, reflux alone is observed in

80%, reflux and obstruction in 17%, and only 29% had obstructive disease alone.164,165 The presence of

obstructive and reflux disease had the worse prognosis for the development of skin changes.166 No

matter the clinical stage, the superficial system is most commonly affected (90%) with GSV involvement

in 70% to 80%, SSV in 15% to 20%, and nonsaphenous veins in approximately 10%. The deep veins are

involved in about 30% and perforator veins in about 20%.164,165 Those with the most severe sequelae of

venous disease have superficial reflux in 74% to 93% with 17% to 54% having only superficial

disease.167–171 In such patients, 50% were noted to have superficial ± perforator disease and less than

10% had isolated deep venous reflux.170–173 In those patients with venous ulcers, two vein systems were

involved in 50% to 70% of patients, and all three systems were involved in 16% to 50% of patients.

Since these duplex imaging studies mainly involve imaging of the lower extremity veins, the influence

of proximal venous occlusive disease may well be underestimated. Reflux allows the transmission of

high venous pressures to the lower leg when standing that cannot be relieved by exercise. Primary

valvular insufficiency is rarely a consequence of congenital absence of valves.174 There are predisposing

genetic factors that can lead to primary disease including Klippel–Trenaunay syndrome, FOXC2 gene

mutation, desmulin dysregulation, the Ehlers-Danlos syndrome, and a CADASIL gene mutation, to name

a few, but these do not reflect the typical patient.175,176 The muscle cell dilating effect of estrogens may

explain the genesis of varicose veins noted in the first trimester of pregnancy. Prolonged exposure to

high venous pressures can cause vein dilation as occurs from an arteriovenous fistula or occupations

requiring prolonged periods of standing. For our standard patient, venous valve prolapse (elongated,

floppy valves) and defects in the vein wall that cause the valve ring to dilate results in malfunctioning

valve cusps with retained valve architecture.177,178 Whether the vein wall changes precede valve

insufficiency or the valve insufficiency causes wall distension and wall changes is less clear.46,175 There

2805

are some data to suggest that sustained local venous hypertension might affect the local venous

microcirculation. Roughly 50% of deep vein valvular dysfunction occurs secondary to DVT whereas the

remainder appears to be of a primary etiology with a 10% to 20% variance, depending on the clinical

experience being reported.153,179–181 Inflammation and thrombosis associated with DVT tend to cause

valve scarring, whether or not recanalization is complete, leaving a damaged valve architecture in

contradistinction to primary valvular insufficiency. This classic differentiation between “primary”

pathology and “secondary” (or postthrombotic) pathology does not clearly exist when subjected to

direct observation of the veins and valves at surgery. In fact, the two conditions can be present in the

same patient as noted some 20 years ago.182 In these cases, the vein wall is thickened and/or fibrotic at

the valve station or there is thickening of the valve cusps and/or intima. Pathologic study of 11 such

veins demonstrated clear postthrombotic changes in 6, but phlebosclerosis of a nonthrombotic origin in

the remaining 5.183 Clearly, preservation of a normal valve architecture can be explained if primary

reflux and sustained high pressure on the wall are the cause of the changes noted. Another theory is that

rapid resolution of acute thrombi, an event known to occur, may have allowed these valves to escape

damage or the valve itself may not have been directly involved in the thrombotic process.184 The

fibrotic process involves only the vein wall and the valve cusps become floppy by virtue of a decrease in

wall diameter resulting from a thickened, noncompliant vein wall.183 The valve remains architecturally

intact and can be repaired surgically.

There can be failure of calf muscle pump function. The pump becomes unable to generate the force

needed to eject blood from the leg while standing, resulted in sustained venous hypertension. Patients

with muscle disuse (e.g., paraplegia, traumatic injury, elderly or bedridden patients) may not have

sufficient muscle for effective exercise. Pathologic conditions that result in muscle fibrosis (e.g.,

muscular dystrophy, multiple sclerosis) can destroy the calf muscle pump. Thrombus and scarring in the

gastrocnemius and soleal veins can prevent blood from entering the pump resulting in a deficient

volume for ejection with contraction. Calf pump function and ankle range of motion are progressively

diminished with increasing severity of CVI.185–188 Physical conditioning improved both pump function

and muscle strength in a small, RCT, demonstrating the influence the pump can have on the lower

extremity.189 With the exception of muscle rehabilitation, very little can be offered to patients with

some of these disorders.

Regardless of the etiology, the sequelae of venous hypertension/stasis are changes observed in the

lower leg skin and subcutaneous tissues, the end organ. Originally, ischemia from various causes was

considered the etiology of the damage noted in the lower leg.190 More recent observations suggest that

far from being simply an ischemic event, the end-organ response to venous hypertension is highly

dynamic. The final answer is likely to involve a complex interaction of multiple factors that favor either

continued destruction or the ultimate healing of the ulcer. Leukocytes, the extracellular matrix,

fibroblasts, and a host of other factors are recruited to heal the early endothelial injury and the more

delayed soft tissue injury.190 In fact, current belief holds that the fundamental basis for CVD and

ulceration is inflammation within the venous microcirculation when subjected to increased hydrostatic

pressure.191 The soft tissue injury may result in a chronic ulcer that requires growth factors to force the

process to healing.192 Research remains active in this component of venous pathophysiology. An

excellent review is available for further information on the current understanding of basis venous

pathophysiology.193

Clinical Signs and Symptoms

Venous disease presents in many ways. A telangiectasia, spider vein, is a confluence of dilated

intradermal venules less than 1 mm in caliber. A reticular vein is a dilated bluish subdermal vein,

usually 1 mm to less than 3 mm in diameter and usually tortuous. These venous abnormalities may or

may not be accompanied by a larger, more deeply located, pathologic vein.

Hereditary varicose veins usually appear during the second decade of life. If the varicosities are due

to a secondary etiology (e.g., thrombosis, trauma), they often present several years after the inciting

event. These veins appear alone or in clusters as dilated, often bluish, serpentine, and palpable

protrusions of branches of the GSV, SSV, or collateral veins lying beneath the skin within the

subcutaneous tissues. Varicose veins generally measure 3 or more millimeters in diameter when

measured in the upright position.194 One finding thought to be an early sign of advanced disease is

corona phlebectatica that is a fan-shaped pattern of small intradermal veins located around the ankle or

doral foot (also called ankle flare or malleolar flare).126,194 If the varicose veins observed are the result

of proximal disease, such as pelvic reflux or obstruction; the location of the varicosities may be scrotal,

2806

perineal, vulvar or posterior/lateral in the lower extremity.126

Symptoms may be those associated with any type of CVD and are described as pain, edema,

hyperpigmentation, stasis dermatitis or eczema, and/or venous ulcers. These changes often occur in the

“gaiter” area just above the medial malleolus. Important perforating veins lay in this area. The observed

hyperpigmentation is thought to result from extruded red blood cells that are degraded by macrophages

leaving hemosiderin deposits. Less definable but described symptoms of CVD include tingling, burning,

muscle cramping, a sensation of throbbing or heaviness, itching, restless or tiredness of the legs, and

fatigue.195 They are more specific indicators of venous disease if made worse with standing and heat

and if relieved by rest and leg elevation.

Venous claudication is a pain syndrome experienced when walking and is associated with cyanosis, a

sensation of increased swelling, and increased prominence of the superficial veins, which is relieved

with rest in combination with elevation of the extremity.152,196,197 It may be so severe in rare cases that

amputation is requested.198 The most severe form is observed when venous incompetence is associated

with obstruction and when the obstructive process is in a more proximal locale.199

4 Critical to patient management and treatment evaluation is an accurate classification of the disease

at any given time. Each patient should be stratified according to the clinical picture, the etiology, the

anatomic distribution, and the pathophysiology (CEAP) classification system (Table 98-2).200 This

classification system helps the physician define the venous disease so that a focused and appropriate

management strategy can be formulated. An extension of the clinical classification system, the Venous

Clinical Severity Score, is available to quantify the extent of venous disease and, therefore, to evaluate

the patient’s clinical response to treatment (Table 98-3).201–203 The anatomic and pathophysiologic

improvement following a treatment of venous disease can be scored using the Venous Segmental

Disease Score.202 While the Venous Disability Score provides some information of what a person can do

while afflicted with venous disease.202 QOL surveys have been developed specifically for patients with

venous disease to help determine the impact of the disease on the patient’s life and the effect therapy

has on the patient’s overall well-being.126,193,204–208 Consistent application of these surveys to the preand postsurgical outcome of patients has yet to be achieved but is imperative to improve our ability to

precisely determine the effect and benefit of a given intervention.

CLASSIFICATION

Table 98-2 Clinical Classification of Chronic Venous Disease

Diagnostic Evaluation

The diagnosis of CVD begins with a thorough history and physical examination. The history is quite

important to provide hints to familial coagulation disorders or events in the patient’s history that may

impact the care of this chronic disorder. Prior DVT, pregnancies, a family history of varicosities,

obesity, or the presence of other factors associated with CDV will add support to the presence of venous

disease. When performing physical examination, the location, distribution and size of varicosities, skin

changes, and/or presence or indication of past ulcers should be noted. Swelling should be quantified, the

location specified, and a determination made whether it is pitting or nonpitting in nature. Inspection,

palpation, and auscultation (presence of a bruit) may be keys to the presence of a vascular

2807

malformation or arteriovenous fistula. Utilization of the CEAP clinical classification (Table 98-2) will

provide a snapshot of the patient being examined, whereas the use of the more detailed Venous Clinical

Severity Score (Table 98-3) will allow some impression of how any therapy is performing as the patient

is being treated.

In addition to determining and classifying the signs and symptoms of venous disease, the history and

physical examination should exclude other potential etiologies for the patient’s complaints such as

arterial occlusive disease, collagen vascular disorders, allergic reactions, infection, or malignancy.

Appropriate confirmatory diagnostic studies may be required to confirm the clinical suspicion, such as a

lower extremity arterial Doppler study, biopsy, or specific laboratory studies when the diagnosis is

unclear. Such studies become most pertinent during the evaluation of advanced venous disease,

especially venous ulcers.193 Only in select patients, such as those with recurrent, early, or unusual sites

of DVT or recurrent venous ulcers, evaluation for thrombophilia is recommended.126,193

Venous duplex ultrasonography provides a B-mode picture of the vein, as well as spectral analysis of

the blood flow within, and is recommended as the first diagnostic test for all patients with suspected

CVD.209 To provide an accurate impression of the venous disease present, a standard technique is

followed and has been outlined in a current review article.126 Venous duplex imaging clearly visualizes

deep, superficial, and perforator veins and often the valves that lie within the veins. The venous duplex

study can help to clarify the etiology (E of CEAP; congenital, primary, or secondary), better define the

anatomic location (A of CEAP; specific veins can be imaged with spectral analysis to determine reflux),

and aid in determining the pathophysiology (P of CEAP; reflux, obstruction, or both) of the venous

problem. Once considered unnecessary in the evaluation of patients with simple varicose veins, it has

become common practice prior to intervention for superficial reflux due to anatomic variability and the

need for precise targeting of veins during endoluminal intervention.121,210–212

DIAGNOSIS

Table 98-3 Venous Clinical Severity Score

Valvular insufficiency is defined as prolonged reflux time through a valve following a provocative test

when duplex imaging is the diagnostic modality. To aid in the standardization of the test, rapidly

deflating distal cuff technique is used in some vascular laboratories, while others use manual

compression of the distal leg after which valve reflux is determined during duplex imaging.132,133 An

2808

abnormal reverse venous flow (reflux) in the saphenous, tibial, and deep femoral veins is 0.5 seconds or

greater while the femoral and popliteal veins have a cutoff value of 1 second 213 Since perforating vein

reflux can also be associated with venous pathology, significant work has gone into determining how to

define abnormal reflux. Current consensus and available data suggest that a “pathologic” perforating

vein is defined as a vein with an outward flow of ≥0.5 seconds, with a diameter of >3.5 mm, which is

located beneath a healed or open venous ulcer.126,209,212,213 The duplex examination for reflux is

performed in the upright position in these reports. Many other provocative maneuvers to generate

venous reflux exist (Valsalva, standardized Valsalva, etc.) in addition to performing the test in different

positions (e.g., 15% Trendelenburg, sitting) and are used in many laboratories for particular patients

who have difficulty standing.214 Each may be acceptable if standardized for an individual laboratory.

Venous obstruction is seen as thickened, scarred, and constricted veins with poor flow and diminished

augmentation following distal and/or proximal compression. Respiratory variation is lost as a result of

local occlusive disease or proximal occlusion. Disease within the SSV should not be ignored because it

can have a significant clinical impact as an isolated finding.215 By imaging the entire lower leg venous

system, the surgeon is provided a detailed roadmap of all veins with determination of obstruction or

reflux within segments separated by valves. Isolated venous valvular insufficiency or obstruction may

have little clinical impact on the patient, and therefore clinicians have attempted to quantify the

pathology by adding up segmental disease, determining mean duration of reflux, determining peak

reverse flow velocity, and so forth.133,198 Although average scores correlate with disease severity,

individual results have little predictive value and, therefore, these methods have not been widely

adapted. This is often the only diagnostic tool needed for the evaluation of superficial and even

perforator disease requiring treatment as a first stage in patient management.

A difficult area of investigation from a noninvasive perspective is the pelvic, abdominal, and chest

veins. CT and MRI can provide details of anatomy and the effect of surrounding structures in areas not

visualized by duplex evaluation.193,216–219 These studies can be particularly useful in evaluating for

pelvic congestion syndrome.220 However, as with all vascular laboratory studies, clinical correlation is

mandatory because anatomic presence does not necessarily translate into a clinical problem. For

example, iliac vein compression is commonly seen in an asymptomatic population.155–160

Plethysmography assesses the overall hemodynamics of the lower extremity venous system. Air

plethysmography (APG) can measure several venous hemodynamic parameters. A plastic cylinder filled

with air is fitted over the calf and foot and changes in leg volume with positional change or exercise are

detected by pressure changes in the cylinder. The venous filling index is 90% of resting standing VV

divided by the time it takes to reach 90% of VV as the patient shifts from the supine to standing position

(mL/second). A venous filling index of 2 mL/second or less is indicative of competent venous system

and higher values suggest venous insufficiency.221,222 After an erect baseline reading, patients exercise

by dorsiflexion or heel raises to empty the calf veins. The ejection fraction is the amount of blood

propelled cephalad with a single muscle contraction divided by VV. After a series of 10 ankle flexions,

the volume remaining in the leg is referred to as the residual volume and, when divided by the VV, is

called the residual volume fraction. An ejection fraction of greater than 60% and residual volume

fraction of less than 35% suggest that the calf pump is working well.187,223 The residual volume fraction

is relatively equivalent to the AVP.142,224 Significant outflow obstruction is determined by occluding

venous outflow until a stable plateau is reached. The thigh cuff causing the venous occlusion is rapidly

deflated, and the difference between maximal volume and that volume present 1 second later divided

by the total calf volume is called the outflow fraction. Normally, 38% or more of venous blood is

expelled from the leg in 1 second.222 Several other plethysmographic methods (e.g., impedance, photo)

and even light reflex rheography have evaluated similar venous parameters. The accuracy of these

techniques to reliably eliminate the presence of significant venous occlusive disease is poor.225 Although

these plethysmographic methods can differentiate patients with severe CVI (class 3 or greater) from

those without disease, stratification by symptom severity is not possible and, therefore, its use in the

treatment of patients with minor symptoms, such as varicose veins or telangiectasias, is also

questionable.214 In current clinical practice, it is being used only in complex cases or for research

purposes. Current consensus encourages the use of plethysmography in the patient with advanced CVD

if duplex scanning cannot provide a definitive diagnosis often underlying pathophysiology.126

As in acute venous disease, venography has no significant role in the initial evaluation of patients

with CVD. Ascending venography can suggest venous occlusion when duplex imaging clearly

demonstrates an open system.226 Even the presence of significant collaterals on transfemoral

venography may underestimate the degree of venous occlusion as documented by intravascular

2809

ultrasound.152,227 The use of ascending venography is selectively used in specific cases to complement

noninvasive studies when considering intervention in the deep venous system or in research protocols.

The technique of descending venography has been well described.228 Descending venography is used

to determine valve leaflet integrity and anatomic location and demonstrate the extent of reflux.228

Assessment of the competence of the profunda femoris venous system in addition to the femoral system

is imperative. If it is a competent system, it may be a source for a valve transposition or may predict

success with an isolated proximal femoral vein repair.229–231 Certainly, descending venography is not

infallible in determining the presence or absence of a normal valve.183 Raju et al.183 report that

descending venography misrepresented the presence of a valve in 11% of cases (a valve considered

present was not at operation) and missed an intact valve in 25% of cases (a valve thought absent was

actually present). However, when combined with a careful venous duplex examination, it is currently

the best method available to determine preoperatively if an in situ reconstruction will be possible.

Intravenous pressure measurements can aid in the diagnosis of venous disease but is invasive and

generally used only when invasive surgery of the deep system is being considered. This study can help

to determine the overall magnitude of reflux and can be correlated with the incidence of venous

ulceration.142,232 Direct lower limb IV pressure measurements before and after reactive hyperemia and

when compared to arm IV pressure has not consistently determined the significance of proximal venous

occlusive disease such that the authors of this technique now recommend IV ultrasonography as a more

reliable diagnostic tool.225 Although IV pressure measurements and venography were once the gold

standard for evaluating venous disease, duplex scanning with the addition of intravascular

ultrasonographic techniques when required is the anatomic and functional test of choice in current

medical practice.

Treatment Options and Results

Medical Therapy

Compression has been the mainstay of the medical treatment for all stages of CVI for centuries. The

goals are to manage clinical symptoms and to control venous hypertension. Roughly speaking, there are

two types of compression: elastic (e.g., support stockings or long stretch bandages) and inelastic (e.g.

Unna’s paste boot, short stretch bandages, multilayer [four-layer] bandage, or Velcro band devices). A

graduated compression stocking is a single-layer elastic compression often used to control edema. The

term multilayer when dealing with compression denotes a bandage that covers the leg with more than

one layer because of overlapping during placement. The term multicomponent is a multilayer bandage

with several components, such as an Unna’s boot, underlying paste layer covered by an elastic wrap. In

general, the more layers the less elastic and more stiff the compression. The degree to which any

particular bandaging is one or the other will depend on the care provider who applies the compression

along with other factors. The mechanical effect is dependent on the level and type of compression and

the desired amount of compression is influenced by the underlying venous pathology being treated.

Initial narrowing of deep and superficial calf veins on standing as determined by duplex imaging is

observed at 20 mm Hg with improved venous hemodynamics and improved QOL data when used to

treat mild disease.233–237 Consistent narrowing of superficial and calf veins occurs at a median of 30 to

40 mm Hg pressure on standing while complete occlusion occurs at a median pressure of 70 mm Hg.

Complete occlusion is not the goal. Therapeutic calf compression improves calf muscle pump function

expressed as a reduction in residual volume fraction during walking.238 Duplex imaging has

demonstrated that thigh compression was helpful in reducing great saphenous and femoral vein

diameter at a constant pressure of ≥40 mm Hg and reduced venous reflux (by APG) at 60 mm Hg.239

Overall, these effects on the underlying veins help to improve the venous pump and decrease the VV in

the lower extremity. It is interesting that elastic stocking maintain a rather constant pressure during

exercise and at rest. Alternatively, inelastic wraps demonstrate a more dramatic increase in pressure

during exercise since they do not stretch but have decreasing pressure with recumbence as the edema

exits the leg and the bandage maintains its shape.240 This difference in performance helps to explain

why inelastic wraps are much better tolerated when left on for days and especially at night when the

constant compression is not required and may be perceived as discomfort. It also explains why

compression should be changed more frequently early in treatment and less frequent latter as the

degree of edema requiring control lessens.

Although there has been concern that compression may impede microcirculatory flow and thereby

jeopardize tissue viability,241 it is known that compression, when used to treat edema, has a positive

influence on the local skin and soft tissues by improving capillary filtration rate, decreasing the

2810

subcutaneous pressure in the perimalleolar area, promoting extracellular fluid reabsorption, and

improving sodium subcutaneous tissue clearance.242,243,244 Compression improves skin transcutaneous

oxygen tension and skin capillary density in patients with venous insufficiency.245,246 Compression can

increase microcirculatory flow velocity and ameliorate the inflammatory injury and fibrosis associated

with CVI.240,245,247,248 Cytokines, such as vascular endothelial growth factor and tumor necrosis factor,

decrease with compression therapy and correlate with ulcer healing.249 Furthermore and in

contradistinction to the first statement in this paragraph, standard compression can actually increase

arterial blood flow in some circumstances.240,250 The lymphatic system is often involved in the overall

pathophysiologic state of patients afflicted with venous insufficiency and performance of this outflow

system is improved with compression.246 In patients with concomtant arterial occlusive disease with an

ankle to brachial systolic blood pressure ratio (ABI) of 0.80 or greater, the use of standard compression

is safe and effective and actually increases arterial perfusion in affected tissues.251–253

In those with more advanced arterial occlusive disease defined as an ABI ≥0.50 (but <0.80) or an

ankle systolic pressure ≥60 mm Hg or toe pressure ≥30 mm Hg as a minimum; modified compression

dressings with lower pressure ratings not to exceed the tissue perfusion pressure can improve tissue

perfusion and aid in healing ulcers of mixed etiology.253–255 These data support the current SVS/AVF

practice guideline that suggests that in a patient with a venous leg ulcer and underlying arterial disease,

compression bandages or stockings are not indicated if ABI is 0.5 or less or if the absolute ankle

pressure is less than 60 mm Hg.193

Evidence-based medicine confirms our clinical impression and basic science findings regarding the

potential benefits of compression garments for the treatment of CVI. Substantial evidence exists to

demonstrate that compression is statistically beneficial for most clinical stages of symptomatic venous

disease (C2–6

). A recent large systematic review evaluating the use of compression for varicose veins

(C2

) demonstrated that symptoms were improved, but the analysis could not confirm that its use

decreased progression of disease or prevented recurrence after invasive treatments.256 Whether

compression stockings should be the primary treatment for symptomatic varicose veins has been

challenged by the recent RCT titled the Randomized Clinical Trial, Observational Study and Assessment

of Cost-Effectiveness of the Treatment of Varicose Veins (REACTIV) trial.257 This study randomized 246

patients with class C2 disease into conservative management including compression versus high ligation,

stripping, and phlebectomy. Over the span of a 2-year follow-up, there was a statistically significant

benefit from surgery in quality-adjusted life-years when analyzed by two scoring systems in addition to

improvements in symptomatic and anatomic measurements. Cost-effective analysis demonstrated a

benefit for the surgical intervention as well. Therefore, in contradistinction to current third-payer

policies, and based on available statistical data, the SVS/AVF Guidelines Committee recommends against

compression therapy being considered the primary treatment of symptomatic varicose veins in those

patients who are candidates for saphenous vein ablation as a grade 1B recommendation.126 Certainly in

those not candidates or those who do not desire interventional options, the Guidelines Committee

suggests compression therapy (20 to 30 mm Hg) for symptomatic benefits (grade 2C).

Compression is the standard of care for patients with advanced CVD (C3–6

) and the majority of the

evidence-based data investigate the benefits of treating venous ulcers since the rate and degree of

healing are measurable. The SVS/AVF commissioned a comparative systematic review and meta-analysis

of compression modalities and venous ulcer healing.258 Nine RCTs provided objective data on initial

ulcer size and outcomes as measured by time to complete healing or proportion of ulcers healed. The

evidence suggests that venous ulcers heal more quickly with compression therapy than without

compression. Most RCTs demonstrated a benefit in healing rate with various compression methods

used.259–261 In addition, the SVS/AVF commissioned analysis of compression and venous ulcer healing

demonstrated low-quality evidence to support the effect of compression on ulcer recurrence.258

Compliance with compression is a challenge for patients with chronic disease and noncompliance is

associated with recurrence while the ability to maintain compression demonstrated less recurrence in

most studies.262–264 Compression comes in many forms and is a factor in venous ulcer healing potential.

The SVS/AVF commissioned analysis found moderate-quality evidence to support multicomponent

compression over single component compression to treat venous ulcers.258 The best studies evaluated a

multilayer (four-layer) bandage versus a single-layer bandage and demonstrated improving overall

healing rates with faster closure rates.265,266

However, the skill of those applying the single-layer dressing might improve these results to mimic

the multilayer compression.267 These data have led the SVS/AVF Guidelines Committee to recommend

that compression be used to heal venous ulcers (grade 1A), to decrease recurrence (grade 2B), and it is

2811

suggested that multicomponent compression bandages be used to treat venous ulcers (grade 2B).126

One last comment on the use of compression in the treatment of venous ulcers, although surgical

intervention is suggested over the use of compression alone to heal venous ulcers, post–interventional

compression does help to prevent recurrence. This has been demonstrated in two RCTs and in the

SVS/AVF commissioned comparative systematic review and meta-analysis of surgical interventions

versus conservative therapy for venous ulcer treatment.268–270

In the final analysis, multilayer relatively inelastic wraps are preferred for the therapy phase of

venous disease (ulcer healing). When the ulcers are healed, elastic wraps, such as compression

stockings, are used to maintain a stable clinical condition (maintenance phase). In addition, elevating

the legs when possible during the day, avoiding prolonged periods of standing or sitting, and elevating

the foot of the bed 4 to 6 in above the heart while sleeping are adjuvant components of conservative

therapy.271,272

Intermittent pneumatic compression (IPC) provides pulsatile emptying of the venous system via

compressive bladder(s) that inflate and deflate. Some data suggest a positive impact on the

inflammatory injury and associate fibrosis when IPC is used to treat CVI.240,247 A Cochrane review

suggests that there is advantage in using IPC compared to no compression, but there is little evidence to

suggest that the addition of IPC to compression therapy is beneficial.273 Certainly, one RCT of 45

patients has demonstrated its use in patients with long-standing ulcers (at least 3 months’ duration)

comparing standard ambulatory compression with or without the addition of IPC. At 3 months, 10 of 21

ulcers healed with the addition of IPC, while only 1 of 24 healed with standard care.274 One study

suggests that a rapid cycle method improves ulcer healing compared with a slow cycling regimen.275

This data is the basis for a practice guideline, suggesting that IPC be employed when compression has

failed, is unavailable, or cannot be used.276

Lifestyle changes, including exercise, improved mobility, and foot exercises, can aid in lowering the

incidence of venous ulcer recurrence as demonstrated by a recent literature review.277 Structured

exercise can improve dynamic muscle strength and calf muscle pump function in patients with

essentially all levels of CVI from varicose veins to venous ulceration.189,278,279 It is unclear whether such

exercise improves ulcer healing rates per se. The use of supervised active exercise to improve muscle

pump function and to reduce pain and edema in patients with leg ulcers is a guideline recommendation

(grade 2B).276 In Europe and other countries, various oral agents (e.g., diosmin, rutosides) have been

touted to improve the feeling of heaviness, fatigue, and even edema of CVD but these agents are not

available in the United States.126,276 A Cochrane review selected 44 studies of such agents for metaanalysis and concluded that there was insufficient evidence to support the global use of these drugs in

the treatment of CVD.280 Drugs potentially useful in treating patients with venous ulcers are available in

the United States. Pentoxifylline does provide an incremental benefit in ulcer healing and has an

improved outcome with higher doses but the trade-off is more gastrointestinal adverse effects.265,281–283

For long-terms effects and as an adjunct to compressive therapy when standing or large venous ulcers,

pentoxifylline, in combination with compression therapy, is recommended (grade 1B).276 Current

practice is to prescribe 400 mg of pentoxifylline three times per day and, if tolerated, the higher dose is

800 mg three times per day. Prophylactic use of systemic antibiotics in the treatment of venous ulcers is

not recommended and may only select resistant organisms. One randomized clinical trial in 47 patients

compared elastic support bandages only versus those also treated with systemic antibiotics. There was

no statistical difference in healing rates of ulcers or in changes of the microbiologic flora.284 Clinically,

evident disease with supportive quantitative wound cultures has demonstrated beneficial effects when

systemic antibiotics are used, but the data are meager.285 Certainly, an established infection (cellulitis

or deeper) must be treated as it would be at any site and is recommended best care by the SVS/AVF

Guidelines Committee. In addition, the recommendation is for oral agent use for 2 weeks unless

evidence of clinical infection continues (grade 1C).276 Limb cellulitis with or without a venous ulcer

generally requires systemic gram-positive antibiotic coverage as demonstrated by several studies and is

a grade 1B recommendation for patient care.276,286

Surgical Therapy

The use of surgical intervention in the realm of venous disease as in all areas of vascular surgery is

driven by the documented presence of disease, the risk of the intervention planned, and the expected

outcome (Algorithm 98-1).

Telangiectasia, Reticular Veins, and Branch Varicose Veins. Percutaneous laser energy (a lamp

that produces laser light that is shined on the blemish) can be used to treat telangiectasias up to 0.7 mm

2812