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29
Lower Extremity Venous Disease
James Laredo, MD, PhD, and Anton N. Sidawy, MD, MPH
Lower extremity venous disease is extremely common, with varicose veins remaining the most frequently
encountered venous condition followed by chronic
venous insufficiency.1,2 The two conditions often occur
together, but each condition may also be present clinically without the other. Lower extremity venous disease
comprises a clinical spectrum ranging from completely
asymptomatic telangiectasias to symptomatic varicose
veins to debilitating venous ulcers.1,2 The most frequently
encountered symptoms associated with varicose veins
include leg swelling, pain, itching, nocturnal cramping,
and leg heaviness. Patients with chronic venous insufficiency often present with leg edema, skin hyperpigmentation, stasis dermatitis of the skin involving the ankles,
fibrosis of the subcutaneous fat (lipodermatosclerosis),
and ulceration.1,2 Lower extremity venous ulceration
remains a significant worldwide health problem resulting
in significant morbidity.1,2
Deep venous thrombosis (DVT) of the lower extremities is another highly prevalent venous condition encountered by health care providers of all disciplines.3 Much has
been published regarding venous thromboembolic disease4-8; therefore, the content of this chapter is limited to
the intrinsic venous disorders of the lower extremities.
• EPIDEMIOLOGY
Prevalence estimates of lower extremity venous disease
vary widely by geographic location, with the highest
reported rates observed in Western countries. The variability in estimates is likely attributable to population differences in risk factor distribution, methods of measurement,
variability in diagnosis, and disease definition.1,2,9,10 The
prevalence of lower extremity varicose veins is estimated
29_Dieter_Ch29_p001-026.indd 1
to be as high as 56% in men and 73% in women.9,10 The
prevalence of chronic venous insufficiency is estimated
to be as high as 17% in men and 40% in women.10 Lower
extremity venous ulceration has been reported to occur
in approximately 0.3% to 1% of the adult population
worldwide.9,11
Risk factors associated with the development of lower
extremity venous disease are listed in Table 29-1. Family
history, female gender, age, and pregnancy have been well
established as risk factors for developing varicose veins.9,10
These risk factors have also been shown to contribute to the
development of chronic venous insufficiency.9,10 Regarding
the development of venous ulceration, in addition to the
risk factors shown in Table 29-1, history of lower extremity phlebitis, lower extremity trauma, DVT, and congestive
heart failure have been shown to be associated with the
development of venous ulceration.11
WITH
Chronic venous insufficiency with venous ulceration AU:
ok as
changed
is extremely prevalent in the United States and is also here ?
the seventh leading cause of chronic debilitating disease.2 Chronic
venous
ciency
Approximately 10% to 35% of the U.S. population has insuffi
WITH
venous
1,2
some form of chronic venous insufficiency. More than ulceration
500,000 men and women experience chronic venous ……….
debilitating
ulcers.1,2,11 Venous ulcers are associated with significant disease
health care costs and substantial economic effects in
terms of days of work lost and diminished quality of
life.2,11 The population-based cost in the United States
for treatment of chronic venous insufficiency and venous
ulcers has been estimated to be more than $1 billion a
year.2 In addition, more than 6 million days of work are
lost each year because of complications associated with
chronic venous ulcers.11 Furthermore, patients’ quality of
life is significantly impacted by the loss of workdays and
debilitating symptoms.2,11
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2 • CHAPTER 29
TABLE 29-1. Risk Factors Associated
with the Development of Lower Extremity
Venous Disease
Older age
Female gender
Pregnancy
Family history of venous disease
Obesity
Prolonged standing
• EMBRYOLOGY
The development of the blood vessels occurs between
the third and eight weeks of embryonic gestation.12 The
primitive circulation begins to develop toward the end of
the third week after appearance of the newly fused heart.
This is followed by rapid changes in the fourth week when
extensive remodeling occurs and continues through the
final month of the embryonic period.12 Development at
the cephalad end of the embryo proceeds more rapidly
than at the caudal end as the arteries and veins change and
interact with the growing thoracoabdominal organs, parietes, and extremities.12
Primitive vascular channels appear in the limb during
the third gestational week, when a capillary network is
initially present during the undifferentiated stage.13 This is
followed by large plexiform structures present during the
4 weeks
retiform stage, and finally, large channels, arteries, and veins
appear during the maturation stage.12,13
The earliest veins that develop are the vitelline veins
from the yolk sac, the umbilical veins from the chorion,
and the cardinal veins from the body proper.12 Venous
developmental changes are more complex than arterial changes and involve additions, deletions, interconDo you
nections, positions, and flow changes.12 The vitelline and AU:
mean positions
and flow
umbilical veins eventually become the hepatic sinusoids, changes here?
hepatic veins, portal vein, superior mesenteric vein, and
left umbilical vein.12 The paired cardinal veins undergo a
series of changes leading to the mature venous drainage of
the body.12,13 The left-sided cardinal veins regress, leaving
the right-sided veins, which become the superior vena cava
(SVC) and inferior vena cava (IVC)12,13 (Figure 29-1). The
distal ends of the post cardinal veins persist after regression
and eventually become the iliac veins.
Persistence of the left subcardinal vein results in a double IVC in as many as 2% to 3% of individuals and a single
left-sided IVC in 0.2% to 0.5%.13,14 Renal vein anomalies
include a retroaortic left renal vein (2%) with or without
a normal anterior left renal vein and a circumaortic renal
collar (1%).13,14
Persistence of embryonic veins after birth results in
venous malformations of the pelvis and lower extremities.13 The marginal vein, often seen in patients with
Klippel-Trenaunay syndrome, is a persistent large, lateral,
superficial embryonic vein that contributes to the development of chronic venous insufficiency.13 Other developmental anomalies include a persistent sciatic vein,
valvular agenesis, venous aneurysms, and primary valvular
insufficiency.13
6 weeks
7 weeks
8 weeks
Postcardinal v’s
Supracardinal v’s
Caudal
extension of
hepatic v’s
Azygous v.
Subcardinal v.
Intersubcardinal
anastomosis
IVC
Subsupraanastomosis
Renal v’s
Illiac v’s
• FIGURE 29-1. Embryology of the venous system. Development of the inferior vena
cava and iliac veins.
(Adapted from Valentine RJ, Wind GG: Embryology of the arteries and veins. In Valentine RJ, Wind
GG (eds). Anatomic Exposures in Vascular Surgery, 2nd ed. Philadelphia: Lippincott Williams and
Wilkins, 2003:1–19.; with permission.)
29_Dieter_Ch29_p001-026.indd 2
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LOWER EXTREMITY VENOUS DISEASE • 3
• ANATOMY
resulting in left iliofemoral vein thrombosis (May-Thurner
syndrome), which is often caused by a chronic stenosis or
occlusion of the vein.13
The superficial veins include the subpapillary venous
plexus, the reticular venous plexus, and all of the veins in
the superficial compartment (see Figure 29-2). The great
saphenous vein and its tributaries comprise the major
superficial venous system of the thigh and medial leg
(Figure 29-4). The small saphenous vein and its tributaries
comprise the major superficial venous system of the lateral
leg (see Figure 29-4). The great saphenous vein drains into
the common femoral vein at the confluence of the superficial inguinal veins (formerly known as the saphenofemoral junction). The confluence of the superficial inguinal
veins is made up of the great saphenous vein, superficial
circumflex iliac, superficial epigastric, and external pudendal veins.13,15 The small saphenous vein originates from the
lateral side of the foot and drains into the popliteal vein.
Below the level of the gastrocnemius muscle, the small
saphenous vein runs adjacent to the sural nerve, which is
prone to injury during surgical stripping procedures.
The perforating veins traverse the muscle fascia connecting the superficial venous system to the deep venous
system (Figure 29-5). Competent valves within the perforating veins ensure superficial to deep, unidirectional flow
in the calf and thigh. Perforating vein valvular incompetence may result in venous congestion, varicosities, and
chronic skin changes, including ulceration.1,2,13,15 The most
important perforating veins of the lower extremity are the
medial calf perforators.13,15 There are two main groups of
Superficial
compartment
Epidermis
Dermis
Subcutis
Subpapillary
venous plexus
a
Fascia
Deep
compartment
Saphenous
compartment
The muscle fascia divides the lower extremity soft tissues
into a superficial compartment and deep compartment
(Figure 29-2). The venous system of the lower extremities include both the deep veins that lie below the muscular fascia and drain blood directly into the IVC and the
superficial veins that lie above the muscular fascia and
drain the superficial compartment. The saphenous fascia
covers the saphenous subcompartment and separates the
great saphenous vein and small saphenous vein from other
veins in the superficial compartment. Connecting the two
venous systems are the perforating veins that traverse the
muscular fascia and normally drain blood from the superficial system into the deep venous system (see Figure 29-2).15
Also present within the superficial compartment is the
reticular venous plexus and subpapillary venous plexus.
Communicating veins connect veins within the same compartment.13 The deep, superficial, and most perforating
veins contain bicuspid valves that maintain unidirectional
venous flow. The nomenclature of the lower extremities
veins has recently been updated (Table 29-2).13,15
The deep veins comprise the venous component of the
neurovascular bundle of the lower extremities. The deep
veins are adjacent to the similarly named arteries and often
occur as paired structures at the popliteal, calf, and ankle
levels (Figure 29-3).13,15 The major pelvic veins include the
common iliac, internal iliac, and external iliac veins, all of
which drain directly into the IVC. The overlying right common iliac artery may compress the left common iliac vein,
Muscle
b
Reticular
venous plexus
a
b
Saphenous
fascia
DISTAL
PROXIMAL
Deep veins
•
FIGURE 29-2. Relationship between the fascia and veins of the lower extremity. The
fascia covers the muscle and separates the deep from the superficial compartment. Superficial veins (a) drain the subpapillary and reticular venous plexuses and are connected to
deep veins through perforating veins (b). The saphenous fascia invests the saphenous
vein. The saphenous compartment is a subcompartment of the superficial compartment.
(From Mozes G, Gloviczki P: New discoveries in anatomy and new terminology of leg veins: clinical
implications. Vasc Endovasc Surg, 2004;38:367–374; with permission.)
29_Dieter_Ch29_p001-026.indd 3
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4 • CHAPTER 29
TABLE 29-2. The Most Common “Old” Anatomic Terms Describing Lower
Extremity Veins and Their “New” Counterparts15
Old Term
New Term
Greater or long saphenous vein
Great saphenous vein (GSV)
Smaller or short saphenous vein
Small saphenous vein (SSV)
Saphenofemoral junction
Confluence of the superficial inguinal veins
Giacomini’s vein
Intersaphenous vein
Posterior arch or Leonardo’s vein
Posterior accessory great saphenous vein of the leg
Superficial femoral fein
Femoral vein
Cockett perforators (I, II, III)
Posterior tibial perforators (lower, middle, upper)
Boyd’s perforators
Paratibial perforators
Sherman’s perforators
Paratibial perforators
“24-cm” perforators
Paratibial perforators
Hunter’s and Dodd’s perforators
Perforators of the femoral canal
May’s or Kuster’s perforators
Ankle perforators
A
B
• FIGURE 29-4. The superficial veins of the lower
• FIGURE 29-3. The deep veins of the lower extremities.
(From Mozes G, Gloviczki P: New discoveries in anatomy and new
terminology of leg veins: clinical implications. Vasc Endovasc Surg,
2004;38:367–374; with permission.)
29_Dieter_Ch29_p001-026.indd 4
extremities. (A) The great saphenous vein and tributaries. Note
the course of the vein running medially from the groin to the
medial ankle. (B) The small saphenous vein (SSV) and tributaries. Note the close proximity of the SSV to the sural nerve.
The SSV usually arises from the popliteal fossa and continues
down to the lateral ankle.
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LOWER EXTREMITY VENOUS DISEASE • 5
in the superficial, deep, and perforating venous systems;
and the underlying pathophysiology (P), which is attributable to reflux, obstruction, or both (Table 29-3).17 Basic
CEAP classification designates only the highest clinical (C)
classification based on symptoms. Advanced CEAP clinical classification includes all symptoms present and further designates any of 18 involved venous segments with
the pathophysiology (P) (Table 29-4).17 A symptomatic
patient presenting with varicose veins, leg pain, leg edema,
and lipodermatosclerosis and is found to have reflux of
the great saphenous veins above and below the knees
bilaterally, with incompetent calf perforating veins, would
have a basic CEAP classification of C4bs, Ep, As,p, Pr, and an
advanced CEAP classification of C2,3,4bs, Ep, As,p, Pr2,3,18.
TABLE 29-3. CEAP Classification of
Chronic Venous Disease17
Clinical classification
C0: no visible or palpable sign of venous disease
C1: telangiectasis or reticular veins
C2: varicose veins
C3: edema
C4a: pigmentation of eczema
C4b: lipodermatosclerosis or atrophic blanche
C5: healed venous ulcer
•
FIGURE 29-5. The superficial and perforating veins of
the lower extremities.
(From Mozes G, Gloviczki P: New discoveries in anatomy and new
terminology of leg veins: clinical implications. Vasc Endovasc Surg,
2004;38:367–374; with permission.)
C6: active venous ulcer
S: symptomatic, including ache, pain, tightness, skin
irritation, heaviness, muscle cramps, and other
complaints attributable to venous dysfunction
A: asymptomatic
Etiologic classification
medial calf perforators, the posterior tibial and the more
proximal paratibial perforating veins. The posterior tibial
perforating veins (Cockett perforators) connect the posterior accessory great saphenous vein with the posterior
tibial veins (see Figure 29-5).
• CEAP CLASSIFICATION OF LOWER
EXTREMITY VENOUS DISEASE
The CEAP (clinical, etiology, anatomy, pathophysiology)
classification of chronic venous disorders was developed
and adopted worldwide to facilitate meaningful communication about chronic venous disorders and to serve as a basis
for more scientific analysis of treatment alternatives.16,17 An
international ad hoc committee of the American Venous
Forum developed the first CEAP consensus document in
1994.16 This document was later revised in 2004.17
The CEAP classification includes a description of the
clinical class (C) based on objective findings—the etiology
(E); the anatomical (A) distribution of the affected veins
29_Dieter_Ch29_p001-026.indd 5
Ec: congenital
Ep: primary
Es: secondary (postthrombotic)
En: no venous cause identified
Anatomic classification
As; superficial veins
Ap: perforator veins
Ad: deep veins
An: no venous location identified
Pathophysiologic classification
Pr: reflux
Po: obstruction
Pr,o: reflux and obstruction
Pn: no venous pathophysiology identifiable
CEAP, clinical, etiology, anatomy, pathophysiology.
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6 • CHAPTER 29
TABLE 29-4. CEAP Classification of
18 Named Venous Segments Used as
Locators for Venous Pathology17
Superficial veins
1: Telangiectasias or reticular veins
2: Great saphenous vein above the knee
3: Great saphenous vein below the knee
4: Small saphenous vein
5: Nonsaphenous vein
Deep veins
6: Inferior vena cava
7: Common iliac vein
8: Internal iliac vein
9: External iliac vein
10: Pelvic: gonadal, broad ligament veins, other
11: Common femoral vein
12: Deep femoral vein
13: Femoral vein
14: Popliteal vein
15: Crural: anterior tibial, posterior tibial,
peroneal veins (all paired)
16: Muscular: gastrocnemial, soleal veins, other
Perforating veins
17: Thigh
18: Calf
CEAP, clinical, etiology, anatomy, pathophysiology.
• VENOUS DISEASES
Reticular veins are flat, incompetent, dilated blue and
green veins (usually ≤3 mm in diameter) that arise from
the reticular venous plexus and are found in the subdermal space (see Figure 29-6).1 Reticular veins serve as
incompetent feeding veins to telangectasias.18
Primary varicose veins are those that develop in patients
without a previous history of an underlying venous condition. In contrast, secondary varicose veins develop as a
result of a prior DVT, congenital venous malformation,
or arteriovenous malformation.19 The majority of patients
presenting with varicose veins have primary varicose veins.
Approximately 25% to 40% of patients with primary varicose veins report symptoms that include aching, itching,
heaviness, tiredness, cramping, and swelling.2,10,19,20 In the
Edinburgh Vein Study, a cross-sectional population study,
32% of women and 40% of men had lower extremity varicose veins ,and 19% of all patients were found to have
valvular incompetence of the great saphenous vein.9,10,21
In another study of patients with varicose veins, the vast
majority (60%–70%) had valvular incompetence of both
the saphenofemoral junction and great saphenous vein.22
Furthermore, superficial venous insufficiency is found in
up to 80% of women with varicose veins.23 The likelihood
of concomitant superficial venous insufficiency being present in patients with varicose veins increases with the presence of symptoms.2,10,19,20 Clearly, a significant percentage
of patients presenting with lower extremity varicose veins
have underlying venous insufficiency. By definition, dilated,
tortuous varicose veins demonstrate valvular incompetence.
However, not every patient with primary varicose veins
presents with venous insufficiency. Therefore, treatment of
patients with primary varicose veins without underlying
venous insufficiency should be limited to approaches and
procedures that are aimed at treating the varicosities. In
contrast, treatment of patients with primary varicose veins
associated with underlying venous insufficiency requires
treatment of both the varicosities and the underlying
chronic venous insufficiency.
OF THE LOWER EXTREMITIES
Varicose Veins
Lower extremity varicose veins are extremely prevalent.
Varicose veins are dilated, palpable, tortuous superficial veins (usually >3 mm in diameter) that are found
beneath the dermis (subcutaneous space) and drain into
communicating veins, incompetent tributaries, and truncal (saphenous) veins (see Figure 29-2 and 29-6).1 Dilatation of the varicose vein results in valvular incompetence.
In addition to varicose veins, patients often present with
telangiectasias (usually <1mm in diameter) that arise
from the subpapillary venous plexus and are found in the
dermis.1,18 Commonly know as spider veins, telangiectasias are dilated postcapillary venules demonstrating backflow from incompetent reticular (feeder) veins or directly
from incompetent tributary or truncal veins.18 Telangiectasias associated with venous insufficiency are usually
dark red or blue (see Figure 29-6). Larger bluish vessels
that are raised above the skin are termed venulectasias.18
29_Dieter_Ch29_p001-026.indd 6
Diagnosis. A careful history and physical examination
is usually sufficient to make a diagnosis of primary and
secondary varicose veins. The clinical evaluation should
focus on the patient’s symptoms and cosmetic concerns,
the extent and distribution of the varicose veins (including reticular veins and telangiectasias), and the severity and
location of the stigmata of chronic venous insufficiency
(edema, hyperpigmentation, stasis dermatitis, lipodermatosclerosis, ulceration).19 Patients should be questioned
regarding a family history of varicose veins and their history of DVT and superficial thrombophlebitis as well as
the time of onset of varicose veins and progression of
symptoms and past and anticipated future pregnancies.19
Patients with primary varicose veins presenting with
secondary skin changes associated with chronic venous
insufficiency may be indistinguishable from patients with
secondary varicose veins. For proper diagnosis, the sequence
of varicose vein development and skin changes is important.19 Patients with primary varicose veins will report the
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LOWER EXTREMITY VENOUS DISEASE • 7
A
B
C
• FIGURE 29-6. (A) Varicose veins of the left lower extremity. Varicose veins are
dilated, tortuous, palpable subcutaneous veins. (B) Red and blue telangiectasias and
venulectasias. Commonly known as spider veins, telangiectasias are dilated postcapillary
venules demonstrating backflow from incompetent reticular veins. Venulectasias are raised
bluish vessels that often appear with nonraised telangiectasias. (C) Telangiectasias and
reticular veins. Also known as feeder veins, reticular veins are flat, dilated blue and green
veins that arise from the reticular venous plexus.
appearance of varicose veins occurring many years before
the onset of the secondary skin changes of chronic venous
insufficiency. In contrast, patients with secondary varicose
veins may not recall a DVT but do describe having normal
legs followed by the development of secondary skin changes
and the appearance of varicose veins at a later time.19
Because a significant percent of patients with primary
varicose veins have underlying venous insufficiency, venous
duplex ultrasound examination is essential for proper
diagnosis and treatment planning. Patients with secondary varicose veins also require a venous duplex ultrasound
examination for thorough assessment of the superficial,
deep, and perforating venous systems. Diagnosis of venous
insufficiency via venous duplex ultrasound examination is
discussed in the Chronic Venous Insufficiency section.
Complications. The major complications of varicose
veins are thrombophlebitis and bleeding in addition to
those complications associated with concomitant venous
insufficiency (frequently found in patients with primary varicose veins), which include hyperpigmentation, stasis dermatitis, lipodermatosclerosis, and ulceration.1,2,19,21,22,24,25
Varicose Vein Bleeding. Bleeding associated with varicose veins and venous insufficiency is uncommon and usually occurs from a varix in an area where the overlying skin
is thin and prone to breakdown because of long-standing
venous insufficiency. The true incidence of bleeding is
unknown. Fatal hemorrhage from bleeding varicose veins
is exceedingly rare, with only a handful of cases reported in
the world’s medical literature.25
29_Dieter_Ch29_p001-026.indd 7
Superficial Thrombophlebitis. Thrombophlebitis or super-
ficial thrombophlebitis is thrombosis of the superficial veins,
which most often occurs in the veins of the lower extremities
but may occur in other areas as well. Thrombophlebitis may
occur in both varicose veins and nonvaricose veins, with the
saphenous veins and their tributaries being the most commonly affected veins.26,27 The incidence of thrombophlebitis
in patients with varicose veins varies widely in published
reports from 4% to 59%.26 Thrombophlebitis presents with
pain, erythema, and swelling around a superficial vein that
becomes firm and on palpation feels like a cord. Varicose
tributaries of the great saphenous vein and small saphenous
vein are most commonly affected.28 When thrombophlebitis involves the saphenous trunks, the great saphenous vein
is involved in 60% to 80% of cases, and the small saphenous vein in 10% to 20% of cases.26 Because of the risk of
thrombus propagation into the deep venous system via the
saphenofemoral and saphenopopliteal junctions, development of saphenous thrombophlebitis has a higher risk of
DVT and pulmonary embolism.26–28 Propagation into the
deep venous system has been reported to occur in 2.6% to
15% of cases.26 In addition, all patients with thrombophlebitis should undergo venous duplex ultrasound examination
to determine the extent of the superficial thrombosis and
to assess the deep venous system. Furthermore, in patients
without a history of varicose veins or an underlying venous
condition who develop saphenous thrombophlebitis, thrombophilia and malignancy should be suspected and the appropriate workup performed.26
In the majority of patients with thrombophlebitis, the
clinical course is benign and self-limiting with resolution
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8 • CHAPTER 29
of symptoms in 10 to 14 days. Conservative treatment
consists of compression stockings, ambulation, warm compresses, and nonsteroidal antiinflammatory drugs. Failure
of conservative treatment or propagation of thrombophlebitis is an indication for anticoagulation.26 In cases of
saphenous thrombophlebitis in which thrombosis involves
the saphenofemoral or saphenopopliteal junction without extension into the deep vein, surgical treatment with
saphenous ligation and anticoagulation are equally good
treatment options.26 Saphenous thrombophlebitis propagation into the deep venous system requires standard anticoagulation for DVT.
Treatment. Indications for treatment of varicose veins
include patient desire for treatment and symptoms associated with varicose veins, namely pain, edema, leg heaviness, and itching. Thrombophlebitis and bleeding are also
indications for varicose vein treatment. The majority of
patients with primary varicose veins present with superficial venous insufficiency. Patients with clinically significant
venous insufficiency (i.e., hyperpigmentation, stasis dermatitis, lipodermatosclerosis, and ulceration) should also
be offered treatment.
Treatment of patients with primary varicose veins without underlying venous insufficiency should be limited to
approaches and procedures that are aimed at treating the
varicosities. In contrast, treatment of patients with primary
varicose veins associated with underlying venous insufficiency requires treatment of both the varicosities and
the underlying chronic venous insufficiency. In addition,
treatment of secondary varicose veins also requires treatment of the underlying cause of the chronic venous insufficiency (i.e., valvular incompetence or venous obstruction).
Treatment of patients with chronic venous insufficiency is
discussed in the next section.
Compression Therapy. Graduated compression stock-
ings improve both the symptoms and venous hemodynamics in patients with varicose veins.29,30 Grade II
compression (20–30 mm Hg) is recommended and has
been shown to confer maximal relief of varicose vein
symptoms.29,30 The benefit of the compression therapy
depends on the compliance of the patient.30 Compliance
is variable and difficult to assess.24 In addition, compression stockings not only provide symptom relief but may
also prevent progression of the venous disease.29,30 In the
Bonn Vein Study, a cross-sectional population study of
3072 randomly recruited residents from Bonn, Germany,
23% received venous disease treatment and 15% wore
graduated compression stockings (range, 1% with C0 to
82% with C5/6 CEAP clinical classification). Compliance
was high: compression stockings were worn 5 or more
days per week by 73% of patients and 8 or more hours
a day by 83% of patients. On average, 71% of the participants said that the disease for which the compression
stockings were prescribed had improved as a result of the
compression therapy.31,32
Sclerotherapy. Sclerotherapy involves the injection of a
liquid or foam sclerosing agent for the targeted elimination
of telangiectasias, reticular veins, varicose veins, and perforating veins.33 Sclerotherapy is considered to be the treatment of choice for small-caliber varicose veins, reticular
veins, and telangectasias.34 The various available sclerosing
agents produce an endothelial injury of the vein, resulting in transformation into a fibrous cord, a process known
as sclerosis.33 This fibrous cord is eventually absorbed over
time (Figure 29-7).
The available sclerosing agents include three different classes: hyperosmotic, chemical, and detergent.34,35
Although each class offers individual advantages, the
A
he
A
B
• FIGURE 29-7.
Sclerotherapy of telangiectasias using 0.2% sodium tetradecyl sulfate
before (left) and 8 weeks after treatment (right).
29_Dieter_Ch29_p001-026.indd 8
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LOWER EXTREMITY VENOUS DISEASE • 9
detergent sclerosing agents such as sodium tetradecyl sulfate and polidocanol have long been recognized as the
preferred class of agents because of their low side effect
profile and proven efficacy.35 Polidocanol is the best-known
sclerosing agent worldwide and is manufactured by several countries outside the United States. It has not been
approved by the Food and Drug Administration (FDA),
and its use in the United States is illegal. Sodium tetradecyl sulfate is the only FDA-approved detergent sclerosing
agent available in the United States. Hypertonic saline and
glycerol are hyperosmotic agents with FDA approval that
are used off label for sclerotherapy. Table 29-5 list the most
commonly used sclerotherapy agents and typical concentrations required for treatment of different vein diameters.
Successful sclerotherapy requires that any underlying
venous insufficiency be treated initially to obtain maximal
results. Sclerotherapy is often performed after treatment of
superficial venous insufficiency and for recurrent varicose
veins after initial treatment with surgical saphenectomy
and phlebectomy. Untreated reflux can be the obvious
cause for recurrent varicosities, persistent symptoms, and
poor patient satisfaction.36
Sclerotherapy using both liquid and foam type sclerosing agents has been show to be efficacious in the treatment
of varicose veins.33,34 Foam sclerotherapy is usually used for
treatment of larger diameter varicose veins (≥6 mm). Foam
displacement of blood within the vein lumen, allowing a
longer duration within the vein, is the major advantage over
liquid sclerotherapy. In addition, the foam bubbles provide
increased surface area and contact with the vein endothelium. This action promotes sclerosis of the treated vessel
with a lower concentration of sclerosing solution.36 The Tessari method of producing foam sclerosant has become the
most popular method of preparation (Figure 29-8). Foam
sclerosant is produced by taking a syringe of detergent sclerosant (polidocanol or sodium tetradecyl sulfate) and mixing it with a syringe of air (1:3 ratio of liquid:air) using a
three-way stopcock. After 10 to 20 passages, a high-quality
foam is produced.
After sclerotherapy, compression therapy is applied to
the treated limb using graduated compression stockings
or compression bandaging. Complications associated with
sclerotherapy are infrequent and include allergic reaction,
skin necrosis, thrombophlebitis, pigmentation, nerve injury,
and telangiectatic matting.33
Surgery. Traditional surgery for varicose veins addresses
both the varicosities and underlying superficial venous insufficiency (most often involving the great saphenous vein)
found in the majority of patients. The standard operation
performed consists of two procedures, ligation and stripping of the great saphenous vein (Figure 29-9), followed
by stab phlebectomy of the varicose veins. This approach
to varicose veins is based on the traditional pathophysiologic description of varicose vein disease, which is considered to develop from the junctions between the deep
venous system and the saphenous veins.37 According to
this theory, the appearance of reflux at the terminal valve
of the saphenous vein is the key point in the progression
of saphenous insufficiency, leading to the appearance of
varicose veins in the tributaries throughout the saphenous
vein from proximal to distal.38 Unfortunately, this theory
TABLE 29-5. Most Frequently Used
Sclerotherapy Agents and Typical
Concentrations Used for Treatment
Vein Diameter (mm)
Sclerosant Concentration
<1
Hypertonic saline 11.7%
Sodium tetradecyl sulfate
0.1 to 0.3%
Polidocanol 0.2% to 0.5%
Glycerin 72% or lidocaine
with epinephrine
1–3
Hypertonic saline 23.4%
Sodium tetradecyl sulfate
0.5% to 0.75%
Polidocanol 0.5 to 1%
4 –6
Hypertonic saline 23.4%
Sodium tetradecyl sulfate
0.75% to 1.5%
Polidocanol 2 to 3%
AU: OR correct
here for Glycerin
72%?
>6
29_Dieter_Ch29_p001-026.indd 9
Hypertonic saline 23.4%
Sodium tetradecyl sulfate
1.5% to 3%
Polidocanol 3 to 5%
• FIGURE 29-8. Tessari method of producing foam
sclerosant. A detergent sclerosant (0.5 mL) in one 3-mLsyringe
and room air (1.5 mL) in another 3-mL syringe and a three-way
stopcock were used to make foam sclerosant after 20 quick
passages of solution. This technique produces a high-quality
foam very quickly.
4/26/10 6:29:00 PM
10 • CHAPTER 29
A
1
2
B
• FIGURE 29-9. Traditional ligation and stripping of
the great saphenous vein (GSV). (A) After ligation of the
saphenofemoral junction, one stripper is passed from the
knee to the groin and another from the ankle to the knee.
(B) The vein is stripped, removing the specimens from the
lower extremity. GSV stripping is usually performed only on
the above-knee segment because of the close proximity
of the great saphenous nerve to the below-knee GSV. The
below-knee nerve is prone to injury during stripping.
does not explain the presence of varicose veins alone
without saphenous reflux. In patients without superficial
venous insufficiency, only stab phlebectomy is performed
(Figure 29-10).
The traditional surgical treatment of patients with varicose veins and great saphenous reflux is associated with
a 20% rate of varicose vein recurrence at 5 years, and up
to 24% of patients require additional treatment.24,39–41
Small saphenous varicose vein recurrence rates have been
reported to be as high as 50% at 5 years.41 In addition,
reported complications include hematoma, infection,
pain, scarring, and saphenous nerve injury in 4% to 7%
of patients.24,39–41 Less frequent complications include
DVT, femoral artery injury, and lymphatic complications.41 Other disadvantages of combined varicose vein
and saphenous vein surgery include the need for general
or spinal anesthesia, prolonged recovery time, and significant postoperative pain.24,39–41
Phlebectomy is the surgical removal of varicose veins
through small skin incisions.24,40 The underlying varicosities are removed using fine mosquito hemostats or hooks,
and the veins are either avulsed or ligated. The procedure
is performed with tumescent anesthesia or under general
anesthesia in an outpatient setting. Transilluminated powered phlebectomy (Trivex) is an alterative to traditional
phlebectomy.24,40 The technique involves an irrigated
transilluminator positioned deep to the varicosities and
a powered suction resector, each introduced through a
skin incision. On activation, the vein is suctioned into the
resector under direct vision, morcellated, and removed by
suction. Trivex is as effective as traditional phlebectomy
in removing varicosities with no significant difference in
pain and morbidity.24,40 One main advantage of this technique is the reduced number of incisions required for
complete phlebectomy. This technique has not gained
widespread acceptance.
• FIGURE 29-10. Phlebectomy of varicose veins. Appearance before (left) and 2 weeks
after phlebectomy (right). Phlebectomy was performed using a #64 Beaver blade.
29_Dieter_Ch29_p001-026.indd 10
4/26/10 6:29:01 PM
LOWER EXTREMITY VENOUS DISEASE • 11
CHIVA. A more recent pathophysiologic description of varicose vein disease is based on the premise that varicose veins
are the consequence of a pathological venovenous shunt
that creates recirculation of blood between the deep and
the superficial system (Figure 29-11).42,43 In this pathophysiologic theory, varicose veins originate in venovenous shunts
with an escape point of reflux, which in turn propagates
retrograde flow from one venous network into another.43
Four venous networks have been classified that depend on
their relationships to the fascial planes of the lower extremity (see Figure 29-11).42,43 The primary venous network,
referred to as R1, comprises all the veins located inside
the deep fascia and belongs to the deep venous system.
Major saphenous
vein
Superficial
fascia
jor
Ma
Superficial femoral vein
us
o
en
ph
sa in
ve
R2
R1
Popliteal vein
R3
Superficial
fascia
Venous
network
R4 longitudinal
R2
R4 transversal
Mino
Superficial
fascia
r sap
heno
us
vein
R1
R3
Perforator
vein
• FIGURE 29-11. The conservative hemodynamic cure of
venous insufficiency (CHIVA). The hemodynamic theory behind
the CHIVA cure is based on the premise that varicose veins
are the consequence of a pathological venovenous shunt that
creates recirculation of blood between the deep and the superficial system.43 The CHIVA strategy redistributes the superficial
venous reflux to the deep veins using a system of shunts
that correct the hemodynamic abnormalities by breaking the
pressure column and suppressing venovenous shunting.
29_Dieter_Ch29_p001-026.indd 11
The secondary venous network, or R2, comprises the veins
contained between the deep and superficial fascia, mainly
the greater and lesser saphenous veins, their major branches,
and the Giacomini vein. The tertiary venous network, or R3
(see Figure 29-11), corresponds to the veins located outside
the superficial fascia, mostly tributaries of the saphenous
vein. Finally, the quaternary venous network, or R4 (see Figure 29-11), comprises the veins located superficially to the
superficial fascia as the tertiary network but that connect
veins from the secondary network. These R4 veins may be
longitudinal if they connect a saphenous vein, or R2, to itself
at different levels, or may be transverse if they communicate
two different veins from the secondary network (e.g., the
great saphenous with the small saphenous vein).43
In 1988, Franceschi described the Conservative Hemodynamic cure of Venous Insufficiency, known by the French
acronym CHIVA.44 The minimally invasive CHIVA strategy redistributes the superficial venous reflux to the deep
veins using a system of shunts that correct the hemodynamic abnormalities by breaking the pressure column and
suppressing venovenous shunting.44 This hemodynamic
surgical approach is based on four strategic principles: fragmentation of the venous pressure column, interruption of
the venovenous shunt, preservation of reentry perforating veins, and suppression of the tertiary and quaternary
venous networks that remain undrained.43 Varicose veins
and symptoms disappear while runoff from the superficial
tissue is preserved via the superficial vein network.42–44
The CHIVA strategy requires specially trained ultrasound technologists, very precise venous duplex ultrasound mapping, and hemodynamic study. The complex
nature of the CHIVA approach and difficult execution
combined with variable results with high recurrence
rates may explain why this approach has not gained
widespread acceptance.37
Ambulatory Selective Varices Ablation under Local
Anesthesi. Another pathophysiologic description of
varicose vein disease is based on the premise that varicose disease originates in the reticular venous plexus (see
Figure 29-2), resulting in the development of subcutaneous varicose veins.45 These subcutaneous veins are the
first to dilate, creating a refluxing venous network. When
this refluxing network becomes large enough, it could
create an aspiratory effect in the interfascial saphenous
vein, leading to decompensation of the vein wall, moving
in an ascending manner to reach the saphenofemoral or
saphenopopliteal junction.37 The great saphenous vein and
the small saphenous veins would be the last veins to experience decompensation as varicose disease progresses.37,45
This may explain the presence of varicose veins without
saphenous reflux.
This pathophysiologic theory has two consequences. If
there were no saphenous reflux, early treatment of varicose
veins would be useful to prevent reflux from spreading to
the saphenous veins.37,45 If there were saphenous reflux,
and up until a certain stage of the disease, the first-line
therapy should include ablation of the superficial varicose
4/26/10 6:29:03 PM
12 • CHAPTER 29
reservoir rather than elimination of saphenous reflux,
which is potentially reversible. Saphenous stripping would
only be indicated in cases in which saphenous reflux is
irreversible.37,45
The ASVAL (Ambulatory Selective Varices Ablation under Local anesthesia) method involves the selective management of superficial venous reflux, depending
on the clinical and hemodynamic context found in each
case.45 Only the superficial varicose reservoir is treated by
phlebectomy; the refluxing saphenous vein is preserved in
the ASVAL method.37
The saphenous vein–sparing ASVAL method results
in significant improvement in saphenous reflux in 90% of
cases and improvement in varicose vein symptoms, with a
16% varicose vein recurrence rate at 3 years.37 In cases in
which the saphenous vein required stripping, a recurrence
rate of 6.3% at 2 years was observed.37
Endovenous
Ablation
of
the
Saphenous
Vein.
Endovenous ablation of the saphenous vein using laser
energy or radiofrequency energy is marketed to practitioners
and patients as a treatment for varicose veins. Endovenous
ablation of the saphenous vein does not directly treat the
varicose veins. Instead, the varicose veins are indirectly
treated by eliminating the underlying saphenous reflux.
Analogous to saphenous vein ligation and stripping, this
procedure treats the superficial venous insufficiency by
ablating the great saphenous vein or small saphenous vein
using an endoluminal technique.24,39–41 The saphenous
vein is not removed. The ablated saphenous vein undergoes coagulative necrosis, shrinkage, and fibrosis. At 6 to
9 months the vein is no longer visible on venous duplex
ultrasound examination.24,39,41 Often combined with phlebectomy of the varicosities, the procedure is most commonly performed using tumescent anesthesia in an office
setting, eliminating the need for general anesthesia and an
operating room setting.24,39–41
VNUS Medical Technologies Inc. (San Jose, CA) received
AU: radio freFDA
approval in 2000 to market its radiofrequency ablaquency ablation ok with
tion
(RFA)
endovenous catheter system. With RFA, the
lowercase…it
is not a trade
catheter
applies
high-frequency alternating current by
name?
direct contact with the vein endothelium, leading to loss
of vessel wall architecture, disintegration, and carbonization of the vessel wall.39 Tissue destruction is precise with
minimal thrombus formation.39
Diomed Inc. (Andover, MA) received FDA approval in
2002 to market its endovenous laser therapy (EVLT) catheter system. With EVLT, the laser catheter delivers laser
energy directly into the vein lumen, resulting in collagen
contraction and destruction of the vein endothelium. Similar to RFA, the treated vein wall thickens and contracts,
and the end result is fibrosis of the vein.39 Since Diomed’s
initial FDA approval, several other competing manufacturers have marketed similar laser ablation systems.
Compared with ligation and stripping, no or minimal scars are created, and the risk of wound infection
is minimal, but RFA and EVLT may be associated with
29_Dieter_Ch29_p001-026.indd 12
local cutaneous side effects.24,39–41 Skin burns have been
reported in fewer than 1% of the RFA and EVLT procedures and can be easily avoided by applying sufficient
tumescent fluid.41 The risk of DVT and saphenous nerve
injury is less than 1%.24,39–41 Small, short-term comparative
studies suggest that EVLT and RFA are equally effective
compared with vein stripping.24,39–41 Long-term studies
are likely to show a clinical benefit for these new procedures compared with ligation and stripping, especially
in the treatment of the small saphenous vein.41 A recent
meta-analysis reported that the success rates (measured
in terms of freedom from recanalization of the treated
great saphenous vein) of RFA and EVLT are about 84%
and 95% after 3 years, respectively.41
Endovenous Ablation Technique. The technique of
both RFA and EVLT is similar. The patient is positioned
supine for treatment of the great saphenous vein, and
venous duplex ultrasonography is used to image the vein
from the saphenofemoral junction to the level of the
medial knee. The great saphenous vein is then punctured
under ultrasound guidance, and a guidewire is inserted into
the vein and advanced into the saphenofemoral junction
(Figure 29-12A). The treatment catheter is then inserted
into the great saphenous vein, and the tip is position 2 cm
distal to the saphenofemoral junction (Figure 29-12B).
Tumescent anesthetic is then infiltrated into the perivenous
tissues (Figure 29-12C). The tumescent anesthetic compresses the vein around the treatment catheter and acts
as a heat sink to protect the perivenous tissues from the
laser or radiofrequency energy delivered to the vein. The
vein is then ablated as the treatment catheter is withdrawn
(see Figure 12D). The treated limb is then wrapped with
an ace wrap, and the patient is instructed to wear a thighlength (20–30 mm Hg) graduated compression stocking
for 2 weeks.
Effect of Saphenous Ablation on Varicose Veins. Similar to the
traditional surgical approach to varicose veins and saphenous reflux, in which ligation and stripping of the saphenous vein is combined with phlebectomy, RFA and EVLT
are often combined with phlebectomy of the varicosities.
However, recent data suggest that phlebectomy may not be
required in most patients with symptomatic varicose veins
and saphenous reflux who undergo endovenous saphenous ablation46–48 (Figure 29-13). In one study, 44 limbs in
45 patients underwent RFA of the great saphenous vein
for symptomatic varicose veins and saphenous reflux.46 The
majority of patients (88.7%) experienced a decrease in the
size of their varicose veins and improvement in symptoms.
Thirteen percent of limbs had immediate resolution of varicose veins, and an additional 28.4% had resolution of varicose veins within 6 months. Forty-one percent of patients
required no additional treatment, and 59% of patients had
sclerotherapy of their residual varicose veins. No patients
required phlebectomy.46 In another study, 184 limbs in
146 patients underwent RFA of the great saphenous vein
4/26/10 6:29:04 PM
LOWER EXTREMITY VENOUS DISEASE • 13
for symptomatic varicose veins and saphenous reflux.47
The majority (65%) of patients had complete resolution of
varicose veins and symptoms; only 25% of patients required
phlebectomy, and 10% had sclerotherapy.47
In our experience with EVLT, 157 procedures were performed in 154 limbs in 139 patients for symptomatic varicose veins and saphenous reflux.48 The majority of treated
patients (n = 123, 88.5%) reported significant improvement
of symptoms and varicose veins and required no further
therapy. Subsequent sclerotherapy of residual symptomatic
varicose veins was required in only 16 patients (11.5%).
No patients required phlebectomy.48
In addition to being an excellent treatment option for
saphenous reflux in patients with symptomatic varicose
A
B
• FIGURE 29-12. Technique of endovenous ablation of the great saphenous vein
(GSV). (A) Ultrasound-guided puncture of the GSV and placement of the guidewire in
the longitudinal view (left) and transverse view (right). (B) Positioning of the treatment
catheter at the saphenofemoral junction. The catheter tip is at the junction (left) and is
positioned 2 cm distal to the junction (right). (C) Infiltration of tumescent anesthetic into
the perivenous tissues. Appearance before (left) and after infiltration (right). (D) The GSV
is ablated as the treatment catheter is withdrawn.
29_Dieter_Ch29_p001-026.indd 13
4/26/10 6:29:04 PM
14 • CHAPTER 29
C
D
• FIGURE 29-12. (continued)
veins, the endovenous ablation procedure is also an excellent treatment option for chronic venous insufficiency of
the superficial venous system.
Chronic Venous Insufficiency
Venous insufficiency is a condition of the veins in which
the one-way valves present within the lumen of the vessel
no longer function properly, leading to valvular dysfunction and incompetence (Figure 29-14). Patients presenting
with venous insufficiency may have either primary chronic
venous insufficiency in which the cause of the valvular
incompetence is unknown (as is the case for the majority of
patients) or secondary chronic venous insufficiency in which
the cause of the valvular dysfunction is most often attributable to an episode of DVT.1,2,49 Although reflux alone is
responsible for primary chronic venous insufficiency, secondary chronic venous insufficiency most often results from
a combination of deep venous obstruction and reflux.
29_Dieter_Ch29_p001-026.indd 14
The underlying pathophysiology in all patients with
chronic venous insufficiency is elevated venous pressure
(venous hypertension).1,2,13,49 In the majority of cases,
venous hypertension is caused by reflux through incompetent valves, but other causes include venous outflow
obstruction and failure of the calf muscle pump because
of obesity or leg immobility. Reflux may occur in the
superficial, deep, or perforator venous systems. It may
occur in one, two, or all three venous systems. A review of
1153 cases of ulcerated legs with reflux found superficial
reflux alone in 45%, deep reflux alone in 12%, and reflux
in both in 43%.1,50
Dysfunction. Valvular incompetence was
originally believed to originate at the saphenofemoral or
saphenopopliteal junctions. The retrograde development
theory of reflux requires incompetence of valves above
the saphenofemoral junction, which in turn causes dilatation and valvular incompetence sequentially in the great
Valvular
4/26/10 6:29:06 PM
LOWER EXTREMITY VENOUS DISEASE • 15
A
B
• FIGURE 29-13. Endovenous laser ablation treatment of varicose veins and superficial venous insufficiency. (A) The right great saphenous vein was treated in this patient
with symptomatic varicose veins and saphenous reflux. Appearance before (left) and
2 weeks after treatment (right). (B) The bilateral small saphenous veins were each treated
2 weeks apart in this patient with symptomatic varicose veins and saphenous reflux.
Appearance before (left) and 3 months after treatment (right). Both patients experienced
complete resolution of symptoms and varicose veins. No further treatment was required.
saphenous vein and its tributaries.1,2,38 This theory has been
found to be inaccurate in a number of patients in whom
saphenous reflux exists without saphenofemoral junction
or saphenopopliteal junction incompetence.51 The theory,
which suggests that valvular incompetence is a consequence of intrinsic structural and biochemical abnormalities of the vein wall, hypothesizes that varicose veins and
29_Dieter_Ch29_p001-026.indd 15
valvular incompetence develop because of underlying
connective tissue defects and altered venous tone.1,2 Varicose and incompetent veins demonstrate diverse histologic abnormalities, including irregular thickening of the
intima, fibrosis between the intima and adventitia, atrophy and disruption of elastic fibers, thickening of individual collagen fibers, and disorganization of the muscular
4/26/10 6:29:09 PM
16 • CHAPTER 29
•
FIGURE 29-14. Valvular incompetence found in patients
with venous insufficiency. Normally functioning vein valves
allow one-way blood flow and prevent back-flow (left and
middle). Incompetent vein valves no longer promote one-way
blood flow but do allow backflow of blood (right).
layers that are heterogeneously distributed throughout
the great saphenous vein and its tributaries.1,2 In addition,
histologic changes suggest that varicose and incompetent
veins have reduced contractility and compliance. Varicose
saphenous veins show an increased collagen and reduced
elastin content. Saphenous smooth muscle content, as
well as total protein content, is reduced, and effective
contraction may be further compromised by fragmentation of the muscle layers.1,2 All of these biochemical and
physiologic changes ultimately result in the development
of valvular incompetence.
Consistent with this hypothesis of valvular incompetence arising from vein wall abnormalities are clinical studies demonstrating a higher likelihood of reflux in patients
with varicose veins compared with patients without varicose veins. Valvular incompetence was found to be present
in 15% of asymptomatic patients without varicose veins.51
The presence of reflux increased to 77% in asymptomatic
patients with prominent, nonvaricose veins and to 87% in
asymptomatic patients with varicose veins. These findings
support involvement of a local or multifocal process in the
development of valvular incompetence.51 Valvular incompetence ultimately leads to venous hypertension.
Tissue Injury Caused by Venous Hypertension. The
clinical findings associated with chronic venous insufficiency and venous hypertension include hemosiderin
pigmentation, stasis dermatitis, lipodermatosclerosis, and
ulceration (Figure 29-15). The incidence of venous ulceration has been shown to be directly related to the ambulatory venous pressure.52 In a study of 153 limbs with
superficial venous insufficiency and 83 limbs with deep
venous insufficiency, no ulceration occurred in limbs with
29_Dieter_Ch29_p001-026.indd 16
ambulatory venous pressures below 30 mm Hg. In contrast, there was a 100% incidence of ulceration in patients
with ambulatory venous pressures above90 mm Hg.52 In
the groups studied, an increased incidence of ulceration
was associated with an increase in ambulatory venous
pressure irrespective of whether the venous problem was
the result of superficial or deep venous insufficiency.52 It is
clear that elevated venous pressure results in tissue injury
and venous ulceration.
The pathophysiologic mechanism for the development of tissue injury and eventual ulceration is unknown;
however, the prevailing theory suggests that prolonged
exposure to venous hypertension causes extravasation of
macromolecules and red blood cells, which in turn leads to
microvascular endothelial cell activation, leukocyte diapedesis, extracellular matrix alterations, and intense collagen
deposition.1,2 The changes in the dermal microcirculation
and interstitium are partially mediated by increased levels
of transforming growth factor β1,, which causes increased
extracellular matrix and collagen production and altered
tissue remodeling by affecting matrix metalloproteinases
and tissue inhibitors of matrix metalloproteinase production.2 The exact cause of ulcer formation is unknown, but
the presence of mast cells suggests that they may play an
important regulatory role.2
Diagnosis. The diagnosis of chronic venous insufficiency
can often be made after a careful history and physical examination. In addition, the clinical evaluation should also determine the nature and the severity of the underlying venous
problem and its impact on the patient’s quality of life.2 The
physical examination should note the presence of varicose
veins, telangiectasias, edema, and the stigmata of chronic
venous insufficiency (pigmentation, dermatitis, lipodermatosclerosis, ulceration, healed ulceration). Measurement
of the ankle-brachial index by Doppler ultrasonography
is essential in excluding arterial insufficiency, which may
be present in up to 20% of patients with chronic venous
insufficiency.1,2,49 Further evaluation requires a venous
duplex ultrasound examination. The venous duplex ultrasound examination helps define the cause of the problem
as congenital, primary, or secondary; the anatomic location
of the problem in the superficial, perforator, or deep systems; and the pathophysiologic mechanism as pure reflux,
reflux with obstruction, or obstruction alone.2
Duplex Ultrasound Examination. Venous
duplex ultrasound examination allows precise anatomic
evaluation and assessment of reflux and obstruction of the
deep, superficial, and perforator venous systems. Venous
duplex ultrasonography also allows accurate determination
of the etiologic, anatomic, and pathophysiologic elements
of the CEAP classification.
Retrograde flow in the lower extremity veins occurs
physiologically just before valve closure and pathologically
as a result of valve absence or incompetence.53 The duration of retrograde flow is also known as the reflux time, or
valve closure time.53 Evaluation of valvular incompetence
Venous
4/26/10 6:29:14 PM
LOWER EXTREMITY VENOUS DISEASE • 17
A
C
B
D
• FIGURE 29-15. Skin changes associated with chronic venous insufficiency.
(A) Hemosiderin pigmentation. (B) Stasis dermatitis. (C) Lipodermatosclerosis.
(D) Ulceration.
in the lower extremities requires that the venous duplex
ultrasound examination be performed with the patient
in the standing position (Figure 29-16). A rapid inflation pneumatic cuff is placed distal to the venous segment under investigation. Augmentation of venous flow
29_Dieter_Ch29_p001-026.indd 17
is observed with inflation, and retrograde flow duration
is measure with cuff deflation. Normal valve closure
time in the deep calf veins and superficial veins is typically 0.5 seconds or less and is 1.0 second or less in the
femoropopliteal veins. Venous reflux is defined as a reflux
4/26/10 6:29:14 PM
18 • CHAPTER 29
Inflation
Deflation
B
A
C
• FIGURE 29-16. Assessment of retrograde flow and valve closure time using the
distal cuff method. (A) A rapid inflation cuff is placed distal to the vein under investigation. Augmentation of flow is observed with inflation, and retrograde flow is observed
with deflation. (B) The duration of retrograde flow (reflux time or valve closure time) is
measured. The valve closure time in this example is greater than 3 seconds. (C) Valve
closure time of less than 1 second in a popliteal vein without reflux (left) and a prolonged
valve closure time of 1.2 seconds in a popliteal vein with reflux (right).
time or valve closure time of more 0.5 seconds in the deep
calf veins and superficial veins and more 1.0 second in the
femoropopliteal veins.53
Assessment of perforator vein reflux requires measurement of the diameter of the perforator vein and the duration of outward flow with calf compression.54 A perforator
vein with a diameter larger than 3 mm and outward flow
duration longer than 0.5 seconds is considered to be incompetent54 (Figure 29-17). The location of the perforator vein
should be noted and distance in centimeters from the floor
should be measured and recorded.
Limitations of venous duplex ultrasound examination are that the detection and assignment of reflux and
obstruction to the various venous segments may be both
operator and equipment dependent, making detection of
29_Dieter_Ch29_p001-026.indd 18
subtle degrees of postthrombotic partial obstruction and
early valve reflux difficult to discern.2
Venography. Venography as a means for assessing the
lower extremity veins for reflux and obstruction has been
replaced by venous duplex ultrasound examination. However, venography will always have its place in the evaluation
and assessment of complex venous conditions. Ascending
venography provides an overall anatomic map of the lower
extremity veins and pathways of venous return. Descending venography is valuable for investigating the venous
valves, distinguishing primary valve disease from secondary
disease, and estimating the severity of reflux. Venography
is also required for planning deep venous reconstructive
surgical procedures.
4/26/10 6:29:20 PM
LOWER EXTREMITY VENOUS DISEASE • 19
• FIGURE 29-17. Assessment of perforating vein reflux.
A perforator vein with a diameter larger than 3 mm and outward
flow duration longer than 0.5 seconds is considered to be
AU: Spell out incompetent. This perforator vein arising from the posterior tibial
PT in this
figure. vein has a diameter of 6 mm and demonstrates outward flow.
Treatment. Venous ulceration remains the most common
indication for treatment of chronic venous insufficiency.49
Leg edema, pigmentation, stasis dermatitis, and symptomatic varicose vein disease with concomitant venous insufficiency are additional indications for the treatment of
patients with venous insufficiency. The goal of treatment
is aimed at lowering the venous pressure to allow optimal
healing of the underlying tissue injury. Prevention of ulcer
recurrence and improvement of patient quality of life are
additional therapeutic goals.
Venous ulcer treatment requires two components, treatment of venous hypertension and aggressive local wound
care. The following discussion addresses the available treatments aimed at reducing venous pressure. For a comprehensive discussion of local wound care of venous ulcers,
readers are referred to several excellent reviews.11,55–57
Compression Therapy. The benefit of compression
therapy in the treatment of patients with chronic venous
insufficiency is well documented. Compression therapy
is essential for wound healing and is often sufficient to
heal the majority of venous ulcers. Compression can be
accomplished with a variety of techniques and devices.
Healing, however, may be prolonged, and ulcer recurrence
remains a major problem. Patient education is important,
and patients must understand that they have a chronic disease that can only be managed and not necessarily cured.
29_Dieter_Ch29_p001-026.indd 19
Compliance with compression therapy is essential to heal
ulcers and minimize recurrence.
Patients with venous insufficiency experience the same
benefits from graduated compression stockings as patients
with varicose vein disease. Compression stockings have
been shown to improve symptoms and venous hemody- AU: refs 58
and 29 were
namics in patients with venous insufficiency. 29,49, 58,59 The the same, so
deleted 58
benefits of graduated compression stockings in venous and renumbered from
ulcer healing were demonstrated in a study of 113 patients here on.
29
with venous ulcers. Healing occurred in 93% of patients
treated with 30 to 40 mm Hg, below-knee elastic compression stockings. Compliance with therapy was crucial. Ulcer
healing occurred in 97% of compliant patients compared
with 55% of noncompliant patients. The mean time to
achieve healing was 5 months. Ulcer recurrence was 29%
at 5 years in compliant patients and 100% at 3 years in
noncompliant patients.29 The guidelines for the appropriate use of graduated compression stocking in patients with
chronic venous disorders are shown in Table 29-6.49
Other forms of compression therapy available include
multilayer compression wrappings, medicated compression therapy such as Unna’s boot, and intermittent pneumatic compression devices.29,49,58,59 Multilayer compression
wrappings provide sustained, graduated compression to the
affected lower extremity. Most wrappings are applied for
1 week at a time or less. Compression wrappings are useful
when stockings cannot be put on by the patient because of
arthritis of the hands or obesity. Unna’s boot is a medicated
compression boot that is used for treating venous ulcers of
the ankle and calf. It is a rolled gauze bandage impregnated
with calamine, zinc oxide, glycerin, sorbitol, gelatin, and
magnesium aluminum silicate that is applied from the base
of the toes to the knee.49,58,59 A Kerlix gauze is then applied
followed by an elastic bandage (ACE wrap). Unna’s boots
are changed weekly and have been shown to be beneficial
in the treatment of venous ulcers. A number of pneumatic
compression devices designed for the treatment of lymphedema are also useful in patients with chronic venous
insufficiency. These devices are especially useful in patient
with limited ambulation.49 All compression devices apply
external compression to the lower extremities. Patient
compliance is critical for successful therapy.
Surgical and Endovenous Treatment. After careful
assessment of the patient with chronic venous insufficiency,
venous duplex ultrasound examination usually identifies the source of the underlying valvular incompetence.
The superficial, deep, or perforator venous system may be
the source of valvular dysfunction, ultimately resulting in
venous hypertension. One, two, or all three venous systems
may be involved. In addition to compression therapy, additional surgical or endovenous treatment may shorten the
time to healing and prevent venous ulcer recurrence.
The site(s) of valvular incompetence usually dictate the
treatment options available to the patient. Table 29-7 lists
the surgical and endovenous treatment options available
according to the venous system involved. Ablative surgical
4/26/10 6:29:23 PM
20 • CHAPTER 29
TABLE 29-6. Indications for Graduated Compression Stockings49
Indication
Compression Pressure (mm Hg)
10–20
20–30
Duration
≥40
30–40
Chronic Venous Disorders
C0s
First choice
If necessary
Symptomatic
C1s
First choice
If necessary
Symptomatic
C2
First choice
If necessary
C3
If possible
First choice
If necessary
Symptomatic
C4
First choice
If necessary
Routine
C5
If possible
First choice
C6
Symptomatic
If necessary
First choice or bandages
After procedures
If possible
First choice
Always in deep CVD
Until healing
If necessary
Variable
Venous Thromboembolism
Prevention
First choice
At risk
Therapy
First choice or bandages
If necessary
4 wks
Postthrombotic Syndrome
AU: Please
spell out
CVD?.
AU: What
page numbers?
Prevention
First choice
If necessary
Therapy
If possible
First choice
>1 y after DVT
If necessary
Indefinite
CVD, ; DVT, deep venous thrombosis.
Adapted from Partsch H: Evidence-based compression therapy. VASA. 2003;32(suppl 3).
TABLE 29-7. Chronic Venous Insufficiency
Treatment Optionsa
and endovenous procedures are all that is needed for treatment of superficial and perforator valvular incompetence,
but treatment of the deep venous insufficiency requires
more complex reconstructive surgical procedures.
Superficial venous incompetence
Ligation of the saphenous veins
Ligation and stripping of the saphenous veins
Ultrasound-guided foam sclerotherapy
Endovenous ablation
Perforator vein incompetence
Linton procedure
Subfascial endoscopic perforator surgery
Ultrasound-guided foam sclerotherapy
Endovenous ablation
Deep venous incompetence
Valvular reconstructive procedures
Axillary vein valve transfer
a
The surgical and endovenous treatment options listed are
based on the location of valvular incompetence.
29_Dieter_Ch29_p001-026.indd 20
Superficial Venous System. Great saphenous vein reflux
has long been treated with ligation and stripping.24,39–41
Because of the close proximity of the sural nerve to the
small saphenous vein (see Figure 29-4), ligation alone has
traditionally been the preferred treatment of small saphenous vein reflux. A recent study of small saphenous vein surgery demonstrated no difference in nerve injury incidence
when the small saphenous vein was ligated and stripped
compared with ligation alone (28% numbness in both
groups).60 Recurrent reflux at 1 year, however, was significantly higher in the ligation only group (32% versus 13%)
compared with ligation and stripping.60
Our own experience with EVLT of the small saphenous vein in 95 limbs in 82 patients demonstrated a 98.8%
small saphenous ablation rate at 6 months with significant
improvement in symptoms.61 Complications were minimal, and postprocedure numbness was seen in only 1.2%
of patients.61
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LOWER EXTREMITY VENOUS DISEASE • 21
Endovenous ablation of the saphenous veins using
EVLT or RFA as a treatment of superficial venous insufficiency has essentially replaced the traditional surgical
approach (Figure 29-18). Short term studies have shown
that EVLT and RFA are equally effective compared with
vein stripping.24,39–41
Ultrasound-guided foam sclerotherapy is also an excellent method to obliterate incompetent segments of the
great and small saphenous veins, which is frequently followed by accelerated healing of venous ulcers.49 Ultrasound-guided foam sclerotherapy in 1411 limbs showed
occlusion in 88% of great saphenous veins and 82% of small
saphenous veins after a mean follow-up of 11 months.
Smaller series showed 69% complete sclerosis in
99 limbs after 24 months of follow-up, 44% occlusion in
211 limbs after 5 years of follow-up, and 88% occlusion
in 143 limbs after 6 weeks of follow-up.39,41
Surgical and endovenous procedures available for treatment of perforator vein reflux
include the traditional Linton procedure (open subfascial
perforator vein interruption), subfascial endoscopic perforator surgery (SEPS), ultrasound-guided foam sclerotherapy, and endovenous radiofrequency or laser ablation.49,54
Perforator Venous System.
The Linton procedure is no longer performed because of
the wound healing problems and ulcer recurrence associated with the longitudinal incision required for exposure
of the subfacial perforator veins.54 SEPS is a laparoscopic,
closed approach to the treatment of incompetent perforator veins that uses micro instruments, carbon dioxide
insufflation of the subfacial space, and visualization of the
operative field on a video screen. Incompetent perforator
veins are then clipped and divided.62 The North American
SEPS registry reported an 88% ulcer healing rate at 1 year
and a recurrence rate of 13% at 2 years.63 When combined
with great saphenous vein stripping, ulcer recurrence was
13% at 5 years.63
Ultrasound-guided foam sclerotherapy of incompetent
perforator veins achieves ablation of the refluxing perforator vein without the need for general anesthesia or an operating room setting. Initial reports appear promising with
one study reporting excellent ulcer healing rates of 83%
at 6 months in 113 patients.64 Newer endovenous ablative
procedure using radiofrequency and laser energy to ablate
incompetent perforator veins have recently become available. Similar to RFA and EVLT of the saphenous veins,
the perforator vein is accessed percutaneously under ultrasound guidance and ablated with a special radiofrequency
ablative stylet or a laser fiber. Both endovenous ablation
procedures appear to be promising.65,66
Deep venous reconstructive procedures are routinely performed in only a few specialized
centers. In patients with incompetent deep venous valves
amenable to surgical repair (i.e., the majority of primary
valvular incompetence patients) versus valves that have
been destroyed because of DVT (secondary valvular incompetence), valvuloplasty has been shown to be a clinically
valuable procedure associated with venous ulcer healing
rates in the range of 65% to 80% at 5 years and longer.67,68
In patients with secondary deep vein incompetence,
axillary vein transfer is the main surgical option for the
treatment for deep venous valves that have been destroyed
by DVT. In this procedure, a competent valve-bearing
segment of axillary vein is taken and sutured to the deep
venous system (common femoral vein or popliteal vein)
as an interposition graft. Ulcer healing rates have been
reported to be 40% to 65% at 5 years or longer.69,70
Deep Venous System.
A
Deep Venous Obstruction. Chronic deep venous
obstruction of the lower extremities is most commonly
caused by absent or incomplete vein recanalization after
an episode of DVT.49 The majority of patients (70%–80%)
with iliac vein thrombosis have incomplete recanalization
even with appropriate anticoagulation.71,72 In addition,
deep vein obstruction has been shown to occur with reflux
in 55% of symptomatic patients and is the principle cause
of symptoms in one-third of all patients presenting with
the postthrombotic syndrome.72
May-Thurner syndrome, or iliac vein compression syndrome (nonthrombotic iliac vein occlusion), was found to be
the cause in 40% of patients treated for iliocaval obstruction.73
Chronic
B
• FIGURE 29-18. Treatment of superficial venous insufficiency in a patient with below-knee, great saphenous vein
reflux and a venous ulcer. (A) A 54-year-old man with a right
medial ankle venous ulcer for 6 months. Before laser ablation
of the below-knee great saphenous vein. (B) Complete healing
had occurred within 2 weeks after the procedure.
29_Dieter_Ch29_p001-026.indd 21
4/26/10 6:29:24 PM
22 • CHAPTER 29
The occlusion typically occurs in the left common iliac vein
at the point where the right common iliac artery crosses over
the proximal left common iliac vein. A web or intraluminal
band is sometimes present.49,73 Other less common causes
of chronic iliocaval obstruction include benign or malignant
tumors, retroperitoneal fibrosis, iatrogenic injury, irradiation,
cysts, and aneurysms.49
Chronic deep venous obstruction of the lower extremities is described as a blockage of the outflow of blood from
the lower limbs.74 In contrast to the arterial system, peripheral resistance in the venous system is low, so a venous
stenosis would likely become hemodynamically significant at a lower degree of stenosis compared with an artery
with the same degree of stenosis.74 Critical venous outflow
obstruction has not been defined; therefore, the diagnosis is
made by morphologic investigation. Morphologic obstruction greater than 50% as measured by intravascular ultrasonography has arbitrarily been chosen for stenting.75,76
success approaches 100% in patients with postthrombotic
iliocaval obstruction and in patients with May-Thurner
syndrome (Figure 29-19).77 In one report, revascularization of the iliac vein was performed in 38 limbs with
iliocaval obstruction.78 In 28 of 38 limbs, stenting was
extended into the common femoral vein. Large-caliber
(14 or 16 mm for the iliac vein), flexible, self-expanding
stents were used. Primary, primary assisted, and secondary patency rates at 24 months were 49%, 62%, and
76%, respectively. There was significant symptomatic
improvement in the stented group. Morbidity was minimal. In another report by the same investigators, stents
were placed in 455 limbs with chronic, nonmalignant
obstruction (stenosis or occlusion). At 3 years, primary
patency, primary assisted, and secondary patency rates
were 75%, 92% and 93%, respectively. Nonthrombotic
limbs had better primary patency than thrombotic limbs
(89% versus 65%).79
Venoplasty and Iliocaval Stenting. Venoplasty and
Surgical Bypass Procedures. Before the advent of
venoplasty and iliocaval stenting, patients with iliocaval
obstruction were treated with surgical bypass reconstruction. Iliac vein obstruction was usually managed by Palma
iliocaval stenting has become the first-line therapy in the
treatment of patients with chronic deep venous obstruction because of its minimally invasive nature. Procedural
A
B
C
• FIGURE 29-19. May-Thurner syndrome. A 42-year-old woman had recurrent
episodes of deep venous thrombosis in the left lower extremity. (A) An antegrade common
femoral vein approach was used, and an ascending venogram showed narrowing of
the left common iliac vein (arrow) along with venous collateral vessels consistent with
May-Thurner syndrome. (B) Two 20- × 55-mm self-expanding stents were placed.
(C) A completion venogram shows the position of the stent in the inferior vena cava and
satisfactory venographic resolution of the left common iliac lesion.
(From Mussa FF, Peden EK, Zhou W, et al: Iliac vein stenting for chronic venous insufficiency.
Tex Heart Inst J. 2007;34:60–66; with permission.)
29_Dieter_Ch29_p001-026.indd 22
4/26/10 6:29:25 PM
LOWER EXTREMITY VENOUS DISEASE • 23
femorofemoral bypass or a unilateral bypass between the
femoral vein distal to the obstruction and the contralateral iliac vein or IVC.80 These major surgical procedures
often required lifelong anticoagulation and a temporary
or continuous adjunctive arteriovenous fistula to keep the
bypass patent. Furthermore, indications for surgical intervention were symptoms associated with severe postthrombotic syndrome, namely debilitating, refractory venous
ulceration. Although reports on the crossover bypass technique claim durable symptomatic relief, most studies lack
consistent follow-up with venography.81,82 At the present
time, the only two indications for surgical bypass are failure of endovascular intervention and the need for venous
reconstruction after resection for malignancy.
Analysis of 412 Palma operations published in nine series
revealed clinical improvement in 63% to 89% of patients.
Patency rates ranged between 70% and 85%.49 Experience
with femorocaval or iliocaval bypass is limited; however
2-year primary and secondary patency rates of 37% and
54%, respectively, have been reported.49
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