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M. C. Siah et al.
tions enrolled in BTK angioplasty studies present
a selection bias based on matching the target
lesion length on the type of studied device.
Studies on stenting, evaluating balloon
expandable and self-expandable stents, bare
metal and DESs, were focused on short and proximal BTK lesions, while studies on uncoated and
DCBs enrolled longer BTK lesions extended to
the distal third of the tibial vessels.
In summary, for short (<5cm) and proximal
BTK lesions DCBs have demonstrated better
results in terms of patency, TLR, and amputations and improved wound healing compared to
uncoated balloon angioplasty and bare metal
stent (100–102).
Treatment ofBelow theAnkle (BTA)
Arteries
If the best strategy in revascularizing patients
with CLTI is restoration of pulsatile in-line ow
to the foot vessel, possibly a DR to the wounded
angiosome, BTA vessel disease represents the
nal obstacle. Many authors proposed BTA intervention as a new strategy to improve clinical success of revascularization.
A recent systematic review and meta-analysis
concluded that the currently available evidence
suggests that additional BTA angioplasty is a safe
and feasible procedure, and there is a potential
benet in wound healing (103).
Despite these positive ndings, before going
aggressively into BTA vessels, we believe it
extremely important to consider a critical
appraisal of this literature.
Studies on FP and BTK endovascular treatment include thousands of patients, many randomized control trials, and long-term follow-up.
The amount of data on BTA vessel angioplasty is
much lower: the only metanalysis by Huinzig
et al. included 10 studies of moderate quality,
reporting a total of 478 patients with BTA angioplasty performed in 524 legs (103). Moreover,
these studies are heterogeneous, the authors
applied different techniques such as endoluminal
or subintimal approaches, antegrade, retrograde
and pedal-plantar loop technique, plain old bal-
loon angioplasty with uncoated balloons and
DCBs, and stenting. We lack data on restenosis
rate and long-term follow-up and no randomized
control trials are available. In conclusion BTA
angioplasty is still in an artisanal era, and we can
share only anecdotal advice based on our
experience.
In line with the GVGs, the rst advice is to
study BTA vessel disease with high-quality imaging. BTA vessels represent the main obstructive
target of SAD, which is strongly associated with
diabetes, hemodialysis, and CLTI (104). To evaluate the presence and the degree of SAD is a key
point in dening the prognosis and the strategy of
any revascularization procedure in patients with
CLTI.Due to the difculty of obtaining a highquality imaging of the BTA vessels and quantifying SAD (repeated contrast dye injection,
movement artifacts), we proposed a calcium
score on the plain radiographs of the foot, which
has demonstrated a high sensitivity and specicity for SAD (105). SAD and MAC scores are
both strong predictors of major adverse limb
events in patients with CLTI.
The second advice is to respect what is, more
or less, function. After treating big artery disease
to the ankle level, before going BTA, consider the
disease extension and the collateral vessel function. We suppose that SAD is not a yes or no phenomenon; it should take months or years to
slowly progress in the vascular tree. The quantitative evaluation of SAD is an open question, for
which we lack standardized angiographic systems, and we rely on peripheral perfusion tests
such as transcutaneous oxygen tension and toe
pressure. In case of doubts, stop the procedure
and wait days or weeks for the clinical response
to big artery disease treatment, looking at wound
evolution and tissue perfusion indexes. Go BTA
only with clear clinical indications and angiographic targets.
“No-Option” Patients withCLTI
Not every patient with CLTI can be revascularized due to vascular and clinical factors. The fate
of these no-option patients with CLTI is poor,
21 Arterial Disease Management intheLimb Salvage Patient: Endovascular andOpen Bypass
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283
with rates of limb loss up to 46% at 1year (106–
111). Moreover, these patients suffer from a low
quality of life and higher rates of mortality in
comparison to other patients with CLTI (106,
110).
Kim etal. proposed a new classication of no-
option patients with CLTI in ve types: type I—
severe and pedal occlusive disease (desert foot
anatomy) for which there is no accepted method
of repair; type II—lack of suitable venous conduit for bypass in the setting of an acceptable target for bypass; type III—extensive tissue loss
with exposure of vital structures that renders salvage impossible; type IV—advanced medical
comorbidities for which available revascularization options would pose a prohibitive risk; and
type V—presence of a nonfunctional limb (106).
Type I no-option patients are characterized by
the desert foot anatomy, which is the nal expression of SAD-MAC.Their prevalence in patients
with CLTI varies from 20% to 45% and is associated with aging, diabetes, and ESRD (110). In
these patients, alternative therapies should be considered such as primary major amputation, palliative care, or foot vein arterialization (FVA). FVA
was proposed as the last attempt, obtaining a limb
salvage rate between 55% and 75% at 1year, with
very with few complications.
In recent years, following the evolution of the
therapy toward less invasive approaches, some
authors proposed totally percutaneous techniques
of FVA, describing positive single center case
series, treated with off-label devices (111–113).
These are quite complex and difcult maneuvers,
whose reproducibility is as yet unknown.
The main attempt in developing a totally percutaneous deep vein arterialization was realized
by the LimFlow company through a series of
dedicated tools designed to perform an arteriovenous stula at the tibial artery level, diverting
blood ow to the deep venous plantar system
through dedicated covered stents. The preliminary studies showed >96% technical success rate
and 70% amputation-free survival at 1year and
multicentric studies are ongoing. In the near
future, FVA could be proposed as a standard procedure in no-option patients with CLTI, before
proceeding with a major amputation (114–117).
Conclusion
The management of a CLTI patient is exceedingly challenging. Interventionalists are armed
with a host of medical, open surgical, and endovascular tools to treat this complex disease process. The decision between open and endovascular
therapy delivery is nuanced, and even in the best
interventionalists hands, avoiding major amputation and cardiovascular morbidity remains a challenge. Continued developments and
advancements may provide new options for the
treatment of CLTI, in the hopes of achieving
effective and durable therapies for patients.
Venous Disease Management
flows in one direction
allow blood to drain and pool
intheLimb Salvage Patient:
Diagnostics, Compression,
andAblation
BiancaCutler, NikitaPatel, andMisakiKiguchi
Introduction
Chronic venous disease (CVD) of the lower
extremities encompasses a wide range of disease
pathologies. Venous hypertension generally
occurs as a result of either a structural or obstructive pathophysiology, or a combination of both.
Structural obstruction of venous outow is seen
in various disease states including MayThurner’s, deep vein thrombosis (DVT), and retroperitoneal brosis, whereas CVD related to
functional reux occurs due to a dysfunction of
vein valves. Healthy veins carry blood towards
the heart, and competent valves prevent retrograde venous ow. However, the failure of vein
valves to close appropriately allows backow
(e.g., reux) of blood, preventing the reduction in
venous pressure that normally occurs with walking or exercising. This reux of venous blood
ultimately results in venous hypertension [1]
(Fig. 22.1). Excessive venous hypertension can
produce a wide distribution of symptoms
B. Cutler · M. Kiguchi (*)
Department of Vascular Surgery, MedStar
Washington Hospital Center, Washington, DC, USA
e-mail: Misaki.M.Kiguchi@medstar.net
N. Patel
Piedmont Heart Institute, Division of Vascular
Surgery, Piedmont Atlanta Hospital,
Atlanta, GA, USA
22
NORMAL VEIN
Valves ensure blood
Fig. 22.1 Valves in a normal vein and diseased vein.
(Reprinted with permission from Medtronic, Inc.)
described by the CEAP classication, ranging
from asymptomatic to clinical ndings of edema,
skin changes, or venous ulcers to the legs [2].
The progression and sequelae of venous
insufciency in the setting of chronic venous
disease contributes signicantly to the economic
healthcare burden and negatively impacts patient
quality of life [3]. Fortunately, the emergence of
minimally invasive, safe, and effective ofcebased treatments has signicantly improved outcomes in chronic venous disease progression
and has largely improved patient satisfaction.
DISEASED VEIN
Valves that cannot close
© Springer Nature Switzerland AG 2023
C. E. Attinger, J. S. Steinberg (eds.), Functional Limb Salvage,
https://doi.org/10.1007/978-3-031-27725-2_22
285
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B. Cutler et al.
Anatomy
The lower extremity venous system is divided
into three major components: the supercial,
deep, and perforating systems. The supercial leg
veins are located between the dermis and muscle
fascia, while the deep veins run just below the
muscle fascia. The deep and supercial systems
are connected by a network of perforating veins.
Supercial veins include major truncal veins:
the great saphenous vein (GSV) and the small
(lesser) saphenous vein (SSV), accessory veins
(anterior and posterior), and any tributaries or
branches that originate from the supercial
venous system [4]. Excluding any anatomical
variants, the GSV is a continuation of the dorsal
venous arch in the foot, traveling anteriorly along
the medial malleolus and ascending along the
medial aspect of the leg. It drains into the deep
system via the saphenofemoral junction (SFJ) and
perforating veins. The SSV begins on the lateral
aspect of the foot and travels posteriorly along the
back of the calf, ultimately draining into the popliteal vein at the saphenopopliteal junction (SPJ).
Anatomical variants include draining into a posterior medial tributary of the GSV, femoral vein or a
vein of Giacomini [5] (Fig.22.2).
Deep veins include the iliac, femoral, profunda, popliteal, peroneal (bular), soleal, tibial,
and plantar (foot) veins. These veins course from
the foot to the upper thigh. Approximately 85%
of the total lower extremity blood volume is
transported via the deep venous system [4].
Perforating veins are bridging channels that
link the supercial and deep venous systems
through the fascia (Fig.22.3). Competent perforator veins support unidirectional blood ow
from the supercial to the deep system. They are
Femoral Vein
(Deep System)
Saphenofemoral
Junction
(SFJ)
Great
Saphenous
Vein
(GSV)
Popliteal Vein
(Deep System)
Small
Saphenous
Vein
(SSV)
Fig. 22.2 Supercial venous anatomy. (Reprinted with
permission from Medtronic, Inc.)
Fig. 22.3 Perforator
veins. (Reprinted with
permission from
Medtronic, Inc.)
Failed valve
Perforator vein
Superficial vein
Deep vein
22 Venous Disease Management intheLimb Salvage Patient: Diagnostics, Compression, andAblation
287
integral in equilibrating blood ow during calfmuscle contraction (walking) by facilitating
venous outow from supercial veins as the deep
system pressure drops. However, it is important
to note that perforators may have physiologic
bidirectional capabilities depending on the phase
of the calf-pump activity, and thus “reux” of the
perforator veins alone is not considered a cause
for venous hypertension [5]. There are approximately 60 perforating veins in a lower extremity,
excluding anatomical variants [6]. However,
there are four clinically important perforator
groups that have been identied, grouped by distribution: upper thigh (Hunterian), lower thigh
(Dodd’s), at knee level (Boyd’s), and in the calf
region (Cockett’s) [5].
Normal Venous Valves
Venous valves are integral in maintaining unidirectional venous circulation against gravity
and intra-abdominal pressure [7]. Normal
venous valves are bicuspid and promote blood
ow from peripheral supercial veins to the
central deep veins, preventing pathologic
reux [5]. These valves are more frequent in
distal veins, located the farthest from central
venous circulation. There are approximately
10–20 valves in the GSV and 10–12 valves in
the SSV [8].
Valves in the deep system vary in number and
location as well; both the tibial and the peroneal
veins have numerous valves, spaced apart at
approximately 2 cm intervals. Most popliteal
veins have one to two valves. The femoral veins
may contain an average of ve valves across the
mid and distal femoral veins, though there are
generally one or no valves in the common femoral vein above the level of the saphenofemoral
junction. The inferior vena cava and the external
iliac veins may be absent of valves altogether [9,
10]. Thus, the deep system relies heavily on ade-
quate use of the calf-pump muscle contraction
that occurs with walking to promote venous
return.
Perforating veins have been shown to have
between one to three venous valves [9].
Dysfunction of these critically important valves
in any component of the lower extremity veins
causes retrograde ow, ultimately resulting in
chronic venous insufciency.
Pathophysiology
The etiology of valvular incompetence resulting
in venous hypertension is generally classied as
either venous reux or venous obstruction, or a
combination of both derangements [4]. Venous
disease from reux results from progressive
venous remodeling due to persistent hemodynamic stress. Obstructive incompetence occurs
due to valve damage and limited venous recanalization after deep venous thrombosis or due to
extrinsic compression [5]. Mechanical contributions to venous hypertension include the failure
of an effective calf muscle pump, thus limiting
effective venous return [11].
Inammatory changes to the venous vessel
wall are thought to be largely involved in the
development and progression of venous reux
and related valve incompetence. There is evidence to suggest that inammatory changes
precede the development of observable valvular
incompetence and varicose veins [5]. Low shear
stress within the vein as a result of vein dilation
and venous reux can promote release of
inammatory markers, increased collagen, and
decreased elastin content. The resulting chronic
inammation ultimately progresses to the clinical manifestations of chronic venous insufciency (CVI) [4].
Deep system valvular venous disease has multiple etiologies, the most common of which
(approximately 30%) is primary valvular incompetence. Deep venous reux may also occur due
to post-thrombotic injury after DVT, extramural
compression (most commonly left common iliac
vein compression by the right common iliac
artery, e.g., May-Thurner’s syndrome), and more
rarely, congenital valve agenesis or hypoplasia
[12–14].
Regardless of a reux-related or obstructive
pathology, the resulting inammation and dysfunction of vein walls and valves within both the
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B. Cutler et al.
supercial and deep venous systems cause
chronic venous hypertension and dilation, resulting in a repeating cycle of pathologies that potentiate one another (abnormal venous ow,
increased local venous pressure, damaged venous
valves, and continued inammatory response to
the venous endothelial cells), ultimately contributing to CVD progression [15].
Epidemiology
CVD is a common condition, although its overall reported prevalence is difcult to capture as
the disease clearly remains underdiagnosed.
The European Society of Vascular Surgery estimates the prevalence of CVD in the adult population to be as high as 60%, particularly among
populations in developed countries [16]. There
is great variability depending on the study population and demographics, and the condition
itself is thought to be largely underreported due
to variability of symptoms. To better detect and
stratify an accurate diagnosis, venous disease is
stratied according to severity using the CEAP
classication system, which is recommended
for clinical practice. The CEAP classication
was introduced in 1994 by the American Venous
Forum (AVF) (later revised in 2020). The classication is based on clinical signs of venous
disease (C), etiology (E), anatomy (A), and the
underlying pathophysiology (P) (Fig. 22.4)
[17].
The linchpin of appropriate diagnosis and
subsequent management of CVD is establishing
the accurate clinical class of the disease. Clinical
class describes the full spectrum of venous disorders, ranging from no physical signs of venous
disease to venous ulceration, which represents
the most severe form of venous disease. The clinical classication stratications are as follows:
no signs of visible or palpable venous disease
(C0), telangiectasia or reticular veins (C1), varicose veins (C2), edema (C3), skin changes,
including hyperpigmentation or eczema (C4a),
lipodermatosclerosis, atrophie blanche (C4b) or
corona phlebectatica (C4c), presence of healed
ulceration (C5), or presence of active ulceration
(C6). The presence or absence of symptoms is
documented as S (symptomatic) or A (asymptomatic). Etiology is either congenital (Ec), primary (Ep), secondary (Es), or no cause identied
(En). Anatomic classication refers to the supercial system (As), perforator involvement (Ap),
deep system (Ad), or no location identied (An).
Pathophysiology is classied under reux (Pr),
obstruction (Po), or both [16].
With standardized clinical reporting (using the
C of the CEAP scale), it is possible to provide
more accurate reports of disease prevalence for
each clinical class, as well as progression rates
though clinical classes over time and the relation-
C class Description
C
0
C
1
C
2
C
2r
C
3
C
4
C
4a
C
4b
C
4c
C
5
C
6
CVD, Chronic venuous disease.
Each clinical class subcharacterized by a subscript indicating the presence (symptomatic, s) or absence (asymptomatic, a) of symptoms attributable
to venous disease.
Fig. 22.4 CEAP classication system. (Reprinted with permission from the Journal of Vascular Surgery: Venous and
Lymphatic Disorders. License Number 502659091955 [18])
No visible or palpable signs of venous disease
Telangiectasias or reticular veins
Varicose veins
Recurrent varicose veins
Edema
Changes in skin and subcutaneous tissue secondary to CVD
Pigmentation or eczema
Corona phlebectatica
Lipodermatosclerosis or atrophie blanche
Healed
Active venous ulcer
Recurrent active venous ulcer
22 Venous Disease Management intheLimb Salvage Patient: Diagnostics, Compression, andAblation
289
ship to risk factors, which impacts the development of CVD. The European Society for Vascular
Surgery published the most recent and comprehensive data in 2015 from updated epidemiologic
studies: telangiectasia and spider veins (C1) have
been reported to affect up to 80% of the population. Varicose veins (C2) are common, with a variable reported incidence ranging from 20% to 64%.
C3-C6 affects approximately 5% of the population, with the prevalence of severe symptoms (C5-
6) estimated at approximately 1–2% [16].
Causes andRisk Factors
While the development of primary CVI of the
supercial or deep venous system can be idiopathic, there are many known risk factors that
contribute to its progression.
Obstructive disease affecting the deep system
is generally due to the aforementioned postthrombotic disease and/or extramural compression of the iliac vein. After development of DVT,
spontaneous lysis occurs in the acute period,
while venous recanalization occurs over months
to years after sustaining the thrombus [19].
Although the extent of recanalization depends on
a myriad of factors (including extent of original
thrombus, location, inammation and inammatory mediators), the process itself generates relative obstruction and reux in the deep and
supercial systems. Incomplete recanalization
may lead to outow obstruction, further potentiating venous hypertension [20].
Primary valvular incompetence that occurs in
the supercial system is thought to be due to a
variety of factors. The European Society for
Vascular Surgery’s 2015 updated clinical practice
guidelines report older age as the most important
risk factor for both symptomatic and asymptomatic varicose veins and CVI [16]. Historically,
gender was thought to be a signicant risk factor,
although more recent studies demonstrate inconclusive gender inuence. While several studies
have highlighted that women have a higher risk
for development of varicose veins (approximately
2–3 times higher risk) than men, a similar prevalence of varicose veins has been documented
among both men and women who have not been
pregnant, which suggests that pregnancy is an
inuential risk factor in development of C2 disease [21]. However, existing literature remains
conicted in gender inuence: the notable
Edinburg Vein study reports that C2 disease may
be even more common among male subjects in
the general population. While there is no obvious
gender inuence concerning development of
venous disease, the gender inuence diminishes
with age [16].
Obesity is known to have a damaging effect on
venous return. A body mass index greater than
25 kg/m2 signicantly increases the risk for
CVI. Excess weight, particularly around the
abdominal area, increases intra-abdominal pressure and thus alters the hemodynamics of the
lower extremity veins that are already under
stress to counteract gravity [22]. Additionally, a
positive family history also increases the prevalence of CVI among individuals. Many studies
have revealed a correlation between positive family history and the risk of developing venous disease; however, a responsible specic genetic
disturbance has not been identied to explain the
heredity [16].
Ethnicity is thought to play a role in CVI, but
most studies are based on gures from developed
countries in the western world. More studies are
needed to evaluate evidence from other geographical locations. Existing data reveals prevalence of C1-C6 disease in all demographics, with
unequal distributions of C5-C6 by region [16].
Some recent studies on the impact of race on CVI
demonstrate that African-American patients
present with more advanced venous disease at a
younger age, compared to Caucasians [23]. In
addition, lower socioeconomic status portended
to a more advanced venous disease presentation,
reecting a possible delay in diagnosis and intervention [24]. Other risk factors for CVI include
damage to the deep veins (secondary to DVT or
trauma), and poor function of the calf muscle
pump through inactivity, immobility, or abnormal gait [1]. Thus, lifestyles or careers that
include prolonged periods of standing or sitting,
with limited use of the calf-muscle pump,
increase the risk for vein damage.
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B. Cutler et al.
Clinical Presentation ofVenous
Hypertension
The clinical presentation of CVI and resulting
CVD runs the gamut from asymptomatic to
lifestyle- limiting subjective symptoms. While
objective manifestations of CVD are encompassed in the CEAP classication system, the
subjective symptoms often correlate to disease
severity.
CEAP C0-C2 patients may often be asymptomatic. Symptom presentation becomes prevalent in CEAP C1-C2 with spider veins,
telangiectasias, and development of small varicosities <3 mm [4]. Varicosities are manifestations of CVD, dened as dilated subcutaneous
veins (arising from supercial veins: GSV, SSV,
or tributaries) measuring >3mm in the upright
position. While often a result of primary venous
disease, varicosities can also manifest due to secondary causes including venous obstruction, previous DVT, supercial thrombophlebitis, or
arteriovenous stula [17]. Varicosities may be
tender or nontender.
Subjectively, patients with CVI at the CEAP
C3 score often report lower extremity heaviness,
achiness, fatigue, and edema that is progressive
throughout the day or with prolonged leg exertion, with improvement of symptoms with leg
elevation [16]. There is a tendency for these
patients to report pruritus, pain, and/or nocturnal
leg cramps. As venous disease progresses to the
CEAP C4 level, the increased truncal vein diameter in conjunction with erythrocyte extravasation and dermal hemosiderin deposition result in
hyperpigmentation [4]. These trophic skin
changes are generally seen in the gaiter distribution of the lower leg, dened as the circumferential region between the medial malleolus and
upper part of the calf [7]. Severe CEAP C4 manifestations include lipodermatosclerosis, atrophie
blanche, and stasis dermatitis, often presenting as
erythema, brosis, and induration. Patients often
describe symptoms of pruritus and pain to the
affected area [4].
CEAP C6 patients may present with a combination of any of the subjective and objective
ndings from previous CEAP classications;
however, criteria for this category is presence of
an ulceration. CEAP C5 classication is reserved
for those with successful healing of venous
ulcers; however, the patient may continue to
have subjective symptoms consistent with CVI/
CVD [4].
Diagnostic Workup
The Society of Vascular Surgery (SVS) guidelines recommend a comprehensive workup of
venous disease including a thorough review of
HPI and clinical exam, in combination with noninvasive diagnostic imaging techniques.
Symptoms that suggest CVD may include throbbing, heaviness, edema, fatigue, restlessness of
the lower extremities, often exacerbated with
standing and sitting for prolonged periods of time
and relieved with elevation. Venous claudication
symptoms occur in both primary and secondary
venous diseases. Pertinent medical history
includes a review of DVT or thrombophlebitis
history, self or family history of thrombophilia
and hypercoagulable disorders, tobacco or hormone use (including pregnancy), and family history of venous diseases. Physical exam should be
comprehensive for varicosities, discoloration
(including atrophie blanche, lipodermatosclerosis, pigmentation), edema, telangiectasias, ulcer
(active or healed), and ankle mobility. Pedal
pulses and sensory/motor function of the leg and
foot should be evaluated to rule out any arterial
insufciency and neuropathy etiologies, respectively. The patient should also be evaluated for
compressive abdominal masses or lymphadenopathy for consideration of extrinsic venous
compression.
22 Venous Disease Management intheLimb Salvage Patient: Diagnostics, Compression, andAblation
291
The SVS recommends using the CEAP classication system to evaluate CVD severity on
clinical exam. If CVD is suspected, a duplex scan
should be completed. Venous duplex is the gold
standard, rst-line diagnostic imaging test to
evaluate for valvular incompetence and obstructive disease, with or without the presence of acute
venous thrombosis. A comprehensive duplex
scan includes visibility, compressibility, venous
ow, and augmentation of the venous vessels.
The SVS denes venous reux in the supercial
system veins as >500ms, which aligns with previous international consensus recommendations
of 0.5s as a cutoff value for lower extremity vein
incompetence. The iliac, femoral, and popliteal
veins of the deep system cutoff are slightly longer
at 1 s. Perforating veins have previously suggested cutoff values of 350 and 500ms, and thus,
perforator vein diameter is included in dening
pathologic reux. The SVS and AVF Guideline
Committee denes pathologic perforating veins
as those with an outward ow of ≥500ms, with a
diameter of ≥3.5mm, with presence of a current
or previous ulceration (CEAP class C5-C6).
CT venography is recommended for patients
in which deep venous obstruction, iliac vein
compression, or post-thrombotic syndrome is
suspected, as well as for patients planning to
undergo endovenous or surgical treatment of
deep system veins [17].
Economic Burden andQuality
ofLife
Although a condition of low mortality, venous
insufciency and its complications signicantly
impact patient quality of life and the overall economic healthcare burden. Varicose veins affect up
to 40% of the population, with up to 4% of
patients older than 65 suffering from venous
ulcers [26]. It is estimated that the direct medical
cost of CVD may exceed over $1 billion annually
in the United States [17]. A systematic review
published in the European Journal of
Endovascular Surgery suggests that venous
ulcers alone contribute to 2% of the total healthcare budget in developed countries [26]. This gure is expected to increase with the rising
population of older adults and the growing prevalence of obesity [27]. Symptomatic varicosities
alone can be a source of chronic pain, discomfort,
loss of working days, disability, and decreased
quality of life. Infrequently, severe CVD can lead
to loss of limb or life [17]. An increased awareness among healthcare providers of venous disease, early detection, lifestyle coaching, and
prompt referral to vein specialists will aid in preventing the progression of venous disease and
curb treatment expenditure [27].
Recognizing the quality of life burden of
severe venous insufciency and disease, numerous standardized outcomes of patient reported
quality of life measures are used to quantify the
degree of venous disease disability. The Venous
Clinical Severity Score (VCSS), for example, is a
scoring tool that standardizes the clinical assessment of venous- specic disease severity. The tool
uses ten gradable symptom categories that may
change in response to treatment, rendering the
VCSS an ideal instrument for longitudinal surveillance and evaluation of venous disease. The
ten clinical descriptors include: pain, varicose
veins, venous edema, skin pigmentation, inammation, induration, number of active ulcers,
duration of active ulcers, ulcer size, and compression use. Each category is scored from 0 to 3 with
a total possible score of 30 (Fig.22.5). With the
introduction of the VCSS and other venous disease specic quality of life measures, both venous
clinical severity and its impact on quality of life
can be quantied, allowing for an outcomes evaluation that cannot be captured by a CEAP score
alone. The venous disease specic quality of life
measures are being increasingly studied and used
in the clinical setting [28].
292
Clinical descriptor
Pain
wer 1/3 calf
wer 1/3 calf
wer 1/3 calf
Varicose veins
Venous oedema
Skin pigmentation
Inflammation
Induration
Number of active ulcers
Ulcer duration
Active ulcer size
Compression therapy
Absent (0) Mild (1) Moderate (2) Severe (3)
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B. Cutler et al.
Fig. 22.5 Venous Clinical Severity Score (VCSS) Tool. License Number: 5444480868116
Conservative Management
All treatment and management strategies for
venous disease have a common aim of achieving
reduced venous hydrostatic pressure. When
supine, and not counteracting effects of gravity,
lower extremity venous pressure is around
10–20mmHg. Hydrostatic pressure changes dramatically during postural changes from supine to
erect, as the body must now counteract an
increased gravitational column. Thus, the lower
extremity veins are subject to a pressure increase
as high as 90–100mmHg. In the absence of any
functional venous pathology, utilization of the
calf muscle pump of the leg can reduce hydrostatic
pressure in the lower legs to as low as 22mmHg,
after an average of only 7–12 steps [29, 30].
Elevation
Leg elevation is recommended to mitigate venous
stasis, provide symptomatic relief, reduce edema
and inammation, and promote ulceration heal-
None
None
None
None
None
None
None
None
None
None
Occasional Daily not limiting Daily limiting
Few
Foot and ankle
Limited perimalleolar
Limited perimalleolar
Limited perimalleolar
1
< 3 month
< 2 cm
Intermittent
Calf or thigh
Below knee
Diffuse lower 1/3 calf Wider above lo
Diffuse lower 1/3 calf
Diffuse lower 1/3 calf
2
3-12 month
2-6 cm
Most days
ing in CVD patients. Leg elevation in patients
with C3-C6 disease has been shown to reduce leg
swelling and venous pressures [16, 31]. While
there is no correlation between elevation and
compression use regarding ulcer size reduction,
elevation remains recommended for patients
unable to tolerate compressive therapy alone.
Some studies suggest that patients who elevate
their legs throughout the day have reduced ulcer
healing times [32, 33]. Additionally, elevation
can help reduce lower extremity edema prior to
donning compressive garments or bandages,
allowing for easier application and compliance.
Compression Therapy
Compression therapy remains the gold standard
in the conservative management of CVD and has
been shown to improve the healing rate of ulcers.
Compression modalities include elastic stockings, non-elastic bandages, non-elastic compression systems (self-adjusted Velcro devices), and
intermittent pneumatic compression pumps
Calf and thigh
Knee and above
Wider above lo
Wider above lo
≥ 3
> 1 year
> 6 cm
Fully comply
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