practice
Chronic venous insufficiency: a
comprehensive review of management
Abstract: Chronic venous insufficiency is an extensive progressive
disease in need of public health attention. This insidious disease is a
growing burden on patient quality of life and the health economy.
Chronic venous insufficiency has become more pronounced in global
populations, especially in regions exhibiting a higher rate of risk
factors. It is critical for healthcare providers to recognise and
ablation ● chronic venous disease ● chronic venous insufficiency ● CVI ● management
venous anatomy ● venous ulcers ● wound ● wound care ● wound healing
C
hronic venous disease is a commonly
underdiagnosed disease that progressively
reduces a patient’s quality of life (QoL) as
well as placing an increasing burden on
healthcare resources. Chronic venous
disease involves telangiectasias, reticular veins, varicose
veins, chronic venous insufficiency (CVI) and chronic
venous hypertension. Symptoms of CVI include pain,
skin discolouration, oedema and ulceration.1–3 More
specifically, CVI is a condition affecting the lower
extremity venous system and involves complex venous
pathology.2,3 Prevalence of chronic venous disease
should raise concern, especially as trends in longevity
and obesity continue to rise.4 This article provides an
overview of the anatomy, pathophysiology, clinical
presentation and diagnosis of CVI, with a focus on
management options to help improve early recognition
and intervention.
The global prevalence of CVI varies widely, from
<1–17% in men and <1–40% in women. These ranges
are likely attributed to variations in the application of
diagnostic criteria, the availability of medical resources
to diagnose and treat, as well as the dispersion of risk
factors unique to global populations.5 Common risk
factors for CVI include: increasing age; family history of
venous disease; smoking; obesity; prolonged standing
or sitting; history of venous thrombosis; pregnancy;
history of lower extremity trauma; or surgery.6 Women
also show a higher incidence and prevalence of CVI
than men at any age.1
Globally, 1–2% of the adult population present with
lower limb ulceration, increasing to 3% for 70–90% of
Julian Azar,1 BS*; Amit Rao,2 MD; Alisha Oropallo,1,2 MD
*Corresponding author email: aoropallo@northwell.edu
1 Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY,
US. 2 Comprehensive Wound Healing & Hyperbarics Center, Northwell Health, Lake
Success, NY US.
510
intervene early to prevent ongoing and debilitating complications.
This article provides a comprehensive review of chronic venous
insufficiency outlining the anatomy, pathophysiology, clinical
presentation, assessment and management options.
Declaration of interest: The authors of this manuscript declare no
conflicts of interest.
● varicose veins ● veins ●
patients aged >65 years. It is estimated that prevalence
of CVI is higher in Western Europe, the US and other
industrialised nations, likely due to lifestyle and levels
of inactivity. CVI is a common medical condition as a
source of morbidity.5,7 It is important for healthcare
providers to educate patients, especially those
with high-risk factors, on the prevention and
management of CVI, to reduce prolonged treatments
and hospitalisations.4
Method
A comprehensive literature review of medical textbooks
and journals was undertaken. Chapters and articles
discussing the pathophysiology of CVI and its sequelae
were included. A PubMed search of journal articles
discussing the management and treatment of CVI
sourced a vast amount of information. The multitude
of search combinations required for a thorough study
of this topic prompted us to focus our investigation on
PubMed articles to maximise article yield and
reproducibility. We restricted the PubMed data
collection to the last 10 years because classification,
management and treatment of CVI have changed
within the last decade.
A literature search of the PubMed database from
January 2011 to January 2021 was performed using
combinations of the following search terms: ‘chronic
venous insufficiency’; ‘venous stasis ulcers’; ‘the
pathophysiology of venous disease’; ‘anatomy of
venous disease’; ‘management’; ‘treatment of venous
disease’; ‘compression therapy’; ‘CEAP and venous
severity score classifications’; ‘pharmacologic
interventions in venous disease’; ‘sclerotherapy,
radiofrequency ablation’; ‘endovenous laser vein
© 2022 MA Healthcare Ltd
ablation’; ‘cyanoacrylate-based adhesives’; ‘venous
surgery’; and ‘venous ligation’.
Removal of duplicates from our original search total
of 1750 records yielded 1152 articles. We then screened
these articles and assessed 188 full-text articles for
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eligibility. Sources were selected based on merit,
comprehensive knowledge base and chronicity. The
information was synthesised and formulated into the
following review.
Patient consent
The patients gave signed consent to have their
photographs taken at clinic.
Anatomy
Venous anatomy is classified into three components:
superficial, deep and perforating veins. The venous
groups are classified according to their relation to the
muscular fascia surrounding the lower leg muscles. The
superficial veins course above the fascia between the
dermis and deep fascia, draining cutaneous
microcirculation, while the deep veins are located
beneath the muscle fascia. Perforator veins connect the
superficial and deep veins by penetrating through the
muscular fascia.1,3,8,9 Fig 1 illustrates the superficial,
deep and perforator venous systems, respectively.1
The superficial veins of the leg include the great
saphenous vein (GSV) and the small saphenous vein
(SSV). The GSV, the longest vein in the body, arises from
the dorsal venous arch on the medial side of the foot
and courses anterior to the medial malleolus along the
medial calf and thigh, communicating with the
common femoral vein in the groin. The SSV begins on
the dorsolateral side of the foot ascending to the
posterolateral side of the calf where it most commonly
joins the popliteal vein.1,8,9
The deep veins of the calf are present in pairs and
course along both sides of major arteries. These include
the anterior tibial, posterior tibial and peroneal veins
which converge to form the popliteal vein. As the vein
Fig 1. Lower extremity superficial veins (a,b), deep veins (c) and perforating veins (d). ACV—anterior circumflex vein;
PCV—posterior circumflex vein; GSV—great saphenous vein; SPJ—saphenopopliteal junction; SSV—small saphenous
vein; EIV—external iliac vein; CFV—common femoral vein; DFV—deep femoral vein; FV—femoral vein; PV—popliteal
vein; PTV—posterior tibial vein; ATV—anterior tibial vein; PEV—peroneal vein; PV—perforating veins
a b
© 2022 MA Healthcare Ltd
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ascends through the adductor hiatus it becomes the
femoral vein. The femoral vein joins the deep femoral
vein to form the common femoral vein found medial to
the common femoral artery. Upon crossing the inguinal
ligament, it is referred to as the external iliac vein,
which then joins with the internal iliac veins, becoming
the common iliac vein before reaching the vena
cava.1,8,9 These landmarks are helpful in diagnostic
testing and surgical intervention.
The superficial and deep venous systems are
connected by perforating veins, which direct blood
from the superficial to deep veins. Perforator and
tributary veins are present throughout the leg and are
named according to their longitudinal location, such
as the ankle, leg, knee and thigh perforators. Although
tributaries may be seen visually, perforators are
commonly identified by using ultrasonography.
Perforators are also subgrouped according to side
(anterior, posterior, medial, lateral). For example,
perforator veins are named as the posterior leg
perforator or medial thigh perforators. Medial thigh
and medial leg perforators are further subdivided into
groups. The medial thigh consists of the inguinal
perforating vein and the perforating vein of the femoral
canal. The medial leg perforators are segmented into
paratibial perforator veins and posterior tibial perforator
veins. 9,10 This improved classification helps to
specifically identify which vein is involved when
treatment is needed.
Pathophysiology
The peripheral venous system of the lower extremity
normally functions to transport deoxygenated blood
from the periphery to the heart. Blood flows from the
superficial veins to the perforator veins into the deep
c d
5 11
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 practice
venous system. The movement of blood against gravity
while in the upright position requires the assistance of
one-way valves and muscle contraction to pump and
return blood to the heart. The one-way bicuspid valves
located throughout the superficial, deep and perforator
veins ensure that blood flows in one direction towards
the heart while limiting backflow and pooling of blood
in the lower extremities.2,3 Together with the valve
system, contraction of lower extremity muscles, such as
the gastrocnemius, helps propel the blood upwards.
Upon muscle contraction, the external venous wall is
squeezed inwards forcing blood anterograde. Upon
muscle relaxation, the vessel opens and physiologic
reflux of blood occurs, closing the sinuses of the
bicuspid valve.2,3,8
Damage to these physiological mechanisms can lead
to pathological venous reflux, which contributes to
venous valve incompetence and dilation, venous
hypertension secondary to blood pooling for prolonged
periods, and inflammation of the vessel wall from
damage.3 Vein dilation can force healthy, undamaged
bicuspid valves apart worsening venous hypertension
and affecting pressure on normal veins. On a molecular
level, venous hypertension causes a release of vasoactive
substances from the endothelium, greater expression of
adhesion molecules, such as E-selectin and intercellular
adhesion molecule 1 (ICAM-1), and an influx of
chemokines and inflammatory mediators. Venous
insufficiency with concomitant diabetes results in
endothelial dysfunction from hyperglycaemia.10 In
addition to venous reflux, obstruction of the vessel from
thrombosis or venous stenosis can limit blood flow and
further cause venous hypertension and endothelial
damage.2,3 Over time, venous hypertension and
chronic vessel inflammation lead to CVI, with greater
risks of hyperpigmentation, lipodermatosclerosis,
extravasation of fluid into the tissue and leg ulcers.1,3
Venous pump weakness and/or ankle hypomobility also
add to the formation of CVI.
Varicose veins are defined as dilated veins >3mm in
diameter, with characteristic bulging and tortuosity.
The global prevalence of varicose veins ranges from
2–56% in men and 1–73% in women, with the US and
Western Europe representing the higher percentages.5
Varicose veins are classified as either primary or
secondary. Primary varicose veins result from pathology
in the superficial venous system of the saphenous veins
with structural damage to the bicuspid valves, weakened
vessel walls and elevated luminal pressure. Risk factors
for primary varicose veins include family history,
ageing, obesity, prolonged standing and sitting,
hormonal therapy and pregnancy. Secondary varicose
veins emerge from insufficient or obstructed deep veins
and/or perforator veins, creating a backflow of pressure
to the superficial venous system.1
CVI is a result of venous hypertension, insufficiency
and subsequent inflammation. Disease progression
occurs as a consequence of incompetent veins found
mainly in the deep venous system. Though the deep
512
venous system involvement occurs less often in
superficial venous system insufficiency, patients with
varicose veins may have a component of CVI and
should be assessed. CVI is categorised as primary deep
venous insufficiency and secondary deep venous
insufficiency.1 Primary or idiopathic CVI corresponds to
non-thrombotic causes, with structural and functional
problems in the vein wall or bicuspid valves. Secondary
CVI is a result of obstruction or post-thrombosis from a
prior deep vein thrombosis (DVT). After a venous
occlusion, the valve leaflets thicken and become
contracted, and unable to effectively prevent retrograde
flow.1,11,12 Venous reflux, obstruction, or a combination
of each, can take place in either primary or secondary
deep venous insufficiency. Patients can be asymptomatic
in isolated segments of venous reflux. However, patients
will show more symptoms with additional venous
reflux sites.11,12 Valve failure at the saphenofemoral and
saphenopopliteal junctions can also lead to CVI.2,3 Less
common causes of CVI include failure of the muscle
pump with neurological movement disorders, iliocaval
compression from physiologic compression or
thrombosis, or arteriovenous fistulas increasing venous
pressures, venous malformations, and congenital deep
vein agenesis or hypoplasia.1–3
Venous leg ulcers (VLUs) occur as a complication of
CVI and represent the most common type of hard-to-
heal wound in the lower extremity, approximately 80%
of all leg ulcers.13–15 The exact mechanism of ulcer
formation as a consequence of venous hypertension
remains unclear, but different theories, (such as the
fibrin cuff theory, inflammatory trap theory, and
dysregulation of proinflammatory cytokines and
growth factors), have been proposed. The fibrin cuff
theory suggests that excess fibrin is deposited along the
capillary bed, thereby increasing pressure and dilation
of endothelial pores which further exacerbates
fibrinogen deposition. These pericapillary ‘fibrin cuffs’
create a barrier that decreases oxygen diffusion to
tissues. Healing is delayed as inflammatory cells and
growth factors become trapped in the fibrin cuff,
constituting the inflammatory trap theory. Trapped
leukocytes release proteolytic enzymes and oxygen
radicals, damaging the endothelium and increasing the
permeability. The influx of leukocytes can cause
occlusion, leading to local ischaemia, tissue hypoxia,
and reperfusion injury.15–17
VLUs are commonly located on the medial one-third
of the lower leg anterior to the medial malleolus, with
irregular margins that can be flat or slightly raised. The
ulcer bed is shallow and red in appearance, and may
show granulation tissue and/or exudate.1,15–17 Other
surrounding signs that suggest a VLU due to CVI
include venous dermatitis, lipodermatosclerosis and
© 2022 MA Healthcare Ltd
atrophie blanche (white atrophy). 15 VLUs are
burdensome to patients as they generally recur and
have prolonged healing times.13 Annually, the
prevalence of VLUs affecting patients in the US is about
600,000.17 Moreover, the incidence of VLU is about
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2.2% for patients aged 65 years and older.17 In a study

Fig 2. Varicose veins of Fig 3. Large venous leg
comparing patients with a VLU to patients without a the thigh and calf ulcer
VLU from 2007–2011, patients with a VLU were
generally older and had higher rates of comorbidities,
hospitalisations, emergency department and outpatient
visits.18 The estimated annual cost for VLUs in the US,
while taking into account resource use and treatment
costs, is $14.9 billion USD, with roughly $6391
spent per Medicare patient and $7086 per privately
insured patient.19

Clinical presentation
CVI ranges from asymptomatic to cosmetic concerns to
severe symptoms, such as ulceration.11,12 Patients may
present with asymptomatic complaints showing signs
of simple telangiectasia (diameter <1mm) or reticular
veins (diameter 1–3mm). Varicose veins (diameter
>3mm) are typically asymptomatic but may cause
discomfort to the patient (Fig 2). As the disease
progresses, patients often complain of heaviness,
throbbing, dull aching, and/or swelling of the legs
which worsens with prolonged standing by the end of
the day and improves with leg elevation. Additional
patient concerns include itching, burning, pain,
nocturnal leg cramps and skin ulceration.2,3,16,17
When evaluating a patient, the legs should be
examined in the upright and supine position beginning
with visual inspection for cutaneous changes such as
hyperpigmentation, stasis dermatitis, erythema,
eczema, and VLUs (Fig 3). It is thought that the
pigmentation is mainly due to haemosiderin or melanin
deposition as a result of venous hypertension.20 The
legs should be palpated for detection of varicose veins,
oedema and tenderness. Observations of increased leg
circumference, pitting oedema and skin changes
consistent with venous stasis indicate deep venous
insufficiency (Fig 4). Over time, oedema may transition
from pitting to becoming more indurated. Advanced
skin findings include lipodermatosclerosis (Fig 5),
atrophie blanche or livedoid vasculopathy (white
scarred ulcer), corona phlebectatica (superficial dilated
perimalleolar area), and ulceration near the medial and
lateral malleolus.2,3,16,17
Clinical diagnosis of CVI is based on history, signs
and symptoms, and diagnostic tests. The differential
diagnosis must be considered to rule out other
significant disease processes, such as arterial pathology
and acute DVT. It is important to assess for mixed
arterial and venous aetiology. Compression management
intended for the venous disease could lead to worsened
outcomes in a patient who also has severe peripheral
arterial disease (ankle–brachial index <0.5). Providers
should ask and review patient history for intermittent
claudication, cardiovascular disease and stroke, while
also assessing for absent or diminished pedal pulses and
irregular blood pressures.1,16,17 Duration of leg oedema
can help differentiate CVI from an acute DVT. Other
causes of bilateral lower leg swelling include myxoedema
from hypothyroidism, pretibial myxoedema from
Graves’ disease, congestive heart failure,
hypoalbuminemia, or a medication side‑effect, such as
from dihydropyridine calcium channel blockers
and thiazolidinediones.1

Assessment
CVI manifestations are organised according to the Fig 4. Pitting oedema (a,b) due to chronic venous insufficiency can lead
CEAP Classification (clinical, etiological, anatomical, A changes (c)
to pigment B C
pathophysiological), which was created in 1994 and .
updated in 2004 to standardise the diverse a b c

manifestations of chronic venous disorders (Table 1).

The categories identify: clinical signs and symptoms
(C0–C6); aetiology divided into congenital, primary or
secondary causes; location of venous anatomy
involved whether superficial, perforator or deep; and
© 2022 MA Healthcare Ltd

pathophysiology denoting reflux, obstruction, both or

neither.1 This international classification system was
created to improve consistency and homogeneity for
describing, diagnosing and treating venous disease.1–3
Classifications of C3 and above constitute CVI.3

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After a review of patient history and however, PPG is more often utilised towards subcutaneous
Fig 5.Lower extremity
exhibiting lipodermato- clinical presentation, venous tests can venous plexus. PPG does not address the superficial and
sclerosis help confirm the diagnosis of CVI. The deep system reflux.3 Computerised tomography (CT) and
gold standard diagnostic test is the magnetic resonance imaging (MRI) venography are
venous duplex ultrasound, which mostly used for visualisation of proximal veins and
combines B-mode imaging and spectral surrounding structures that attribute to vessel external
Doppler to detect venous reflux or compression.1–3 A rarely used invasive test, known as
obstruction in superficial and deep phlebodynamometry, measures intravascular peripheral
veins.1,3 Visualisation or change in venous pressure to determine whether a patient needs
spontaneous flow may indicate chronic surgery for evaluating conditions such as post‑thrombotic
DVT or stenosis.2,3 The 2020 Appropriate syndrome or deep vein incompetence.3 Intravascular
Use Criteria (AUC) guidelines21 suggest ultrasound is a minimally invasive device helpful in
the patient should be in the upright detecting intravenous disease and compression of the
position, assuming the patient can safely iliocaval veins.
stand, while performing the duplex As a way to measure disease severity, the Venous
ultrasound during the evaluation of Severity Scoring system was developed in 2000 and
venous reflux. Patients placed in the revised in 2010. It includes three components:
supine or steep reverse Trendelenburg ● The Venous Clinical Severity Score (VCSS)
positions were deemed less appropriate ● The Venous Segmental Disease Score (VSDS)
measures. Venous reflux of an ● The Venous Disability Score (VDS).
incompetent valve correlated with a Doppler waveform The VCSS estimates the severity of CVI and serves as a
reflux duration time of >0.5 seconds in the superficial guide for evaluating response to treatment. Its purpose is
veins and >1.0 seconds in the deep veins, such as the to complement the CEAP classification system by
femoral and popliteal.2 To elicit venous reflux, distal illustrating changes in the disease over time. The
compression at the calf is performed. Whereas the following 10 attributes of venous disease are graded from
Valsalva manoeuvre is commonly used to assess the 0–3 (0=absent, 1=mild, 2=moderate, 3=severe): pain;
common femoral vein or saphenofemoral junction.2,3,22 varicose veins; venous oedema; skin pigmentation;
Colour‑assisted Doppler ultrasound may help visualise inflammation; induration; active ulcer number; active
venous flow patterns.1 ulcer duration; active ulcer size; use of compression
Air plethysmography (APG) is used to assess venous therapy (Table 2). The revised version provided
reflux, obstruction and muscle pump dysfunction by more descriptors for grading.2,3,23
measuring venous volume and refilling time while the The VSDS grades major venous segments using
legs are moved from the supine to standing position, and anatomical and pathophysiological components
after calf muscle pump exercises. These changes are to assess for reflux or obstruction based on
measured by air displacement in a cuff wrapped around imaging studies.24
the calf. Though less commonly used, the APG can assist VDS estimates a patient’s ability to work an eight‑hour
in the diagnosis of CVI when the duplex ultrasound fails day with or without assistance. The score determines the
to provide an adequate evaluation. Photoplethysmography level of disability in venous disease.25,26 Providers can
(PPG) detects venous filling times by measuring the use the venous severity scoring system to monitor
amount of infrared light reflected by haemoglobin; treatment outcomes.23

Table 1. CEAP classifications

Clinical signs Aetiology Anatomy Pathophysiology

C 0: no visible signs of venous disease Ec: Congenital A s: Superficial Pr: Reflux

C2: Varicose veins Es: Secondary A p: Perforator Pr,o: Reflux and obstruction

C3: Oedema En: Aetiology not identified A n: Anatomy not specified Pn: Not identified

C4A: Pigmentation or eczema

C4B: Lipodermatosclerosis or atrophie blanche

C4C: Corona phlebectatica

C5: Healed venous ulcer

© 2022 MA Healthcare Ltd

C6: Active venous ulcer

C6r: Recurrent active venous ulcer

Descriptors A (asymptomatic) or S (symptomatic) are placed after the C clinical class26–28

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Table 2. Venous clinical severity score

Attribute Absent=0 Mild=1 Moderate=2 Severe=3

Pain None Occasional Daily Daily

Pain does not restrict daily Pain interferes but does not Pain limits most daily activity
activity prevent daily activity

Varicose veins None Few, scattered, isolated Confined to calf OR thigh Involves calf AND thigh
branch varices, or clusters
including corona phlebectatica
(ankle flare)

Venous oedema None Limited to foot and ankle Extends above the ankle but below Extends to knee and above
the knee

Skin pigmentation None or focal Limited to perimalleolar area Diffuse over the lower third of the The wider distribution above
calf the lower third of the calf

Inflammation None Mild cellulitis, ulcer margin Diffuse over the lower third of the Wider distribution over the
limited to perimalleolar calf lower third of the calf

Induration None Limited to perimalleolar Diffuse over the lower third of the Wider distribution over the
calf lower third of the calf

Ulcer number 0 1 2 ≥3

Ulcer duration NA <3 months >3 months to <1 year >1 year unhealed

Ulcer size NA Diameter <2cm Diameter 2–6cm Diameter >6cm

Compressive therapy Not used Intermittent Most days Full compliance

NA—not applicable2,3,30

Management of hard-to-heal Table 3. Treatment based on CEAP classification

venous wounds CEAP classification Recommended therapy
Conservative therapies
Management of vascular insufficiency can be Asymptomatic C1 Conservative

challenging and requires an individualised approach. Symptomatic C1 Conservative and/or sclerotherapy

Patients may have mobility limitations and
comorbidities, such as arterial disease and diabetes.
After a thorough evaluation of the patient, conservative,
pharmacological and interventional therapies may be
utilised, or a combination of therapies (Table 3). Initial
therapy often involves conservative measures with
compression, elevation, exercise and gait training to
optimise the venous pump. These conservative therapies
can improve oxygenation of the subcutaneous tissue
and skin by augmenting venous flow.
Compression therapy
Compression therapy is often the standard initial
treatment in venous insufficiency classes C2–C6. There are
a variety of ambulatory compression methods available
such as medicated paste gauze boots (the Unna boot),
elastic compression stockings and Velcro leg wraps,
multilayer compression systems and static dressings.27–29
Pneumatic compression devices are also used for patients
with VLUs and refractory oedema after a failed six-month
trial of standard therapies.30 A recent article comparing a
© 2022 MA Healthcare Ltd
Symptomatic C2–C6 with reflux Superficial venous thermal or non-thermal
ablation or foam sclerotherapy, phlebectomy,
vein stripping or ligation, or iliac venous stent
placement
required by most insurance companies before definitive
treatment is offered. However, data is not sufficient to
determine the effectiveness of compression therapy in
the treatment of symptomatic varicose veins. 31–33
Compression therapy can help manage symptoms but
cannot correct the source of reflux; it has been
recommended as appropriate when treating patients
with superficial disease with an unknown or
uncorrectable source of reflux. A compression stocking
or sock at 20–30mmHg graded compression can be used
in the maintenance of varicose veins.27,28 Patients with
symptomatic varicose veins (C2) with significant venous
reflux should be evaluated for treatment with
endovenous intervention in the case of failure of medical
management, such as compression therapy.27,28,34

compression device to compression stockings in previously
non-adherent patients with CVI C3–C6 found the devices
were comparable for adherence and outcomes.30
For C2, compression therapy is usually the initial
therapy and a trial of compression therapy is often
For CVI (C3–C6), long-term compression therapy is
effective in patients with oedema and venous
stasis ulcers. A multilayer compression bandage, leg
wrap or graded compression stocking of 30–40mmHg
should be used in patients with VLUs.27,28 A systematic

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review of compression therapy healing VLUs found
that compression therapy increased healing rates
compared with no compression therapy, and
multicomponent systems were more effective than
single‑component systems.35
Pharmacological interventions
Non-adherence rates of compression therapy have been
reported as high as 60–70%, and pharmacological
interventions may offer an alternative for patients
unable or unwilling to use compression therapy.36,37
Various drugs targeting venous disease are available
with some demonstrating beneficial effects on CVI
symptoms, such as oedema, paraesthesia and VLUs.
Micronised purified flavonoid fraction (MPFF) is
available in the US as Diosmiplex, a medical food that
requires a prescription. MPFF is beneficial in the
treatment of VLUs alone and as an adjunctive to
compression therapy, and for symptoms including
oedema caused by CVI.3,38 A systematic review of the
use of flavonoids for the treatment of VLUs found that
flavonoids including MPFF and hydroxyethylrutosides
(HR) improved the rate of healing ulcers. However, the
authors determined the majority of the studies were
poorly reported and there was an unclear risk of
publication bias in one trial.39
Horse chestnut seed extract (HCSE) contains aescin
with saponin as its active component. HCSE has been
shown to inhibit an enzyme involved in proteoglycan
degradation and stimulate the release of prostaglandins,
creating a vasoactive effect.40,41 An updated systematic
Cochrane review from 2012 found HCSE improved
signs and symptoms of CVI compared with placebo.
Signs and symptoms assessed were leg pain and oedema
evaluated by leg volume. The review suggested
short‑term treatment with HCSE as effective; however,
it recommended larger and more long-term studies were
needed to be conclusive.41
A trial using the Widmer Classification for assessing
CVI suggested that HCSE may be as effective as
treatment with compression stockings in reducing leg
volume in patients with early and mild CVI, Grade 1.
However, compression therapy was found to be superior
in treating patients with CVI Grades 2 and 3.42
Limitations of these studies were the small sample size
and unreported adherence.41,42
Interventional therapies
Corrective treatment should be offered for patients with
advanced CVI. The use of conservative therapy alone
may only be applied in exceptional cases or if a patient
refuses further interventional therapy. The type and
approach for corrective treatment are dependent on the
vessel anatomy, source of reflux, symptoms, severity of
reflux and vessel size. There are many interventional
options such as sclerotherapy, endovenous laser and
radiofrequency ablation, or surgical ligation and
stripping. Endovenous vein ablation and sclerotherapy
are current methods used in perforator and tributary
516
varicose vein involvement. The CEAP classification of
the vein will dictate the method of treatment.
Sclerotherapy
Sclerotherapy is minimally invasive and involves a
percutaneous injection of chemical irritants, most
commonly polidocanol or sodium tetradecyl sulfate
(STS), into small superficial visible veins. Many
sclerosant mediums are available in liquid or foam. The
liquid agents are used in the cosmetic treatment of
telangiectasias, reticular veins and small varicose veins.
Foam sclerotherapy agents are often used for veins
>5.5mm. Patients with CVI can be treated with
sclerotherapy primarily or in conjunction with a
surgical procedure. Treatment with liquid sclerotherapy
is generally cosmetic and most often used for
asymptomatic C1–C2, and is generally not covered
by insurance.43
Superficial endovenous ablation
Superficial endovenous ablation is appropriate for
symptomatic superficial venous disease when a source
of reflux has been determined.22 A retrograde flow of
>0.5 seconds’ duration is recommended for
intervention.22,34 Several ablation techniques are
available and include thermal, chemical and
mechanical. The intervention method is dependent on
physician preference, vein location, tortuosity and
vessel size.
A variety of non-thermal ablation methods is available
for use, such as endovenous mechanochemical ablation
(MOCA), cyanoacrylate adhesive and sclerosant foam.
MOCA induces mechanical damage to the vessel while
simultaneously injecting a sclerosant. Cyanoacrylate
adhesive is injected endovascularly and works by
causing inflammation and fibrotic occlusion of the
vessel.44 The two most commonly used foam sclerosants
are polidocanol and sodium tetradecyl sulphate (STS),
which are delivered intravenously under ultrasound
guidance. Foam is preferred over liquid sclerotherapy
for larger vessels and can be created manually with a
three-way stopcock or purchased separately.45
The two main thermal ablation methods are
radiofrequency ablation (RFA) and endovenous laser
ablation (EVLA). Thermal ablation is generally the
preferred method over traditional surgery for patients
who are candidates due to less pain, reduced anaesthesia
risk and shorter recovery period.46 EVLA is achieved
under ultrasound guidance and uses a laser that is a
bare-tipped or jacketed laser optical fibre to emit energy
as heat, thus causing thrombotic occlusion of the vessel.
Various lasers using different wavelengths are available.
Longer wavelengths have demonstrated fewer adverse
effects, such as post-procedural discomfort and bruising,
© 2022 MA Healthcare Ltd
which usually resolves over time.47 RFA causes occlusion
of the vessels by creating a closed-loop alternating
electrical current generating heat and injuring the
vessel endothelium. Steam vein sclerosis is a more
recent ablation method for the treatment of varicose
JOURNAL OF WOUND CARE VOL 31, NO 6, JUNE 2022
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veins and promises to be a safer and simpler technique
compared with traditional thermal methods; however,
insufficient evidence exists to determine its effectiveness
and place in the management of venous insufficiency.45
Saphenous vein ligation and stripping
Open surgical GSV and SSV ligation and stripping have
been the standard of care for treating symptomatic
varicose veins. With the evolution of surgical
techniques, this standard procedure continues to be the
main reference of comparison for minimally invasive
surgical (MIS) procedures today. The procedure begins
with a small incision made along the groin crease at the
confluence of the GSV with the common femoral vein.
The GSV is ligated near the saphenofemoral junction
and an extended segment is removed (stripping) ending
near the knee joint. Below the knee stripping is not
typically performed due to the potential for saphenous
nerve injury; however, it can be appropriate in a patient
with CEAP classification C4–C6 with skin or
subcutaneous changes, or for healed or active ulcers
when there is segmental GSV reflux below the knee
directed to the affected area.22,27,28
An alternative method to conventional stripping of
the GSV is cryostripping and ligation. Cryostripping
involves division and high ligation of the saphenous
vein and using a specialised instrument to freeze the
vein, which adheres to the device and is removed along
with the device. A possible benefit of cryostripping is
decreased postoperative bruising compared with
conventional stripping.48 A randomised controlled trial
(RCT) comparing patient outcomes of EVLA to
cryostripping of the GSV at five years demonstrated
noninferiority.49 Thus, cryostripping may be an adequate
alternative to conventional ligation and stripping.
Venoplasty and stenting
Deep vein abnormalities causing CVI may be primary
or secondary. Primary causes are non-thrombotic
lesions compressing the vein, thereby causing outflow
obstruction. Secondary causes are post-thrombotic;
DVT can cause obstruction and irreversible damage to
the valves which can lead to post-thrombotic syndrome
(PTS).50 Venoplasty and stenting are therapies that can
be employed when deep venous insufficiency of the
lower extremities results in obstructive disease with
≥50% reduction of vessel area by intravascular
ultrasound. Iliac vein or inferior vena cava (IVC)
stenting for obstructive disease without superficial
truncal reflux is recommended in patients with CEAP
classes C4–C6 as first-line treatment.22
Cyanoacrylate-based adhesives treatment
The use of cyanoacrylate-based adhesives for cyanoacrylate
© 2022 MA Healthcare Ltd
embolisation (CAE) to block the lumen of the vein has
been an alternative approach to the treatment of CVI in
recent years. The CAE technique involves the catheter-
guided infusion of glue to ablate the insufficient vein
without heat generation. Studies have demonstrated
JOURNAL OF WOUND CARE VOL 31, NO 6, JUNE 2022
practice
successful occlusion with low postoperative complication
and recanalisation rates.51–53 A small subset of individuals
can experience hypersensitivity reactions, including
phlebitis, to the procedure, but the occurrence is rare.53 A
study using six-month follow-up data found a
100% efficacy rate.51 Patients with multiple allergies or
who are immunosuppressed may consider another
alternative therapy.
CVI management during COVID-19
The COVID-19 pandemic has devastated hospitals and
depleted resources in unprecedented ways, greatly
affecting patients receiving routine care for their
chronic conditions. Due to the recommendations of
social distancing and stay-at-home orders across the
world, venous insufficiency patients have experienced
a delay in their care, which has decreased their quality
of life. This shift in priority to minimise COVID-19
exposure and minimise hospitalisation for non-urgent
procedures, such as venous ablation, has allowed for
redistribution of resources such as personal protective
equipment (PPE), staffing and intensive care unit (ICU)
beds during the global pandemic.54
These delays in care, however, can result in severe
complications for patients, such as DVT or VLUs.55
Although the risks of COVID-19 exposure are high,
studies have shown how lack of access to wound care
visits can lead to more severe complications, such as
limb infection followed by loss of limb and patient
life.56 Thus, a balance must be met where the frequency
of wound care visits minimises COVID-19 exposure
while meeting the minimum frequency of visits
necessary to promote wound healing or, at a minimum,
prevent wound deterioration, as studies have shown
that increased frequency of wound care clinic visits
increases the healing of hard-to-heal wounds.57
To achieve this balance, hospitals have searched for
ways to triage and prioritise the high-patient volume
during the pandemic. For example, one study developed
the ‘MeNTS’ (medically necessary, time-sensitive) score
to measure the urgency for procedures based on factors
leading to poorer perioperative outcomes, risk of
COVID-19 transmission to health professionals and
increased hospital resource use. 54 Another study
rescheduled all elective procedures, including all venous
cases, and postponed all venous insufficiency ultrasound
studies, while allowing patients with suspected VLUs or
DVTs to undergo appropriate testing and, in some cases,
be seen at the clinic. The postponed clinic visits were
recorded in a database to allow for rescheduling once
COVID-19-related restrictions are lifted.55
For non-urgent venous cases, some clinics have
implemented virtual methods to accommodate patient
care, including patients sending photographs of affected
areas, and secured video calls with providers, treating
non-urgent patients with compression, elevation and
exercise.51 A study demonstrated the efficacy and high
patient satisfaction of these telehealth initiatives in
patients with hard-to-heal wounds.57
517
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 practice
Conclusion
CVI is a common disease with a significant health and
financial burden on the population, and can be
challenging to identify and treat. Appropriate diagnosis
with a thorough understanding of venous anatomy and
utilisation of diagnostic ultrasound is imperative to
determine optimal management. Prevention and early
intervention is the best approach for treating CVI.
Physicians should be cognisant of managing underlying
venous hypertension while treating VLUs. In addition,
ulcer management should be in conjunction with
interventional therapy at the source of reflux. The
expansion of newer and less invasive treatment methods
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www.journalofwoundcare.com
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practice
Reflective questions
● How would you apply the principles of compression therapy
in your practice?
● Given the parameters discussed, how do you approach
patients with recalcitrant venous leg ulcers?
● How do address issues of obesity, immobility and nutrition
in relation to venous insufficiency in your practice?
● How are advanced therapies such as cellular tissue-based
products (CTP) incorporated into your practice?
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