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139
Chronic Venous Insufficiency
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11
VarunN.Kumar andRameshK.Tripathi
11.1 Introduction andEpidemiology
The prevalence of leg edema (Fig.11.1) as a manifestation of chronic venous insuf-
ciency has been reported between 7.4 and 17.1% in men and 4.9–20.3% in women.
Furthermore, the prevalence of CVI has been estimated from between <1 and 17%
in men and between <1 and 40% in women [1]. Some of the variance in these values
is due to differing criteria for what constitutes chronic venous insufciency and
sampling bias in the epidemiological studies. However, it is also known that different populations with exposure to different genetic and environmental factors show
signicant differences in the incidence of chronic venous insufciency [2].
Regardless of the exact percentages, venous insufciency is a common cause of
both unilateral and bilateral leg edema. Its peak incidence is in the 5th decade of
life, and it is approximately twice as common in females compared to males.
11.2 Anatomy andPhysiology
Approximately 90% of blood from the lower limb is drained directly by deep veins,
which follow the arteries supplying the lower limb. 10% is drained by supercial
veins, which run above the deep fascia for most of their course [3] The physiological ejection fraction of the calf muscle pump is 65% and 15% for the thigh muscle
pump [3–5]. When calf muscle dysfunction occurs, it impacts on the valve function
too. One must keep in mind that treating valve function without addressing calf
pump may lead to treatment failure.
V. N. Kumar · R. K. Tripathi (*)
Faculty of Medicine, School of Biomedical Sciences, University of Queensland,
Brisbane, QLD, Australia
e-mail: ramesh.tripathi@vascularsurgeon.org
© The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2022
S. K. Tiwary (ed.), Approach to Lower Limb Oedema,
https://doi.org/10.1007/978-981-16-6206-5_11
141
142
Fig. 11.1 CEAP C3
varicose veins with edema
V. N. Kumar and R. K. Tripathi
The supercial venous system is responsible for temperature regulation, as a
reservoir of blood and to deliver blood to the deep venous system. Medially, the
great saphenous vein (GSV) originates from the dorsal venous arch at the ankle and
runs to the pelvis, emptying into the femoral vein at the sapheno-femoral junction
(SFJ). Its notable tributaries include the anterior accessory saphenous vein and the
lateral accessory saphenous vein [3, 6]. The small saphenous vein (SSV) arises just
underneath the lateral malleolus and travels up the leg posteriorly to join the popliteal vein at the sapheno-popliteal junction (SPJ). There are a multitude of perforators through which blood ows from supercial to deep vessels in physiological
conditions [3] (Fig.11.2a and b).
The common pathway of drainage of all the blood of the lower limb is through
the femoral vein, up the external followed by the common iliac, into the inferior
vena cava. In the case of IVC obstruction blood can drain through the ascending
lumbar veins to the azygous and hemiazygos veins, as well as up the epigastric veins
to the superior vena cava [7, 8].
Obstruction of the main pathways of venous return and the use of these small
diameter collaterals results in a higher pressure distal to the pathology. More blood
Digital veins
Small
saphenous
vein
Fibular
(peroneal)
vein
Dorsal
venous
arch
Dorsal
metatarsal
veins
© 2012 Pearson Education, Inc.
11 Chronic Venous Insuciency
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143
is pushed into the supercial venous system, which is more capable of distention as
it is not constricted within muscle and dense fascia. However, in a system that only
handles 10% of the lower limb blood ow, the introduction of more blood volume
can lead to the maladaptive changes characteristic of chronic venous insufciency.
11.3 Etiopathophysiology ofLower Leg Edema inCVI
The mechanism behind chronic venous insufciency (CVI) is fundamentally an
inammatory state induced by the stress that venous hypertension places on cells of
the vessel wall. As with injury in regions elsewhere in the body, vasoactive substances are released from the endothelium, adhesion molecules, chemokines, matrix
metalloproteinases, and inammatory mediators are expressed to create a local
inammatory response. Adhesion factors such as ICAM-1 have been associated
a
a
Schematic flowchart of the anterior and posterior veins
Internal
iliac
vein
External iliac vein
Femoral
vein
Anterior Posterior
Great
saphenous
vein
Popliteal
vein
Anterior
tibial
vein
Posterior
tibial
vein
Dorsalis
pedis
vein
Inferior
vena cava
Common iliac vein
Femoral
vein
Small
saphenous
vein
Fibular
(peroneal)
vein
Plantar
veins
Deep
plantar arch
Digital
veins
b
c
Popliteal
vein
Small
saphenous
vein
Fibular
vein
Anterior
tibial vein
Dorsalis
pedis vein
Dorsal
venous
arch
Dorsal
metatarsal
veins
Anterior view Posterior view
Common iliac vein
Internal iliac vein
External iliac vein
Inguinal ligament
Femoral vein
Great saphenous
vein superficial)
Great
saphenous
vein
Popliteal
vein
Anterior
tibial vein
Fibular
vein
Small
saphenous
vein
(superficial)
Posterior
tibial
vein
Plantar
veins
Deep
plantar arch
Fig. 11.2 (a) Anatomy of venous system of lower limbs; (b) Varicose veins and vein valve
function
144
b
Normal veins Varicose veins
V. N. Kumar and R. K. Tripathi
Incompetent
valves
Fig. 11.2 (continued)
with the invasion of venous vales and vessel walls by monocytes and macrophages
[9]. The overall result is disruption and disorganization of vessel walls with brosis,
all of which leads to decreased vein compliance and further damage [5, 9].
Furthermore, stretching of the vessel wall may lead to a vicious cycle of further
valvular incompetence causing more hypertension, dilation, and uid leakage setting up a negative cycle in which the condition chronically progresses (Fig.11.3).
Following from the pathophysiology, anything that increases lower limb venous
pressure may contribute to the development of chronic venous insufciency. These
may include prolonged standing, musculo-venous pump failure, thoraco-abdominal
pump failure, heart failure, decreased sympathetic tone, and obesity (increased
intra-abdominal pressure) [2, 10].
An important cause of increased capillary hydrostatic pressure is estrogen.
Estrogen inhibits vascular smooth muscle tone and proliferation, resulting in a
greater diameter of vessels. The result is more uid and hence more capillary hydrostatic pressure. This is why chronic venous insufciency has a much greater prevalence in the female population [11]. During pregnancy, levels of estrogen are further
elevated, and the developing fetus obstructs the inferior vena cava resulting in an
increased risk of developing symptoms of chronic venous insufciency.
•Failure of the calf-muscle pump
11 Chronic Venous Insuciency
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Damaged or
weakened
valves
Reflux
Vasoactive
factors
Vein wall
changes
145
Increased
venous tone
Altered
shear
stress
Hypoxia
Venous
hypertension
Flavonoids
Capillary hypertension
Other causes for venous hypertension
•Obstruction of venous outflow
Dilated veins
•Varicose veins
•Reticular veins
•Telangiectasias
Inflammation
•Leukocyte infiltration & activation
•Inflammatory mediators
•TGF-β
•MMP-2, MMP-9 and other proteases
Symptoms
•Pain
•Itching
•Etc.
Inflammation?
Tissue changes
•ECM remodelling
•Fibrosis
•Degradation
•Hypertrophy
Skin changes
•Dermatitis
•Lipodermatosclerosis
•Atrophie blanche
•Venous ulcers
Oedema
Pigmentation
•Melanocytic stimulation
•Hemosiderin deposition
Fig. 11.3 Pathophysiological mechanisms in venous hypertension
While these underlying conditions may certainly contribute to chronic venous
insufciency, the most common cause of venous hypertension is deep venous
obstruction (DVO). The etiology of DVO is broadly classied into deep vein thrombosis or scarring after DVT, or non-thrombotic iliac vein lesions (NIVL) [2].
A common cause of NIVL is May-Thurner syndrome. Also known as Cockett
syndrome or Iliac vein compression syndrome, it occurs when the right common
iliac artery compresses the left common iliac vein against the sacral promontory.
This can lead to endothelial irritation and the formation of intraluminal “spurs” or
146
“bands” which further affect blood ow [12]. It has been implicated in the etiology
of leg edema and refractory leg ulcers and has been associated with varicose veins
of the pelvic organs [12, 13]. It is present in 22–32% of the general asymptomatic
population and 18–49% of patients with left lower limb DVT [14].
Other risk factors that make veins more vulnerable or weak to changes in venous
pressure can also contribute to chronic venous insufciency: advancing age, smoking, previous lower extremity trauma, and genetic disorders resulting in abnormal
vein or connective tissue characteristics like Ehlers-Danlos type IV syndrome,
Klippel-Trenaunay syndrome, hyperhomocysteinemia, and FOXC2 mutations
(venous valve failure ➔ varicose veins) [15]. Additionally, a number of multifactorial genetic or epigenetic changes may predispose one to CVI through deformed,
shrunken, or generally abnormal valves in the venous system of their lower limb.
Such a family history of chronic venous insufciency is a risk factor for the development of CVI in an individual. Marfan’s syndrome only affects the arterial system
and as such is not implicated in the development of chronic venous insufciency.
Due to this, the approach to chronic venous insufciency is largely symptom
based, most commonly classied using CEAP scoring, which qualitatively grades
the level of venous disease based on external symptoms, etiology, anatomic distribution, and pathophysiology.
Patients presenting with edema are by denition C3 patients.
V. N. Kumar and R. K. Tripathi
11.4 Diagnosis ofCVI inPatients Presenting withLower
Leg Edema
The general symptoms of chronic venous insufciency include leg pain or cramps,
fatigue, pruritis, and heaviness. When present, edema has a tendency to occur in the
evening and decrease with walking or elevation above the level of the patient’s heart
(e.g., when supine and resting their leg on a pillow). Its likelihood may be further
assessed with questioning directed at the risk factors related to the pathophysiology
of CVI discussed previously. Risk factors for the development of venous insufciency include pregnancy, smoking, obesity, trauma, DVT, supercial thrombophlebitis, and inactivity. Finally, chronic venous insufciency is positively correlated
with age, as are a multitude of other medical conditions that may present with lower
limb edema [16]. Therefore, it is important to consider the individual holistically
and thoroughly assess for comorbid conditions that may contribute to lower
limb edema.
The signs of chronic venous insufciency in the lower limbs manifest as a spectrum, from telangiectasias and spider veins, to edema and varicose veins, lipodermatosclerosis, and nally venous ulcers. Edema is a constant presentation of C3-6
venous insufciency.
Edema due to chronic venous insufciency presents as a pitting edema. If the
disease has been present for a long time however, the edema may be non-pitting or
brawny as lymphatic obstructive elements get involved with subcutaneous
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