Pathophysiology of the chronic venous disease by Jean-Patrick Benigni, MD, General Secretary of the French Society of Phlebology, Paris – FranceChronic venous disease is undoubtedly a multifactorial disease. No main cause has been demonstrated. It is not possible, therefore, to rank the primary physical or biological changes in order of importance.
Valve insufficiency
This may be quantitative or qualitative
- quantitative in the event of congenital insufficiency in terms of valve numbers or massive destruction due to venous thrombosis
- qualitative as a result of a valve being torn or due to permeability of the valve
Venous wall damage
Damage to the venous wall seems to be more common than valve damage. The wall becomes thinner at the level of the valve. The vein is dilated and pushes the valve cusps apart, compromising their impermeability. This wall damage may be related to damage to the innermost layer of the vein: the endothelium.
The exact causes leading to the development of Chronic Venous Disease are not clearly known, but we do know that the following factors play a role:
- Hereditary factors, sedentary lifestyle, age,
- Deficiency of the muscle and joint pump
- Female sex hormones, enzymatic factors,
- Sequestration of leukocytes and their adhesion to the endothelium
- Microcirculatory problems
- Defective vasoconstriction in the standing position
- Hypercoagulability of blood in the event of a thrombosis
Damage to valves and the venous wall under the influence of one or more of the above factors will lead to impairment of the venous network of the lower limbs. It causes venous hypertension which can lead to a chronic venous disease with tissue decompensation: chronic venous insufficiency.
Paradoxically, we do not know why some people develop microcirculatory and tissue decompensation while others tolerate major venous hypertension very well.
Venous hypertension: the cause of chronic venous insufficiency
This excessive pressure has variable consequences, depending on its extent. It can be measured directly at the ankle.
Visible morphological changes
As a result of this excessive pressure and defective peripheral vasoconstriction, the venous wall gradually stretches. Varicose veins appear.
Tissue changes
This excessive pressure can lead to tissue compensation and the development of true chronic venous insufficiency with repercussions for the tissue surrounding the varicose vein. The permeability of the affected vein is increased. The leg swells; this is the oedema stage. To begin with, this oedema regresses when the person lies down or raises the leg, but it gradually becomes permanent. This is the start of tissue manifestations. Tissue manifestations are self-sustaining (stasis, extravasation, interstitial flooding and local ischaemia) and mutually exacerbate one another. Without appropriate management, this vicious circles progresses and the CVD becomes more and more severe.
Altered cellular exchanges and the consequences of this
Tissue manifestations lead to impaired cellular exchanges.
The series of phenomena that occur following venous hypertension (stasis, extravasation, interstitial flooding, intoxication and local ischaemia) are self-perpetuating and mutually aggravating.
Without appropriate management, this vicious circle progresses and the CVD becomes more and more severe.
