Normal Venous Physiology [8]
Peripheral veins are both a reservoir to store blood and a conduit for blood return to the heart. Normal functioning requires the vessels to be patent, the presence of a series of 1-way valves to be competent and a muscle pump system. In the erect position blood in the legs is pumped back to the heart by the muscles, predominantly calf muscles, as they contract around the deep venous system providing enough pressure to move the blood up against gravity and any other pressures (physiological or pathological) working against venous return. Venous valves are bicuspid and the 1-way valves in the venous system permit blood to flow as it is pumped back to the heart and then close to prevent blood falling back down the leg.
The superficial system also has valves and communicates with the deep system, via a series of interconnections and perforators, but it lies superficial to the muscular fascia and does not have a muscular pump surrounding these veins. The superficial system receives blood from the foot and the deep system and acts as a “capacitance” system to temporarily hold blood and/or move blood up and along into the truncal veins until it’s returned to the deep system via perforators or SFP/SPJ into the deep system and onto the heart.
Venous Dysfunction and Pathophysiology
Dysfunction of the peripheral venous system occurs when the pressure in the system (superficial or deep) increases and/or there is impairment of venous return of blood to the heart. This can be due to various mechanisms [2, 5]. The mechanism affecting the superficial veins, resulting in chronic superficial venous disease, relates to changes in the biochemistry and haemodynamics of the vein wall and dysfunction of the superficial valves.
The valves of the superficial veins can also be incompetent or dysfunctional. This results in retrograde flow or reflux of blood within the superficial system and increase in hydrostatic pressures. Failure of superficial valves can be primary, related to weakness in the vessel wall or valve leaflet, or secondary due to damage from direct injury, superficial phlebitis, venous distension secondary to hormonal effects or increased venous pressure. Damage to the valves at the junctions of the deep and superficial veins or saphenofemoral and saphenopopliteal junction results in development of CVI. Valve incompetence and reflux of the superficial veins is identified in 70-80% of patients with incompetence of the GSV and over 80% of patients presenting with venous ulcers.
Superficial vein wall changes associated with VV formation and CVI include: 1) the actions of various growth factors produced from macrophages and monocytes, in particular TGF-β, 2) changes in vein wall collagen production, including decreased collagen type III, and 3) increased expression of matrix metalloproteinase that promotes degradation of matrix proteins[1]. These changes result in tissue remodelling of the vein wall, including successive zones of hypertrophy and atrophy and degradation of vein wall matrix proteins. When combined with perturbation in vein haemodynamics this enables the development of microangiopathic changes including elongation and dilatation of the capillary bed, thickening of the basement membrane with increased collagen and elastic fibres and formation of venous varicosity. Progression of cellular changes can result in endothelial damage and increased pericapillary oedema, increased venous permeability, accumulation of fluid, macromolecules and extravasation of red blood cells into interstitial tissues commonly seen in advanced CVI.
Other conditions that can increase pressure and/or decrease blood flow in the superficial system include: deep vein thrombosis, prolonged increase in intra-abdominal pressure due to physiological causes (i.e. pregnancy) or pathological causes (i.e. obesity, pelvic tumour, etc). Rare congenital abnormalities of the blood vessels (Klippel-Trenaunay syndrome) and collagen disorders (Ehlers-Danlos) can predispose to the development of varicose veins[8].
