Pathophysiology

The major venous plexuses in the lower leg and foot are anatomically positioned so that they are compressed during normal ambulation, thus pumping venous blood towards the heart. Their position, between the soleus and gastrocne-mius muscles in the calf and between the first and second muscle layers of the sole of the foot, is such that even muscle contractions while stationary are sufficient to pump blood proximally. The investing deep fascia surrounding the calf muscles ensures that much of the pressure generated by the muscular contractions, in excess of 200 mmHg, is transmitted directly to the deep calf veins. This force is also transmitted to the superficial veins via the connective tissue.

The muscle pumps are at their most efficient during normal ambulation, any deviation from this reducing their activity. Such gait abnormalities may be caused by:

• Localised or generalised muscle weakness;

• Localised or generalised neurological disorders;

• Ankle joint stiffness, due to an arthropathy, the effect of trauma or under-use;

• Knee, hip or spinal pathology;

• Frailty in elderly patients;

Bicuspid valves throughout the venous system maintain the unidirectional flow of blood towards the heart. These counteract the effect of gravity on the column of blood from the head to the foot. The term venous reflux describes the flow of blood, towards the feet and occurs to a minor degree in normal subjects, as the valves are closing. When prolonged, due to valve malfunction, it is termed venous insufficiency and

Figure 15.18. Thrombectomy specimen showing foci of white thrombus from within the value cusps and dark consecutive thrombosis between.

leads to venous hypertension. Valve damage is usually primary (i.e. of unknown aetiology), but may be secondary to previous thrombus formation and subsequent recanalisation and scarring within the vein (Fig. 15.18).

The walls of varicose veins have been shown to be deficient in elastin and collagen and are dilated and tortuous. It is not known whether these changes are primary, leading to valve failure and venous hypertension, or if these changes are secondary to the effect of high venous pressure following valvular insufficiency.

Venous hypertension is responsible for the symptoms and skin complications of varicose veins. Many of the early symptoms may be related to venous congestion but as the hypertension becomes established microcirculatory changes occur. There has been much debate as to the exact mechanism by which they lead to tissue damage and poor tissue healing. Perivascular fibrin cuffs, seen in tissue biopsies from lipoder-matosclerotic skin, might provide a barrier to the diffusion of oxygen, causing local necrosis. White cell trapping within tissues exposed to high venous pressures is well documented, causing neutrophil degranulation and activation of various inflammatory cascades leading to tissue damage.

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