Treating Venous Stasis Ulcers In The Lower Extremity

By Mark Beylin, DPM

A Guide To Normal Venous Anatomy
And Physiology
Venous stasis disease has been a challenging problem to treat for centuries. Fabricius, an Italian surgeon, was the first to recognize the structure and function of the venous valve, which lead to the understanding of the pathophysiology of venous stasis ulcers. With this in mind, it is important to have a strong grasp of normal venous anatomy and physiology.
The great saphenous vein is the main superficial vein in the leg. It begins just anterior to the medial malleolus and rises obliquely and posteriorly. The saphenous vein is joined by the posterior arch vein just below the knee. The superficial anterior vein in the lower leg and the anterolateral and posteromedial veins in the thigh join the saphenous vein near the inguinal ligament.
The lesser saphenous vein is located posterior to the lateral malleolus advancing upward, lateral to the Achilles tendon. As it reaches the popliteal space, it is situated between the heads of the gastrocnemius muscle.
The communicating veins are the connection between the superficial and deep veins. Blood flows through one-way valves from the superficial venous system to the deep venous system of the lower extremity.
In the calf, the deep veins are paired and accompany their corresponding arteries with venous tributaries intertwining over the surface of the artery. At the knee, the veins usually join to form the popliteal vein. The function of the deep veins is to carry blood from the muscles of the extremity providing carrier function for the calf muscle pump.
The calf muscle veins are covered with a tight fascia, similar to that of an elastic support stocking. This prevents dilation of the deep veins in contrast to the superficial veins, which are contained within loose non-supportive tissue. The popliteal vein becomes the superficial femoral vein.
As far as physiology goes, the calf muscle pump cycle has two phases of blood pumping: systolic and diastolic. During the systolic phase, contraction of the calf muscles compresses the blood within the deep venous system, pumping it in the direction of the heart. Valves of the communicating veins act as the bridge between the deep and superficial systems. These valves are closed as they prevent the back flow of venous blood. At this time, the pressure within the deep venous system can reach 120 mm Hg.1
During the diastolic phase of the muscle pump, the muscle relaxation allows the deep venous system of the calf to refill. This facilitates blood flow from the superficial veins to the deep venous system through the perforating veins that now have open valves. At this point, the higher pressure in the superficial venous system favors flow to the deep venous system.

Understanding The Etiology Of Venous Ulcers
When venous insufficiency goes untreated, whether it is in the deep or superficial venous system, it can lead to leg pain, swelling, characteristic skin changes and eventual ulcer formation.
Venous stasis ulcerations can result from sustained elevated pressure in the venous system of the lower extremities. Higher than normal pressures damage either the deep or superficial veins or both. A rise in the venous pressures and subsequent venous stasis leads to more permeability of capillaries. Protein leaks out of the vascular bed into the surrounding tissues. Subsequently, fibrinogen is converted into fibrin that coats the capillaries, thus interfering with the exchange of oxygen and nutrients.3 Tissue breakdown is almost inevitable and venous ulceration can occur.

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