Venous incompetence — deep vein incompetence
Valvular incompetence of the deep veins may develop in the same way as in the superficial venous system, with the degeneration of the valve cusps resulting in reverse flow in these veins. In other patients it may develop following a deep vein thrombosis. When the deep veins• fill with thrombus a new channel appears (recanalisation) after a number of weeks or months. However, the deep vein valves are destroyed by this process and, although the veins carry blood, the valves no longer work and reverse flow is allowed. Some veins are severely scarred by the recanalisation process so that they also become very narrow and ineffective at carrying blood. Occasionally veins fail to recanalise at all. This is sometimes seen following a venous thrombosis in the iliac veins. Under these conditions the blood must find an alternative way round the blockage and collateral veins develop. In the leg the long and short saphenous veins may act as collateral channels and may double in size to accommodate the additional blood flow. In patients with chronic iliac vein occlusion large suprapubic or abdominal varices may be seen carrying the collateral flow.
Clinical features of deep vein incompetence
A number of patients with severe deep vein damage has little to show for their problems. In patients with venous valvular
incompetence the calf muscle increases in size, apparently in response to the greater work in returning blood from the leg. There may be some ankle oedema, especially in those patients who have persistent venous obstruction. A proportion of patients develops skin complications. These may range from mild eczema to severe ulceration. An early sign of skin injury is brown pigmentation due to haemosiderin deposition in the skin. This occurs because the high venous pressures which result from damage to the muscle pumping mechanism cause red blood cells to be forced out of capillaries in the skin where their haemoglobin breaks down to form haemosiderin. A later and more serious stage is lipodermatosclerosis in which palpable induration develops in the skin and subcutaneous tissues. This particularly affects the gaiter area of the leg, just above the malleoli, and may be the precursor of leg ulceration. Contraction of the skin and subcutaneous tissues is seen and the ankle becomes narrower. The combination of a narrow ankle and prominent calf is often referred to as a ‘champagne bottle leg’. Atrophie blanche may also develop. In this condition the superficial blood vessels are lost from the skin and white patches develop. These indicate that the skin has been severely damaged by the venous valvular incompetence. Venous ulceration may develop in these areas.
Patients may remain untroubled by many of these symptoms and may not seek medical advice until venous ulceration develops. Even then, it is thought that less than half of the patients with venous leg ulcers are known to their general practitioners.
Effects of deep and superficial venous
Incompetence on the vascular physiology of the leg
When the venous valves fail, the ability of the muscle pumps to reduce the pressure in the leg is decreased. Following muscle contraction blood may return to the leg rapidly by flowing in the reverse direction along deep or superficial veins. Incompetence of the deep veins usually has a more severe effect on the venous physiology than does superficial venous incompetence as the deep veins are much larger than the superficial veins. The effect of reverse flow in the deep or superficial veins is to prevent the superficial venous pressure from falling during exercise. This is referred to as ‘ambulatory venous hypertension’ and is the main cause of venous leg ulceration. Persistently raised venous pressure tracks back to the microcirculation of the skin and causes skin damage that eventually may result in venous ulceration.
In some patients veins remain permanently blocked following a deep vein thrombosis leading to the blood experiencing difficulty leaving the leg. This usually causes worse symptoms than venous valvular incompetence alone. Swelling of the leg, especially ankle oedema, is often a feature in patients with persistent venous obstruction. In many cases the passage of time allows deep veins to recanalise and the ankle oedema may then become less severe. However, the recanalised veins are likely to be incompetent and the features of venous hypertension may then predominate.
How does ambulatory venous hypertension cause leg ulceration?
The damage caused by venous hypertension in patients with venous disease is confined to the skin and subcutaneous tissues. The main focus of the damage is in the capillaries in the skin. These increase in size and length, and become very convoluted and are described as ‘glomerulus like’. The amount of capillary endothelium is increased in the skin and many more capillary loops are cut on histological sections of damaged skin. This results in the development of a fibrotic process affecting the skin and subcutaneous fat which comprise the condition of lipodermatosclerosis. Around the capillaries are many inflammatory cells, especially macrophages. The combination of capillary proliferation and inflammation accounts for the appearance of liposclerotic skin, which looks inflamed. A perivascular cuff is present around the capillaries, which is made up of many connective tissue proteins including fibrin, collagen IV and fibronectin. This perivascular cuff is probably the result of chronic inflammation and occurs in many other types of inflammatory processes. It was originally thought that the fibrin cuff acted as a barrier to diffusion preventing nutrient exchange between the capillaries and the tissues. The ‘flbrin cuff’ hypothesis was accepted for many years as the explanation for venous ulceration. Research and theoretical calculations have shown that there is no physical barrier to the diffusion of nutrients to the tissues in this condition.
The factors which cause the inflammatory process have been sought. It has been shown that venous hypertension causes leucocyte sequestration in the microcirculation of the leg. Patients with chronic venous disease resulting in lipodermatosclerosis and venous ulceration trap more leucocytes than do subjects with normal limbs. It has been shown that these ‘trapped’ leucocytes become activated and release the proteolytic enzymes that are normally used in defence against infection. This, in turn, causes injury to the capillary endothelium. It seems likely that inappropriate activation of leucocytes instigates the series of events that results in leg ulceration. The frill mechanism is incompletely understood and further investigation of the processes involved may eventually lead to the development of better treatments for venous ulceration. This mechanism is referred to as the ‘white cell trapping hypothesis’ and was first proposed in 1988.
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