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’ (Fig.
16.10). 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 (Fig. 16.11).
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’ (Fig.
16.12). 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 (Fig. 16.13).