The drop in pressure caused by the calf-muscle pump dur- cient blood can no longer be withdrawn and the intravas-
ing walking is reduced or completely absent (venous cular pressure increases. The continuous build-up of back
hypertension), and the functional capacity of the venous pressure in turn results in metabolic derangements in the
valves is progressively impaired. The effects manifest as peripheral skin areas, and in the worst case to ulceration.
chronic venous insufficiency, characterized by the patho- Moreover, the increased pressure stress not infrequently
physiological disorders of microcirculation in the cutis leads to leakage of the valves of the perforating veins,
and subcutis already described, which can culminate in causing blood to flow back from the subfascial into the
the formation of a venous leg ulcer. suprafascial system.
When the valvular apparatus is still sufficient in primary The consequences are secondary varices and edematous
varicosis, however, ulcerations can also develop as a infiltration of the cutis and subcutis with the known sec-
result of injuries, blunt traumas or varicose ruptures. Their ondary complications. Postthrombotic syndrome (PTS) is
prognosis is correspondingly more favourable. the commonest cause of venous leg ulcer (postthrombotic
venous leg ulcer).
Subfascial venous insufficiency /
postthrombotic syndrome
Insufficiency of subfascial veins can also occur in a pri-
mary form consecutive to valve agenesia or congenital
underdevelopment of the venous valves, but in most
cases appear as the secondary form after deep leg vein
1 thrombosis (phlebothrombosis).
Thrombosis of the deep veins not treated immediately by
thrombolysis or thrombectomy usually heals leaving a
2
defect. The thrombus becomes organised like connective
3 tissue, and this collagenous remodelling results in scar
formation. Incomplete obstruction of the venous volume
may often be followed by recanalisation, but because of
the scar formation the vein loses elasticity and can no
Poststhrombotic vascular and
longer adapt to the variable blood volumes. The venous
flow situation: the deep vein is
valves also can no longer fully perform their closure func-
scarred and recanalised after the
thrombosis (1). “Blow out”
tion and often create additional flow obstacles which pro-
through dilated communicating
mote turbulence of the blood. The alterations in the
veins (2), resulting in secondary
lumen due to scarring in the deep veins create new dead
varices (3).
space for the calf-muscle pump, with the result that suffi-
Causes [14.15]
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