Chronic Venous Insufficiency

Wikis > Peripheral Vascular Disease > Chronic Venous Insufficiency

Muscular action of calf becomes inefficient during its ‘systolic’ phase and blood flows to superficial veins. Valves in superficial system become inefficient  reverse flow

Basic underlying mechanism is venous hypertension due to:
• the outflow being obstructed (eg thrombosis, congenital abnormality, tight bandage, tight garters)
• backflow/reflux due to valve dysfunction/incompetence (eg valves damaged by thrombi)
Both or either of these mechanisms leads to an increase in venous pressure during the systole phase of the calf muscle pump.

The venous hypertension  affects microcirculation of dermis

Pathological changes include an increase in pericapillary space and enlargement of capillary diameter . Reduced number of capillaries in those with severe CVI.

Clinical Features:
Veins are dilates; there may be pain/aches in the leg
Progressive pitting oedema - tends to occur early; initially limited to area just above skin line and resolves with elevation and rest; does not involve forefoot initially (lymphoedema does) later can progress to mid-calf. When chronic  subcutaneous fibrosis  non-pitting
Superficial veins are dilated (common early – especially medial calf)
Usually skin is thin; shiny; atrophic; cyanotic; brownish pigmentation
Haemosiderin deposits – due to venous hypertension  distends local capillaries  leakages of red blood cells metabolism of haemoglobin  ‘brawny’ appearance of skin
May get eczema with superficial weeping dermatitis
May have symptoms of ‘fullness’, heaviness, aching, tired legs – especially after prolonged standing
Up to a third may have signs of neuropathy (reduced vibration and temperature sensation)

• Support hose/external compression with elastic stockings
• intermittent pneumatic compression
• foot elevation
• foot health promotion – skin care (eg use of emollients)
• surgical (see Varicose Veins)

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