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PH-CV20

Varicose veins and chronic venous insufficiency

How failed valves turn the calf muscle pump against the leg: reflux at the saphenous junctions dilates the superficial veins, and pressure that stays high during walking leaks into the skin, causing oedema, brown staining, hard skin and ulcers.

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  • 4 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain how the calf muscle pump, venous valves and perforating veins lower venous pressure in the leg during walking.
  • Distinguish primary valve failure from secondary (post-thrombotic) disease, and relate reflux at the saphenofemoral and saphenopopliteal junctions to varicose veins.
  • Explain how ambulatory venous hypertension injures the skin microcirculation, and relate it to haemosiderin staining, venous eczema, lipodermatosclerosis, atrophie blanche and ulcers in the gaiter area.
  • Contrast varicose veins of the leg with the oesophageal and anorectal varices of portal hypertension.
  • Recognise the CEAP classes, duplex findings and differential diagnoses of venous disease, and explain how compression, ablation and the other main treatments act on its mechanism.

What it is

Chronic venous disease is long-standing dysfunction of the leg veins, usually from valves that leak (reflux) and less often from obstruction, which keeps venous pressure high while a person stands and walks (ambulatory venous hypertension). Varicose veins are dilated, twisted superficial veins; chronic venous insufficiency is the advanced stage in which the raised pressure damages the skin and fat of the lower leg, with oedema, skin changes and ulcers.

3 types to tell apart
Primary
No previous clot: the vein wall weakens and dilates and its valves leak. The commonest form, mainly in the superficial veins.
Secondary (post-thrombotic)
After deep vein thrombosis the deep valves are scarred or destroyed and the vein may stay partly blocked, so reflux and obstruction combine. Often more severe.
Congenital
Rare: absent or malformed valves and veins present from birth, sometimes as part of a vascular malformation syndrome such as Klippel–Trénaunay syndrome.

US spelling: oedema → edema.

Normal function

How walking empties the leg veins

The leg has two sets of veins. Superficial veins run in the fat under the skin: the climbs from in front of the medial malleolus along the inner leg and thigh to join the in the groin (the saphenofemoral junction), and the climbs the back of the calf to join the , usually behind the knee (the saphenopopliteal junction). Deep veins run with the arteries inside the muscle compartments, wrapped in tight deep fascia, and carry most of the blood. Perforating veins pierce the fascia between the two sets; their valves let blood pass only inwards, from superficial to deep.

Standing still, the pressure in an ankle vein equals the weight of the column of blood up to the heart, roughly 80–100 mmHg. Walking changes this. Each contraction of the calf muscles squeezes the deep veins and the venous sinuses inside soleus and drives blood upwards: the calf muscle pump. As the muscles relax, the valves below close, the emptied deep veins draw blood in from the superficial veins through the perforators, and the column of blood is broken into short segments. After a few steps the pressure in the ankle veins has fallen to a fraction of its standing value.

This fall protects the skin. Pressure in the skin capillaries of the foot and ankle follows the venous pressure, so a working pump and competent valves keep them at low pressure for most of a walking day. Lying with the legs raised removes the column altogether, which is why the symptoms of venous disease ease overnight.

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