Venous disorders of the lower limb

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Venous disorders of the lower limb

Venous thrombosis and the post-thrombotic limb

Anatomy of the lower limb venous system

Blood is drained from the lower limb via two separate systems. The deep venous system drains the deep tissues of the foot and muscles of the lower leg and thigh. These deep veins lie within the mass of lower limb muscles and include the large soleal venous sinuses. Muscle contraction during walking and other exercise pumps blood back towards the heart against gravity (the muscle pump). Reverse flow is prevented by valves in the system.

The skin and other tissues superficial to the deep fascia drain into the superficial system with two main vessels, the long (great) saphenous vein and the short (small) saphenous vein. The long saphenous vein receives tributaries from the antero-medial aspect of the limb (and lower anterior abdominal wall), and penetrates the fascia lata in the groin to drain into the (deep) femoral vein (Figs 43.3). The short saphenous vein drains the posterior part of the leg and passes through the deep fascia into the popliteal vein of the deep venous system. There is a network of interconnecting superficial veins that drain blood from the limb if long or short saphenous veins are removed or ablated. The superficial system has no muscle pump to aid venous return but the valves normally prevent retrograde flow, particularly at sapheno-femoral and sapheno-popliteal junctions. Several perforating veins drain superficial blood into the deep system; valves on these normally ensure one-way flow. Most perforators lie medially on the calf above the ankle but there is a fairly constant ‘Hunterian perforator’ in the medial mid-thigh.

Presentation and consequences of venous thrombosis (Table 43.1)

Thromboembolic disease and its consequences are common and include acute deep vein thrombosis (DVT), pulmonary embolism and superficial thrombophlebitis (‘phlebitis’). Deep venous thrombosis most commonly occurs as a complication of major surgery, lower limb fractures, myocardial infarction or other severe illness. About one-third of DVTs present with no apparent cause, though many of these patients have a detectable prothrombotic state. The risk factors, clinical presentations and management of acute DVT and pulmonary embolism are discussed in Chapter 12, p. 167.

Deep venous thrombosis is an acute local problem, and often causes major long-term limb complications but has the added risk of pulmonary embolism. The affected extremity is known as a post-thrombotic limb or, less accurately, a post-phlebitic limb. Often patients present with a post-thrombotic limb without a symptomatic or diagnosed DVT previously, though many have had major surgery or lower limb fractures.

Pathophysiology of post-thrombotic problems

Following a DVT, the clot gradually undergoes inflammation, organisation and then recanalisation of the vein. During this process, valves are often damaged and become incompetent. This is because valve cusps fail to meet and interrupt the column of blood, allowing blood to reflux downwards causing increased pressure distally. This is chronic deep venous insufficiency and can take months or years to develop.

In the normal adult limb, ankle venous pressure while standing is about 125 cm of water. This falls markedly during walking as a result of the calf pump and valve function. In the post-thrombotic limb, where blood refluxes or veins remain occluded, ankle venous pressure remains high during walking. This leads secondarily to valve incompetence in perforating veins. Blood is forced into the superficial system causing local venous hypertension, disrupting normal vascular dynamics in skin and subcutaneous tissues. This may impair skin vitality and healing ability. Characteristic local signs of a gross post-thrombotic limb are listed in Box 43.1 (see also Fig. 43.1).

The following factors contribute to the clinical features:

Investigation of venous insufficiency

Chronic venous insufficiency usually presents with a chronically swollen limb and/or typical skin changes of venous insufficiency around the ankle, and sometimes with ankle ulceration. This may be due to superficial or deep venous reflux (post-thrombotic or congenital absence of valves) or a combination of both.

The diagnostic pathway depends on responses to the following questions: