Venous disorders of the lower limb
Venous thrombosis and the post-thrombotic limb
Anatomy of the lower limb venous 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.
Table 43.1
Pathophysiology of post-thrombotic problems
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:
• Venous stagnation restricts arterial replenishment of capillary blood
• Arteriovenous shunts beneath the affected skin divert blood away from dermal capillaries
• Venous hypertension causes dilatation of local venules and the capillary network, allowing plasma proteins to leak into the interstitial spaces. Fibrin polymerises forming pericapillary cuffs which may interfere with metabolic exchange between blood and tissues
Investigation of venous insufficiency
The diagnostic pathway depends on responses to the following questions:
• Is the condition venous in origin? This is suggested by a history of DVT, prolonged bed rest in the past or lower limb fractures, or a finding of varicose veins or a ‘champagne-bottle’ leg (i.e. proximal limb swelling due to oedema and distal narrowing due to fat atrophy and fibrosis). If the condition is not venous, another cause of ulceration and swelling should be sought
• If it is venous, is there superficial (Fig. 43.2