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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 (LSV) receives tributaries from the anteromedial aspect of the limb (and lower anterior abdominal wall), and penetrates the fascia lata in the groin to drain into the (deep) femoral vein (see Fig. 43.3 ). The short saphenous vein (SSV) 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 LSVs or SSVs are removed or ablated. The superficial system has no muscle pump to aid venous return, but the valves normally prevent retrograde flow, particularly at saphenofemoral and saphenopopliteal 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 midthigh.

Presentation and Consequences of Venous Thrombosis

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 .

TABLE 43.1
Summary of Lower Limb Venous Disorders
Basic Disease Pathophysiological Process Clinical Manifestations
Varicose veins —incompetent valves in veins connecting deep and superficial venous systems; often begins with saphenofemoral valve incompetence Failure of muscle pump means blood is forced from deep venous system to superficial system through incompetent valves causing slowly progressive tortuous dilatation of superficial veins Slowly progressive development of prominent purple, dilated, tortuous superficial veins. Patient often complains of aching, especially after long period of standing. Patients may be distressed by cosmetic appearance or, if there is a family history, fear of progression or ulceration. Pain relieved by elevation. Dilated vessels are vulnerable to trauma and may bleed profusely
Venous hypertension may cause chronic skin changes and sometimes ulceration. Women more often affected than men; varicosities often first appear during pregnancy
Superficial venous thrombosis (i.e., thrombophlebitis)— usually occurs in tortuous dilated varicose veins; more common in pregnancy. Occasionally, affects normal veins in thrombophlebitis migrans occurring in patients with visceral malignancy Spontaneous thrombosis in superficial veins; excites an inflammatory response in the vessel wall and surrounding tissues Rapid onset of acute, highly localised pain and tenderness, associated with varicose veins. Overlying skin red and oedematous; underlying veins hard and nodular. Infection is not a feature so antibiotic treatment is illogical. Treatment is with nonsteroidal anti-inflammatories. Occasionally, ligation of the superficial vein at its junction with the deep vein is required to prevent thrombus propagating into the deep venous system
Deep venous thrombosis— predisposed to by previous deep vein thrombosis, pregnancy, oestrogen therapy, major surgery, trauma, obesity, abdominal or pelvic malignancy, immobility, a thrombophilia and increasing age. Long haul flying can be a factor, may be complicated by pulmonary embolism Thrombosis in deep venous system of calf; may propagate proximally into iliofemoral veins. Can obstruct venous return in both short and long term
Spontaneous recanalisation may cause deep vein valvular incompetence, that is, chronic venous insufficiency, and local swelling. Late complication is postthrombotic venous hypertension. This obstructs capillary flow and inhibits metabolic exchange; leakage of red cells causes subcutaneous deposition of haemosiderin
Combined effects cause atrophy of skin and subcutaneous fat, fibrosis, poor healing and predisposition to ulceration		 Classic acute presentation is pain and swelling of calf and ankle with calf tenderness but is often asymptomatic. Dorsiflexion may cause pain (Homans sign). Leg usually warm and normal in colour, but pulses may be impalpable because of oedema. If iliofemoral veins involved, thigh also swollen. Late complication is post-thrombotic limb with chronic brawny oedema and narrow ankle because of lipodermatosclerosis. Skin atrophic, scaly and pigmented (varicose/venous eczema). Skin above medial malleolus most vulnerable to chronic ulceration after minor trauma

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 postphlebitic 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 back 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 out 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 (also see Fig. 43.1 ).

BOX 43.1
Signs of a Gross Post-thrombotic Limb

  • Chronic lower leg swelling with brawny oedema

  • Varicose veins with incompetent perforating veins

  • Inflammation and haemosiderin pigmentation in the area above the medial malleolus (the ‘gaiter’ area) and other parts of the lower half of the leg. This is known as varicose or venous eczema and may be complicated by low-grade cellulitis

  • Active or healed venous ulceration above the medial malleolus

  • Lipodermatosclerosis around the ankle (replacement of soft subcutaneous fat with firm collagenous scar tissue). This causes the ‘champagne-bottle leg’ with oedema above and a narrow atrophic ankle below

BOX 43.2
Initial Examination of Varicose Veins

  • Severity —examine the extent and severity of varicose veins with the patient standing. Many patients attend with unsightly ‘spider veins’, which are not varicose. Others attend for advice because they are worried they will develop ulcers (‘like my mother’).

  • Skin changes —examine the leg for swelling, ulcers and varicose eczema. If present, could indicate a post-thrombotic limb.

  • Long or short saphenous —examine the distribution of varicose veins. Are there varicosities above knee, indicating probable saphenofemoral incompetence? Could these be short saphenous system varicosities, that is, posterolateral calf veins feeding towards popliteal fossa, where short saphenous may be palpable?

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

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 caused by 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:

  • 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 caused by oedema and distal

    Case Histories

    Fig. 43.1, Post-thrombotic Limbs and Venous Eczema. (A) Healed venous ulcer showing local loss of subcutaneous fat and surrounding pigmentation. (B) Man of 66 years with no history of deep vein thrombosis showing marked swelling of the left leg with pigmentation in the lateral gaiter area representing venous eczema. The right leg has moderate varicose veins; the blue discolouration around both ankles is an age change, caused by dilated venules and is of no clinical consequence. On colour duplex ultrasound examination, there was evidence of deep venous thrombotic damage in the left leg. (C) Bilateral post-thrombotic limbs in a woman of 57 years with gross venous eczema, fat atrophy, signs of healed venous ulceration and varicose veins.

    narrowing caused by 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 (see Fig. 43.2 ) or deep venous insufficiency, or a combination of both?

  • If a combination, how much is caused by superficial venous insufficiency and therefore likely to respond to surgery (unlike deep venous reflux).

Patients should undergo colour-flow duplex Doppler ultrasound investigation, now the ‘gold standard’. This can give detailed information on the presence and severity of reflux in deep and superficial veins, as well as determining whether there is venous obstruction. Functional detail will also be gleaned about the superficial system to enable targeted and appropriate treatment.

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