Venous disorders of the lower limb

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43

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:

Patients should undergo a 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.

Management of post-thrombotic problems

The main post-thrombotic problems requiring active treatment are chronic venous ulcers and acute cellulitis.

Venous ulcers: Ulcers may develop spontaneously but are more commonly initiated by minor trauma which fails to heal, often complicated by secondary infection. Most venous ulcers can be healed by non-operative methods provided treatment is applied skilfully. Even if operative treatment is needed, conservative measures are used to prepare the limb. These include reducing swelling by multi-layer bandaging, removing necrotic tissue from the ulcer base and controlling cellulitis.

The systolic arterial pressure in the leg should be measured relative to the upper limb (i.e. ankle brachial pressure index (ABPI)—see Ch. 41, p. 497). If the ABPI is < 0.8, the arterial circulation may be inadequate; it should be assessed and necessary treatment instigated before compression therapy as (a) poor arterial supply may be part of the reason for non-healing of an ulcer and (b) compression bandaging with low arterial pressure will make ulceration worse.

Properly applied support and compression of skin and superficial tissues is the mainstay of treatment, provided initially by elastic bandages and when healed, by correctly fitting graduated compression stockings. In both cases, the aim is for pressure to be greatest at the ankle (up to 40 mmHg), reducing progressively up the limb. Great care must be taken that pressure does not cause ischaemia, or abrasions over tendons or bony prominences. Most venous ulcers can be healed rapidly whilst keeping the patient ambulatory by competent four-layer bandaging, avoiding the need for hospital care unless complications occur or skin grafting is required.

Spreading cellulitis should be treated with systemic antibiotics. Infection confined to the ulcer may be treated by saline soaks and perhaps excision of dead tissue; antiseptics are avoided as they may retard granulation tissue production and epithelialisation. Local antibiotics have no place in the management of ulcers.

Venous surgery may be indicated if there is superficial venous incompetence. Varicose veins should be ligated, treated endovenously or removed unless there is gross deep venous incompetence. Effective treatment of superficial venous reflux reduces the healing time for ulcers and halves the recurrence rate. Surgical disruption or ligation of incompetent perforating veins is of doubtful value, even if performed by subfascial endoscopic surgery (SEPS). Intractable or large ulcers may require skin grafting once the ulcer base is clean. Deep venous reflux is treated conservatively as there are no satisfactory surgical options that deliver long-term success.

Long-term care and prevention: As soon as a post-thrombotic limb is recognised, the patient should use graduated compression stockings and take care to avoid even minor trauma, especially to the gaiter area above the medial malleolus. Flaking and dryness of the skin should be treated with a moisturiser.

For minor venous insufficiency, well-fitting class I elastic stockings or tights provide suitable support. In more severe insufficiency, class II or III compression stockings may reverse tissue damage or arrest its progress. They also provide protection from minor trauma. Ideally they should be worn at all times except in bed. Correctly fitted stockings are vital; proximal constricting bands impair venous return and stockings sometimes need to be custom made. Effective elastic support will often be required for life but may not prevent further episodes of cellulitis or ulceration.

Axillary vein thrombosis

Axillary vein thrombosis is uncommon and is the upper limb equivalent of DVT. It usually presents with a sudden onset of swelling of hand, forearm and arm, and aching pain in the whole arm. The limb often has a bluish tinge and sensation is preserved. The cause can be primary or secondary. A primary presentation often has no detectable cause but may be associated with visceral malignancy (thrombophlebitis migrans), or a thrombotic predisposition. Paget–Schroetter syndrome is also referred to as ‘effort-induced thrombosis’. It usually occurs in younger people as a result of external compression of the subclavian vein between first rib and clavicle. The space may be congenitally narrow or physical activity such as weight-lifting may cause muscle hypertrophy or local trauma. Treatment options include anticoagulation to prevent propagation of thrombus and to encourage spontaneous clot lysis, or thrombolysis to restore vessel patency. Following successful lysis, patients may benefit from surgical excision of the first rib via an axillary or supraclavicular approach.

Secondary causes include long-term venous catheters, commonly employed in renal dialysis patients, and patients requiring long-term venous access for chemotherapy or parenteral nutrition. Catheter problems are usually managed with formal anticoagulation.

Varicose veins

Varicose veins are dilated, tortuous and prominent superficial veins in the lower limb (see Fig. 43.5). Varicose veins are common worldwide, being present in about 20% of people aged 20, increasing to 80% at 60 years. Nevertheless, only about 12% have symptoms or develop complications.

Pathophysiology of varicose veins

Abnormal communication between deep and superficial venous systems is crucial in the development of varicose veins. The process probably begins with failure of the valve at the sapheno-femoral junction, leading to an uninterrupted column of blood from the heart which progressively dilates superficial veins down the limb (see Fig. 43.5a). Varicose veins usually develop slowly over 10–20 years, so surgical treatment is rarely urgent. The long saphenous system is involved in about 90% and the short saphenous in 25% (some have both systems involved).

Women are affected about six times more often than men, with most developing during or soon after the second or third pregnancy. An important factor is probably the high level of progesterone, causing changes in collagen structure (which may not fully recover), as well as smooth muscle relaxation. Pressure on the pelvic veins by the enlarging uterus may contribute by restricting venous return.

Hereditary factors appear to play a part in some patients, especially in men and in those who develop varicosities in their teens. Predisposing anatomical factors may include congenital absence of valves in iliac veins or abnormal vein wall elasticity. DVT plays little part in causing varicose veins. Rarely, multiple congenital arteriovenous fistulae (Klippel–Trenaunay and other syndromes) cause gross varicose veins. In these patients, there is gigantism of the lower limb and often venous ulceration (see Ch. 46). A technique of examining varicose veins is shown in Figure 43.6.

Investigation of varicose veins

Traditional investigation of varicose veins includes clinical examination and tourniquet techniques (Fig. 43.6). As a screening investigation in clinic, hand-held ultrasound Doppler allows assessment of reflux at sapheno-femoral (SFJ) and sapheno-popliteal junctions (SPJ) and within the long and short saphenous veins. The probe is placed over either junction, the calf is pressed and the examiner can hear if there is significant reflux outwards through the junction on release of calf pressure. Formal duplex scanning is now advocated for all cases where intervention is planned. This gives accurate assessment of superficial and deep systems, determining anatomical areas of reflux and allowing appraisal for endovenous therapy.

Management of varicose veins

Most patients with longstanding varicose veins do not have venous complications. For these, surgical treatment is not usually necessary but advice can be given to elevate the legs when sitting and to wear supporting elastic stockings when standing for long periods.

Indications for surgical treatment of varicose veins

The main indications are aching legs after standing, relieved by elevation or when in bed at night (particularly with unilateral ankle oedema), haemorrhage from a varicose vein, superficial thrombophlebitis and venous skin changes due to superficial venous insufficiency. All of these can be treated with support bandages or stockings, but surgery is often preferable and more permanent.

Injection sclerotherapy (e.g. Fegan’s technique) is used for treating small cosmetically unattractive varicose veins below the knee but is unsuitable for major varicosities, particularly in the thigh. This type of injection sclerotherapy and surgery for varicose veins is shown in Figure 43.7.

Endovenous treatment of varicose veins

Newer endovenous treatments of main trunk varicose veins (i.e. LSV and SSV) have been introduced. These aim to ablate the main incompetent superficial vein using foam sclerotherapy, or laser or radiofrequency ablation. All can be performed under local anaesthesia without a groin incision, using ultrasound to give accurate guidance, and give a quicker return to normal activities.

Foam sclerotherapy involves injecting a sclerosant into a vein (e.g. sodium tetradecyl sulfate or polidocanol). It is first mixed with air or a physiological gas such as carbon dioxide in a syringe to create foam. Foaming increases the surface area of the sclerosant and ensures it displaces the blood, allowing it to act directly on the vein wall. For catheter ablation, the distal truncal vein is located by ultrasound and cannulated using a Seldinger technique to place a sheath into the vein. A laser fibre or a radiofrequency catheter is positioned just distal to the sapheno-femoral or sapheno-popliteal junction using ultrasound guidance. Before treatment, a tumescent mixture of local anaesthetic and normal saline is injected around the length of the vein for analgesia and to act as a heat sink. The vein is then heated internally by drawing the laser fibre or the ablation catheter along its length.

Results of all three techniques appear at least comparable with surgery but longer-term evaluation is in progress.

Perioperative management of the patient having varicose vein surgery

Varicose veins must be marked out indelibly on the legs before operation, ideally by the surgeon doing the operation. The patient must stand first, often for some minutes, to allow veins to fill, and marking performed in this position. Most surgeons mark all prominent veins that are visible or palpable. Extra marks are often added for areas needing special surgical attention such as suspected perforating veins. Duplex scanning is often employed to assist marking of perforators or of the sapheno-popliteal junction, well known to have a variable anatomy.

Patients with a history of deep or superficial venous thrombosis should be prescribed low-dose subcutaneous heparin, as should those with other risk factors for DVT, especially obese patients. The first dose should be given 1–2 hours before operation.

Immediately after operation, the whole leg is bandaged firmly with an elastic bandage. The patient should then be mobilised and encouraged to walk about. All dressings can be removed 24 hours later, and the bandage exchanged for a graduated elastic stocking (class 2) which should stay on for a minimum of 2 weeks. On return home, patients should be encouraged to be active, walking several times a day for at least the first 2 weeks. The legs should be elevated when sitting, and the patient should get up and walk around about every half-hour. All these measures are designed to discourage venous stagnation and venous thrombosis. Most patients can drive a car 24 hours after operation and return to work after a week. The patient should be warned that the legs will be bruised when bandages are removed.