Editorials

Avoiding the consequences of deep vein thrombosis

Elevation and compression are importantand too often forgotten 

Deep vein thrombosis has never been managed well. Before the use of anticoagulants it carried a substantial mortality, rising to over 50% for pulmonary embolism.¹ Doctors were slow to adopt anticoagulation before a small randomised trial showed dramatic reductions in mortality and recurrence.² Since then, however, anticoagulants have been widely used, but simple physical measureselevation followed by mobilisation with elastic compressionare too often forgotten.

Our aim should be urgent diagnosis and treatment with the twin objectives of (a) preventing extension of thrombosis, further venous damage, and embolism to the lungs and (b) encouraging clot lysis with restoration of venous function. Studies repeatedly show that clinical diagnosis is unreliable, but this is no excuse for delaying treatment for acute leg swelling associated with calf, popliteal, or femoral vein tenderness. Immediate high elevation and full heparinisation should be started and the diagnosis confirmed urgently. Duplex doppler imaging is ideal, although there is good evidence that simple ultrasound imaging reliably detects iliac or inferior vena caval thrombosis.³ Venography carries a small risk of rethrombosis,⁴ may not adequately show the iliac veins, and is indicated only when the ultrasound image is inadequate or placement of an inferior vena caval filter is planned for free floating thrombus.

Before anticoagulants are started blood should be taken for a thrombophilia screen, including activated protein C resistance associated with factor V Leiden mutation or acquired through taking oestrogen.⁵ Immediate anticoagulation with 5000 units of intravenous heparin may now be followed by subcutaneous heparin fractions administered in a fixed dose per weight, which encourages both early mobilisation and discharge.⁶

Despite good evidence that raising the leg and applying elastic compression prevents stasis and reduces both oedema and postphlebitic symptoms, these are often omitted.⁷ Heparin infusion tends to immobilise patients and, if they are left sitting in a chair, calf compartment pressures may threaten limb ischaemia. If ischaemia occurs high elevation (a Zimmer frame under the mattress) and thrombolytic treatment are urgently required, with three compartment fasciotomies if the foot is critically ischaemic (anaesthetic). Young adults have had above the knee amputations for the lack of simple elevation.

As soon as swelling resolves, usually after only 48 hours' elevation, the patient should be mobilised in class II elastic stockings (generally full length but below knee if only the calf is involved). The patient should be encouraged to walk but when not walking should return to bed with the leg raised, as sitting encourages venous stasis. Changing to oral anticoagulation involves a brief period when anticoagulation may be inadequate, so this should be delayed for at least a week in patients with extensive iliofemoral thrombosis. Venous thrombectomy is rarely helpful, as rethrombosis is usual. Thrombolysis may be accelerated by streptokinase or alteplase, but there is no convincing evidence that venous function is subsequently improved.⁸ The role of regional and systemic thrombolytic therapy needs to be evaluated in clinical trials.

Most patients are discharged with no plan to address postphlebitic symptoms, yet these may precipitate a lifetime of debility. Our practice is to supply class II elastic hosiery (20-25 mm Hg at the ankle) for everyday use, with class III hosiery (35-40 mm Hg) for patients who are on their feet all day or travelling long journeys. Patients should wear these stockings from getting up, having slept with the foot of the bed raised, until either retiring or resting with their legs raised in the evening. A daily walk stimulates the calf muscle pump. These conservative measures are often required for the rest of the patient's life but tend to be abandoned if the leg recovers fully. They are compatible with full employment unless ulceration develops.

As thrombus is lysed, patency is re-established in sclerotic and damaged veins with incompetent valves. Prognosis depends on preserving valve function, particularly in the distal deep veins of the calf, popliteal fossa, and thigh. ^{7 9 10} The risk of venous ulceration is only 6% and is strongly associated with recurrent deep vein thrombosis. Most patients who develop the postphlebitic syndrome have never been given appropriate advice on elevation and elastic stockings. Even if the advice is given years after deep vein thrombosis, symptoms can still be improved.⁷ Advice should also include information on weight loss, as obesity increases intra-abdominal pressure and the fat of the lower abdomen and upper thigh compress the femoral vein on sitting.

The treatment of deep vein thrombosis is largely common sense. Early anticoagulation combined with high elevation, carefully fitted elastic hosiery, and advice on lifestyle may help patients avoid a heavy swollen leg and venous ulceration in later life.