Deep vein thrombosis and pulmonary embolism: diagnosis, treatment and prevention

Abstract

Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major public health issue, with an incidence of 1/1,000 and thousands of VTE-related deaths each year in the UK. The estimated cost of VTE and its complications to the NHS is in excess of £600 million. 1 PE is the most common cause of inpatient mortality, and is the leading cause of death in pregnant women. Common risk factors include hospitalisation, surgery, cancer and immobilisation; and in women, combined oral contraceptive use, hormone replacement therapy and pregnancy. Approximately a quarter of VTE episodes are unprovoked, that is without an identifiable precipitant. 2 Clinical features of DVT include swelling and pain, pitting oedema, increased warmth and superficial venous dilation of the lower limb. PE may present with or without symptoms of a DVT in addition to chest pain, breathlessness, haemoptysis, syncope, hypotension, tachycardia and hypoxia. Without prompt recognition and treatment, PE can lead to death in up to 30%. Clinical diagnosis of VTE can be challenging and, furthermore, clinically silent episodes are not uncommon. Integrated diagnostic strategies have been demonstrated to be safe, efficacious and cost effective. 3 These strategies employ the use of a clinical pretest probability score (Table 1) in combination with D-dimer to inform the need for further diagnostic imaging. Patients at low risk of DVT/PE with a negative Ddimer result (using a high sensitivity assay) require no further investigation. However, those identified as moderate or high probability, or with a raised D-dimer require definitive imaging to confirm or exclude the diagnosis. Non-invasive compression ultrasonography is increasingly used first line for investigation of DVT, with advantages over venography including superior safety and portability. Sensitivity can be adversely affected by operator experience and poor views may be obtained in the presence of severe obesity, gross oedema or a plaster cast. However, its sensitivity for symptomatic proximal DVT remains up to 97%. 4 Computed tomography (CT) pulmonary angiography is currently accepted as the investigation of choice for PE diagnosis 5 ; its increased resolution allows detection of PE to subsegmental levels, in addition to detection of alternate diagnoses, such as, infection or cancer. Treatment for VTE is primarily aimed at prevention of clot extension, embolisation and symptom relief, with additional long-term aims of minimising recurrence and preventing postthrombotic syndrome. 6 Anticoagulation is the mainstay of treatment and should be initiated at confirmation of diagnosis or when first suspected if there is a delay in diagnostic imaging. Thrombolysis or surgical thrombectomy/embolectomy should be reserved for selected patients with haemodynamic instability due to massive PE or critical limb ischaemia secondary to DVT. Low molecular weight heparins (LMWHs) are the preferred agents for initiation of anticoagulation due to improved efficacy, safety and ease of administration with once daily subcutaneous injection. 6 Monitoring of the anticoagulant effect is not required routinely with LMWH and rates of early mortality, recurrence and major bleeding are reduced compared to unfractionated heparin, as is the risk of heparin-induced thrombocytopenia. Warfarin should be initiated once the diagnosis of VTE is confirmed, in the absence of contraindications,