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Deep Vein Thrombosis (DVT) is a common cause of morbidity and mortality. Timely diagnosis and prompt treatment can be lifesaving, as death may result from Pulmonary Embolism (PE).

Patients presenting at a primary care setting with unilateral swelling, pain and erythema of a lower limb should be viewed with high suspicion of DVT. However, the diagnosis of DVT can be very challenging as many skin and musculoskeletal disorders can mimic such presentation. The diagnosis of DVT rests on 3 pillars of (i) clinical suspicion, (ii) a blood test called d-dimer and (iii) compression ultrasound (CUS). While a clinical diagnosis can be difficult, an astute physician can judge the patient to be at low, moderate or high risk of DVT, based on Well’s score of pre-test probability. D-dimer is often considered unreliable as a raised level can be seen in many other conditions and a normal value does not rule out DVT reliably. CUS has become the diagnostic modality of choice for the diagnosis of DVT.

Anticoagulation remains the cornerstone of DVT management. The anticoagulant agents available for use include (i) Heparin — unfractionated heparin (UFH) and low molecular weight heparin (LMWH), (ii) Vitamin K antagonists (VKA) — the all too familiar warfarin and (iii) Non-vitamin K antagonists (NOACs) which include direct thrombin inhibitors like dabigatran and factor Xa inhibitors like rivaroxaban and apixaban. Over the years there has been a shift in management of DVT in selected patients from inpatient to outpatient departments (OPD). The patients suitable for OPD treatment should be haemodynamically stable, have low bleeding risk and have normal renal function.

Traditional approach of treating DVT with warfarin, overlapped with a short course of LMWH till INR stabilises in target range of 2-3 is marred with difficulties in keeping INR in stable range over a longer period often due to various food and drug interactions.

Deep Vein Thrombosis

NOACs have revolutionised the management of DVT and there is now the possibility for the complete management of selected patients with DVT to be undertaken by primary care. NOACs (rivaroxaban and apixaban) can be given in a fixed dose, without initial treatment with heparin. Rivaroxaban is given as 15 mg x twice a day for 3 weeks and 20 mg x once a day for the next 9 weeks. These drugs additionally enjoy minimal drug and food interactions and require no monitoring. However, NOACs are expensive, not safe in patients with compromised renal function and cannot be easily reversed in case of bleeding or at the time of urgent surgery.

Other therapies of DVT including thrombolysis (usually catheter directed) and throbectomy (surgical or percutaneous mechanical) are rarely employed in cases of massive illeofemoral thrombosis (Phlegmasia Cerulea Dolens) with risk of venous gangrene.

By Dr Pankaj Handa, Senior Consultant, Department of General Medicine, Tan Tock Seng Hospital

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