Lucan · Conditions

Deep vein thrombosis

Australian guidance: Thrombosis and Haemostasis Society Australia VTE Guidelines

1. Definition and epidemiology

Deep vein thrombosis (DVT) is thrombotic occlusion of the deep venous system, most commonly involving the veins of the calf, popliteal fossa, femoral, or iliac segments of the lower limb. DVT forms part of the broader venous thromboembolism (VTE) spectrum that encompasses distal DVT, proximal DVT, and pulmonary embolism (PE). Symptomatic VTE affects approximately 1 per 1,000 Australians per year, and hospitalisation is a major independent risk factor, with up to 75% of all VTE arising as a consequence of hospital admission. PE accounts for an estimated 7% of all in-hospital deaths in Australia, and in almost 25% of cases sudden death is the first clinical sign.

2. Pathophysiology

DVT arises from Virchow's triad of venous stasis, endothelial injury, and a hypercoagulable state, as described in Robbins Ch 4. Reduced blood flow, as occurs with prolonged immobility or external compression of a vein, allows activated clotting factors to accumulate locally rather than being diluted by flowing blood. Endothelial disruption from surgery, trauma, or indwelling catheters exposes subendothelial collagen and tissue factor, triggering the extrinsic coagulation cascade and platelet adhesion. Hypercoagulability may be inherited (factor V Leiden gene mutation causing activated protein C resistance, prothrombin 20210A gene mutation, deficiencies of antithrombin or proteins C and S) or acquired (antiphospholipid antibodies, malignancy, oestrogen therapy, pregnancy, myeloproliferative disorders). The resulting thrombus is composed of a platelet-rich white head at the site of endothelial injury and an erythrocyte-fibrin red tail propagating proximally. Proximal extension from distal calf veins, or thrombus fragmentation, may precipitate PE.

3. Clinical presentation and diagnostic criteria

Classic lower limb DVT presents with unilateral calf or thigh pain, pitting oedema, erythema, warmth, and dilation of superficial veins. Homans sign has poor sensitivity and specificity and should not be relied upon. Up to 50% of DVTs are clinically silent, particularly when distal. Provoked DVT follows an identifiable precipitant (surgery within the preceding month, trauma, hospitalisation, immobility, oestrogen therapy, or active cancer). Unprovoked DVT occurs without a clear trigger and carries a higher recurrence risk. Pre-test probability is stratified using the Wells DVT score: two or more points places the patient in the high probability category. Key Wells criteria include active cancer, paralysis or recent plaster immobilisation, bedridden for more than three days, localised tenderness along the deep venous system, entire leg swelling, calf swelling greater than 3 cm versus the asymptomatic leg, pitting oedema confined to the symptomatic leg, collateral superficial veins, and a previous DVT. An alternative diagnosis being at least as likely as DVT subtracts two points.

4. Investigations and AU-specific cutoffs

The investigation sequence follows a pre-test probability guided pathway. In patients with low to moderate Wells score (less than 2 points), a D-dimer assay is the first investigation. A negative age-adjusted D-dimer (threshold of 10 micrograms/L multiplied by age in patients over 50 years, as recommended in Australian practice per Thrombosis and Haemostasis Society of Australia and New Zealand guidelines) effectively excludes DVT without the need for imaging. In patients with high pre-test probability or a positive D-dimer, bilateral lower limb compression ultrasonography is the imaging of choice. Non-compressibility of a vein segment on ultrasound is diagnostic of DVT. Magnetic resonance venography or CT venography may be used when ultrasound is technically limited (pelvic DVT, obesity) or when iliac segment involvement is suspected. Repeat ultrasound at 5 to 7 days is indicated when the initial scan is negative but clinical suspicion remains high. Thrombophilia testing should not be performed in provoked DVT secondary to surgery or major trauma. Testing may be considered in patients under 45 years with unprovoked proximal DVT, and antiphospholipid antibody testing is reasonable in all patients with unprovoked VTE.

5. Management

Management depends on whether DVT is provoked or unprovoked, proximal or distal, and on individual patient bleeding risk. The Thrombosis and Haemostasis Society of Australia and New Zealand (THANZ) guidelines, published in the Medical Journal of Australia in 2019, recommend anticoagulation for a minimum of three months for provoked proximal DVT and for at least three to six months for unprovoked proximal DVT. For isolated distal DVT, surveillance with serial ultrasound is an acceptable alternative to anticoagulation if the patient is at low risk of propagation and has no severe symptoms. Anticoagulation is initiated with either a direct-acting oral anticoagulant (DOAC) as monotherapy or with low molecular weight heparin (LMWH) followed by a vitamin K antagonist. DOACs are first-line for most patients with DVT without active cancer, given their fixed dosing, predictable pharmacokinetics, and absence of routine monitoring requirements. For patients with active cancer-associated DVT, LMWH or a DOAC (apixaban or rivaroxaban) is preferred over a vitamin K antagonist; dabigatran data in this setting are lacking. DOACs are contraindicated in pregnancy; LMWH is the agent of choice throughout pregnancy and the postpartum period and is the only anticoagulant considered safe while breastfeeding alongside warfarin. Early mobilisation with graduated compression stockings reduces symptoms and may reduce the incidence of post-thrombotic syndrome.

6. Pharmacology and AU PBS notes

Rivaroxaban (Xarelto): 15 mg orally twice daily with food for the first 21 days, then 20 mg once daily. PBS streamlined authority item for treatment of DVT and PE. Avoid if creatinine clearance (CrCl) less than 15 mL/min.

Apixaban (Eliquis): 10 mg orally twice daily for the first 7 days, then 5 mg twice daily. PBS listed for VTE treatment. Avoid if CrCl less than 25 mL/min.

Dabigatran (Pradaxa): requires initial parenteral anticoagulation for at least 5 to 10 days, then 150 mg twice daily (110 mg twice daily for patients aged 80 years or older or on verapamil). PBS listed. Avoid if CrCl less than 30 mL/min.

Enoxaparin (Clexane): 1 mg/kg subcutaneously twice daily or 1.5 mg/kg once daily for treatment dose. Dose reduction to 1 mg/kg once daily required if CrCl less than 30 mL/min. Not renally cleared via same pathway as dabigatran; preferred parenteral agent in renal impairment when other agents cannot be used.

Warfarin: Requires INR monitoring with a therapeutic target of 2.0 to 3.0. Has largely been replaced by DOACs for DVT treatment in non-pregnant patients. Remains PBS-listed and appropriate when DOACs are contraindicated or unavailable. Warfarin is suitable while breastfeeding. Interactions with vitamin K-containing foods and many medications require ongoing clinical review.

For VTE prophylaxis in nonsurgical hospital inpatients: LMWH is preferred over DOACs due to a higher bleeding risk with DOACs in this setting. Enoxaparin 40 mg subcutaneously once daily (20 mg once daily if CrCl less than 30 mL/min) is the standard regimen.

7. Complications and monitoring

Pulmonary embolism: The most immediately life-threatening complication. Proximal DVT carries the highest risk of PE; approximately 50% of patients with proximal DVT have asymptomatic PE on ventilation-perfusion scanning. Patients must be monitored for dyspnoea, haemoptysis, pleuritic chest pain, and haemodynamic instability throughout admission and in the weeks following discharge.

Post-thrombotic syndrome (PTS): Occurs in 20 to 50% of patients after proximal DVT. Results from valvular incompetence and chronic venous hypertension. Presents as chronic leg pain, swelling, heaviness, skin discolouration, and in severe cases venous ulceration. Properly fitted below-knee graduated compression stockings (30 to 40 mmHg) worn for at least two years after proximal DVT are recommended to reduce severity.

Recurrent VTE: Unprovoked DVT carries a 10-year recurrence risk of approximately 30 to 40%. Patients with identified thrombophilia, active cancer, or two or more unprovoked events should be assessed for indefinite anticoagulation. Risk of recurrence is reassessed at completion of the index treatment period using clinical features, D-dimer off anticoagulation, and patient preference.

Monitoring on anticoagulation: DOACs do not require routine coagulation monitoring. Renal function should be checked at baseline and annually (or more frequently if clinically indicated) given dose adjustments required with declining CrCl. Platelet count should be monitored in patients receiving LMWH to detect heparin-induced thrombocytopenia (HIT), particularly between days 4 and 14 of therapy. Patients on warfarin require INR monitoring with titration to target range of 2.0 to 3.0. The ACSQHC VTE Prevention Clinical Care Standard mandates reassessment of thrombosis and bleeding risk at intervals of no longer than every seven days during hospitalisation, and at any transition of care.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.