DVT - Ix

For the lung side of venous thromboembolism, see Pulmonary Embolism; for ongoing anticoagulation — duration, monitoring, procedures, bleeding — see VTE Treatment & Anticoagulation Management.

Risk factors and clinical assessment

VTE (DVT and PE) is the third most common cardiovascular disease; at least 17,000 Australians develop it each year, with a lifetime risk of 8%. Classify an event as provoked (surgical, or non-surgical transient/persistent) or unprovoked — this drives both recurrence risk and anticoagulation duration decisions. Common risk factors: recent trauma/surgery/immobilisation, travel >6 hours, previous VTE or family history, pregnancy/postpartum/oestrogen therapy, active cancer (~15% of cancer patients develop DVT), obesity, age >60, inherited thrombophilia, antiphospholipid antibodies, inflammatory bowel disease, and various medications (glucocorticoids, tamoxifen, testosterone, some antidepressants).

History: unilateral (occasionally bilateral, especially with cancer or very proximal DVT) leg or arm pain, tightness, swelling, warmth, redness. Examination: tenderness/swelling, dilated superficial veins, erythema, a palpable venous cord; check distal perfusion; assess for signs of PE (breathlessness, pleuritic chest pain, tachycardia, hypotension). Consider differentials — cellulitis, muscle strain, ruptured Baker’s cyst, lymphatic obstruction, venous stasis unrelated to DVT.

Diagnostic approach

Only around 20% of patients with clinically suspected VTE have it confirmed objectively, so objective testing is required — clinical impression alone is not reliable enough given the consequences of both over- and under-diagnosis (unnecessary long-term anticoagulation vs missed life-threatening PE).

Clinical prediction rules + D-dimer. Complete a Wells score (simplified: score 0–1 = DVT unlikely, ≥2 = DVT likely — not validated in pregnancy or upper-limb DVT). In people not known to have DVT, the diagnosis can usually be ruled out using any 2 of: a low-risk Wells score, a negative D-dimer, and a negative ultrasound.

• Low probability (Wells 0–1): arrange D-dimer. A negative D-dimer with a low-risk score has ~99% sensitivity to rule out DVT/PE. D-dimer has only ~50% specificity and can be falsely positive in pregnancy, older age, heart failure, recent surgery, malignancy, renal disease, or infection — it is not useful for diagnosing DVT in the presence of superficial venous thrombosis (not sensitive/specific enough), and there is no Medicare rebate when a GP requests it. A positive D-dimer needs a leg vein ultrasound.
• High probability (Wells ≥2): arrange an urgent leg vein ultrasound directly. If ultrasound isn’t available within 4 hours, start parenteral anticoagulation (e.g. enoxaparin), send a D-dimer, and get the ultrasound within 24 hours. If ultrasound is negative but symptoms persist, repeat in 1 week.
• Duplex ultrasound is the mainstay imaging test — a negative single whole-leg ultrasound excludes DVT and anticoagulation can be withheld. Diagnosing recurrent ipsilateral DVT is harder (incomplete thrombus resolution in 30–50%), so a single repeat scan at 3–6 months is reasonable as a comparator for future imaging; serial scanning without symptoms adds nothing.
• For suspected PE: CTPA is the preferred, most accurate test but involves significant radiation (3–5 mSv) and iodinated contrast (up to 14% nephrotoxicity risk, <1% allergic reaction). VQ scanning avoids contrast (useful in renal impairment or pregnancy, where it’s preferred) but is non-diagnostic in 27–55% of cases, requiring further testing.

Types of DVT and superficial thrombosis

• Distal DVT — thrombus confined to the calf veins (tibial, peroneal, gastrocnemius, soleal). ~10% extend proximally (especially in the first 2 weeks), more likely with thrombus close to proximal veins, active cancer, prior VTE, or hospitalisation.
• Proximal DVT — popliteal vein or more central (femoral, iliac, IVC). Higher risk of PE and of an underlying serious medical condition (active cancer, heart failure, respiratory disease) — investigate accordingly. Severe presentations (whole-leg swelling, cyanosis, venous gangrene, compartment syndrome) need urgent escalation.
• Upper-limb DVT — axillary/subclavian; less likely to embolise than lower-limb DVT. Wells score and D-dimer are not validated/recommended for this. Consider thoracic outlet syndrome if unprovoked.
• Superficial venous thrombosis (SVT), formerly “thrombophlebitis” — 5% of patients presenting with SVT also have a concurrent DVT; the other 95% have a 10% risk of extension to the deep system within 10 days. Risk-stratify by distance from the saphenofemoral junction: high risk (within 3 cm of the junction) needs full anticoagulation as for DVT (≥3 months, seek haematology advice); intermediate risk (>5 cm long, >3 cm from the junction) gets 4–6 weeks of anticoagulation (enoxaparin or rivaroxaban); low risk (<5 cm, >3 cm from the junction) can be managed conservatively with limb elevation, compression, and analgesia, with follow-up at 7–10 days.

Management

Anticoagulation reduces thrombus extension/recurrence by at least 80% and is indicated for most VTE. Oral factor Xa inhibitors (apixaban, rivaroxaban) are preferred first-line over dabigatran or warfarin for proximal DVT and PE, since they don’t need parenteral lead-in and require no routine monitoring, with few food/drug interactions. Use enoxaparin (not a DOAC) for: pregnancy/breastfeeding, cancer-associated VTE (discuss with oncology/haematology — DOACs may be considered in some), antiphospholipid syndrome (warfarin + enoxaparin, discussed with haematology), or severe renal impairment (apixaban needs CrCl ≥25 mL/min, rivaroxaban CrCl ≥15 mL/min — use CrCl, not eGFR, e.g. Cockcroft-Gault).

Duration of anticoagulation:

• Proximal DVT and PE: at least 3 months. Events provoked by major surgery/trauma can usually stop at this point.
• Distal DVT: uncertainty remains, but most distal DVT can be treated for 6–12 weeks; serial ultrasound (2 scans over 2 weeks) instead of anticoagulation is reasonable if bleeding risk is raised. HNE HealthPathways gives more specific timing: isolated distal DVT with a transient provoking factor → 6 weeks (if no persistent risk factor remains); unprovoked distal DVT → 3 months.
• Extended anticoagulation (beyond 3–6 months): consider for unprovoked VTE or VTE from a non-surgical (transient or persistent) risk factor, weighing recurrence risk against bleeding risk (roughly <1%/year extra bleeding risk on extended therapy). It does not reduce recurrence risk after stopping — once stopped, recurrence risk is the same regardless of how long treatment ran. Key recurrence predictors: unprovoked/non-surgical event, proximal DVT or PE (vs distal), prior VTE, male sex. If extending, low-intensity dosing is an option: apixaban 2.5 mg twice daily is as effective as 5 mg twice daily for preventing recurrence beyond 6 months, with a trend to less bleeding; rivaroxaban 10 mg once daily is similarly as effective as 20 mg once daily. Aspirin reduces recurrence less effectively than anticoagulants (though better than nothing) and should be avoided unless anticoagulation genuinely cannot be used.

Red flags needing urgent escalation (arrange ambulance transport and immediate assessment, with vascular surgery input): proximal DVT extending into the iliofemoral segment or IVC; upper-limb DVT with no provoking factor; evidence of gangrene or phlegmasia cerulea dolens (marked swelling, pain and cyanosis that can progress to arterial ischaemia and gangrene). Also seek urgent review for contraindications to anticoagulation (active bleeding, severe thrombocytopenia <50, recent intracranial haemorrhage or high-risk GI bleeding, uncontrolled severe hypertension, recent neurosurgery) or severe symptoms with no timely access to investigation.

Investigation after an unprovoked DVT

Thrombophilia testing is not routinely recommended. Inherited thrombophilia does not influence initial anticoagulant choice or mortality, and testing rarely changes management: Factor V Leiden and prothrombin gene mutation heterozygosity should not be routinely sought — they don’t change treatment duration or advice for family members. The one situation where testing is reasonable is antiphospholipid syndrome screening (lupus anticoagulant, anticardiolipin antibodies, anti-beta2-glycoprotein-1) in unprovoked VTE under age 45, or with recurrent events — results can be affected by anticoagulants, so seek specialist advice on timing/interpretation. Only rare deficiencies of the natural inhibitors (antithrombin, protein C or S) meaningfully raise recurrence risk enough to influence extending anticoagulation; family history alone is a poor predictor of thrombophilia and can often inform relatives’ prophylaxis advice without testing.

Malignancy screening: up to 10% of patients with unprovoked VTE are diagnosed with cancer in the following year. Assessment should be a thorough history, examination, and age-appropriate cancer screening (e.g. FBC, EUC, LFTs, calcium, urinalysis ± chest X-ray, and standard bowel/cervical/ breast/ovarian/prostate screening where relevant) — routine additional abdominopelvic CT does not identify more early-stage cancers or improve outcomes and is not recommended as an extra screening step.

Baseline work-up for any confirmed DVT should also include FBC, EUC, LFTs, and coagulation studies, plus a pregnancy test if anticoagulation is being considered in a person of childbearing age (oral anticoagulants are contraindicated in pregnancy — use enoxaparin, and arrange emergency antenatal assessment for a pregnant patient with confirmed DVT).

Complications

Post-thrombotic syndrome (PTS) affects around 1 in 3 patients after DVT (swelling, discomfort, hyperpigmentation, lipodermatosclerosis); iliofemoral DVT and ipsilateral recurrence are the main risk factors. Anticoagulation does not prevent PTS; evidence for compression stockings is mixed, though a trial of graduated compression (20–30 mmHg at the ankle) is reasonable for symptomatic relief. Chronic thromboembolic pulmonary hypertension (CTEPH) is rarer (3.4% incidence after acute PE) but has a poor untreated prognosis (30% five-year survival) — investigate with VQ scanning if suspected, and refer patients with persistent unmatched perfusion defects to an expert centre; pulmonary endarterectomy is potentially curative.