📋 Key Information Summary
- Use the Wells score to stratify clinical probability before ordering D-dimer or compression ultrasound (CUS) for suspected DVT.
- In low-probability Wells score, a negative high-sensitivity D-dimer safely excludes DVT without imaging.
- Whole-leg compression ultrasound is the first-line imaging modality; proximal CUS is preferred when serial testing is planned.
- Direct oral anticoagulants (DOACs) — apixaban or rivaroxaban — are first-line for most patients with acute DVT, without the need for initial parenteral heparin bridging.
- LMWH (enoxaparin) remains first-line for cancer-associated VTE, pregnancy, and severe renal impairment (CrCl <30 mL/min may require unfractionated heparin).
- Outpatient management is appropriate for most low-risk DVT; use the Vienna Prediction Model or VTE-BLEED to identify suitable patients.
- Graduated compression stockings (20–30 mmHg) may reduce swelling and improve comfort but are no longer mandated to prevent post-thrombotic syndrome based on current evidence.
- Provoked DVT (surgery, trauma, immobilisation, oestrogen) warrants 3 months of anticoagulation; unprovoked DVT requires individualised risk–benefit assessment for extended therapy.
- Routine thrombophilia screening is NOT recommended after a first provoked DVT; consider testing only if it will change management (e.g., unprovoked VTE, family history, young age).
- All patients with unprovoked VTE should be assessed for occult malignancy with age-appropriate cancer screening; extensive thrombophilia panels are not routinely indicated.
- Extended anticoagulation (beyond 3–6 months) reduces recurrence by ~80% but carries ongoing bleeding risk; use reduced-dose apixaban (2.5 mg BD) or rivaroxaban (10 mg daily) for extended prophylaxis.
- Upper extremity DVT (UEDVT) is most commonly catheter-related or effort-related; treat with anticoagulation for ≥3 months and consider thrombolysis in severe cases.
- Pregnancy-associated VTE requires LMWH throughout pregnancy and 6 weeks postpartum; DOACs are contraindicated in pregnancy and breastfeeding.
- Aboriginal and Torres Strait Islander Australians have higher VTE rates and later presentations; ensure culturally safe care, community-based follow-up, and awareness of geographic barriers to anticoagulation monitoring.
Introduction & Australian Epidemiology
Deep vein thrombosis (DVT) is the formation of a blood clot within the deep venous system, most commonly in the lower extremities. Together with pulmonary embolism (PE), DVT constitutes venous thromboembolism (VTE), which is the third leading cause of cardiovascular death in Australia after myocardial infarction and stroke.
In Australia, the annual incidence of VTE is estimated at 52–82 per 100,000 population, with approximately half presenting as DVT. The incidence rises sharply with age — from ~5 per 100,000 in those aged 15–29 to over 500 per 100,000 in those aged ≥75 years. Hospital-associated VTE accounts for approximately 50–60% of cases, highlighting the importance of thromboprophylaxis in line with NSQHS Standards.
Key Australian data sources include the AIHW National Hospital Morbidity Database, the Thrombosis Australia Registry, and the Australasian Society of Thrombosis and Haemostasis (ASTH). Recurrence rates in Australia parallel international data: ~10% at 1 year and ~30% at 10 years after a first unprovoked DVT. Post-thrombotic syndrome (PTS) develops in 20–50% of patients, and chronic thromboembolic pulmonary hypertension (CTEPH) occurs in 2–4% following PE.
NSQHS Clinical Deterioration Standard: All hospitalised patients should receive VTE risk assessment and appropriate thromboprophylaxis within 24 hours of admission, in accordance with the Australian Commission on Safety and Quality in Health Care (ACSQHC) Clinical Deterioration Standard and the National VTE Prevention Clinical Care Standard (2018).
In-hospital case fatality for DVT alone is low (<1%), but rises to 3–8% for PE and up to 30% for massive PE with haemodynamic instability. Early recognition and risk-appropriate management are essential to prevent these complications.
Diagnosis
The diagnostic approach to suspected DVT integrates clinical probability assessment (Wells score), D-dimer testing, and compression ultrasound to efficiently confirm or exclude DVT while minimising unnecessary imaging.
Clinical Probability — Wells Score
The modified Wells score stratifies patients into low, moderate, or high clinical probability categories, guiding subsequent investigations.
| Clinical Feature | Points |
|---|---|
| Active cancer (treatment within 6 months or palliative) | +1 |
| Paralysis, paresis, or recent plaster immobilisation of lower limb | +1 |
| Recently bedridden ≥3 days or major surgery within 12 weeks | +1 |
| Localised tenderness along deep venous system | +1 |
| Entire leg swollen | +1 |
| Calf swelling ≥3 cm compared with asymptomatic leg (measured 10 cm below tibial tuberosity) | +1 |
| Pitting oedema confined to symptomatic leg | +1 |
| Collateral superficial veins (non-varicose) | +1 |
| Previously documented DVT | +1 |
| Alternative diagnosis at least as likely as DVT | −2 |
Low
Score ≤1
DVT prevalence ~5%. Perform high-sensitivity D-dimer. If negative, DVT excluded. If positive, proceed to CUS.
Setting: GP / ED
Moderate
Score 2–6
DVT prevalence ~17%. D-dimer or direct CUS. Age-adjusted D-dimer cutoff (>50 years: age × 10 µg/L) improves specificity.
Setting: ED / Hospital
High
Score ≥7
DVT prevalence ~53%. Proceed directly to compression ultrasound. D-dimer does not exclude DVT at this probability.
Setting: ED / Hospital
D-Dimer
High-sensitivity D-dimer (ELISA or immunoturbidimetric assay, threshold <500 µg/L FEU) is most useful for excluding DVT in low-to-moderate probability patients. A negative result (<500 µg/L) has a negative predictive value of >97%.
Age-adjusted D-dimer: In patients aged >50 years, using an age-adjusted cutoff (age × 10 µg/L) substantially improves specificity without sacrificing safety. For example, a 65-year-old patient has a cutoff of 650 µg/L rather than 500 µg/L. This approach is endorsed by the European Society of Cardiology (ESC) and is increasingly adopted in Australian practice.
D-dimer is less specific in hospitalised patients, pregnant women, the elderly, post-operative patients, and those with active malignancy, infection, or inflammation. It should not be used as a standalone test to rule in DVT.
Compression Ultrasound (CUS)
Compression ultrasound is the gold-standard imaging modality for DVT diagnosis. It is non-invasive, widely available across Australian metropolitan and regional centres, and does not require contrast.
Essential
Proximal (2-point) CUS
Assesses common femoral and popliteal veins. Sensitivity 97%, specificity 94% for proximal DVT. Preferred when serial testing is planned (e.g., initial CUS negative in moderate probability — repeat in 5–7 days). MBS Item 55716.
Available
Whole-leg CUS
Extends assessment to calf veins (peroneal, posterior tibial, gastrocnemius, soleal). Detects isolated distal DVT, which accounts for 20–25% of all DVTs. Eliminates need for serial testing. Preferred by many Australian EDs.
Available
CT venography
Useful for suspected iliac vein or IVC thrombosis, or when CUS is equivocal. MBS Item 57321. Higher radiation dose; reserved for complex cases.
Referral
MR venography
Gold standard for iliac vein and IVC thrombosis. No radiation. Limited availability outside tertiary centres. Useful in pregnancy and young patients.
Proximal vs Distal DVT
| Feature | Proximal DVT | Distal (Calf) DVT |
|---|---|---|
| Location | Popliteal, femoral, iliac veins | Peroneal, posterior tibial, gastrocnemius, soleal veins |
| Proportion of all DVT | ~75% | ~25% |
| PE risk | High (25–50% if untreated) | Lower (~10%), but may extend proximally |
| Treatment | Anticoagulation recommended | Anticoagulation if symptomatic, high-risk features, or extension on serial CUS |
| Serial CUS | Not needed if positive | If not anticoagulating: repeat in 5–7 days to assess for proximal extension |
Isolated distal DVT — clinical vigilance required: Patients with isolated distal DVT who are not anticoagulated require repeat proximal CUS in 5–7 days to detect proximal extension. Those with active cancer, reduced mobility, D-dimer >1000 µg/L, extensive clot (≥5 cm or involving multiple veins), or no reversible provoking factor should be considered for anticoagulation even for distal DVT.
Diagnostic Algorithm
1
Assess Clinical Probability
Apply modified Wells score. Classify as low (≤1), moderate (2–6), or high (≥7).
2
Low Probability
High-sensitivity D-dimer → if negative, DVT excluded → if positive, proceed to CUS.
3
Moderate Probability
D-dimer (with age-adjusted cutoff) or direct CUS. If D-dimer negative, DVT excluded.
4
High Probability
Proceed directly to compression ultrasound. Do not rely on D-dimer to exclude.
5
CUS Positive → Treat
Initiate anticoagulation. Assess for PE if symptoms present (chest pain, dyspnoea, haemoptysis).
6
CUS Negative, High Suspicion
Consider CT/MR venography for iliac vein thrombosis. Serial CUS in 5–7 days if distal DVT not excluded.
Acute Management
The goals of acute DVT management are to prevent thrombus extension, reduce PE risk, and minimise post-thrombotic syndrome. Treatment has been revolutionised by DOACs, which allow most patients to be managed entirely in the outpatient setting.
Anticoagulation Choice
Anticoagulation is the cornerstone of DVT treatment. The choice of agent depends on clinical context, renal function, drug interactions, patient preference, and cost.
Apixaban
Eliquis® · DOAC (Factor Xa inhibitor)
Acute dose
10 mg PO BD for 7 days, then 5 mg PO BD
Extended prophylaxis
2.5 mg PO BD (after ≥6 months of treatment)
Renal adjustment
No dose change for CrCl ≥15 mL/min. Avoid if CrCl <15 mL/min or on dialysis
Key interactions
Strong dual CYP3A4/P-gp inhibitors/inducers (ketoconazole, rifampicin, phenytoin, carbamazepine)
PBS status
✔ PBS General Benefit
Rivaroxaban
Xarelto® · DOAC (Factor Xa inhibitor)
Acute dose
15 mg PO BD with food for 21 days, then 20 mg PO daily with food
Extended prophylaxis
10 mg PO daily (after ≥6 months of treatment)
Renal adjustment
Avoid if CrCl <15 mL/min. Use with caution CrCl 15–30 mL/min
Key interactions
Must be taken with food to ensure absorption. Strong CYP3A4/P-gp inhibitors/inducers
PBS status
✔ PBS General Benefit
Enoxaparin (LMWH)
Clexane® · Low-molecular-weight heparin
Adult dose
1.5 mg/kg SC once daily OR 1 mg/kg SC BD
Bridging
Use when transitioning to warfarin (target INR 2.0–3.0 for ≥24 hours and ≥5 days overlap)
Renal adjustment
Reduce to 1 mg/kg SC OD if CrCl <30 mL/min. UFH preferred if CrCl <15 mL/min
Monitoring
Anti-Xa levels if renal impairment, extremes of weight (<50 kg or >120 kg), pregnancy
PBS status
✔ PBS General Benefit
Warfarin
Marevan® · Vitamin K antagonist
Adult dose
Individualised dosing; typically 5 mg PO daily for 2–3 days, then adjusted per INR. Target INR 2.0–3.0
Duration
Minimum 3 months; overlapped with LMWH/UFH for ≥5 days AND until INR ≥2.0 for ≥24 hours
Renal adjustment
No renal dose adjustment required. Monitor INR closely
Key interactions
Numerous (amiodarone, antibiotics, azole antifungals, rifampicin, cranberry juice, St John's wort)
PBS status
✔ PBS General Benefit
Unfractionated Heparin (UFH)
DBL Heparin · Parenteral anticoagulant
Adult dose
80 units/kg IV bolus, then 18 units/kg/hr IV infusion. Adjust per APTT (target APTT 1.5–2.5× control)
Indications
Severe renal impairment (CrCl <15 mL/min), massive PE with haemodynamic instability, peri-procedural bridging when rapid reversal needed
Reversal
Protamine sulfate (1 mg neutralises ~100 units UFH)
PBS status
✔ PBS General Benefit
Preferred Anticoagulation Strategy
First-line for uncomplicated DVT: Apixaban or rivaroxaban are preferred over warfarin for most patients due to comparable efficacy, lower bleeding risk, no routine INR monitoring, and simpler dosing. These DOACs do not require initial parenteral bridging (the AMPLIFY and EINSTEIN-DVT trials demonstrated non-inferiority with a simplified single-drug approach).
Warfarin remains appropriate for patients with mechanical heart valves, antiphospholipid syndrome (triple-positive), severe renal impairment where DOACs are contraindicated, and patient preference. LMWH bridging is required when initiating warfarin.
Outpatient vs Inpatient Management
Evidence from the OTIS-DVT, OASIS, and other trials demonstrates that most patients with acute DVT can be safely managed as outpatients with equivalent outcomes to inpatient care.
| Criteria | Outpatient Suitable | Consider Inpatient |
|---|---|---|
| Haemodynamic status | Stable | Hypotension, shock (suspected PE) |
| Symptoms | Isolated leg DVT, manageable pain | Severe limb ischaemia (phlegmasia), massive iliofemoral DVT |
| Bleeding risk | Low bleeding risk | High bleeding risk, recent GI haemorrhage |
| Comorbidities | Few or well-managed | Decompensated heart failure, severe renal/hepatic disease |
| Social factors | Reliable, can attend follow-up | No fixed address, cognitive impairment, no access to medication |
| Anticoagulant plan | DOAC (no monitoring needed) | Warfarin initiation with LMWH bridging |
LMWH Bridging
LMWH bridging is required when warfarin is used rather than a DOAC. Enoxaparin (Clexane®) 1.5 mg/kg SC once daily or 1 mg/kg SC BD is commenced immediately and continued for a minimum of 5 days AND until the INR is ≥2.0 for at least 24 hours (typically 2 consecutive INR results in range).
LMWH bridging is NOT required for DOACs: Apixaban and rivaroxaban have rapid onset of action (peak levels within 2–4 hours) and do not require parenteral bridging. This is a major advantage for outpatient management. Starting a DOAC with LMWH bridging adds bleeding risk without benefit.
Compression Therapy
Graduated compression stockings (GCS, 20–30 mmHg) have traditionally been recommended to reduce post-thrombotic syndrome. However, the SOX trial (2014) showed no significant reduction in PTS with compression stockings versus placebo. Current recommendations are nuanced:
- Symptom relief: GCS may reduce acute leg swelling, pain, and heaviness. They may be offered for symptom management on a case-by-case basis.
- PTS prevention: Routine use of GCS specifically to prevent PTS is no longer universally recommended (referenced in eTG and 2024 ISTH guidance).
- Application: 20–30 mmHg thigh-high stockings, fitted 1–2 weeks after acute DVT onset when swelling has improved. Wear during the day, remove at night.
- Contraindications: Peripheral arterial disease (ABPI <0.8), diabetic neuropathy with skin breakdown, severe peripheral oedema.
Adjunctive Measures
- Early mobilisation: Bed rest is NOT required. Patients should be encouraged to mobilise as tolerated from the time of diagnosis. A Cochrane review (2014) showed no increased PE risk with early ambulation.
- Elevation: Elevate the affected limb when resting to reduce swelling.
- Analgesia: Paracetamol, short-course NSAIDs (if no contraindication to concurrent anticoagulation), or mild opioids for severe pain.
- PESI/sPESI for concomitant PE: If PE is also present, use the Pulmonary Embolism Severity Index to guide disposition (outpatient management for class I–II).
Provoked vs Unprovoked DVT
The distinction between provoked and unprovoked DVT is fundamental to determining anticoagulation duration, the need for thrombophilia testing, and cancer screening.
Definitions
| Category | Examples | Anticoagulation Duration |
|---|---|---|
| Major provoked | Surgery (within 6 weeks), significant trauma (within 6 weeks), lower-limb plaster cast/immobilisation (within 6 weeks), hospitalisation with reduced mobility | 3 months (sufficient in most cases) |
| Minor provoked | Oestrogen therapy (HRT, OCP), long-haul travel (>8 hours), minor illness with reduced mobility, pregnancy/puerperium | 3 months (consider extension if ongoing risk factor) |
| Unprovoked | No identifiable provoking factor, or only minor transient risk factor (e.g., minor infection) | ≥3 months, then reassess for extended therapy |
| Cancer-associated | Active cancer (diagnosis within 6 months, metastatic, on treatment, or recurrent) | Minimum 6 months, ongoing as long as cancer active (LMWH or DOAC) |
Thrombophilia Testing
Thrombophilia testing is frequently over-requested. Routine testing after a first provoked DVT is not recommended, as it rarely changes management and can cause unnecessary anxiety.
When to consider thrombophilia testing:
- First unprovoked VTE in a young patient (<50 years) — if results would influence duration of anticoagulation
- Recurrent VTE, particularly if unprovoked
- VTE at unusual sites (cerebral, splanchnic, portal vein)
- Strong family history of VTE (first-degree relatives with VTE <50 years)
- Planning to stop anticoagulation — test while on treatment may be informative for genetic tests (Factor V Leiden, prothrombin G20210A); functional tests (protein C, S, antithrombin) should be deferred until ≥2 weeks after stopping anticoagulation
Available
Factor V Leiden mutation
Genetic test — can be performed on or off anticoagulation. Present in ~5% of Caucasians. Heterozygous: 3–5× increased VTE risk. Homozygous: 50–80× increased risk.
Available
Prothrombin gene mutation (G20210A)
Genetic test — can be performed on or off anticoagulation. Present in ~2% of Caucasians. ~2–3× increased VTE risk.
Available
Antiphospholipid antibodies
Lupus anticoagulant, anticardiolipin antibodies, anti-β2 glycoprotein I. Requires testing on TWO occasions ≥12 weeks apart to confirm antiphospholipid syndrome. Lupus anticoagulant testing unreliable on DOACs — test on LMWH or warfarin.
Available
Antithrombin, Protein C, Protein S
Functional assays — must be performed OFF anticoagulation (≥2 weeks post-stop). Acquired deficiencies common in acute VTE, liver disease, DIC. Hereditary deficiency prevalence <1% but high VTE risk.
Cancer Screening After Unprovoked DVT
Approximately 7–12% of patients with unprovoked VTE will be diagnosed with cancer within 12 months. Age-appropriate cancer screening is recommended.
1
Basic Screening (All Patients)
Thorough history and physical examination (including breast, testicular, prostate, lymph nodes, rectal). Age-appropriate screening per National Cancer Screening Register (bowel, breast, cervical). FBC, LFTs, calcium, urinalysis. Chest X-ray.
2
Extended Screening (Selective)
CT abdomen/pelvis if clinical suspicion or abnormal bloods. Tumour markers are NOT routinely recommended for screening. PET-CT not recommended as a screening tool in asymptomatic patients.
3
Ongoing Vigilance
Patients should remain cancer-aware for 12 months post-DVT. New symptoms should prompt investigation. Routine whole-body CT without clinical indication is not recommended (INSIGHT study showed low yield).
Anticoagulation Duration Decisions
The decision to continue or stop anticoagulation beyond the initial treatment period is one of the most important clinical decisions in DVT management.
Provoked DVT — Stop at 3 Months
When the provoking factor has resolved (e.g., post-surgical immobilisation ended, OCP ceased), the recurrence risk returns to baseline (~1–3% per year). Extended anticoagulation offers minimal additional benefit and exposes patients to bleeding risk. Discontinue anticoagulation at 3 months with a clear plan for patient education regarding recurrent symptoms.
Unprovoked DVT — Individualise
Recurrence risk is ~10% per year if anticoagulation is stopped after 3 months. Factors favouring extended therapy: male sex, elevated D-dimer after stopping (D-dimer positive at 1 month off anticoagulation predicts high recurrence), persistent residual vein obstruction on CUS, post-thrombotic syndrome, and patient preference. Factors favouring stopping: female sex, high bleeding risk, falls risk, low D-dimer off anticoagulation, patient preference.
Recurrent VTE Prevention
After stopping anticoagulation for a first unprovoked DVT, recurrence rates are approximately 10% at 1 year, 25% at 5 years, and 36% at 10 years. Extended anticoagulation is highly effective at reducing recurrence, but the decision must balance this benefit against ongoing bleeding risk.
Extended Anticoagulation
For patients in whom the decision is made to continue anticoagulation indefinitely, reduced-dose regimens provide a favourable balance between efficacy and safety:
Apixaban (reduced dose)
Eliquis® · Extended prophylaxis dose
Dose
2.5 mg PO BD (after ≥6 months of standard-dose anticoagulation)
Evidence
AMPLIFY-EXT: 81% reduction in recurrent VTE vs placebo; major bleeding not significantly increased
PBS status
✔ PBS Authority Required
Rivaroxaban (reduced dose)
Xarelto® · Extended prophylaxis dose
Dose
10 mg PO daily with food (after ≥6 months of standard-dose anticoagulation)
Evidence
EINSTEIN-CHOICE: rivaroxaban 10 mg superior to aspirin for recurrence prevention with similar bleeding rates
PBS status
✔ PBS Authority Required
Aspirin
Cardiprin® / Cartia® · Antiplatelet
Dose
100–150 mg PO daily (alternative when anticoagulation contraindicated)
Evidence
WARFASA/ASPIRE: modest ~30% reduction in VTE recurrence; inferior to DOACs
PBS status
✔ PBS General Benefit
Risk–Benefit Assessment Tools
Several validated tools assist in the decision to extend or stop anticoagulation:
| Tool | Components | Application |
|---|---|---|
| D-dimer after stopping AC | Repeat D-dimer 1 month after stopping anticoagulation. If elevated, high recurrence risk (≥8%/yr) | If negative: consider stopping. If positive: consider restarting extended therapy |
| Vienna Prediction Model | D-dimer, sex, site of VTE, provoked status | Estimates recurrence risk to guide duration decision |
| HERDOO2 (women only) | Hyperpigmentation, oedema, D-dimer >250, obesity, age ≥65 | Women with ≤1 point may safely stop anticoagulation after 5–12 months |
| DOAC Score / VTE-BLEED | Bleeding risk factors including age, cancer, anaemia, renal disease, antiplatelet use | Assess bleeding risk to contextualise recurrence risk |
| Residual vein obstruction (RVO) | CUS at 3–6 months: presence of non-compressible residual thrombus | RVO modestly increases recurrence risk; used in some European protocols, less in Australian practice |
Thrombophilia Management
Thrombophilia-specific management considerations:
- Antiphospholipid syndrome (APS): Lifelong warfarin (target INR 2.0–3.0). DOACs are generally avoided in triple-positive APS based on the TRAPS trial (rivaroxaban was inferior with increased thrombotic events). May consider DOACs in single/double-positive APS if warfarin is impractical (shared decision-making).
- Factor V Leiden / Prothrombin mutation: Heterozygous — does not mandate lifelong therapy alone but supports extended therapy in unprovoked VTE. Homozygous or compound heterozygous — generally lifelong anticoagulation.
- Antithrombin deficiency: High thrombotic risk. Consider lifelong anticoagulation. LMWH or UFH during high-risk periods (surgery, pregnancy). Antithrombin concentrate available for critical situations (PPTA supply).
- Protein C / S deficiency: Moderate thrombotic risk. Consider extended therapy after unprovoked VTE. Warfarin-induced skin necrosis risk — always bridge with LMWH.
Warfarin-induced skin necrosis: Patients with protein C or S deficiency who start warfarin without adequate LMWH bridging are at risk of warfarin-induced skin necrosis (typically occurs days 3–5). Always overlap warfarin with enoxaparin for a minimum of 5 days and until INR is therapeutic. Start warfarin at a low dose (5 mg, not 10 mg) in high-risk patients.
Special Situations
Upper Extremity DVT (UEDVT)
Upper extremity DVT accounts for ~10% of all DVT cases. It is classified as primary (effort-related/Paget-Schroetter syndrome or idiopathic) or secondary (catheter-related, malignancy-related, or due to thoracic outlet syndrome).
- Diagnosis: CUS of the axillary and subclavian veins has good sensitivity for axillary DVT but limited sensitivity for subclavian and innominate vein thrombosis. CT or MR venography is preferred for proximal UEDVT. D-dimer is less validated in this context.
- Treatment: Anticoagulation with a DOAC (apixaban or rivaroxaban) or LMWH/warfarin for a minimum of 3 months. If catheter-related and the catheter is still needed, anticoagulate with the catheter in situ; remove if no longer required.
- Thrombolysis: Consider catheter-directed thrombolysis or surgical decompression for severe effort-related UEDVT (Paget-Schroetter syndrome) with significant symptoms, particularly in young, active patients. Refer to vascular surgery.
- Paget-Schroetter syndrome: First rib resection should be considered after initial thrombolysis and anticoagulation to prevent recurrence, typically at 3–6 months. Refer to cardiothoracic/vascular surgery.
Available
Duplex CUS (upper limb)
First-line for axillary and proximal subclavian veins. Limited sensitivity for central subclavian and innominate veins. MBS Item 55716.
Referral
CT venography (upper thorax)
CT with contrast from arm to SVC. Preferred for central UEDVT. MBS Item 57321.
Referral
MR venography
No radiation. Useful for young patients and those with contrast allergy. Requires tertiary centre access.
Specialist
Catheter-directed thrombolysis
Interventional radiology. Indicated for severe Paget-Schroetter syndrome. Tissue plasminogen activator (tPA) delivered directly to thrombus.
Superficial Thrombophlebitis (Superficial Vein Thrombosis — SVT)
Superficial vein thrombosis (SVT) is common and often self-limiting, but can be associated with concurrent DVT in 6–40% of cases and carries a risk of extension into the deep venous system.
| Risk Category | Features | Management |
|---|---|---|
| Low risk | SVT >3 cm from saphenofemoral junction (SFJ), no prior VTE, no active cancer, varicose vein-related | Compression stockings, NSAIDs, warm compresses. Consider fondaparinux 2.5 mg SC daily for 45 days (CALISTO trial) |
| High risk | SVT within 3 cm of SFJ, prior VTE, active cancer, SVT in non-varicose veins, extensive SVT (>5 cm), pregnancy | Anticoagulation as for DVT — therapeutic-dose DOAC or LMWH for 6 weeks–3 months. CUS to exclude DVT |
Fondaparinux
Arixtra® · Synthetic Factor Xa inhibitor
SVT dose
2.5 mg SC once daily for 45 days
Evidence
CALISTO trial: 85% reduction in DVT/PE extension vs placebo with low bleeding risk
Renal adjustment
Contraindicated if CrCl <30 mL/min
PBS status
✘ Not PBS listed for SVT (may be Authority Required for DVT/PE)
Catheter-Related Thrombosis (CRT)
Central venous catheters (CVCs), peripherally inserted central catheters (PICCs), port-a-caths, and haemodialysis catheters all carry VTE risk. CRT accounts for 30–60% of all UEDVT cases.
- Incidence: PICCs: 2–5%. CVCs: 2–30% depending on catheter type, patient factors, and surveillance method. Higher with femoral vein catheters.
- Diagnosis: CUS is the first-line investigation. If negative and clinical suspicion remains, CT venography is recommended.
- Treatment: Anticoagulation for as long as the catheter is in situ, plus at least 3 months after catheter removal. If the catheter is still required (e.g., chemotherapy, parenteral nutrition), anticoagulate without removing the catheter unless it is non-functional, infected, or no longer needed.
- Catheter removal: Not mandatory if the catheter is still needed and functional. Remove if possible, as this may reduce recurrence.
- Prophylaxis: Routine prophylactic anticoagulation for CVCs is not recommended (Cochrane review). Ensure proper catheter placement, flushing protocols, and aseptic technique.
Pregnancy-Associated VTE
DOACs are contraindicated in pregnancy. Apixaban, rivaroxaban, dabigatran, and edoxaban are teratogenic in animal studies and cross the placenta. All pregnant or potentially pregnant patients with VTE must be treated with LMWH. Warfarin is teratogenic in the first trimester (warfarin embryopathy) and crosses the placenta in the third trimester.
VTE is a leading cause of maternal morbidity and mortality in Australia. The risk is 5–10× higher than in non-pregnant women of the same age, with the highest risk in the postpartum period (6-week postpartum window).
Enoxaparin (Pregnancy)
Clexane® · LMWH — pregnancy anticoagulant of choice
Treatment dose
1 mg/kg SC BD or 1.5 mg/kg SC OD (adjusted to weight; check anti-Xa levels)
Prophylactic dose
40 mg SC OD (or 20 mg BD in extreme obesity)
Monitoring
Anti-Xa levels (target 0.5–1.0 IU/mL for treatment dose, 4 hours post-dose). Monthly FBC. Anti-Xa levels every 4 weeks due to changing renal clearance and weight gain
Postpartum
Can transition to warfarin if preferred (compatible with breastfeeding). Total treatment: 6 weeks postpartum minimum (≥3 months total from acute event)
PBS status
✔ PBS General Benefit
Neuraxial anaesthesia caution: LMWH must be withheld for ≥12 hours after prophylactic doses and ≥24 hours after treatment doses before epidural/spinal anaesthesia. Timing must be coordinated with obstetric and anaesthetic teams. This is critical for patients approaching term.
Pregnancy VTE Risk Stratification
| Risk Level | Features | Thromboprophylaxis |
|---|---|---|
| Low | No risk factors, or single minor transient risk factor | Early mobilisation, hydration, consider risk reassessment in each trimester |
| Moderate | Prior provoked VTE (not hormone-related), BMI >30, age >35, IVF, varicose veins, smoking | Consider LMWH 40 mg SC OD from first trimester |
| High | Prior unprovoked VTE, heritable thrombophilia with family history, antiphospholipid syndrome, multiple risk factors | LMWH 40 mg SC OD throughout pregnancy + 6 weeks postpartum |
| Very High | Prior VTE in pregnancy, known antithrombin deficiency, multiple thrombophilias | LMWH treatment dose throughout pregnancy + 6 weeks postpartum |
Phlegmasia Cerulea Dolens and Phlegmasia Alba Dolens
These are severe, limb-threatening presentations of extensive DVT requiring urgent intervention:
- Phlegmasia alba dolens: Extensive iliofemoral DVT with severe leg swelling, pain, and pallor but preserved arterial inflow. Treat with anticoagulation and consider catheter-directed thrombolysis.
- Phlegmasia cerulea dolens: Massive DVT with complete venous outflow obstruction leading to arterial compromise, cyanosis, and threatened limb. Medical emergency requiring immediate systemic anticoagulation, catheter-directed thrombolysis, or surgical thrombectomy. Fasciotomy may be needed for compartment syndrome. Refer urgently to vascular surgery.
Limb-threatening DVT: Phlegmasia cerulea dolens has a mortality rate of 20–40% and amputation rate of 20–50% if untreated. Immediate vascular surgery referral, systemic anticoagulation (UFH for rapid titration), and consideration of catheter-directed thrombolysis or surgical thrombectomy are required. Transfer to a tertiary centre if not already at one.
Monitoring
Monitoring requirements vary by anticoagulant type. DOACs require less monitoring than warfarin but still warrant regular clinical review.
| Anticoagulant | Routine Monitoring | Frequency | Special Monitoring |
|---|---|---|---|
| Apixaban / Rivaroxaban | FBC, renal function (eGFR/CrCl), LFTs | Baseline, 1 month, then every 6–12 months | More frequently if CrCl 15–30 mL/min, age ≥80, weight <60 kg, drug interactions |
| Warfarin | INR (target 2.0–3.0) | Until stable: 2–3× weekly. Stable: every 2–4 weeks (up to 12 weeks if very stable per TTR >70%) | TTR (time in therapeutic range) calculation every 6 months; aim for >65% |
| LMWH | Anti-Xa levels, FBC, creatinine | Baseline, then as indicated | Anti-Xa if: CrCl <30 mL/min, weight <50 or >120 kg, pregnancy, extremes of age |
| UFH (IV) | APTT (target 1.5–2.5× control) | 6 hours after bolus, then every 6 hours during infusion, with each rate change | Platelet count at baseline and every 2–3 days (monitoring for HIT) |
Heparin-induced thrombocytopenia (HIT): Suspect HIT if the platelet count falls >50% from baseline within 5–14 days of starting heparin (or sooner if recent heparin exposure). Stop all heparin immediately and switch to an alternative anticoagulant (e.g., argatroban IV). Do NOT give warfarin until platelet count recovers. HIT antibody testing (PF4 ELISA) is available through Australian pathology services. Incidence: ~1–3% with UFH, <0.1% with LMWH.
Clinical Follow-Up Schedule
Week 1–2
Review medication adherence, assess for bleeding complications, pain management, confirm outpatient safety. Repeat INR if on warfarin.
Month 1
Renal function and FBC. Assess for PE symptoms. Review compression therapy. Evaluate provoking factors and whether they have resolved.
Month 3
Critical decision point: continue or stop anticoagulation. Review Wells/provoked status. Consider D-dimer testing off anticoagulation if stopping. Repeat CUS if indicated.
Month 6
If on extended therapy: reassess bleeding risk (HAS-BLED), recurrence risk. Switch to reduced-dose DOAC if appropriate. Cancer screening review if unprovoked.
Annually
Renal function, FBC, LFTs. Reassess ongoing need for anticoagulation. Patient education regarding bleeding precautions, travel advice, and when to seek emergency care. Assess for post-thrombotic syndrome.
Special Populations
Pregnancy
Treatment: LMWH (enoxaparin) throughout pregnancy and ≥6 weeks postpartum. DOACs contraindicated. Warfarin contraindicated in first trimester (embryopathy) and late third trimester (fetal haemorrhage).
Monitoring: Anti-Xa levels every 4 weeks. Dose adjustment required as pregnancy weight and renal clearance change. Platelet count monthly.
Labour plan: Switch from twice-daily to once-daily LMWH from 36 weeks to allow predictable timing. Stop LMWH ≥24 hours before planned induction/CS. If labour begins on treatment-dose LMWH, neuraxial anaesthesia contraindicated for 24 hours.
Breastfeeding: LMWH and warfarin are compatible with breastfeeding. DOACs should be avoided.
Paediatrics
Epidemiology: VTE in children is rare (0.07–0.14 per 10,000) but increasing with improved survival of complex conditions. Most are catheter-related (70–80%). Risk factors: central venous catheters, malignancy, congenital heart disease, nephrotic syndrome.
Treatment: LMWH (enoxaparin 1.5 mg/kg SC OD or 1 mg/kg SC BD) is first-line. Monitor anti-Xa levels (target 0.5–1.0 IU/mL for treatment). Warfarin is an alternative for long-term therapy. DOACs: rivaroxaban now TGA-approved for paediatric VTE (body weight-based dosing); apixaban trials ongoing.
Duration: Minimum 3 months for provoked VTE. Consider extended therapy for ongoing risk factors (e.g., unresected malignancy, ongoing CVC use). Neonatal VTE: often provoked by CVC; 6 weeks to 3 months of anticoagulation.
Elderly (≥75 years)
Bleeding risk: Significantly increased with age. Falls risk, polypharmacy, renal decline, and comorbidities increase bleeding on anticoagulation. Use age-adjusted D-dimer cutoffs. HAS-BLED score helps quantify risk.
DOACs: Apixaban may be preferred due to lower GI bleeding risk compared with rivaroxaban. Rivaroxaban and apixaban require dose assessment based on age, weight (<60 kg), and renal function (e.g., rivaroxaban 15 mg OD if CrCl 15–49 mL/min).
Warfarin: More difficult to control in the elderly (lower starting dose, e.g., 2.5–3.5 mg). Higher TTR variability. Falls alone are not a contraindication to anticoagulation (risk of intracranial haemorrhage from falls is lower than the stroke/VTE recurrence risk in most cases).
Renal Impairment
CrCl >50 mL/min: All DOACs at standard dose. No dose adjustment for apixaban or rivaroxaban.
CrCl 30–50 mL/min: Apixaban: no dose change. Rivaroxaban: 15 mg OD for extended therapy (for active VTE treatment, use standard dose with caution). Enoxaparin: reduce to 1 mg/kg OD if CrCl <30 mL/min.
CrCl 15–30 mL/min: Apixaban usable with caution (limited data). Rivaroxaban — avoid or use with extreme caution. LMWH — dose-adjust and monitor anti-Xa levels. UFH may be preferred in haemodialysis patients.
Haemodialysis: UFH is the mainstay during dialysis. Warfarin is the preferred long-term oral anticoagulant. DOACs are generally not recommended. Consider nephrology co-management.
Hepatic Impairment
Mild (Child-Pugh A): Apixaban and rivaroxaban can be used with caution. Monitor LFTs.
Moderate (Child-Pugh B): Rivaroxaban contraindicated (impaired metabolism). Apixaban — use with extreme caution. Warfarin sensitivity is increased (reduced synthesis of clotting factors); use lower doses and frequent INR monitoring.
Severe (Child-Pugh C): All DOACs contraindicated. LMWH has altered pharmacokinetics (reduced clearance of anti-Xa). UFH with APTT monitoring may be the safest option. Complex cases require haematology input.
Immunocompromised
Cancer: LMWH (enoxaparin 1.5 mg/kg SC OD) has been the traditional standard based on the CLOT trial. DOACs (edoxaban, rivaroxaban) are now non-inferior based on SELECT-D and Hokusai VTE Cancer trials. Apixaban also effective (ADAM VTE, Caravaggio). Caution with GI and GU malignancies (higher GI bleeding with DOACs).
HIV: Increased VTE risk (4–10× baseline). Drug interactions with antiretrovirals: protease inhibitors increase DOAC levels (avoid rivaroxaban with ritonavir); integrase inhibitors generally safe with DOACs. LMWH is safe. Consult infectious diseases.
Transplant: VTE risk increased. DOAC interactions with calcineurin inhibitors (tacrolimus, cyclosporine) and mTOR inhibitors require careful assessment. LMWH or warfarin often preferred. Coordinate with transplant team.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Quick Reference — Anticoagulation Duration
Major provoked DVT
Apixaban or Rivaroxaban
3 months
Stop if provoking factor resolved
Minor provoked DVT
Apixaban or Rivaroxaban
3 months
Remove ongoing risk factor; consider extension
First unprovoked DVT
Apixaban or Rivaroxaban → reduced dose
≥3–6 months, then reassess
Consider extended reduced-dose DOAC if recurrence risk high
Recurrent unprovoked VTE
Apixaban 2.5 mg BD or Rivaroxaban 10 mg OD
Indefinite
Annual bleeding risk reassessment
Cancer-associated DVT
LMWH or DOAC (apixaban/rivaroxaban)
Minimum 6 months, while cancer active
GI/GU malignancy: prefer LMWH (lower GI bleed risk)
Pregnancy-associated DVT
Enoxaparin (LMWH)
Throughout pregnancy + 6 weeks postpartum
DOACs contraindicated. Monitor anti-Xa levels
Catheter-related UEDVT
Apixaban or Rivaroxaban
While catheter in situ + ≥3 months
Remove catheter if no longer needed
Isolated distal DVT (treated)
Apixaban or Rivaroxaban
3 months
Serial CUS if not anticoagulating
📚 References
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