📋 Key Information Summary
- Venous thromboembolism (VTE) encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE), with an annual incidence of approximately 1–2 per 1,000 in Australia.
- Confirm DVT with compression Doppler ultrasound of the affected limb; a negative D-dimer with low Wells score can safely exclude DVT in the outpatient setting.
- Confirm PE with CT pulmonary angiography (CTPA) as first-line imaging; ventilation–perfusion (V/Q) scanning is an alternative when CT contrast is contraindicated.
- Assess provoking factors — recent surgery (<6 weeks), trauma, immobilisation ≥3 days, pregnancy/puerperium, oestrogen therapy (HRT or OCP), active malignancy, and hospitalisation all increase VTE risk.
- First-line anticoagulation for most patients is a direct oral anticoagulant (DOAC): apixaban or rivaroxaban (single-drug approach) preferred over LMWH→warfarin.
- LMWH (enoxaparin) bridged to warfarin remains appropriate for severe renal impairment (eGFR <15 mL/min), antiphospholipid syndrome, and where DOACs are contraindicated.
- Duration of anticoagulation: 3 months for provoked VTE with a transient risk factor; extended (indefinite) anticoagulation should be considered for unprovoked VTE after individual bleeding–recurrence risk assessment.
- Massive PE with haemodynamic instability requires emergency systemic thrombolysis (alteplase) and urgent referral to a tertiary centre or ICU.
- Submassive PE (right ventricular dysfunction without hypotension) warrants close monitoring, and a low threshold for multidisciplinary escalation including cardiology and respiratory medicine.
- Cancer-associated VTE is best managed with LMWH (dalteparin or enoxaparin) as first-line; edoxaban or rivaroxaban are DOAC alternatives for non-gastrointestinal malignancy.
- Refer immediately for massive PE, submassive PE, unusual-site VTE (cerebral venous sinus, splanchnic), pregnancy-related VTE, and cancer-associated VTE requiring specialist co-management.
- Aboriginal and Torres Strait Islander Australians have significantly higher VTE rates and poorer access to anticoagulation monitoring; culturally safe care and point-of-care INR testing in remote communities improve outcomes.
Introduction & Australian Epidemiology
Venous thromboembolism (VTE) is a collective term for deep vein thrombosis (DVT) and pulmonary embolism (PE). It is a leading cause of preventable morbidity and mortality in Australian hospitals and the community. The management of a first VTE event requires accurate diagnosis, identification of provoking factors, appropriate anticoagulant selection, and a clear plan regarding treatment duration.
In Australia, VTE affects an estimated 30,000 people annually, with an incidence of approximately 1–2 per 1,000 person-years. The incidence increases sharply with age, rising to over 1% per year in those aged ≥65 years. PE accounts for approximately 5,000 deaths per year nationally. Hospital-acquired VTE remains a major patient safety concern; the Australian Commission on Safety and Quality in Health Care (ACSQHC) mandates VTE risk assessment and appropriate thromboprophylaxis in all admitted patients under the National Safety and Quality Health Service (NSQHS) Standards.
Patient safety standard: All Australian hospitals must conduct VTE risk assessment on admission and prescribe appropriate thromboprophylaxis in accordance with ACSQHC Standard 5 (Comprehensive Care). Failure to provide prophylaxis is considered a quality and safety breach.
Risk factors for VTE are broadly categorised as provoked (identifiable transient or persistent risk factor present) or unprovoked (no identifiable risk factor). This distinction is critical as it directly influences the recommended duration of anticoagulation and the risk of recurrence after treatment cessation.
Confirm VTE — Diagnostic Approach
A structured diagnostic approach is essential to confirm or exclude VTE efficiently. The pre-test probability guides the choice and sequence of investigations, minimising unnecessary imaging while ensuring high diagnostic sensitivity.
Clinical Pre-Test Probability — Wells Score
The Wells score stratifies patients into low, moderate, or high probability of DVT or PE. In low-probability patients, a negative high-sensitivity D-dimer (<500 ng/mL or age-adjusted for patients >50 years) effectively excludes VTE without the need for imaging.
| Wells Criteria — DVT | Score |
|---|---|
| Active cancer (treatment within 6 months or palliative) | +1 |
| Paralysis, paresis, or recent cast immobilisation of lower limb | +1 |
| 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 to asymptomatic side | +1 |
| Pitting oedema confined to symptomatic leg | +1 |
| Collateral superficial veins (non-varicose) | +1 |
| Previously documented DVT | +1 |
| Alternative diagnosis as likely or more likely than DVT | −2 |
Interpretation: ≤1 point = low probability (≈5% DVT prevalence); 2–6 points = moderate probability (~17%); ≥7 points = high probability (~53%).
Wells Criteria — Pulmonary Embolism
| Wells Criteria — PE | Score |
|---|---|
| Clinical signs/symptoms of DVT | +3 |
| PE is the most likely diagnosis, or equally likely | +3 |
| Heart rate >100 bpm | +1.5 |
| Immobilisation (≥3 days) or surgery in the previous 4 weeks | +1.5 |
| Previous DVT/PE | +1.5 |
| Haemoptysis | +1 |
| Active cancer | +1 |
Interpretation: ≤4 points = PE unlikely (≈12%); >4 points = PE likely (~37%).
Diagnostic Investigations
Essential
Compression Doppler Ultrasound (DVT)
First-line imaging for suspected DVT of the lower limb. Sensitivity >95% for proximal DVT; lower sensitivity for distal (calf) DVT. Available at all Australian public hospitals and most radiology practices (MBS item 55058). Repeat in 5–7 days if initial scan is negative but clinical suspicion remains moderate–high for isolated distal DVT.
Essential
CT Pulmonary Angiography (CTPA)
First-line imaging for suspected PE. High sensitivity (>95%) and specificity (>97%) for segmental and larger pulmonary emboli. Requires IV iodinated contrast; avoid in severe contrast allergy or eGFR <30 mL/min without nephrology input. Available at all major Australian hospitals (MBS item 56400). Radiation exposure ~3–5 mSv.
Available
Ventilation–Perfusion (V/Q) Scan
Alternative to CTPA when iodinated contrast is contraindicated (severe allergy, significant renal impairment). High sensitivity for PE when the result is "high probability." Available at most tertiary and many regional hospitals. More likely to yield a non-diagnostic result in patients with pre-existing lung disease. MBS item 61348.
Available
D-dimer (High-Sensitivity Assay)
High negative predictive value in low pre-test probability patients. Age-adjusted D-dimer cutoff (age × 10 ng/mL for patients >50 years) improves specificity. Cannot be used alone to diagnose VTE. Available at all Australian pathology services (MBS item 65140).
Essential
Baseline Bloods
FBC, renal function (eGFR), LFTs, coagulation (INR, APTT). Required prior to initiating anticoagulation. Haemoglobin and platelet count inform bleeding risk. INR baseline needed if warfarin is planned.
Referral
Echocardiography (Transthoracic)
For risk stratification in acute PE: assess right ventricular (RV) size and function. RV dilatation/dysfunction with preserved blood pressure defines submassive PE. Available at most hospitals but urgent availability may be limited in regional centres.
1
Low Wells Score (≤1 DVT / ≤4 PE)
Order D-dimer. If negative → VTE excluded. If positive → proceed to Doppler US (DVT) or CTPA (PE).
2
Moderate–High Wells Score
Proceed directly to imaging (Doppler US for DVT; CTPA for PE). D-dimer does not need to be ordered — a negative result cannot reliably exclude VTE in this group.
3
Haemodynamically Unstable PE
If CTPA cannot be performed immediately, bedside echocardiography showing RV dilatation/dysfunction supports emergency thrombolysis. Do not delay treatment for confirmatory imaging if clinical probability is high.
Identify Provoking Factors
Identifying a provoking factor is one of the most important determinants of anticoagulation duration and recurrence risk. VTE is classified as provoked if a major transient or persistent risk factor is identified, and unprovoked (idiopathic) if no risk factor is found.
Why this matters: The annual recurrence risk after stopping anticoagulation is approximately 1% for provoked VTE (with a transient risk factor) versus 5–10% for unprovoked VTE. This distinction drives the decision on whether to stop anticoagulation at 3 months or continue indefinitely.
| Risk Factor | Classification | Notes |
|---|---|---|
| Major surgery (within 6 weeks) | Transient — Major | Especially orthopaedic (hip/knee replacement), abdominal, pelvic surgery. VTE risk highest in first 4 weeks post-op. |
| Significant trauma / lower limb fracture | Transient — Major | Immobilisation in a cast increases risk 5–10×. |
| Immobilisation ≥3 days | Transient — Major | Bed rest, prolonged sitting (e.g. long-haul flight >8 hours), hospitalisation. |
| Hospitalisation with acute illness | Transient — Major | ACSQHC mandates VTE prophylaxis for all acutely ill medical inpatients. |
| Pregnancy and puerperium (up to 6 weeks postpartum) | Transient — Major | VTE risk 5–10× baseline. Highest in the third trimester and first 6 weeks postpartum. |
| Oestrogen-containing therapy (OCP, HRT, SERMs) | Transient — Minor | Combined OCP increases VTE risk 3–5×. Risk persists for 4–6 weeks after cessation. Levonorgestrel IUD has minimal risk. |
| Active cancer | Persistent — Major | Accounts for ~20% of all VTE. Highest with pancreatic, brain, lung, and ovarian cancers. Cancer treatment (chemotherapy, surgery) independently increases risk. |
| Antiphospholipid syndrome (APS) | Persistent — Major | High recurrence risk. DOACs are contraindicated in triple-positive APS; use warfarin (INR 2–3). |
| Hereditary thrombophilia (Factor V Leiden, prothrombin mutation, protein C/S deficiency, antithrombin deficiency) | Variable | Testing not routinely recommended for first VTE unless strong family history or unusual site. Does not independently change duration of treatment for provoked VTE. |
| Obesity (BMI ≥30) | Persistent — Minor | Modest increase in VTE risk (2–3×). Relevant as a contributing factor in unprovoked VTE. |
| No identifiable risk factor | Unprovoked | Higher recurrence risk (~5–10% per year). Extended anticoagulation should be discussed. |
Clinical pearl: In patients with apparently unprovoked VTE, consider age-appropriate cancer screening. Current evidence does not support extensive beyond-standard screening (e.g. CT abdomen/pelvis, tumour markers) beyond history, examination, FBC, LFTs, urinalysis, and age-appropriate screening (bowel, cervical, breast, prostate). A structured clinical assessment is recommended over routine exhaustive investigation.
Anticoagulant Choice & Duration
Anticoagulation is the cornerstone of VTE treatment. The goals are to prevent thrombus extension, reduce the risk of PE, and prevent recurrence. Modern management favours DOACs as first-line for most patients, with LMWH→warfarin reserved for specific indications.
Initial Anticoagulation Strategy
Apixaban
Eliquis® · DOAC (Factor Xa inhibitor)
Acute treatment dose
10 mg PO BD for 7 days, then 5 mg PO BD
Extended prophylaxis
2.5 mg PO BD (for secondary prevention after ≥6 months of treatment)
Renal adjustment
No dose adjustment for renal impairment. Use with caution if eGFR <15 mL/min (limited data).
Hepatic adjustment
Contraindicated in severe hepatic impairment (Child-Pugh C). Caution in moderate hepatic disease.
Key interactions
Avoid strong dual CYP3A4 and P-gp inhibitors (e.g. ketoconazole, ritonavir) and inducers (e.g. rifampicin, carbamazepine, phenytoin).
PBS status
✔ PBS General Benefit
Rivaroxaban
Xarelto® · DOAC (Factor Xa inhibitor)
Acute treatment dose
15 mg PO BD with food for 21 days, then 20 mg PO once daily with food
Extended prophylaxis
10 mg PO once daily (for secondary prevention after ≥6 months of treatment)
Renal adjustment
Avoid if eGFR <15 mL/min. Caution if eGFR 15–30 mL/min.
Key interactions
Avoid strong CYP3A4/P-gp inhibitors and inducers. Take with food to ensure absorption.
PBS status
✔ PBS General Benefit
Enoxaparin (LMWH)
Clexane® · Low-molecular-weight heparin
Adult dose (DVT/PE)
1.5 mg/kg SC once daily OR 1 mg/kg SC BD (standard therapeutic dosing)
Renal adjustment
Reduce to 1 mg/kg SC once daily if eGFR <30 mL/min. Monitor anti-Xa levels.
Paediatric dose
Neonates: 1.5 mg/kg SC BD; Children: 1 mg/kg SC BD (monitor anti-Xa 0.5–1.0 IU/mL).
Duration
Usually a bridge to warfarin (minimum 5 days overlap) or used as sole agent in cancer-associated VTE.
PBS status
✔ PBS General Benefit
Warfarin
Marevan® · Coumarin anticoagulant
Adult dose
Commence 5 mg PO daily (3 mg if elderly, low body weight, or hepatic impairment). Titrate to INR 2.0–3.0.
Loading
Overlapped with LMWH for minimum 5 days AND until INR ≥2.0 for ≥24 hours.
Monitoring
INR every 1–2 days during initiation, then weekly when stable, extending to every 4–6 weeks. Point-of-care INR testing available in many Australian community pharmacies and Aboriginal health services.
Key interactions
Extensive — amiodarone, antibiotics (metronidazole, TMP-SMX, fluconazole), NSAIDs, cranberry juice. Requires dietary consistency with vitamin K intake.
PBS status
✔ PBS General Benefit
Edoxaban
Lixiana® · DOAC (Factor Xa inhibitor)
Adult dose
60 mg PO once daily. Reduce to 30 mg PO once daily if eGFR 15–50 mL/min, body weight ≤60 kg, or concurrent use of certain P-gp inhibitors (ciclosporin, dronedarone, erythromycin, ketoconazole).
Prerequisite
Requires initial parenteral anticoagulation (LMWH) for at least 5 days before switching.
PBS status
✔ PBS General Benefit
Anticoagulation Duration by VTE Type
| VTE Category | Recommended Duration | Notes |
|---|---|---|
| Provoked — major transient risk factor (surgery, trauma, immobilisation, OCP) | 3 months | Stopping at 3 months is safe. Recurrence risk ≈1%/year. OCP should be permanently ceased; switch to progestogen-only or non-hormonal methods. |
| Provoked — minor transient risk factor (long-haul flight, minor illness) | 3–6 months | Discuss with patient; consider extended if combined risk factors are present. |
| Unprovoked (idiopathic) — first event | Minimum 3–6 months, then reassess for extended (indefinite) therapy | Annual recurrence risk 5–10% if stopped. D-dimer testing at 1 month post-cessation may help guide decision (elevated D-dimer suggests higher recurrence risk). Menstruate recurrence risk higher than women. |
| Cancer-associated VTE | Indefinite (duration of active cancer and treatment) | LMWH first-line (dalteparin or enoxaparin). DOACs (edoxaban, rivaroxaban) are alternatives but avoid in GI and genitourinary malignancy due to mucosal bleeding risk. |
| Antiphospholipid syndrome | Indefinite | Warfarin (INR 2–3) is first-line. DOACs are contraindicated (inferior efficacy demonstrated in TRAPS trial). Avoid direct thrombin inhibitors. |
Do NOT use DOACs in antiphospholipid syndrome (APS). The TRAPS trial demonstrated significantly higher rates of recurrent thrombosis with rivaroxaban compared to warfarin in triple-positive APS patients. Warfarin with target INR 2.0–3.0 remains the standard of care for APS-related VTE.
When to Consider Extended (Indefinite) Anticoagulation
- Unprovoked proximal DVT or PE
- Recurrent VTE (second or subsequent event)
- Active cancer (unless high bleeding risk)
- Antiphospholipid syndrome
- Residual DVT on ultrasound at 3–6 months in the setting of unprovoked VTE
- Persistent elevation of D-dimer after stopping anticoagulation
- Male sex (higher recurrence rate than female after unprovoked VTE)
When extended therapy is chosen, consider dose reduction after 6 months: apixaban 2.5 mg BD or rivaroxaban 10 mg OD provide effective secondary prevention with a lower bleeding risk (AMPLIFY-EXT and EINSTEIN-CHOICE trials).
Contraindications to DOACs
| Situation | Preferred Agent |
|---|---|
| Severe renal impairment (eGFR <15 mL/min) | LMWH (dose-adjusted) → warfarin |
| Antiphospholipid syndrome (triple-positive) | Warfarin (INR 2–3) |
| Mechanical heart valve | Warfarin (INR 2.5–3.5) |
| Moderate–severe mitral stenosis | Warfarin |
| Concomitant strong CYP3A4/P-gp inducers (rifampicin, carbamazepine, phenytoin) | LMWH → warfarin |
| Active GI malignancy (DOAC-related mucosal bleeding risk) | LMWH (dalteparin or enoxaparin) |
| Pregnancy | LMWH (enoxaparin or dalteparin). DOACs and warfarin are teratogenic. |
Emergency Therapy — Massive PE & Thrombolysis
Massive PE (defined as PE with sustained hypotension — systolic BP <90 mmHg for >15 minutes or requiring inotropic support) carries a mortality rate of 25–65% and is a medical emergency requiring immediate intervention.
Low Risk
Haemodynamically Stable PE
Normal BP, no RV dysfunction on imaging or echocardiography, negative troponin and BNP. sPESI 0.
Setting: Ward or outpatient (if appropriate social support)
Intermediate Risk
Submassive PE
Preserved BP but evidence of RV dysfunction (RV/LV ratio >0.9 on CTPA, RV dilatation on echo) AND/OR elevated troponin or BNP.
Setting: Monitored ward or HDU. Cardiology / respiratory consult.
High Risk
Massive PE
Haemodynamic instability: systolic BP <90 mmHg >15 min, cardiac arrest, or requirement for vasopressors. Marked RV dysfunction and troponin elevation expected.
Setting: ICU. Immediate systemic thrombolysis or surgical/embolectomy.
Systemic Thrombolysis for Massive PE
Alteplase (tPA)
Actilyse® · Thrombolytic agent
Adult dose (massive PE)
100 mg IV infusion over 2 hours (accelerated regimen: 15 mg bolus, then 0.75 mg/kg over 30 min [max 50 mg], then 0.5 mg/kg over 60 min [max 35 mg])
Indication
Massive PE with haemodynamic instability. Consider in submassive PE with clinical deterioration despite anticoagulation.
Contraindications
Active internal bleeding, recent (<3 months) intracranial surgery or trauma, intracranial neoplasm, severe uncontrolled hypertension.
PBS status
✔ PBS General Benefit (hospital use)
Time-critical: In massive PE with cardiac arrest, consider systemic thrombolysis during CPR (alteplase 50 mg IV bolus). Peri-arrest thrombolysis has been shown to improve survival in PE-related cardiac arrest. Administer without delay — do not wait for confirmatory imaging if clinical probability is high.
Monitoring During Anticoagulation
| Anticoagulant | Monitoring Required | Frequency |
|---|---|---|
| DOACs (apixaban, rivaroxaban, edoxaban) | Renal function (eGFR), LFTs, FBC. No routine coagulation monitoring needed. Anti-Xa levels can be measured if clinically indicated (overdose, bleeding, surgery). | Baseline, then every 6–12 months (more frequently if eGFR <50 mL/min or ≥80 years). |
| LMWH (enoxaparin) | Anti-Xa levels only if renal impairment (eGFR <30 mL/min), extremes of body weight (<50 kg or >120 kg), pregnancy. | Target 0.5–1.0 IU/mL for BD dosing; 1.0–2.0 IU/mL for once-daily dosing. Check 4 hours post-dose. |
| Warfarin | INR. Target 2.0–3.0 for VTE treatment. | Every 1–2 days during initiation; every 4–6 weeks when stable. Point-of-care INR available at many Australian community pharmacies (MBS item 65200). |
Bleeding Risk Assessment
Assess bleeding risk before and during anticoagulation. The HAS-BLED score (Hypertension, Abnormal renal/liver function, Stroke, Bleeding, Labile INR, Elderly, Drugs/alcohol) is commonly used. A score ≥3 indicates high bleeding risk — not a contraindication to anticoagulation, but mandates closer monitoring and correction of modifiable risk factors.
- Optimise blood pressure control (<140/90 mmHg)
- Minimise concomitant NSAIDs and antiplatelet agents where possible
- Avoid excessive alcohol intake (≤2 standard drinks/day recommended)
- Maintain consistent vitamin K dietary intake if on warfarin
- Review and deprescribe anticoagulation if recurrent major bleeding (case-by-case MDT decision)
Follow-Up Imaging
Routine repeat imaging of DVT or PE is not recommended. Repeat Doppler ultrasound is indicated only if there is clinical suspicion of recurrence. Repeat CTPA is indicated if there is clinical concern for new or progressive PE. In patients with PE, consider echocardiography at 3–6 months if persistent dyspnoea to assess for chronic thromboembolic pulmonary hypertension (CTEPH).
When to Refer
Most first VTE events can be managed in primary care or general internal medicine with appropriate anticoagulation. However, certain situations require specialist referral or emergency escalation.
Emergency Referral (Call Retrieval / Transfer)
1
Massive PE
Haemodynamic instability (systolic BP <90 mmHg), cardiac arrest, or requirement for vasopressors. Initiate systemic thrombolysis (alteplase 100 mg IV over 2 h) and arrange immediate ICU transfer. Contact retrieval services (RFDS, state retrieval) if in a regional or remote centre.
2
Cerebral Venous Sinus Thrombosis (CVST)
Presents with headache, seizures, focal neurological deficits, or altered consciousness. Requires urgent neuroimaging (CT/MR venogram) and haematology/neurology input. Anticoagulate even in the presence of haemorrhagic venous infarction (discuss with neurology).
3
Splanchnic Vein Thrombosis
Portal, mesenteric, or hepatic vein thrombosis. May present with abdominal pain, ascites, or bowel ischaemia. Requires gastroenterology and haematology input. Assess for underlying liver disease or myeloproliferative neoplasm (JAK2 mutation testing).
Urgent / Semi-Urgent Referral
Submassive PE
Anticoagulation + monitoring
RV dysfunction on imaging or echo; elevated troponin/BNP. Cardiology and respiratory medicine co-management. Consider catheter-directed therapy if deterioration.
Cancer-associated VTE
LMWH or DOAC
Haematology and oncology co-management. Ongoing anticoagulation for duration of active cancer. Monitor for recurrent VTE despite treatment (consider dose escalation of LMWH).
Pregnancy-related VTE
LMWH (weight-adjusted)
Obstetric medicine and haematology co-management. DOACs and warfarin contraindicated. Switch to LMWH as soon as pregnancy confirmed. Plan for delivery — discuss with obstetric anaesthesia team.
Suspected CTEPH
Referral for assessment
Persistent dyspnoea >3 months after PE. Echocardiography may show elevated RVSP. V/Q scan is the preferred screening test (high sensitivity). Refer to CTEPH specialist centre for right heart catheterisation and assessment for pulmonary endarterectomy or balloon pulmonary angioplasty.
Complex comorbidity
Individualised
Patients with multiple anticoagulation indications (e.g. VTE + atrial fibrillation + mechanical valve), dual antiplatelet therapy requirement, or significant bleeding history should be co-managed with haematology.
Special Populations
Pregnancy
LMWH (enoxaparin or dalteparin)
First-line anticoagulant throughout pregnancy. Weight-adjusted dosing. DOACs and warfarin are contraindicated — warfarin is teratogenic (warfarin embryopathy in first trimester; CNS abnormalities in any trimester). Switch from DOAC to LMWH as soon as pregnancy is confirmed.
Monitoring
Anti-Xa levels monthly (target 0.5–1.0 IU/mL 4 h post-dose) due to changing renal clearance and volume of distribution. Platelet count at baseline and every 2–3 weeks (risk of HIT). Dose adjustment with weight changes.
Delivery planning
Cease LMWH 24 hours before planned induction/caesarean (or 12 hours if prophylactic dose). Resume 4–6 hours post-vaginal delivery or 6–12 hours post-caesarean. Epidural anaesthesia requires at least 12-hour gap from last therapeutic dose. Discuss with obstetric anaesthesia team early.
Paediatrics
LMWH (enoxaparin)
First-line for paediatric VTE. Neonates: 1.5 mg/kg SC BD; Children: 1 mg/kg SC BD. Monitor anti-Xa (target 0.5–1.0 IU/mL 4 h post-dose). Difficult to achieve therapeutic levels in neonates — often requires dose escalation.
Warfarin
Can be used in older children when oral therapy is preferred. Monitor INR closely. Challenge: dietary consistency with vitamin K, difficulty with blood sampling.
DOACs
Limited data in children. Rivaroxaban has TGA-approved paediatric indications for VTE treatment in certain age groups. Refer to paediatric haematology for guidance.
Elderly (≥65 years)
DOACs preferred
Apixaban has the most favourable bleeding profile in elderly patients (lower rates of major and GI bleeding compared to warfarin, rivaroxaban, and dabigatran in meta-analyses). Dose reduction criteria: apixaban 2.5 mg BD if ≥2 of: age ≥80, weight ≤60 kg, Cr ≥133 µmol/L.
Warfarin
Start at 2.5–3 mg daily in frail elderly. Falls risk and polypharmacy increase bleeding risk — but falls alone should not preclude anticoagulation if VTE indication is strong. INR monitoring more challenging; point-of-care testing recommended.
Bleeding risk
HAS-BLED score is often ≥3 in elderly patients. Address modifiable risk factors: blood pressure, concurrent antiplatelet/NSAID use, alcohol. Reassess anticoagulation need and bleeding risk at every review.
Renal Impairment
eGFR 30–50 mL/min
Apixaban preferred (least renally dependent DOAC). Rivaroxaban and edoxaban can be used with caution. Monitor renal function every 3–6 months.
eGFR 15–30 mL/min
LMWH (dose-reduced: 1 mg/kg SC once daily) with anti-Xa monitoring, or warfarin. Apixaban may be considered with caution (limited data). Rivaroxaban and edoxaban generally avoided.
eGFR <15 mL/min / Dialysis
LMWH dose-adjusted with anti-Xa monitoring, or warfarin. DOACs not recommended. Haematology consultation advised.
Hepatic Impairment
Child-Pugh A–B
DOACs can be used with caution (all are partially hepatically metabolised). Monitor LFTs every 3–6 months. Warfarin sensitivity is increased — start at lower doses (2–3 mg daily).
Child-Pugh C
DOACs contraindicated. Warfarin difficult to manage due to coagulopathy. LMWH with anti-Xa monitoring preferred, though dosing is unpredictable. Haematology input essential.
Immunocompromised
HIV-positive patients
VTE risk is 2–10× higher than the general population. Antiretroviral drug interactions with DOACs and warfarin — consult HIV pharmacist. Protease inhibitors significantly increase rivaroxaban and apixaban levels.
Post-transplant patients
Ciclosporin and tacrolimus interact with DOACs (P-gp inhibition). Consider warfarin or LMWH. Immunosuppression and thrombocytopenia increase bleeding risk. Haematology co-management recommended.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
📚 References
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