Thrombosis and Thromboembolism

Last updated 1 Jun 2026 · Haematology / Vascular

📋 Key Information Summary

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Incidence: Approximately 30 000 venous thromboembolism (VTE) events occur annually in Australia; pulmonary embolism (PE) is a leading cause of preventable hospital death.
DVT diagnosis: Use Wells score to stratify pre-test probability; a negative high-sensitivity D-dimer effectively excludes DVT in low-risk patients. Compression duplex ultrasound is the confirmatory imaging modality.
PE diagnosis: CT pulmonary angiography (CTPA) is the first-line imaging for suspected PE. V/Q scanning is an alternative when CTPA is contraindicated (e.g. contrast allergy, pregnancy consideration).
Massive PE: Haemodynamic instability (systolic BP <90 mmHg) mandates emergency systemic thrombolysis (alteplase 100 mg IV over 2 hours) or catheter-directed therapy; discuss with tertiary centre immediately.
Initial anticoagulation: Low-molecular-weight heparin (enoxaparin 1.5 mg/kg SC daily or 1 mg/kg SC BD), unfractionated heparin (UFH) for high-risk/renal impairment, or a DOAC lead-in (rivaroxaban or apixaban) are all acceptable first-line strategies.
Warfarin: Target INR 2.0–3.0 for most VTE and atrial fibrillation; INR 2.5–3.5 for mechanical mitral valves. Overlap with parenteral anticoagulation for ≥5 days AND until INR ≥2.0 for ≥24 hours. Monitor with regular INR testing.
DOACs: Apixaban and rivaroxaban are first-line for most VTE treatment and stroke prevention in non-valvular atrial fibrillation. No routine coagulation monitoring required. Dose-adjust for renal function and body weight where indicated.
Duration of anticoagulation: Minimum 3 months for provoked VTE; consider extended (indefinite) anticoagulation for unprovoked proximal DVT/PE after assessing bleeding risk (VTE-BLEED score). Re-assess annually.
Warfarin overdose/reversal: Asymptomatic elevated INR — omit dose, repeat INR; serious/life-threatening bleeding — prothrombin complex concentrate (PCC) 25–50 units/kg IV + vitamin K 10 mg IV slow injection.
DOAC reversal: Idarucizumab (Praxbind®) reverses dabigatran; andexanet alfa (Andexxa®) reverses factor Xa inhibitors (apixaban, rivaroxaban). Access via emergency departments; discuss with haematologist.
Cancer-associated VTE: DOACs (apixaban or rivaroxaban preferred) are first-line over LMWH for most cancer-associated thrombosis, provided no high GI-bleeding risk or drug interactions. LMWH remains an alternative.
Special populations: Pregnancy — use LMWH throughout (warfarin and DOACs contraindicated). Elderly — increased bleeding risk; lower threshold for renal dose adjustment. Renal impairment (eGFR <30) — UFH or dose-adjusted apixaban preferred.
ATSI considerations: Aboriginal and Torres Strait Islander Australians have 1.5–2× higher VTE rates, later presentation, and reduced access to specialist vascular and haematology services in remote areas. Ensure culturally safe communication, use available telehealth pathways, and coordinate with ACCHOs for anticoagulation follow-up.

Introduction & Australian Epidemiology

Venous thromboembolism (VTE), encompassing deep venous thrombosis (DVT) and pulmonary embolism (PE), is a major cause of morbidity and mortality in Australia. Each year an estimated 30 000 Australians develop VTE, with PE responsible for approximately 5 000 deaths — many of which are potentially preventable with timely diagnosis and appropriate anticoagulation. VTE is the leading cause of preventable hospital-acquired death in Australian acute care settings.

The Australian and New Zealand VTE Prevention and Management Clinical Practice Guidelines (2024 update), developed under the auspices of the National Health and Medical Research Council (NHMRC) and supported by the Australasian Society of Thrombosis and Haemostasis (ASTH), provide a framework for risk assessment, prevention, diagnosis, and treatment. This article synthesises current evidence and Australian recommendations for general practitioners and specialists managing thrombotic disease.

Arterial thromboembolism — including ischaemic stroke, transient ischaemic attack (TIA), myocardial infarction, and peripheral arterial embolism — shares overlapping pathophysiology with VTE and is increasingly managed with direct oral anticoagulants (DOACs) in specific clinical contexts such as atrial fibrillation and stable coronary artery disease. This article integrates arterial and venous thromboembolism management to provide a comprehensive, practice-oriented resource.

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Australian burden of disease: The Australian Institute of Health and Welfare (AIHW) reports that VTE-related hospitalisations exceed 15 000 per annum, with a 30-day mortality rate of approximately 5–10% for PE. Risk is heightened following major surgery, prolonged immobilisation, malignancy, and in Aboriginal and Torres Strait Islander communities.

Key Australian organisations contributing to VTE management include the Royal Australian College of General Practitioners (RACGP), the Australasian Society of Thrombosis and Haemostasis (ASTH), Haematology Society of Australia and New Zealand (HSANZ), the Thrombosis and Haemostasis Society of Australia and New Zealand (THSANZ), and state-based anticoagulation services.

Pathophysiology of Venous & Arterial Thromboembolism

Thrombosis occurs when the balance between procoagulant and anticoagulant forces is disrupted. Virchow's triad — endothelial injury, venous stasis, and hypercoagulability — remains the conceptual framework for understanding both venous and arterial thrombosis, although the predominant mechanism differs.

Venous Thromboembolism

Stasis: Immobilisation, hospitalisation, prolonged travel, and paralysis reduce venous return, promoting activation of coagulation factors in the valve sinuses of deep veins (classically the calf veins, propagating proximally).
Hypercoagulability: Inherited thrombophilias (Factor V Leiden, prothrombin G20210A mutation, protein C/S deficiency, antithrombin deficiency) and acquired states (malignancy, antiphospholipid syndrome, oestrogen therapy, pregnancy) shift the balance toward thrombin generation.
Endothelial injury: Surgery, trauma, central venous catheters, and inflammation damage the vessel wall, exposing subendothelial collagen and tissue factor, initiating the coagulation cascade.
PE pathogenesis: Most PE arises from embolisation of proximal (above-popliteal) DVT. Thrombus dislodges, travels through the right heart, and lodges in the pulmonary vasculature, causing ventilation–perfusion mismatch, right ventricular strain, and — in massive PE — obstructive shock.

Arterial Thromboembolism

Atherothrombosis: Rupture of an atherosclerotic plaque exposes thrombogenic material, triggering platelet-rich (white) thrombus formation. This is the mechanism for most myocardial infarction and ischaemic stroke.
Cardioembolism: Atrial fibrillation (AF) causes blood stasis in the left atrial appendage, promoting fibrin-rich (red) thrombus that embolises to the brain (stroke), mesentery, or limbs. AF accounts for ~25% of ischaemic strokes in Australia.
Paradoxical embolism: Venous thrombus crosses to the arterial circulation via a patent foramen ovale (PFO) or atrial septal defect (ASD), causing cryptogenic stroke — particularly in younger patients.

Deep Venous Thrombosis — Risk Factors & Diagnosis

Risk Factors for DVT

Risk factors are cumulative and may be classified as provoking (transient) or unprovoked (idiopathic). Unprovoked VTE requires consideration of occult malignancy and extended anticoagulation.

Category	Risk Factors	Population Attributable Risk
Surgery & Trauma	Major orthopaedic surgery (hip/knee arthroplasty, hip fracture), abdominal/pelvic surgery, major trauma, spinal cord injury	~20%
Medical Immobilisation	Hospitalisation ≥3 days, acute medical illness (heart failure, respiratory failure, sepsis), prolonged bed rest	~20%
Malignancy	Active cancer (especially pancreatic, brain, lung, ovarian, lymphoma), chemotherapy, central venous catheters	~20%
Hormonal	Combined oral contraceptive pill (COCP), hormone replacement therapy (HRT), tamoxifen, pregnancy, postpartum period	~10%
Inherited Thrombophilia	Factor V Leiden (most common in Caucasians), prothrombin gene mutation, protein C/S deficiency, antithrombin deficiency	~5–10%
Other	Obesity (BMI ≥30), age ≥60, previous VTE, long-haul travel (>8 hours), inflammatory bowel disease, nephrotic syndrome, antiphospholipid syndrome, central venous catheters	~20%

Clinical Presentation of DVT

Unilateral leg swelling, pain, warmth, and erythema — classically involving the left lower limb (May–Thurner syndrome: left iliac vein compression by right iliac artery).
Calf DVT: tenderness along the deep venous system, positive Homan's sign (low sensitivity, not recommended as sole criterion).
Proximal (ilio-femoral) DVT: more extensive swelling, may cause phlegmasia cerulea dolens (massive limb oedema with cyanosis) or phlegmasia alba dolens (white, painful leg) — surgical emergencies.
Upper limb DVT: associated with central venous catheters, thoracic outlet syndrome, or Paget–Schroetter syndrome (effort thrombosis in athletes). Presents with arm swelling, pain, and visible collateral veins.
Many DVTs are asymptomatic — detected incidentally on imaging or when PE presents first.

Diagnosis — Wells Score for DVT

Clinical Feature	Points
Active cancer (treatment ongoing or within 6 months)	+1
Paralysis, paresis, or recent cast immobilisation of leg	+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 with asymptomatic leg	+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

Interpretation:

Score ≤1 (low probability, ~5%): Perform high-sensitivity D-dimer. If negative → DVT effectively excluded. If positive → proceed to compression ultrasound.
Score ≥2 (moderate-high probability, ~17–53%): Proceed directly to compression duplex ultrasound. D-dimer is not useful in this group as it does not change management (imaging required regardless).

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Australian practice note: High-sensitivity D-dimer (ELISA-based, cut-off 500 µg/L fibrinogen equivalent units) is Medicare-rebatable (MBS) and available in all Australian hospital laboratories and most community pathology services. Age-adjusted D-dimer cut-off (age × 10 µg/L for patients >50 years) improves specificity without reducing safety.

Pulmonary Embolism

Clinical Presentation

PE has a highly variable presentation, ranging from asymptomatic (incidental finding) to sudden cardiac death. A high index of clinical suspicion is essential.

Symptoms: Dyspnoea (sudden onset, most common), pleuritic chest pain, haemoptysis, tachycardia, pre-syncope/syncope, anxiety.
Signs: Tachypnoea (>20 breaths/min), tachycardia (>100 bpm), hypoxia, raised JVP, right ventricular heave, loud P2, signs of DVT (50% of PE have concurrent DVT).
Massive PE: Haemodynamic instability — systolic BP <90 mmHg for >15 minutes, cardiac arrest, or requiring vasopressors. Mortality 25–65% without treatment.
Submassive PE: Haemodynamically stable but with right ventricular dysfunction (on echocardiography or CT) and/or elevated troponin/BNP. Risk of clinical deterioration.

Wells Score for Pulmonary Embolism

Clinical Feature	Points
Clinical signs/symptoms of DVT	+3
PE is the most likely diagnosis	+3
Heart rate >100 bpm	+1.5
Immobilisation (≥3 days) or surgery within 4 weeks	+1.5
Previous DVT/PE	+1.5
Haemoptysis	+1
Active malignancy	+1

Interpretation:

Score ≤4 (PE unlikely): Apply PERC rule. If all PERC criteria negative → PE excluded without further testing (failure rate <2%). If any PERC criterion positive → order D-dimer. If D-dimer negative → PE excluded.
Score >4 (PE likely): Proceed directly to CTPA. Do not delay for D-dimer.

PERC Rule (Pulmonary Embolism Rule-out Criteria)

All 8 criteria must be negative to safely exclude PE without D-dimer in low-risk patients (Wells ≤4):

Age <50 years
Heart rate <100 bpm
SpO₂ ≥95% on room air
No haemoptysis
No exogenous oestrogen use
No prior DVT/PE
No unilateral leg swelling
No surgery/trauma within 4 weeks

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Massive PE — emergency: If clinical suspicion for massive PE with haemodynamic instability, do NOT wait for CTPA. Perform bedside echocardiography (RV dilation, McConnell's sign) and initiate systemic thrombolysis (alteplase 100 mg IV over 2 hours) or activate catheter-directed therapy pathway. Discuss immediately with on-call intensivist and/or interventional radiologist.

Investigations

MBS Rebateable High-sensitivity D-dimer (ELISA) Cut-off 500 µg/L (age-adjusted >50 yrs: age × 10 µg/L). Negative predictive value >99% in low-risk patients. Available in all Australian pathology services. Not useful if Wells score ≥2 (PE likely) as imaging required regardless. Elevated in malignancy, infection, pregnancy, elderly — reduces specificity.

MBS Rebateable Compression Duplex Ultrasound (Lower Limb) First-line imaging for suspected DVT. Sensitivity 95% for proximal DVT, 60–70% for isolated calf DVT. Non-compressibility of the vein is the diagnostic criterion. Available in all Australian radiology practices and hospital EDs. Can be performed bedside by trained operators. MBS item 55714 (or equivalent).

MBS Rebateable CT Pulmonary Angiography (CTPA) First-line imaging for PE when Wells >4 or D-dimer positive. Sensitivity 83–100%, specificity 89–97%. Requires IV iodinated contrast (check renal function, eGFR >30 mL/min). Available at all major Australian hospitals and many private radiology centres. MBS item for CT angiography applicable.

MBS Rebateable V/Q (Ventilation–Perfusion) Lung Scan Alternative to CTPA when iodinated contrast contraindicated (severe contrast allergy, pregnancy where CTPA radiation to breast is a concern). High-probability scan diagnostic. Normal V/Q scan excludes PE. Less widely available than CTPA — primarily at major hospitals with nuclear medicine facilities.

MBS Rebateable Echocardiography (Transthoracic) Not diagnostic for PE in haemodynamically stable patients but assesses right ventricular function (submassive PE). Findings: RV dilation, RV/LV ratio >1, septal bowing, tricuspid regurgitation, elevated RVSP. Bedside echo essential in cardiac arrest with suspected PE. Available at all major hospitals.

Essential Troponin & BNP/NT-proBNP Risk stratification in PE. Elevated troponin and/or BNP in haemodynamically stable PE indicates submassive (intermediate-risk) PE and higher mortality risk. Not diagnostic. Available at all Australian hospitals.

MBS Rebateable FBC, Coagulation Studies, LFTs, Renal Function Baseline assessment before anticoagulation. INR for warfarin monitoring. aPTT for UFH monitoring. Creatinine/eGFR for DOAC dose adjustment. LFTs to exclude hepatic coagulopathy.

Specialist Consideration Thrombophilia Screen Consider in unprovoked VTE in young patients (<50 years), recurrent VTE, unusual sites (cerebral, splanchnic, portal vein), or strong family history. Tests: Factor V Leiden, prothrombin gene mutation, antithrombin, protein C, protein S, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I). Do NOT test during acute VTE or while on anticoagulation (except genetic tests).

Risk Stratification — Pulmonary Embolism Severity

PE risk stratification guides treatment intensity and disposition. The European Society of Cardiology (ESC) and American Heart Association (AHA) frameworks classify PE into three risk categories:

Low Risk

Low-Risk PE

Haemodynamically stable. No RV dysfunction on echo/CT. Normal troponin and BNP. sPESI = 0 or PESI class I–II. Mortality <1–3%.

Setting: Consider outpatient management or early discharge. Treat with anticoagulation (DOAC preferred).

Intermediate Risk

Submassive PE

Haemodynamically stable BUT: RV dysfunction on echo/CT (RV/LV >1, McConnell's sign) AND/OR elevated troponin and/or BNP. sPESI ≥1. Mortality 3–15%. May deteriorate to massive PE.

Setting: Hospital admission (ward or HDU). Anticoagulation ± close monitoring. Consider escalation to thrombolysis if clinical deterioration.

High Risk

Massive PE

Haemodynamic instability: systolic BP <90 mmHg for >15 min, cardiac arrest, need for vasopressors, or shock. Mortality 25–65% without treatment.

Setting: ICU / critical care. Systemic thrombolysis (alteplase 100 mg IV over 2 h) or catheter-directed therapy. Surgical embolectomy if thrombolysis contraindicated/failed.

Simplified PESI (sPESI) Score

Variable	Points
Age >80 years	+1
History of cancer	+1
Chronic cardiopulmonary disease	+1
Heart rate ≥110 bpm	+1
Systolic BP <100 mmHg	+1
SpO₂ <90%	+1

Score 0 = low risk (30-day mortality ~1%). Score ≥1 = higher risk (30-day mortality ~10%). Used to guide disposition — sPESI 0 patients may be suitable for outpatient management with DOAC (with appropriate follow-up).

Initial (Empirical) Anticoagulation

Anticoagulation should be initiated as soon as VTE is diagnosed or when clinical suspicion is high and imaging is pending. The choice of initial agent depends on clinical severity, renal function, route of administration, and patient factors.

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Enoxaparin (Clexane®)

LMWH · First-line initial anticoagulation for most VTE

Adult dose (VTE treatment) 1.5 mg/kg SC once daily OR 1 mg/kg SC every 12 hours (twice-daily dosing preferred for obesity >100 kg and high-risk PE)

Paediatric dose Neonates: 1.5 mg/kg SC BD. Children: 1 mg/kg SC BD (target anti-Xa 0.5–1.0 units/mL for treatment)

Renal adjustment eGFR <30 mL/min: reduce to 1 mg/kg SC OD (or switch to UFH). Monitor anti-Xa levels in severe renal impairment.

Key monitoring Anti-Xa levels (if obesity >120 kg, renal impairment, pregnancy, extremes of weight). Platelet count at baseline and day 4–5 (HIT risk).

PBS status ✔ PBS General Benefit

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Unfractionated Heparin (UFH)

IV infusion · For massive PE, renal impairment (eGFR <30), peri-procedural bridging

Adult dose 80 units/kg IV bolus, then 18 units/kg/hr infusion. Titrate to aPTT 1.5–2.5× control (laboratory-specific). Weight-based protocol preferred.

Renal adjustment No dose adjustment required — preferred in eGFR <30 mL/min

Key monitoring aPTT every 6 hours until stable. Platelet count at baseline and every 2–3 days (HIT surveillance). Anti-Xa if aPTT unreliable.

Reversal Protamine sulfate 1 mg per 100 units heparin given in preceding 2–3 hours (max 50 mg). Fully reversible.

PBS status ✔ PBS General Benefit

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When to use UFH over LMWH: Use UFH (IV) in massive PE (short half-life, fully reversible with protamine), severe renal impairment (eGFR <30), when urgent surgery is anticipated, or when a patient is haemodynamically unstable and may need rapid reversal of anticoagulation.

Alternative Initial Strategy — DOAC Lead-in

For haemodynamically stable patients with confirmed DVT or PE (not massive), a DOAC can be initiated without parenteral lead-in using a higher initial dose:

Rivaroxaban: 15 mg PO BD with food for 21 days, then 20 mg PO OD with food.
Apixaban: 10 mg PO BD for 7 days, then 5 mg PO BD.

Alternatively, standard DOAC dosing can follow a 5-day parenteral lead-in (enoxaparin or UFH) as per dabigatran and edoxaban regimens.

Warfarin Anticoagulation

Warfarin (Marevan®) remains an important oral anticoagulant in Australia, particularly for patients with mechanical heart valves, antiphospholipid syndrome, severe renal impairment (eGFR <15 mL/min where DOACs are contraindicated), or patient preference. Warfarin requires regular INR monitoring and has extensive drug–food interactions.

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Warfarin (Marevan®)

Vitamin K antagonist · Oral anticoagulant

Adult dose Individualised. Typical initiation: 5 mg PO OD for 2 days, then adjust per INR. Highly variable — pharmacogenomics (CYP2C9, VKORC1) influence dose requirements. Elderly/frail: start 2–3 mg.

Route Oral (tablets: 0.5 mg, 1 mg, 2 mg, 2.5 mg, 3 mg, 5 mg) or IV (rarely used)

Duration (VTE) Provoked VTE: 3 months. First unprovoked proximal DVT/PE: ≥3 months, then reassess for extended therapy. Recurrent unprovoked VTE: indefinite.

Renal adjustment No dose adjustment required — use INR-guided dosing. Preferred in eGFR <15 mL/min (dialysis).

Hepatic adjustment Use with extreme caution in severe hepatic impairment. Contraindicated in active liver disease with coagulopathy. Reduce dose in moderate hepatic impairment; monitor INR closely.

PBS status ✔ PBS General Benefit

INR Targets

Indication	Target INR	Duration
Treatment of DVT/PE	2.0–3.0	Minimum 3 months; extended if unprovoked
Non-valvular atrial fibrillation	2.0–3.0	Indefinite (or until CHA₂DS₂-VASc score no longer favours anticoagulation)
Mechanical aortic valve (low-risk prosthesis)	2.0–3.0	Indefinite
Mechanical mitral valve	2.5–3.5	Indefinite
Antiphospholipid syndrome with VTE	2.0–3.0 (target 2.5)	Indefinite (DOACs generally avoided in triple-positive APS per TRAPS trial)
Bioprosthetic valve (first 3 months)	2.0–3.0	3 months, then cease or switch to aspirin

Warfarin Overdosage & Management

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Life-threatening or intracranial bleeding on warfarin: Administer Prothrombin Complex Concentrate (PCC) 25–50 units/kg IV (4-factor PCC: Octaplex®, Beriplex®) + Vitamin K (phytomenadione) 10 mg IV slow injection over 20 minutes. Target INR correction within 15–30 minutes. Activate major haemorrhage protocol. Discuss with haematologist urgently.

Situation	INR	Action
Below therapeutic range	<2.0	Increase warfarin dose (5–15% increment). Recheck INR in 1–2 weeks. Investigate causes: missed doses, drug interactions, dietary change, increased vitamin K intake.
Mildly elevated, no bleeding	3.0–5.0	Reduce or omit next dose. Recheck INR in 1 week. If consistently elevated, reduce weekly dose by 5–15%.
Moderately elevated, no bleeding	5.0–8.0	Omit 1–2 doses. If no significant bleeding risk: oral vitamin K 1–2.5 mg (Konakion® MM oral solution). Recheck INR in 24 hours. Reduce subsequent warfarin dose.
Significantly elevated, no bleeding	>8.0	Omit warfarin. Give oral vitamin K 2.5–5 mg. Recheck INR in 12–24 hours. If high bleeding risk: consider IV vitamin K 10 mg and admission for observation.
Serious or life-threatening bleeding	Any	PCC 25–50 units/kg IV + vitamin K 10 mg IV. Major haemorrhage protocol. ICU/HDU care. Activated Factor VIIa (rFVIIa) may be considered as rescue therapy in refractory bleeding — haematologist decision.

Major Drug Interactions with Warfarin

Warfarin has extensive interactions due to CYP2C9, CYP3A4, CYP1A2, and protein-binding mechanisms. Always check for interactions when starting or stopping medications.

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Common clinically significant warfarin interactions:
Potentiation (↑ INR, ↑ bleeding risk): Amiodarone, fluconazole/voriconazole, metronidazole, macrolides (erythromycin, clarithromycin), trimethoprim–sulfamethoxazole, NSAIDs/COX-2 inhibitors, SSRIs, omeprazole (CYP2C9 inhibition), paracetamol (>2 g/day regularly), cranberry juice (high intake), St John's Wort (variable).
Antagonism (↓ INR, ↓ efficacy): Rifampicin (most potent inducer — may need 2–5× warfarin dose increase), carbamazepine, phenytoin, cholestyramine (reduces absorption), St John's Wort (CYP3A4 induction), vitamin K supplements, chronic alcohol excess, green leafy vegetables (high vitamin K content — advise consistent intake rather than avoidance).

Perioperative warfarin management: Stop warfarin 5 days before elective surgery. Bridge with LMWH (therapeutic or prophylactic dose depending on thrombotic risk) if high VTE risk (e.g. mechanical valve, recent VTE <3 months). Resume warfarin 12–24 hours postoperatively when haemostasis is secured. For minor procedures (dental extraction, cataract), warfarin may be continued with local haemostatic measures.

Warfarin and Pregnancy

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Warfarin is teratogenic (FDA Category X). Contraindicated in the first trimester (warfarin embryopathy: nasal hypoplasia, stippled epiphyses, limb hypoplasia — risk 5–10% with exposure between 6–12 weeks). Also contraindicated in the third trimester (risk of fetal intracranial haemorrhage during delivery). Switch to LMWH as soon as pregnancy is confirmed, or preferably pre-conception. The only exception is mechanical heart valves where the risk–benefit analysis may favour warfarin in the second trimester under specialist supervision.

Australian INR Monitoring Services

INR monitoring is widely available across Australia through:

Community pathology: All major pathology providers (Pathology Queensland, Douglass Hanly Moir, Sonic Healthcare, etc.) offer walk-in INR testing with MBS rebate.
Point-of-care INR (CoaguChek®): Available for home monitoring. Devices can be purchased or hired. Self-monitoring improves time in therapeutic range (TTR). Suitable for motivated, stable patients. Requires training and quality assurance.
Hospital anticoagulation clinics: Pharmacist- or nurse-led clinics at major hospitals provide structured warfarin management with dose algorithms.
GP anticoagulation management: RACGP-endorsed point-of-care INR in general practice. MBS item for POC coagulation testing available under specific criteria.

Direct Oral Anticoagulants (DOACs) & Arterial Thromboembolism

Direct oral anticoagulants (DOACs) have transformed VTE and atrial fibrillation management in Australia since their PBS listing. They offer predictable pharmacokinetics, no routine coagulation monitoring, fewer drug interactions, and non-inferior or superior efficacy with comparable or lower major bleeding rates compared with warfarin. The four DOACs available on the Australian PBS are:

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Apixaban (Eliquis®)

Factor Xa inhibitor · First-line DOAC for most indications

VTE treatment dose 10 mg PO BD for 7 days → 5 mg PO BD (continued for treatment duration)

AF stroke prevention 5 mg PO BD (reduce to 2.5 mg BD if ≥2 of: age ≥80, weight ≤60 kg, Cr ≥133 µmol/L)

Renal adjustment eGFR >25 mL/min: no adjustment for VTE. eGFR 15–29: use with caution. eGFR <15: not recommended. Haemodialysis: no data — avoid.

Key advantages Lowest major bleeding rate among DOACs (ARISTOTLE trial). Suitable for elderly. With food or without food.

PBS status ⚠ PBS Authority Required

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Rivaroxaban (Xarelto®)

Factor Xa inhibitor · Once-daily dosing for VTE maintenance

VTE treatment dose 15 mg PO BD with food for 21 days → 20 mg PO OD with food

AF stroke prevention 20 mg PO OD with food (15 mg OD if CrCl 15–49 mL/min)

Renal adjustment CrCl 15–49: 15 mg OD for AF. VTE: avoid if CrCl <15. Avoid in haemodialysis.

Key advantages Once-daily maintenance dosing improves adherence. Must be taken with food (for the 15 mg and 20 mg tablets). EINSTEIN trial programme.

PBS status ⚠ PBS Authority Required

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Dabigatran (Pradaxa®)

Direct thrombin inhibitor · Requires parenteral lead-in for VTE

VTE treatment dose 150 mg PO BD (after ≥5 days parenteral anticoagulation with LMWH/UFH)

AF stroke prevention 150 mg PO BD (110 mg BD if age ≥80, on verapamil, or high bleeding risk)

Renal adjustment CrCl 30–49: 100–150 mg BD depending on indication and bleeding risk. CrCl <30: contraindicated. Most renally cleared DOAC.

Key advantages Specific reversal agent (idarucizumab). RE-COVER trial. Capsule — do not crush/open (bioavailability increase).

PBS status ⚠ PBS Authority Required

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Edoxaban (Lixiana®)

Factor Xa inhibitor · Once daily, parenteral lead-in for VTE

VTE treatment dose 60 mg PO OD (after ≥5 days parenteral anticoagulation). 30 mg OD if CrCl 15–50 mL/min, weight ≤60 kg, or concurrent use of certain P-gp inhibitors (ciclosporin, erythromycin, verapamil).

AF stroke prevention 60 mg PO OD (30 mg OD if CrCl 15–50, weight ≤60 kg, or P-gp inhibitor use)

Renal adjustment CrCl 15–50: dose reduction to 30 mg OD. CrCl <15: not recommended. ENGAGE AF-TIMI 48 / Hokusai-VTE trials.

PBS status ⚠ PBS Authority Required

DOAC Reversal Agents

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Idarucizumab (Praxbind®)

Specific reversal agent for dabigatran

Dose 5 g IV (given as 2 × 2.5 g boluses no more than 15 minutes apart)

Onset Within minutes. Complete reversal of dabigatran anticoagulant effect.

Access Available at major Australian hospital EDs. May need to be sourced from hospital pharmacy or blood bank. Contact haematologist/on-call intensivist.

PBS status ✘ Authority Required (hospital only)

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Andexanet Alfa (Andexxa® / Ondexxya®)

Reversal agent for Factor Xa inhibitors (apixaban, rivaroxaban)

Dose Low dose: 400 mg IV bolus then 4 mg/min for 120 min (apixaban ≤5 mg, rivaroxaban ≤10 mg, or >8 hours since last dose). High dose: 800 mg IV bolus then 8 mg/min for 120 min (higher doses/within 8 hours).

Onset Minutes. Reduces anti-Xa activity by >90%.

Access Limited availability in Australia. Discuss with haematologist. May need to be sourced through special access scheme (SAS) or hospital blood product stores.

PBS status ✘ Not PBS-listed (hospital/special access only)

DOACs for Arterial Thromboembolism

DOACs have expanded beyond VTE into arterial thromboembolism management:

Atrial Fibrillation — Stroke Prevention

DOACs are first-line over warfarin for non-valvular AF (NHFA/CSANZ 2024 Australian guidelines). All four DOACs are approved and PBS-listed for this indication.
CHA₂DS₂-VASc score determines anticoagulation need. Score ≥2 in men or ≥3 in women → anticoagulate. Score 1 in men → consider anticoagulation based on bleeding risk and patient preference.
HAS-BLED score assesses bleeding risk. High score (≥3) identifies patients needing closer monitoring but is not an absolute contraindication to anticoagulation.
DOACs are contraindicated in mechanical heart valves and moderate-to-severe mitral stenosis (rheumatic) — warfarin remains the standard.

Stable Coronary & Peripheral Artery Disease

COMPASS trial: Rivaroxaban 2.5 mg BD + aspirin 100 mg OD reduced cardiovascular events (MACE) and major adverse limb events in stable CAD and PAD compared with aspirin alone. PBS authority may apply for this reduced dose in selected patients.
AfACS/AFIRE trial: Rivaroxaban monotherapy (15 mg OD) was non-inferior to combination (rivaroxaban + antiplatelet) for efficacy and safer for bleeding in AF patients ≥12 months after PCI/CABG.
Post-PCI AF patients: Triple therapy (DOAC + aspirin + clopidogrel) for 1 week to 6 months, then DOAC + single antiplatelet (usually clopidogrel) for up to 12 months, then DOAC monotherapy. Minimise triple therapy duration to reduce bleeding.

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When to prefer warfarin over DOACs: Mechanical heart valves, moderate-to-severe rheumatic mitral stenosis, antiphospholipid syndrome (particularly triple-positive APS — based on TRAPS trial showing excess thrombotic events with rivaroxaban), severe hepatic impairment (Child-Pugh C for some DOACs), eGFR <15 mL/min or haemodialysis, and patient inability to afford PBS co-payment (warfarin is the cheapest option).

DOAC Drug Interactions

Interaction	DOACs Affected	Clinical Significance
Potent P-gp/CYP3A4 inhibitors (ketoconazole, itraconazole, posaconazole, HIV protease inhibitors, ciclosporin)	All DOACs	↑ DOAC levels → ↑ bleeding risk. Contraindicated with dabigatran. Avoid or reduce dose with others.
Potent P-gp/CYP3A4 inducers (rifampicin, carbamazepine, phenytoin, St John's Wort)	All DOACs	↓ DOAC levels → risk of treatment failure/thrombosis. Avoid combination.
Verapamil	Dabigatran (major), edoxaban (moderate)	↑ levels. Dabigatran: reduce to 110 mg BD (take at same time as verapamil). Edoxaban: reduce to 30 mg OD.
Antiplatelet agents / NSAIDs	All DOACs	↑ bleeding risk. Dual or triple therapy increases major bleeding 2–3×. Use lowest effective dose and shortest duration.
Antacids / PPIs	Dabigatran (pH-dependent absorption)	PPIs may reduce dabigatran absorption slightly — clinically insignificant in most patients. Antacids: separate by 2 hours.

Directed & Specific Therapy

Cancer-Associated VTE

Cancer increases VTE risk 4–7 fold. Management has shifted from LMWH monotherapy to DOAC-first strategies for most cancer patients:

First-line: Apixaban or rivaroxaban (SELECT-D, ADAM-VTE, CARAVAGGIO trials). Apixaban has lower GI bleeding risk than rivaroxaban in upper GI or colorectal malignancy.
When to use LMWH instead: GI malignancy with high bleeding risk (especially upper GI), mucosal lesions, active GI ulceration, drug interactions with DOACs (e.g. concurrent chemotherapy interacting via CYP3A4), or inability to take oral medications.
Duration: Minimum 6 months. Continue anticoagulation as long as cancer is active or patient is receiving active treatment. Re-assess every 3–6 months for bleeding risk vs thrombotic risk.
Catheter-related thrombosis: Anticoagulate for ≥3 months. DOAC or LMWH. Remove catheter if no longer needed; if still required, anticoagulation continues with catheter in situ.

Thrombolysis for Massive PE

💉

Alteplase (Actilyse®)

Tissue plasminogen activator (tPA) · Fibrinolytic

Dose (massive PE) 100 mg IV over 2 hours (preferred regimen in Australia). Accelerated regimen: 0.6 mg/kg (max 50 mg) over 15 minutes — used in cardiac arrest settings.

Indication Massive PE with haemodynamic instability. Consider for submassive PE with clinical deterioration despite anticoagulation (shared decision with intensivist/haematologist).

Contraindications Active internal bleeding, recent (<3 months) intracranial/spinal surgery or trauma, intracranial neoplasm, AVM or aneurysm, known bleeding diathesis (excluding anticoagulation), severe uncontrolled hypertension (>200/110).

PBS status ✔ PBS General Benefit (hospital use)

Post-Thrombotic Syndrome Prevention

Graduated compression stockings (30–40 mmHg) for 2 years after proximal DVT to reduce post-thrombotic syndrome (PTS). Evidence is mixed (SOX trial was negative) but guidelines still recommend a trial of stockings for symptom relief in patients with persistent swelling.
Early mobilisation — bed rest is NOT recommended for DVT. Patients should ambulate as tolerated.
Elevate affected limb when resting.

Inferior Vena Cava (IVC) Filter

Indications for IVC filter insertion (by interventional radiologist):

Absolute contraindication to anticoagulation in acute proximal DVT/PE (e.g. active life-threatening bleeding, recent CNS surgery).
Recurrent VTE despite adequate anticoagulation.
Retrievable filters should be removed once anticoagulation can be safely resumed (typically within 2–6 weeks).

Monitoring

Warfarin Monitoring

Frequency: Every 1–2 days during initiation, then weekly once stable, then every 2–4 weeks when consistently in therapeutic range. Time in therapeutic range (TTR) target ≥65% — calculated using the Rosendaal linear interpolation method.
If TTR <65%: Investigate causes (adherence, diet, interactions), increase monitoring frequency, consider switching to a DOAC if appropriate.
Point-of-care testing: Home INR monitoring with CoaguChek® is safe and effective for stable patients. Improve TTR and patient satisfaction. PBS does not currently fund home monitoring devices.

DOAC Monitoring

Routine coagulation monitoring is NOT required for DOACs. However, assess the following at regular intervals:

Every 3–6 months: Renal function (eGFR/CrCl) — mandatory for dose adjustment. FBC (anaemia may indicate occult GI bleeding). LFTs at baseline and periodically.
Adherence assessment: Pill counts, pharmacy refill data. DOACs have short half-lives (8–17 hours) — missed doses quickly lead to loss of anticoagulation.
Drug interaction review: At every visit and whenever new medications are prescribed.
Special situations requiring DOAC levels: Acute stroke (need to know residual anticoagulation before thrombolysis), major bleeding, peri-procedural assessment, extremes of body weight (<50 kg or >120 kg), renal deterioration, suspected overdose. Use calibrated anti-Xa assays (for apixaban, rivaroxaban, edoxaban) or dilute thrombin time/ecarin clotting time (for dabigatran).

LMWH Monitoring

Routine treatment: Anti-Xa levels not required for standard-dose enoxaparin in patients with normal renal function and weight 50–100 kg.
Indications for anti-Xa monitoring: Renal impairment (eGFR <30 mL/min), obesity (>120 kg or BMI >40), underweight (<50 kg), pregnancy (therapeutic dosing), extremes of age (neonates, very elderly).
Target anti-Xa levels: Treatment dose: 0.5–1.0 units/mL (measured 4 hours post-dose for BD dosing; 4–6 hours post-dose for OD dosing).

Special Populations

🤰

Pregnancy

Anticoagulation of choice: LMWH (enoxaparin or dalteparin) throughout pregnancy. Warfarin and all DOACs are contraindicated (teratogenic/unknown safety).

Dose: Weight-adjusted enoxaparin 1 mg/kg SC BD (treatment) or 40 mg SC OD (prophylaxis). Adjust doses as weight changes through pregnancy. Monitor anti-Xa levels monthly.

Labour & delivery: Switch to UFH at 36+ weeks or planned induction (UFH has shorter half-life, can be stopped 4–6 hours before delivery). Alternatively, planned delivery with omission of LMWH ≥24 hours prior.

Postpartum: Resume LMWH or commence warfarin (compatible with breastfeeding). Warfarin does not cross into breast milk in clinically significant amounts. DOACs: limited data; not recommended during breastfeeding as a precaution.

VTE risk is 5–10× higher in pregnancy. Prophylactic LMWH indicated for previous VTE, thrombophilia with family history, or other high-risk factors.

👶

Paediatrics

First-line: LMWH (enoxaparin) — the most commonly used anticoagulant in children. Neonates: 1.5 mg/kg SC BD. Children: 1 mg/kg SC BD. Target anti-Xa 0.5–1.0 units/mL.

Warfarin: Used for longer-term anticoagulation. Dosing is highly variable and requires frequent INR monitoring. Can be used from infancy with expertise.

DOACs: Rivaroxaban is now PBS-approved for VTE treatment in children (EINSTEIN-Jr trial). Dosing is weight-based (granule formulation for young children). Apixaban studies ongoing. Other DOACs: limited paediatric data.

Most paediatric VTE is catheter-related (central venous access devices). Refer to paediatric haematology for management. Treatment duration typically 3 months for provoked VTE.

👴

Elderly (≥65 years)

Key considerations: Increased bleeding risk (HAS-BLED ≥3 common). Falls risk does NOT contraindicate anticoagulation (annual ICH risk from falls <1% vs stroke risk 4–15% in AF). Renal decline is common — check eGFR regularly.

Preferred DOAC: Apixaban has the best bleeding profile in elderly (ARISTOTLE subgroup analysis). Standard dose unless criteria for dose reduction are met (age ≥80, weight ≤60 kg, Cr ≥133 µmol/L).

Warfarin: Start at lower doses (2–3 mg). Interacts with polypharmacy common in elderly. INR monitoring may be challenging for patients with limited mobility — use community pathology or home testing.

De-prescribing review is essential. Anticoagulation should be continued if benefits outweigh risks, even in frail elderly, unless life expectancy is very limited (<6 months).

🫘

Renal Impairment

eGFR 30–49 mL/min: Apixaban and edoxaban preferred (least renally cleared). Rivaroxaban: use 15 mg OD for AF. Dabigatran: 100–150 mg BD (higher bleeding risk — use with caution). LMWH: monitor anti-Xa levels.

eGFR 15–29 mL/min: Apixaban (use with caution, limited data). UFH for initial treatment. Warfarin may be preferred for long-term.

eGFR <15 mL/min or haemodialysis: UFH for acute treatment. Warfarin for long-term. DOACs are generally not recommended (insufficient data). Consider nephrology/haematology co-management.

Dabigatran is the most renally cleared DOAC (~80% renal excretion) — avoid in moderate-severe renal impairment.

🫁

Hepatic Impairment

Child-Pugh A (mild): All DOACs can be used with caution. Monitor LFTs. Warfarin: increased sensitivity — closer INR monitoring.

Child-Pugh B (moderate): Apixaban and rivaroxaban: use with caution (limited data). Dabigatran and edoxaban: generally avoid. Warfarin: use with extreme caution, frequent INR checks.

Child-Pugh C (severe): Avoid all DOACs. Warfarin contraindicated if coagulopathy present. LMWH with anti-Xa monitoring may be used cautiously. Seek haematology input.

Hepatic coagulopathy is complex — patients may be both prothrombotic and bleeding-prone simultaneously. Specialist management is recommended.

🧬

Cancer & Immunocompromised

Cancer-associated VTE: DOACs (apixaban preferred) are first-line for most solid tumours and haematological malignancies. LMWH remains an alternative for GI cancers with high bleeding risk or drug interactions.

Drug interactions: Check interactions with chemotherapy (especially TKIs that affect P-gp/CYP3A4). Azole antifungals (common in immunocompromised) interact with all DOACs — may need dose reduction or LMWH.

Thrombocytopenia: If platelets <50 × 10⁹/L, balance bleeding vs thrombotic risk. Consider prophylactic-dose LMWH if platelets 25–50. Hold anticoagulation if platelets <25.

Incidental VTE (found on staging CT) should be treated the same as symptomatic VTE. Mortality risk from untreated incidental PE is similar to symptomatic PE.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of venous and arterial thromboembolism. The AIHW reports that Indigenous Australians are hospitalised for VTE at 1.5–2 times the rate of non-Indigenous Australians, with higher rates of PE-related mortality. Arterial thromboembolism (including rheumatic heart disease-related stroke and AF-related embolism) is also significantly more prevalent. These disparities are driven by complex interactions of remoteness, socioeconomic disadvantage, health literacy, chronic disease burden, and systemic barriers to timely care.

VTE incidence

1.5–2× higher hospitalisation rate for VTE compared with non-Indigenous Australians. Higher rates of PE at presentation, suggesting delayed diagnosis of DVT.

Rheumatic heart disease

RHD remains 5–6× more common in Indigenous Australians, particularly in remote NT, QLD, and WA communities. Mechanical heart valve replacement requires lifelong warfarin with INR monitoring — a significant challenge in remote settings.

Remote access

Compression ultrasound and CTPA are unavailable in most remote communities. Patients may require aeromedical retrieval (Royal Flying Doctor Service) for diagnosis. Point-of-care D-dimer and telehealth-guided clinical assessment can support initial triage.

Anticoagulation monitoring

Regular INR monitoring for warfarin is challenging in remote areas with infrequent pathology collection runs (may be weekly or fortnightly). Point-of-care INR devices (CoaguChek®) deployed in some ACCHOs can improve access. DOACs may be preferred where accessible and affordable, as they eliminate the need for routine INR monitoring.

PBS affordability

PBS co-payments can be a barrier. Aboriginal and Torres Strait Islander patients with a current Centrelink concession card are eligible for PBS scripts at the concessional rate. Closing the Gap PBS co-payment (.70 per script in 2025) applies to Indigenous Australians with, or at risk of, chronic disease — including those on anticoagulants. Ensure patients are aware of and enrolled in these programs.

Health literacy & cultural safety

Anticoagulation education must be culturally appropriate and, where possible, delivered in the patient's first language or with interpreter support. Use visual aids and practical demonstrations. Engage Aboriginal Health Workers (AHWs) and Aboriginal Health Practitioners (AHPs) in anticoagulation counselling and adherence support.

ACCHO integration

Aboriginal Community Controlled Health Organisations (ACCHOs) are best placed to provide ongoing anticoagulation follow-up. Coordinate with ACCHOs for warfarin INR management, DOAC prescriptions, and adherence monitoring. Telehealth haematology consultations (via platforms such as Healthdirect) can support complex cases without requiring patient transfer.

Preventive strategies

VTE prophylaxis during hospitalisation is frequently suboptilised. Strengthen hospital-based VTE prophylaxis protocols with Indigenous health liaison officers. Community-based cardiovascular risk reduction (smoking cessation, rheumatic fever prophylaxis, diabetes management) addresses upstream arterial thromboembolism risk.

ℹ️

Recommendations for clinicians:

Always ask about VTE symptoms proactively in Indigenous patients presenting with leg swelling, breathlessness, or chest pain — delayed presentation is common.
Prioritise DOACs over warfarin where clinically appropriate and PBS-accessible, to reduce the burden of INR monitoring in remote settings.
Ensure all Indigenous patients on anticoagulants are registered for Closing the Gap PBS co-payment reductions.
Engage AHWs/AHPs in anticoagulation education and monitoring — they are trusted intermediaries and essential to culturally safe care.
Use telehealth haematology consultations for complex cases (thrombophilia workup, cancer-associated VTE, mechanical valve management).
Advocate for RHD register compliance and secondary prophylaxis to reduce mechanical valve-related anticoagulation burden.

📚 References

1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603.
2. Stevens SM, Woller SC, Kreuziger LB, et al. Antithrombotic therapy for VTE disease: second update of the CHE

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).