Lucan · Conditions

Pulmonary embolism

Australian guidance: eTG Cardiovascular — VTE + Thrombosis Australia 2019

1. Definition and epidemiology

Pulmonary embolism (PE) is the occlusion of one or more pulmonary arteries by thrombus that has typically embolised from the deep venous system of the lower limbs or pelvis. It sits at the severe end of the venous thromboembolism (VTE) spectrum, which ranges from distal deep vein thrombosis (DVT) through to fatal PE. Symptomatic VTE affects approximately 1 per 1,000 Australians per year, and PE accounts for 7% of all deaths in Australian hospitals; in nearly 25% of cases, sudden death is the first clinical sign. Up to 75% of all VTE in hospitalised patients occurs as a consequence of hospital admission, making PE a leading preventable cause of inpatient mortality in Australia.

2. Pathophysiology

Robbins Ch 4 identifies Virchow's triad as the mechanistic framework: venous stasis, endothelial injury, and a hypercoagulable state. Thrombus typically originates in the deep veins of the calf or thigh; propagation into proximal veins greatly increases embolic risk. When thrombus fragments and migrates through the right heart into the pulmonary vasculature, it raises pulmonary vascular resistance acutely, causing right ventricular pressure overload, dilation, and septal shift that impairs left ventricular filling and reduces cardiac output. Hypoxaemia results from ventilation-perfusion mismatch, intrapulmonary shunting, and low mixed-venous oxygen tension. Pulmonary infarction is uncommon given the dual bronchial blood supply, but can occur peripherally where collateral flow is inadequate. Massive PE carries a case fatality exceeding 30% without rapid intervention, driven by acute right ventricular failure.

3. Clinical presentation and diagnostic criteria

Presentation varies from incidental to catastrophic depending on clot burden and cardiopulmonary reserve. The classic triad of dyspnoea, pleuritic chest pain, and haemoptysis appears in fewer than 20% of confirmed cases. More common presenting features include acute dyspnoea (the most frequent symptom), tachycardia, tachypnoea, hypoxia on pulse oximetry, and pleuritic chest pain suggesting peripheral infarction. Massive PE presents with haemodynamic instability: systolic blood pressure below 90 mmHg or a fall of at least 40 mmHg sustained for more than 15 minutes, syncope, or cardiac arrest. Risk stratification using validated tools is central to the Australian diagnostic approach. The Wells PE score assigns points for clinical DVT signs, PE being the most likely diagnosis, immobilisation or surgery within four weeks, prior VTE, haemoptysis, heart rate above 100 beats per minute, and active malignancy. A score of four or below is low probability; above four is high probability. In low-to-moderate probability patients, a negative age-adjusted D-dimer (upper limit of normal multiplied by age in years divided by 100 for patients aged over 50) safely excludes PE without imaging.

4. Investigations and AU-specific cutoffs

Investigations follow a risk-stratified, sequential approach per Thrombosis and Haemostasis Society of Australia and New Zealand (THANZ) 2019 guidance. First-line assessment includes:

• Wells PE score to determine pre-test probability
• D-dimer: standard cutoff 500 micrograms/L; age-adjusted cutoff (age x 10 micrograms/L) for patients aged over 50 reduces unnecessary computed tomography pulmonary angiography (CTPA)
• ECG: sinus tachycardia is most common; the classic S1Q3T3 pattern and new right bundle branch block suggest right heart strain but are neither sensitive nor specific
• Chest X-ray: typically normal or shows oligaemia distal to obstruction (Westermark sign), Hampton's hump (pleural-based wedge opacity), or an enlarged hilum; most useful to exclude alternative diagnoses
• CTPA: first-line definitive imaging when PE probability is high or D-dimer is elevated; contrast dose requires renal function check (estimated glomerular filtration rate above 45 mL/min/1.73m2 preferred)
• Ventilation-perfusion scan: preferred in pregnancy, significant iodinated contrast allergy, or severe renal impairment
• Bilateral lower limb compression ultrasonography: useful if CTPA unavailable or inconclusive
• Troponin and B-type natriuretic peptide (BNP): elevated values indicate right ventricular strain and identify patients at higher risk of early deterioration; guide intensity of treatment decisions
• Echocardiography: right ventricular dilation or hypokinesis in haemodynamically unstable patients supports diagnosis and guides thrombolysis decisions when CTPA is not immediately obtainable

5. Management

Management is stratified by haemodynamic status and bleeding risk, anchored to the THANZ 2019 guidelines referenced in eTG Cardiovascular.

Haemodynamically unstable (massive PE): Immediate systemic thrombolysis with alteplase 100 mg intravenously over two hours is first-line treatment when there is confirmed or strongly suspected massive PE and no absolute contraindications to thrombolysis. Unfractionated heparin (UFH) infusion should be administered concurrently and continued after thrombolysis. If thrombolysis fails or is absolutely contraindicated, catheter-directed therapy or surgical embolectomy are considered; both require urgent specialist consultation.

Haemodynamically stable (submassive and low-risk PE): Anticoagulation is initiated promptly. Direct-acting oral anticoagulants (DOACs) are the preferred initial and long-term therapy in eligible patients. Rivaroxaban (15 mg orally twice daily for 21 days, then 20 mg once daily with the evening meal) or apixaban (10 mg orally twice daily for seven days, then 5 mg twice daily) are preferred because evidence shows at least equivalent efficacy and lower rates of major bleeding compared with conventional heparin-bridged warfarin therapy. Low molecular weight heparin (LMWH), specifically enoxaparin 1 mg/kg subcutaneously twice daily (or 1.5 mg/kg once daily in selected patients), is appropriate when DOACs are contraindicated, in active malignancy-associated PE, pregnancy, or severe renal impairment where specialist guidance should be sought. Warfarin is now a second-line agent; if used, a therapeutic international normalised ratio (INR) of 2.0 to 3.0 is the target, and LMWH must overlap until two consecutive therapeutic INR readings are confirmed.

Early discharge protocols using the Pulmonary Embolism Severity Index (PESI) or simplified PESI allow low-risk patients to be managed in the outpatient setting with close follow-up.

6. Pharmacology and AU PBS notes

First-line DOACs for VTE treatment (PBS listed under Section 85 for PE):

• Rivaroxaban (Xarelto): 15 mg twice daily for 21 days, then 20 mg once daily. PBS streamlined authority required for VTE treatment; do not use if creatinine clearance (CrCl) is below 15 mL/min
• Apixaban (Eliquis): 10 mg twice daily for seven days, then 5 mg twice daily. Do not use if CrCl is below 25 mL/min
• Dabigatran (Pradaxa): 150 mg twice daily (or 110 mg twice daily for patients aged 80 years or over, or those also taking verapamil); must follow five to ten days of initial parenteral anticoagulation. Do not use if CrCl is below 30 mL/min

Parenteral agents:

• Enoxaparin (Clexane): dose-adjust in renal impairment; avoid in CrCl below 30 mL/min without specialist input; anti-Xa monitoring recommended in extreme body weight or renal impairment
• UFH: preferred in haemodynamic instability, renal failure requiring rapid reversal, or when thrombolysis is planned; titrate to activated partial thromboplastin time (APTT) 60 to 100 seconds

Thrombolysis:

• Alteplase (Actilyse): 100 mg intravenously over two hours for massive PE; absolute contraindications include intracranial haemorrhage, recent intracranial surgery, active internal bleeding, and ischaemic stroke within three months.

Extended anticoagulation: After three months of treatment, consider indefinite reduced-dose anticoagulation for unprovoked PE: apixaban 2.5 mg twice daily or rivaroxaban 10 mg once daily, with lower bleeding risk than full treatment doses.

7. Complications and monitoring

Early complications include haemodynamic collapse from right ventricular failure, cardiogenic shock, cardiac arrest, and PE recurrence. Haemoptysis from pulmonary infarction and pleural effusion may develop within days.

Subacute and late complications:

• Recurrent VTE: risk is highest in the first three to six months and in unprovoked PE; indefinite anticoagulation halves recurrence risk but must be weighed against annual major bleeding risk of approximately 1 to 3%
• Chronic thromboembolic pulmonary hypertension (CTEPH): occurs in 2 to 5% of survivors; presents as progressive dyspnoea months to years after the index event; all patients should be reassessed with echocardiography at three months if symptoms persist
• Post-thrombotic syndrome: less prominent after isolated PE than DVT, but lower-limb oedema and skin changes can occur if concurrent DVT was present

Monitoring schedule:

• Clinical review at seven to fourteen days; repeat imaging as indicated for haemodynamic reassessment
• INR two to three times weekly until stable (warfarin only), then monthly
• Renal function and full blood count at baseline and three months; more frequent with LMWH in renal impairment
• Echocardiography at three months in patients with elevated troponin, right ventricular dysfunction, or persisting symptoms to screen for CTEPH
• D-dimer at three months assists the decision to stop anticoagulation in unprovoked PE; persistently elevated values support continuation per THANZ 2019

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