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Pulmonary embolism

SNOMED: 59282003967 wordsUpdated 03/03/2026
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Exam Tips

  • In OSCE/viva, always combine symptom pattern (sudden dyspnoea, pleuritic pain, haemoptysis) with risk factors and pre-test probability before ordering tests.
  • Normal chest X-ray or non-specific ECG does not exclude PE; they are mainly for differential diagnosis.
  • High-risk PE = hypotension/shock: escalate urgently for reperfusion (thrombolysis/embolectomy) and senior/critical care input.
  • Pregnancy: LMWH is preferred; avoid DOACs and generally avoid warfarin antenatally due to fetal risk.
  • Remember classic but insensitive ECG clue S1Q3T3 and the key imaging diagnosis on CTPA (intraluminal filling defect).
  • For follow-up questions, mention CTEPH in patients with persistent dyspnoea after PE and the need for specialist reassessment.

Definition

Pulmonary embolism (PE) is acute obstruction of the pulmonary arterial circulation, usually by thrombus that has embolized from a deep vein (most often the leg or pelvis). It causes ventilation-perfusion mismatch and can rapidly progress from pleuritic pain or breathlessness to right ventricular (RV) failure, shock, or sudden death. In UK practice, PE is considered part of venous thromboembolism (VTE) alongside deep vein thrombosis (DVT).

Pathophysiology

Most PE arises when thrombus forms under Virchow triad conditions (venous stasis, endothelial injury, hypercoagulability), then embolizes to pulmonary arteries. Mechanical obstruction plus vasoactive mediator release increases pulmonary vascular resistance, acutely raising RV afterload; RV dilatation and ischemia can reduce left ventricular preload and systemic blood pressure. Small peripheral emboli more often cause pleuritic pain/haemoptysis from pulmonary infarction, while large central emboli can cause syncope, hypotension, and obstructive shock. See standard textbook figures showing clot migration from leg veins to pulmonary arteries and RV pressure overload (e. g, VTE/RV-strain diagrams in core medicine texts).

Risk Factors

  • Previous VTE (DVT or PE)
  • Recent surgery (especially major orthopaedic) or trauma/fracture
  • Immobility or hospital bed rest (>5 days), limb paralysis
  • Active cancer (notably pancreatic, GI, lung, brain, haematological malignancy)
  • Pregnancy and puerperium (highest risk in first 6 weeks postpartum)
  • Oestrogen exposure (combined oral contraceptive pill, some HRT regimens)
  • Thrombophilia including antiphospholipid syndrome
  • Increasing age and family history of VTE
  • Obesity, smoking, long-haul travel
  • Comorbid states such as heart failure, COPD, IBD, nephrotic syndrome, sepsis, myeloproliferative disease

Clinical Features

Symptoms

  • Sudden-onset dyspnoea (most common)
  • Pleuritic chest pain, often unilateral
  • Haemoptysis
  • Syncope or presyncope (suggests large/central PE)
  • Cough
  • Retrosternal chest discomfort from RV strain

Signs

  • Tachypnoea
  • Tachycardia
  • Hypoxia (may be normal in smaller PE)
  • Hypotension or shock in massive/high-risk PE
  • Raised JVP, loud P2, tricuspid regurgitation murmur
  • Fever or pleural rub
  • Clinical signs of DVT (unilateral calf swelling/tenderness)

Investigations

Clinical probability assessment (e. g, Wells score; consider PERC only in very low-risk patients):Stratifies pre-test probability to guide D-dimer versus immediate imaging
D-dimer (if PE unlikely/intermediate probability):Raised in many PE cases; a negative high-sensitivity test helps rule out PE in low-risk patients
CT pulmonary angiography (CTPA):Intraluminal filling defect in pulmonary arteries; may show central/saddle or segmental emboli, RV enlargement
Ventilation-perfusion (V/Q) scan:Segmental perfusion defects with preserved ventilation; useful when CTPA is unsuitable
ECG:Often sinus tachycardia; possible right heart strain pattern (e. g, right axis deviation, RBBB, S1Q3T3)
Chest X-ray:Often normal or non-specific (atelectasis, small pleural effusion); mainly to assess differentials
Cardiac biomarkers (troponin/BNP):Elevation suggests RV myocardial strain and higher early risk
Echocardiography (urgent in haemodynamic instability):RV dilatation/dysfunction, pressure overload; supports high-risk PE when unstable
Compression ultrasound of leg veins:Proximal DVT supports VTE diagnosis when chest imaging is delayed/contraindicated
Arterial blood gas:May show hypoxaemia and respiratory alkalosis, but can be normal

Management

Lifestyle Modifications

  • Early mobilisation when clinically stable and use of VTE prophylaxis in future high-risk admissions
  • Stop smoking, optimise weight, maintain hydration, and reduce prolonged immobility/travel stasis
  • Review reversible provoking factors (for example, switch from oestrogen-containing contraception where appropriate)
  • Safety-netting: return urgently for worsening breathlessness, chest pain, syncope, haemoptysis, or bleeding on anticoagulants

Pharmacological Treatment

Direct oral anticoagulants (first-line in many non-pregnant adults)

  • Apixaban 10 mg twice daily for 7 days, then 5 mg twice daily
  • Rivaroxaban 15 mg twice daily for 21 days, then 20 mg once daily with food

Check renal function, drug interactions, and bleeding risk before prescribing. Avoid in pregnancy/breastfeeding; caution or avoid in severe renal impairment and significant hepatic disease with coagulopathy. Consider reduced-dose extended prevention after 6 months in selected patients (e. g, apixaban 2.5 mg twice daily or rivaroxaban 10 mg once daily).

Parenteral anticoagulation (when DOAC unsuitable, in pregnancy, or haemodynamic concern)

  • Enoxaparin 1 mg/kg subcutaneously twice daily (or 1.5 mg/kg once daily in selected patients)
  • Unfractionated heparin IV infusion (weight-based) with aPTT/anti-Xa monitoring

LMWH preferred in pregnancy (weight-adjusted). Use UFH when rapid reversal may be needed (e. g, peri-procedural or high bleeding-risk instability). Monitor platelets for heparin-induced thrombocytopenia and adjust dose in renal impairment.

Vitamin K antagonist pathway

  • Warfarin (typically start 5 mg once daily, then titrate to INR 2.0-3.0) with LMWH/UFH overlap for at least 5 days and until INR >=2.0 for at least 24 hours

Use when DOACs are unsuitable or in specific indications (e. g, antiphospholipid syndrome often managed with VKA). Major interactions and monitoring burden; contraindicated in pregnancy (except specialist circumstances).

Systemic thrombolysis for high-risk (massive) PE with shock/hypotension

  • Alteplase 100 mg IV over 2 hours (or weight-based protocol in lower body weight), plus anticoagulation per protocol

Use only when benefits outweigh bleeding risk. Contraindications include prior intracranial haemorrhage, recent ischaemic stroke, active bleeding, recent major surgery/trauma, and suspected aortic dissection.

Surgical / Interventional

  • Catheter-directed thrombolysis or thrombectomy for selected intermediate/high-risk PE when deterioration occurs or systemic lysis is unsuitable
  • Surgical embolectomy for massive PE when thrombolysis is contraindicated or has failed
  • Inferior vena cava (IVC) filter only if anticoagulation is absolutely contraindicated or recurrent PE occurs despite adequate anticoagulation

Complications

  • Early death, including sudden death before diagnosis
  • Obstructive shock and cardiac arrest in haemodynamically unstable PE
  • Right ventricular failure and myocardial injury
  • Recurrent VTE/PE after stopping anticoagulation (risk depends on persistent risk factors)
  • Chronic thromboembolic pulmonary hypertension (CTEPH) with progressive exertional dyspnoea and possible right heart failure
  • Longer-term post-PE syndrome with reduced exercise tolerance and quality of life

Prognosis

Untreated PE has substantial mortality, while prompt anticoagulation markedly improves outcomes. Prognosis is worst in haemodynamic instability/cardiac arrest, intermediate in stable patients with RV strain or myocardial injury, and best in low-risk stable PE. Recurrence risk is lowest after major transient triggers, higher with persistent factors (especially active cancer or antiphospholipid syndrome), and many recurrences occur within the first year after anticoagulation is discontinued.

Sources & References

💊BNF Drug References(3)

NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 304, 305)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 298)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 304)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 509)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 235)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 252, 253)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1413)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 93)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 70, 71)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 489)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 206, 207)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 832, 833)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 206)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 179)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 833, 834)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 932)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 1417)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 528)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 1080, 1081)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 869, 870)[context]

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