Pulmonary Embolism — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Pulmonary embolism (PE) is the acute obstruction of one or more branches of the pulmonary arterial tree by thrombus material, most commonly originating from deep vein thrombosis (DVT) of the lower limb or pelvis — collectively termed venous thromboembolism (VTE). PE and DVT are manifestations of the same pathophysiological process (Virchow's triad of stasis, endothelial injury, and hypercoagulability) and are often considered together as VTE. PE is the third most common cause of acute cardiovascular death after myocardial infarction and stroke. Approximately 90% of PEs arise from proximal lower limb DVT (popliteal vein and above — femoral, iliac veins); calf DVT is a less common source. The haemodynamic consequences of PE depend on the clot burden and the patient's cardiopulmonary reserve: massive PE (causing haemodynamic compromise — systolic BP below 90 mmHg — shock) carries 40-70% mortality without urgent treatment; submassive PE (right ventricular dysfunction without hypotension — intermediate risk) carries 3-15% mortality; low-risk PE has a mortality below 2%. Classification by risk guides the urgency and intensity of treatment. PE may present acutely (acute PE — hours to days) or with symptoms developing over weeks (subacute) or longer (chronic thromboembolic disease — which can lead to chronic thromboembolic pulmonary hypertension — CTEPH). Without anticoagulation, 30-50% of DVT patients develop symptomatic PE.

PE results from venous thrombus formation in the systemic veins, usually the deep veins of the lower limb, followed by detachment and embolisation to the pulmonary circulation. Virchow's triad: the classic mechanistic framework for thrombosis — venous stasis, endothelial injury, and hypercoagulability — all contribute to VTE. Provoking risk factors: major surgery (particularly orthopaedic surgery — hip and knee arthroplasty; abdominal/pelvic surgery — DVT risk 40-80% without prophylaxis), hospitalisation, prolonged immobility (bed rest, long-haul air travel above 4 hours — economy class syndrome), trauma (pelvic and lower limb fractures), active malignancy (cancer is the single strongest acquired VTE risk factor — Trousseau's syndrome; mucinous adenocarcinomas of pancreas, lung, GI tract, and ovary are particularly thrombogenic; chemotherapy further increases risk), pregnancy and the postpartum period (5-fold increased VTE risk; highest in the first 6 weeks postpartum), oestrogen-containing combined oral contraceptive pill (3-6-fold increased DVT risk, particularly with VTE-prone thrombophilias). Thrombophilias (inherited and acquired): Factor V Leiden mutation (most common hereditary thrombophilia — present in 5% of European populations; increases VTE risk 5-7-fold in heterozygotes); prothrombin G20210A mutation; protein C, protein S, or antithrombin deficiency; antiphospholipid syndrome (APLS — acquired thrombophilia associated with SLE and recurrent VTE — Lupus anticoagulant, anti-cardiolipin antibodies, anti-beta2-glycoprotein I antibodies). Other risk factors: previous VTE (strongest predictor of recurrence), inflammatory bowel disease, nephrotic syndrome, polycythaemia vera, obesity (BMI above 30), smoking, dehydration, heart failure, COPD.

PE presents with a highly variable clinical picture — from incidentally detected asymptomatic PE on CT imaging to sudden haemodynamic collapse and cardiac arrest. The classic triad of dyspnoea, pleuritic chest pain, and haemoptysis is present in fewer than 20% of confirmed PE cases. Dyspnoea: the most common symptom — present in 70-90% of PE; typically sudden onset, at rest or with exertion; accompanied by tachycardia and anxiety. Pleuritic chest pain: sharp, lateralised chest pain worsening with inspiration — caused by pulmonary infarction (occurs in peripheral, smaller PEs where collateral circulation is insufficient to prevent lung infarction); present in 40-50% of PE. Haemoptysis: rust-brown or blood-streaked sputum — occurs with pulmonary infarction; present in 15-30% of PE. Syncope or pre-syncope: sudden loss of consciousness or near-fainting — suggests massive PE with severe haemodynamic compromise from acute right ventricular outflow obstruction. Tachycardia: sinus tachycardia (heart rate above 100 bpm) — the most common physical sign; found in 40-50%. Massive PE: severe dyspnoea, diaphoresis, cyanosis, hypotension (BP below 90 mmHg), tachycardia, elevated JVP (right heart failure), right heart failure signs — and cardiac arrest (pulseless electrical activity — PEA — is the arrest rhythm in massive PE). DVT symptoms (in 20-30% of PE patients): unilateral leg swelling, warmth, erythema, and tenderness of the calf or thigh — the leg with the DVT may not be the symptomatic side. Atypical presentations: PE presenting as apparent pneumonia (consolidative infarction), unexplained heart failure, or new atrial fibrillation.

Clinical probability assessment is the first step — validated scoring systems determine pre-test probability and guide investigation. Wells PE score: assigns points to clinical features (DVT signs +3, PE most likely diagnosis +3, tachycardia +1.5, immobilisation or surgery in last 4 weeks +1.5, previous DVT/PE +1.5, haemoptysis +1, malignancy +1); total score: PE unlikely 0-4, PE likely 5+. PERC rule: in low-risk patients (Wells 0-1), if all 8 PERC criteria are negative, PE can be excluded without D-dimer or imaging. D-dimer: highly sensitive but non-specific for VTE — useful for excluding PE in low-probability patients (if D-dimer below 500 µg/L, PE is excluded in low-probability cases); in intermediate-to-high probability, D-dimer does not exclude PE and imaging is required; D-dimer is elevated in many conditions (infection, malignancy, pregnancy, post-surgery) — clinical utility limited in these contexts; age-adjusted D-dimer (age × 10 µg/L for patients above 50) increases specificity. CT pulmonary angiography (CTPA): the gold standard investigation for PE — identifies thrombus in pulmonary arteries to segmental level; sensitivity 83-90%, specificity 96%; also identifies alternative diagnoses; rapid results in the Emergency Department. Echocardiography (TTE or TOE): not diagnostic for PE but essential for risk stratification — RV dilation, septal bowing (D-shaped septum), tricuspid regurgitation, elevated RVSP (pulmonary hypertension), and McConnell's sign (RV free wall hypokinesis with apical sparing) indicate right heart strain; bedside echo is critical in haemodynamically unstable patients where CTPA may not be feasible. V/Q (ventilation-perfusion) scan: alternative to CTPA — preferred in pregnancy (lower radiation dose to the fetus), young women, and renal impairment; a high-probability V/Q scan is diagnostic. Biomarkers: troponin elevation and NT-proBNP elevation in submassive PE indicate myocardial injury and RV stress — predict adverse outcomes and escalate risk category. PESI score (Pulmonary Embolism Severity Index): guides outpatient vs inpatient treatment decision in haemodynamically stable PE. Leg ultrasound (duplex): confirms DVT in 30-50% of confirmed PE; important when CTPA is contraindicated.

Risk-stratified treatment is the cornerstone of PE management. All PE patients: immediate anticoagulation unless contraindicated — to prevent propagation and recurrence. Low-risk PE (PESI class I-II, no RV dysfunction, no troponin elevation): outpatient treatment appropriate for selected stable patients — reduces hospitalisation without compromising outcomes. Anticoagulation for all PE: direct oral anticoagulants (DOACs) are now first-line for most patients — apixaban 10 mg BD for 7 days then 5 mg BD, or rivaroxaban 15 mg BD for 21 days then 20 mg OD — both oral, no monitoring required, equivalent or superior to VKA in efficacy with lower major bleeding rates (EINSTEIN-PE, AMPLIFY trials). Low molecular weight heparin (LMWH — enoxaparin, dalteparin): subcutaneous injection — used in cancer-associated VTE (dalteparin preferred, edoxaban or rivaroxaban also approved), pregnancy (DOACs contraindicated — warfarin also contraindicated in 1st and 3rd trimesters), and severe renal impairment. Warfarin (VKA): still used when DOACs contraindicated (antiphospholipid syndrome, severe renal failure, mechanical heart valve); INR target 2-3; requires regular INR monitoring; bridging with LMWH until therapeutic INR achieved. Duration of anticoagulation: provoked PE (reversible provoking risk factor) — 3 months; unprovoked PE — minimum 3 months, then individual risk-benefit assessment for extended treatment (indefinite anticoagulation with DOAC at reduced dose reduces recurrence by 80-90% at the cost of bleeding risk); cancer-associated VTE — anticoagulate for cancer duration or for 6 months with reassessment. Intermediate-risk (submassive) PE: anticoagulation plus close monitoring for haemodynamic deterioration; catheter-directed thrombolysis (CDT) or systemic thrombolysis for haemodynamic decompensation. Massive PE with haemodynamic compromise (systolic BP below 90 mmHg or cardiac arrest): emergency systemic thrombolysis — alteplase 100 mg IV over 2 hours; contraindications include active bleeding, recent surgery, stroke within 3 months; in cardiac arrest from PE — CPR and alteplase without delay (50 mg IV bolus, continue CPR for 60-90 minutes post-thrombolysis before declaring futility); surgical embolectomy or catheter-directed embolectomy/pharmacomechanical thrombolysis for thrombolysis failure or contraindication. IVC filter: temporary or permanent inferior vena cava filter for PE with absolute contraindication to anticoagulation, or recurrent VTE despite adequate anticoagulation.

PE causes both acute life-threatening and chronic long-term complications. Acute right ventricular failure: massive PE obstructs pulmonary arterial outflow, causing acute right ventricular pressure overload, RV dilation, tricuspid regurgitation, and septal shift compressing the left ventricle — causing cardiogenic shock and cardiac arrest; mortality 40-70% without urgent thrombolysis or embolectomy. Pulmonary infarction and haemoptysis: peripheral PE with infarction causes pleuritic chest pain, haemoptysis, and occasionally pleural effusion — most infarcts heal without complications, but large infarcts can cavitate. Chronic thromboembolic pulmonary hypertension (CTEPH): the most important chronic complication — develops in 2-4% of PE survivors when thrombus fails to fully resolve, organises into fibrous material, and permanently obstructs pulmonary arterial branches; presents with progressive exertional dyspnoea and right heart failure months to years after acute PE; potentially surgically curable by pulmonary endarterectomy (PEA) — a highly specialised, high-risk procedure at designated CTEPH centres; riociguat (soluble guanylate cyclase stimulator) and balloon pulmonary angioplasty (BPA) for inoperable CTEPH. Post-thrombotic syndrome (PTS): DVT-related complication causing chronic venous insufficiency, leg oedema, pain, and venous ulceration. Anticoagulation complications: major haemorrhage (intracranial, GI, or retroperitoneal bleeding) occurs in 1-3% per year on anticoagulation — requiring urgent reversal (idarucizumab for dabigatran; andexanet alfa for factor Xa inhibitors; vitamin K + PCC for warfarin). Recurrent VTE despite anticoagulation warrants thrombophilia testing and APLS workup.

VTE prophylaxis in hospitalised patients is the most important preventive intervention. NICE recommends VTE risk assessment for all hospital admissions using the DH VTE risk assessment tool — all medical, surgical, and trauma patients should be assessed. Pharmacological prophylaxis: LMWH (enoxaparin 40 mg daily SC, or dalteparin 5000 units daily) for moderate-to-high-risk surgical and medical patients; extended prophylaxis (28 days) for major orthopaedic surgery (total hip and knee arthroplasty), abdominal-pelvic cancer surgery, and oncological patients; DOACs (rivaroxaban, apixaban) are approved for orthopaedic VTE prophylaxis. Mechanical prophylaxis: graduated compression stockings (TED stockings) and intermittent pneumatic compression (IPC) devices — used alongside or instead of pharmacological prophylaxis; IPC reduces DVT risk by 50-60% in high-risk surgical patients. Long-haul air travel: increase hydration, avoid alcohol, perform calf exercises and walk during flight; below-knee compression stockings for journeys above 4 hours; consider LMWH for very high-risk travellers (previous VTE, known thrombophilia, active cancer, recent surgery). Combined oral contraceptive pill: switch to progestogen-only pill or other contraception in women with VTE risk factors — particularly those with known thrombophilia. Extended DOAC therapy: patients with unprovoked VTE, cancer-associated VTE, or thrombophilia benefit from extended anticoagulation reducing recurrence risk by 80-90%; regular reassessment of risk-benefit at 3-6 months.

Pulmonary embolism is a medical emergency that can be rapidly fatal — prompt diagnosis and treatment are life-saving. Call 999 or go to the Emergency Department immediately for: sudden onset breathlessness or worsening breathlessness without explanation; sharp chest pain particularly worsening on breathing (pleuritic); haemoptysis (blood in sputum or coughing blood); collapse, syncope, or loss of consciousness; rapid or irregular heartbeat associated with breathlessness; severe breathlessness in a patient who is pregnant, postpartum, recently had surgery, is on the combined oral contraceptive pill, has active cancer, or has had prolonged immobility. Do not wait to see if symptoms improve — untreated massive PE can cause death within minutes. Also seek urgent medical assessment for: a swollen, red, painful, warm leg — this may represent DVT which can progress to PE if untreated; unexplained breathlessness in a patient with known malignancy or recent orthopaedic surgery; and breathlessness in a patient with a family history of VTE or known thrombophilia. After a PE is treated, report persistent or worsening breathlessness to your respiratory physician — this may indicate CTEPH requiring specialist investigation.