Internal Medicine & Pulmonology & Emergency Medicine
Pulmonary embolism
Pulmonary embolism (PE) is an acute obstruction of one or more pulmonary arteries by thrombotic material—in more than 90% of cases, a thrombus originating from deep vein thrombosis (DVT) of the lower extremities or pelvis. Together with DVT, it constitutes the two clinical manifestations of venous thromboembolism (VTE), a unified pathophysiological entity. PE is the third leading cause of cardiovascular mortality after myocardial infarction and stroke, with an estimated incidence of 60 to 70 cases per 100,000 inhabitants per year. Its short-term mortality varies considerably depending on severity: less than 1% for low-risk PEs treated early, it reaches 30 to 50% for massive PEs with untreated cardiogenic shock. The pathophysiology is based on Virchow’s triad—venous stasis, hypercoagulability, and endothelial injury—and the resulting pulmonary arterial obstruction leads to increased pulmonary vascular resistance → right ventricular (RV) dilation and dysfunction → reduced cardiac output → hypoxemia due to shunting and increased ventilatory dead space → shock if the obstruction is massive. Risk stratification upon admission—distinguishing high-risk PE (shock or hypotension), intermediate-risk (RD dysfunction without shock), and low-risk cases—is fundamental because it determines the urgency and intensity of treatment.
Clinical presentation, risk factors, and diagnostic approach
- Clinical Presentation — From Common Syndrome to Life-Threatening Emergency: sudden unexplained dyspnea (the most common symptom—80% of cases); pleural chest pain (reactive pleurisy—peripheral pulmonary infarction—50% of cases); sinus tachycardia (>100 bpm—most common physical sign); hemoptysis (hemorrhagic pulmonary infarction—10–15% of PE cases); syncope or presyncope (massive PE—acute right ventricular dysfunction—10% of PE cases); signs of concomitant DVT (pain + unilateral calf edema — 30% of PE cases); insidious forms: progressive exertional dyspnea, unexplained tachycardia, exacerbation of heart failure or COPD — PE should be considered in any unexplained cardiorespiratory presentation
- Key risk factors: recent major surgery (<3 months—especially orthopedic: total hip or knee replacement—risk × 40–60 without prophylaxis); prolonged immobilization (bed rest >3 days, air travel >8 hours, limb paralysis); active cancer (paraneoplastic hypercoagulability—risk × 4–6—20% of PE cases have underlying cancer); pregnancy and postpartum (risk × 4–5—PE is the leading cause of direct maternal mortality in Canada); combined oral contraceptives (risk × 3–4—especially if smoking + obesity); history of VTE (risk of recurrence: 10% at 1 year, 30% at 5 years); hereditary thrombophilia (Factor V Leiden, prothrombin G20210A mutation, protein C/S or antithrombin deficiency) or acquired thrombophilia (antiphospholipid syndrome); obesity (BMI >30); chronic heart or respiratory failure; central venous catheter
- Wells Score and Pretest Probability Stratification clinical signs of DVT (3 pts) + PE more likely than the alternative diagnosis (3 pts) + heart rate >100 bpm (1.5 pts) + immobilization or surgery within 4 weeks (1.5 pts) + history of DVT/PE (1.5 pts) + hemoptysis (1 pt) + active cancer (1 pt); score <2 = low probability; score 2–6 = moderate probability; score >6 = high probability; PERC rule (Pulmonary Embolism Rule-out Criteria): if all 8 PERC criteria are negative in a patient with low pretest probability → PE ruled out without D-dimer testing (age <50 years + HR <100 bpm + SpO₂ ≥95% + no DVT + no hemoptysis + no recent use of estrogen + no history of DVT/PE + no recent surgery or trauma requiring hospitalization)
- Diagnostic workup : D-dimers (high-sensitivity ELISA): reference value <500 µg/L — negative predictive value >99.1% if pretest probability is low or moderate → negative D-dimers = PE ruled out; age-adjusted threshold: in those >50 years old, use age × 10 µg/L as the threshold (reduces false positives without loss of sensitivity — Douma 2010 BMJ); Positive D-dimers or high probability → chest CT angiography (CTA): gold standard — sensitivity 83–100% (%), specificity 89–98% (%) — visualizes clots down to the segmental arteries; V/Q (ventilation/perfusion) lung scintigraphy: alternative to CT angiography if contraindicated for iodine (allergy, severe chronic kidney disease) + in pregnant women (lower breast radiation exposure) + if chronic post-embolic pulmonary hypertension (CPEH) is suspected; lower extremity venous ultrasound (proximal DVT): useful adjunct if CT angiography is inconclusive; ECG: sinus tachycardia (most common sign) + S1Q3T3 (15 % — not very specific) + incomplete BBD + T-wave inversion in V1–V4 (right ventricular overload); echocardiography (ETT): assessment of RV function (dilatation + hypokinesis + McConnell’s sign) + estimation of PAPS + search for in situ thrombus + hemodynamic status → essential in high-risk PE
Treatment
| Treatment | Mechanism, diagram, and terms | Duration, effectiveness, and precautions |
|---|---|---|
| Anticoagulation — standard treatment Acute Coronary Syndrome on 1st line - heparin if high risk or pregnant |
Direct Oral Anticoagulants (DOACs) — ESC 2019 first-line treatment / Thrombosis Canada for non-massive PE: rivaroxaban (Xarelto) 15 mg BID for 21 days then 20 mg QD (high-dose initial regimen without prior heparin); apixaban (Eliquis) 10 mg BID for 7 days then 5 mg BID (same principle – without prior heparin); dabigatran (Pradaxa) 150 mg BID after 5–10 days of initial heparin; edoxaban (Lixiana) 60 mg QD after 5–10 days of initial heparin; low molecular weight heparin (LMWH) + vitamin K antagonist (warfarin): classic treatment still used if DOACs are contraindicated (severe CKD GFR <30 + active cancer + pregnancy + antiphospholipid syndrome) — LMWH: enoxaparin (Lovenox) 1 mg/kg SC BID or 1.5 mg/kg QD; tinzaparin 175 IU/kg QD — warfarin: target INR 2–3 — overlap LMWH + warfarin until 2 consecutive INRs ≥2 at 24h interval; IV unfractionated heparin (UFH): indicated for high-risk PE or severe renal impairment — bolus 80 IU/kg + continuous infusion 18 IU/kg/h — target aPTT 60–100 sec (1.5–2.5 × control) | DOACs are superior to warfarin for PE (40–50% reduction in bleeding risk with non-inferior anticoagulant efficacy—van Es 2014 meta-analysis, Lancet Haematol); contraindications for DOACs: eGFR <15–30 mL/min (depending on the drug) + pregnancy + breastfeeding + antiphospholipid syndrome (IgG and IgM positive — increased risk of recurrence with DOACs vs. warfarin — ESC/ISTH recommendation) + active cancer (LMWH or rivaroxaban/apixaban according to the CARAVAGGIO/SELECT-D study) ; reversibility: andexanet alfa (Andexxa) for rivaroxaban/apixaban + idarucizumab (Praxbind) for dabigatran — available in hospitals for major bleeding; Duration of anticoagulation depending on the context: PE caused by a major reversible transient factor (surgery, immobilization) → 3 months; unprovoked PE (idiopathic) → minimum 3 months followed by reassessment of the risk of recurrence vs. hemorrhage; PE in active cancer → indefinite duration as long as the cancer is active |
| Systemic thrombolysis Massive pulmonary embolism with shock - life-threatening emergency |
Formal indication: High-risk PE with cardiac arrest + hemodynamic instability (SBP 15 min otherwise unexplained + cardiogenic shock with signs of organ failure); agent: alteplase (tPA — Activase) 100 mg IV over 2 hours (10 mg IV bolus over 1–2 min + 90 mg IV over 2h) — ESC 2019 reference protocol; in case of cardiac arrest: alteplase 50 mg IV bolus + external chest compressions for a minimum of 90 min (lyse the thrombus during resuscitation); absolute contraindications: hemorrhagic stroke or ischemic stroke <3 months + recent intracranial or spinal surgery + recent severe head trauma + active non-compressible bleeding; relative contraindications (to be weighed against life risk): major surgery <3 weeks + recent gastrointestinal bleeding <1 month + pregnancy + thrombocytopenia 180/110); after thrombolysis: resume anticoagulation with IV UFH without bolus upon completion of infusion (aPTT <80 sec before resuming) or as soon as aPTT <2 × control if infusion stopped | Systemic thrombolysis reduces mortality by 50–60% in massive ischemic stroke with shock (Marti meta-analysis, 2015 — NNT ≈ 8 to prevent one death) at the cost of a major bleeding risk of 10–20 per 1,000 (hemorrhagic stroke 1–3 per 1,000); in high-intermediate-risk PE (right ventricular dysfunction + elevated troponin) without shock — rescue thrombolysis: reserved for hemodynamic deterioration while on anticoagulation alone (PEITHO trial 2014 — reduction in early complications but excess hemorrhagic strokes with systematic thrombolysis); low-dose thrombolysis: alteplase 50 mg over 2 hours (MOPETT study 2013 — submassive PE — reduction in PAPS and HPEC at 28 months — limited data); the decision to perform thrombolysis in intermediate PE must be individualized — consultation between emergency physician, intensivist, and pulmonologist |
| Surgical embolectomy and catheter-directed Alternatives to systemic thrombolysis |
Surgical embolectomy under CPB: indicated if thrombolysis is contraindicated or has failed + massive PE with shock + thrombus in situ in the right heart + patent foramen ovale with paradoxical emboli — emergency cardiothoracic surgery + cardiopulmonary bypass (ECC) + pulmonary artery thrombus extraction — success rate 80–90% in expert centers — operative mortality 20–30% (versus >50% without treatment); catheter-directed thrombolysis (EKOS + CDT): multi-lumen catheter positioned in the pulmonary artery via a percutaneous approach (femoral vein → OD → PA) — local infusion of low-dose alteplase (1 mg/h/catheter × 12–24 h) ± low-frequency ultrasound (EKOS system — ULTIMA trial 2014 — SEATTLE II 2015 — reduction in mean PAP + improvement in RV/LV ratio at 24 hours without excessive bleeding vs. systemic thrombolysis); catheter-directed thrombus aspiration (Penumbra Indigo, AngioVac): less well-evaluated option — specialized centers; caval filters (filter in the inferior vena cava): indicated if PE is confirmed + anticoagulation is strictly contraindicated (major active bleeding) or recurrence of PE despite optimal anticoagulation — retrievable filters preferred over permanent ones — removal as soon as anticoagulation is possible | PERT (Pulmonary Embolism Response Teams) — interdisciplinary teams available in several university hospitals in Quebec (CHUM, MUHC, IUCPQ) — allow for rapid, collaborative decision-making (emergency physician + pulmonologist + hematologist + cardiologist + vascular surgeon) for high- and intermediate-high-risk PEs — their implementation is associated with reduced in-hospital mortality in several cohorts; permanent vena cava filters increase the long-term risk of DVT (Decousus PREPIC trial 1998) and are not a substitute for anticoagulation — their indication should be regularly reassessed with removal if possible; CPAP and non-invasive ventilation can worsen the hemodynamic status in massive PEs (increased RV afterload) — prioritize high-flow O₂ or orotracheal intubation with protective settings (avoid high pressures). |
| Duration of anticoagulation and prevention of recurrence Individualized decision — bleeding benefit/risk balance |
Context-based decision algorithm: PE caused by a major transient surgical factor (surgery ≥30 min + general anesthesia + bed rest >3 days) → stop at 3 months — low risk of recurrence (3 % at 5 years); PE caused by a minor transient factor (travel, brief immobilization, contraceptives) → 3 months — intermediate risk (15 % at 5 years); Unprovoked PE (idiopathic — no identified triggering factor) → minimum 3 months, followed by assessment of the benefit-risk ratio of prolongation — HERDOO2 score in women (hyperpigmentation + edema + lower limb erythema + post-anticoagulation D-dimers + obesity + age ≥65 years) — HAS-BLED score for bleeding risk — ESC recommendation: indefinite prolonged anticoagulation if low bleeding risk + first unprovoked episode + no contraindications; PE in active cancer → LMWH or apixaban/rivaroxaban (CARAVAGGIO 2020 — HOKUSAI VTE Cancer) as long as cancer is active or being treated; major thrombophilia (antiphospholipid syndrome, antithrombin deficiency) → indefinite anticoagulation; recurrent PE → indefinite anticoagulation unless major bleeding risk | Unprovoked PE recurs in 30–50% of cases at 10 years without prolonged anticoagulation—the decision to discontinue anticoagulation at 3 months should be made in consultation with the patient (preferences + individual bleeding risk + quality of life on anticoagulation); reduced dose after 6 months: apixaban 2.5 mg twice daily (AMPLIFY-EXT trial — 67% reduction in recurrences vs. placebo) or rivaroxaban 10 mg once daily (EINSTEIN CHOICE — 74% reduction vs. aspirin) — options for indefinite continuation with lower bleeding risk; aspirin alone (100 mg × 1/day) is insufficient to prevent PE recurrence (only a 30% reduction — ASPIRE/WARFASA) vs. reduced-dose OAC — do not use aspirin as an alternative to anticoagulants; post-anticoagulation D-dimer testing (1 month after discontinuation): Positive D-dimer levels → doubled risk of recurrence → strong argument for extending anticoagulation (DOLORES/PROLONG study) |
| Outpatient management and post-embolic pulmonary hypertension Low-risk EP — long-term sequelae |
Outpatient treatment or early discharge from the emergency department for low-risk cases: simplified PESI (Pulmonary Embolism Severity Index) score = 0 (age <80 years + no cancer + HR <110 + SVR ≥100 + SpO₂ ≥90 % + no heart failure or COPD) → low-risk PE → outpatient treatment possible + ACOD immediately; Hestia criteria (12 exclusion criteria for outpatient treatment) — if all negative → discharge possible; 30-day recurrence and mortality rates for outpatient treatment of low-risk PE: <1–2% (Aujesky 2011 Lancet — non-inferior to hospitalization); chronic thromboembolic pulmonary hypertension (CTEPH): long-term sequela — organized thrombus + pulmonary vascular remodeling → progressive obstruction of the pulmonary arteries → pulmonary hypertension (mean PAP >25 mmHg on right heart catheterization) — incidence: 0.5–3.8 per 1,000 PE cases at 2 years; presentation: progressive exertional dyspnea + exercise intolerance + signs of chronic cor pulmonale; diagnosis: V/Q scan (first step — high sensitivity) + CT angiography + pulmonary catheterization; standard surgical treatment: pulmonary endarterectomy (PEA) — Jamieson procedure — expert centers (Toronto General Hospital — top Canadian center) + riociguat (Adempas — soluble guanylate cyclase stimulator) if inoperable or residual HPTEC post-PEA | HPTEC is underdiagnosed—any patient with PE and persistent dyspnea lasting >3 months who is on optimal anticoagulation should undergo a screening V/Q scan; PAH is curable in 70–80% of operable cases (normalization of pulmonary pressures)—operative mortality is 2–5% in expert centers; riociguat (Adempas) is the only drug treatment approved by Health Canada for inoperable HPTEC—reimbursed by RAMQ under certain conditions; cardiopulmonary rehabilitation after PE is recommended for patients with persistent deconditioning or CTEPH — improves functional capacity and quality of life; 6-minute walk test (6MWT) + echocardiography + NT-proBNP: follow-up evaluations at 3 and 6 months after PE to screen for CTEPH and assess RV recovery |
ℹ️
Thrombophilia testing - when to prescribe it: A thrombophilia workup (Factor V Leiden, prothrombin G20210A mutation, protein C, protein S, antithrombin, antiphospholipid antibodies—lupus anticoagulant + anticardiolipin IgG/IgM + anti-beta2-GP1) is recommended in cases of unprovoked PE before age 50, a first-degree family history of VTE, recurrent PE or DVT, thrombosis in an unusual site (mesenteric, caval, cerebral veins), or suspected antiphospholipid syndrome. It should be performed at least 3 months after the acute event and at a distance from anticoagulation (warfarin falsely alters protein C and S levels; DOACs can interfere with some functional coagulation tests). A positive result modifies the duration of anticoagulation but should not delay treatment of the acute event.
Emergency — Massive pulmonary embolism and shock
Dial 911 immediately if: Sudden severe shortness of breath + chest pain + SpO₂ <90% 1–3 minutes + tachycardia >120 bpm pulmonary embolism until proven otherwise — transfer to ER.
Hypotension (SBP < 90 mmHg) + syncope + signs of shock (pallor, mottling, altered consciousness) in this context → massive PE → emergency thrombolysis or surgical embolectomy for life-threatening condition — high-flow O₂ + IV access + call for resuscitation team.
Patient known for anticoagulation for PE with sudden respiratory worsening → Embolic recurrence or bleeding on anticoagulation - urgent evaluation.
Consult at Clinique Omicron
Clinique Omicron physicians evaluate patients presenting with symptoms suggestive of pulmonary embolism (unexplained shortness of breath, chest pain, tachycardia), apply validated diagnostic algorithms (Wells score, D-dimers, CT angiography referral), initiate anticoagulation, and provide outpatient follow-up for low-risk PEs treated at home. Post-PE follow-up, including monitoring for CTEPH and optimal anticoagulation duration, is coordinated with the pulmonology and internal medicine teams. Consultations are available at our service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not substitute for the advice of a qualified healthcare professional. Any suspicion of pulmonary embolism constitutes a medical emergency requiring immediate hospital evaluation.
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