2026 Guidelines for Pulmonary Embolism
Diagnosis
Clinical Probability Assessment
Use a validated prediction rule (Wells or revised Geneva score) to stratify every patient with suspected PE into low, intermediate, or high clinical probability before ordering any tests. 1, 2
Immediately assess for hemodynamic instability—defined as shock, cardiac arrest, obstructive shock (systolic BP <90 mmHg with vasopressor requirement), or persistent hypotension (systolic BP <90 mmHg or drop ≥40 mmHg lasting >15 minutes not caused by arrhythmia, hypovolemia, or sepsis)—to identify high-risk PE requiring urgent reperfusion therapy 1, 2
The revised Geneva score assigns points for: previous PE/DVT (3 points), heart rate 75-94 bpm (3 points) or ≥95 bpm (5 points), surgery/fracture within past month (2 points), hemoptysis (2 points), active cancer (2 points), unilateral leg pain (3 points), pain on deep venous palpation with unilateral edema (4 points), and age >65 years (1 point) 1
Low probability = 0-3 points; intermediate = 4-10 points; high ≥11 points on the original Geneva score 1
D-dimer Testing
Measure D-dimer only in patients with low or intermediate clinical probability (or "PE unlikely") using a highly sensitive assay; do not measure D-dimer in high-probability patients because a normal result does not safely exclude PE. 1, 2
A normal D-dimer in low- or intermediate-probability patients permits exclusion of PE without further imaging 2
Age-adjusted D-dimer cut-offs (age × 10 µg/L for patients >50 years) can be used as an alternative to the fixed cut-off value 1
Imaging Strategy
Computed tomography pulmonary angiography (CTPA) is the first-choice imaging test for hemodynamically stable patients with elevated D-dimer or high clinical probability. 1, 2
Accept a PE diagnosis when CTPA shows a segmental or more proximal filling defect in patients with intermediate or high clinical probability 1, 2
Reject a PE diagnosis when CTPA is normal in patients with low or intermediate clinical probability 1, 2
For suspected high-risk PE, perform bedside echocardiography or emergency CTPA depending on local availability and patient stability 2, 3
Ventilation-perfusion (V/Q) scintigraphy is a valid alternative when CTPA is contraindicated (e.g., contrast allergy, renal impairment); a normal perfusion scan excludes PE 1, 2
Do not use magnetic resonance angiography to rule out PE 1, 2
A proximal deep-vein thrombosis identified by compression ultrasound in a patient with suspected PE confirms venous thromboembolism and justifies anticoagulation 1, 2
Avoiding Overuse of Testing
- The Pulmonary Embolism Rule-out Criteria (PERC)—age <50 years, pulse <100 bpm, SaO₂ >94%, no unilateral leg swelling, no hemoptysis, no recent trauma/surgery, no history of VTE, and no oral hormone use—can identify emergency department patients with such low PE probability that diagnostic workup should not be initiated 1
Risk Stratification
High-Risk PE
High-risk PE is defined by the presence of shock, cardiac arrest, obstructive shock, or persistent hypotension and carries early mortality potentially exceeding 30%. 1, 3, 4
These patients require immediate reperfusion therapy (systemic thrombolysis or surgical embolectomy) 3, 4
Confirmation can be made with bedside echocardiography showing right ventricular (RV) dysfunction or emergency CTPA 3
Intermediate-Risk PE
Intermediate-risk PE comprises hemodynamically stable patients with evidence of RV dysfunction (on echocardiography or CTPA) and/or elevated cardiac biomarkers (troponin, BNP/NT-proBNP). 1, 3
Intermediate-high risk: both RV dysfunction and biomarker elevation present 3
Intermediate-low risk: only one of the two markers present 3
These patients require hospitalization with close monitoring and rescue thrombolysis if clinical deterioration occurs 3, 4
Low-Risk PE
Low-risk PE is characterized by hemodynamically stable patients without RV dysfunction or myocardial injury markers, with mortality <1%. 3, 4
The Pulmonary Embolism Severity Index (PESI) or simplified PESI (sPESI) should be used to identify patients suitable for outpatient management 3, 4, 5
PESI class I/II or sPESI score of 0 identifies low-risk patients who are candidates for early discharge or outpatient treatment 3, 5
Key PESI predictors include age, cancer, systolic BP <100 mmHg, altered mental status, heart rate >110/min, and SaO₂ <90% 4, 5
Acute-Phase Treatment
High-Risk PE Management
Initiate intravenous unfractionated heparin (UFH) without delay using a weight-adjusted bolus (80 units/kg or 5,000-10,000 units) followed by continuous infusion (18 units/kg/hour or 30,000-40,000 units/24 hours), even before imaging confirmation. 2
Maintain activated partial thromboplastin time (aPTT) at 1.5-2.5 times control, measured 4-6 hours after initiation 2
Administer systemic thrombolytic therapy immediately to all high-risk PE patients who do not have a high bleeding risk. 1, 2, 3
Alteplase (rtPA) is the preferred agent: 100 mg infused over 2 hours, or 0.6 mg/kg over 15 minutes (maximum 50 mg) 2
Thrombolysis reduces mortality or recurrence in massive PE (OR 0.45; 95% CI 0.22-0.92) but carries a 21.9% major bleeding risk versus 11.9% with heparin alone 2
In life-threatening PE, traditional contraindications to thrombolysis should be ignored; the mortality benefit supersedes bleeding concerns. 2
Surgical pulmonary embolectomy is indicated when thrombolysis is absolutely contraindicated or fails to improve hemodynamics within one hour 1, 2
Catheter-based embolectomy or thrombus fragmentation may be considered when surgery is unavailable 2
Provide rescue thrombolysis if hemodynamic deterioration occurs despite anticoagulation 1, 2
Hemodynamic Support
Administer high-flow oxygen for hypoxemia correction 2
Use vasopressor agents (norepinephrine preferred) for hypotensive patients 2
Dobutamine and dopamine may be used in patients with low cardiac output and normal blood pressure 2
Avoid aggressive fluid challenges—this worsens right ventricular failure. 2, 4
Avoid diuretics and vasodilators as they may precipitate cardiovascular collapse 2
Intermediate- and Low-Risk PE Management
Start anticoagulation immediately in patients with high or intermediate clinical probability while diagnostic work-up proceeds. 1, 2
For parenteral anticoagulation in hemodynamically stable patients, prefer low-molecular-weight heparin (LMWH) or fondaparinux over UFH 1, 2
Do not use systemic thrombolysis as routine primary treatment in intermediate- or low-risk PE. 1, 2, 4
Rescue thrombolysis should be considered if hemodynamic deterioration occurs despite anticoagulation 4
Oral Anticoagulation Selection
Prefer a non-vitamin-K oral anticoagulant (NOAC)—apixaban, rivaroxaban, edoxaban, or dabigatran—over a vitamin K antagonist (VKA) when initiating oral therapy. 1, 2, 4, 6
NOACs offer simplified dosing without need for routine laboratory monitoring and have a potentially improved safety profile compared to traditional anticoagulants 6
If a VKA (warfarin) is chosen, overlap with parenteral anticoagulation until the INR reaches 2.0-3.0 on two consecutive measurements taken at least 24 hours apart (target INR 2.5) 1, 2
Do not use NOACs in patients with severe renal impairment (creatinine clearance <25-30 mL/min) or antiphospholipid antibody syndrome; these patients must receive a VKA indefinitely. 1, 2
For cancer-associated PE, edoxaban or rivaroxaban should be considered as alternatives to LMWH, with caution in gastrointestinal cancers due to increased bleeding risk 1, 4
During pregnancy, use therapeutic fixed-dose LMWH based on early-pregnancy weight; NOACs are contraindicated in pregnancy and lactation 1, 2
Duration of Anticoagulation
All patients with PE require therapeutic anticoagulation for a minimum of 3 months, followed by mandatory reassessment at 3-6 months to decide on continuation. 1, 2
Provoked PE
Discontinue anticoagulation after 3 months in patients whose first PE was provoked by a major transient/reversible risk factor (e.g., surgery, trauma, immobilization, pregnancy). 1, 2
Unprovoked PE
Extend anticoagulation indefinitely beyond 3 months for unprovoked PE when bleeding risk is low-to-moderate; the annual recurrence risk exceeds 5% and outweighs bleeding risk. 1, 2
The 2019 ESC guideline no longer supports terminology such as "provoked" versus "unprovoked" PE/VTE, as it is potentially misleading; instead, classify risk factors as high, intermediate, or low recurrence risk 1
A reduced dose of apixaban (2.5 mg twice daily) or rivaroxaban (10 mg daily) for extended anticoagulation should be considered after the first 6 months of treatment 1
Recurrent VTE
Continue oral anticoagulation indefinitely in patients with recurrent VTE (≥1 prior episode of PE or DVT) not related to a major transient risk factor. 1, 2
Antiphospholipid Antibody Syndrome
Continue VKA therapy indefinitely in patients with antiphospholipid antibody syndrome; NOACs are contraindicated. 1, 2
Monitoring During Extended Therapy
Re-assess patients at 3-6 months and then yearly for drug tolerance, adherence, hepatic/renal function, and bleeding risk 1, 2
VTE recurrence scores and bleeding scores should be used in parallel to guide decisions about extended anticoagulation 1
Inferior Vena Cava (IVC) Filter Placement
Do not routinely place IVC filters; reserve them only for patients with absolute contraindications to anticoagulation (e.g., active major bleeding) or who experience recurrent PE despite adequate anticoagulation. 1, 2
Follow-Up and CTEPH Screening
Re-examine all patients 3-6 months after acute PE to evaluate persistent dyspnea, functional limitation, signs of VTE recurrence, cancer, or bleeding complications. 1, 2
An integrated model of patient care after PE is proposed to ensure optimal transition from hospital to community care 1
If persistent or new-onset dyspnea or functional limitation is present at the 3-6 month review, perform ventilation-perfusion (V/Q) scintigraphy to detect mismatched perfusion defects suggestive of chronic thromboembolic pulmonary hypertension (CTEPH) 1, 2
Refer symptomatic patients with persistent perfusion defects to a specialized CTEPH center, considering echocardiography, natriuretic peptide levels, and/or cardiopulmonary exercise testing results 1, 2
Schedule regular follow-up visits at yearly intervals for patients on extended anticoagulation 2
Follow-up imaging is not routinely required in asymptomatic patients but may be considered in those with risk factors for CTEPH (unprovoked PE, large perfusion defects, RV dysfunction, hypothyroidism, diabetes) 2
Critical Pitfalls to Avoid
Never delay anticoagulation in high- or intermediate-probability PE while awaiting diagnostic confirmation. 1, 2
Never measure D-dimer in high-clinical-probability patients; proceed directly to imaging. 1, 2
Never use NOACs in severe renal impairment (<25-30 mL/min) or antiphospholipid antibody syndrome; VKA is mandatory. 1, 2
Never discontinue anticoagulation at 3 months in unprovoked PE without weighing bleeding risk; the annual recurrence exceeds 5%. 2
Never lose patients to follow-up after acute PE; routine reassessment at 3-6 months is essential for detecting CTEPH and guiding anticoagulation duration. 1, 2
Never ignore persistent dyspnea, as it may indicate CTEPH requiring specialized evaluation. 1, 2
Never withhold thrombolysis in massive PE solely because of relative contraindications; contraindications should be set aside in life-threatening situations. 2
Never use aggressive fluid resuscitation in high-risk PE; this worsens right ventricular failure. 2, 4