ESC Guidelines for Acute Pulmonary Embolism

Guidelines Summarised by Mr John Tsao, Yong Loo Lin School of Medicine, NUS


Article Reference: 2019

ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Konstantinides et al. EHJ 2019

The updated 2019 guidelines for the adult management of acute pulmonary embolism (PE) detail new recommendations layering on established practices from the 2014 version published by the European Society of Cardiology (ECS) in collaboration with the European Respiratory Society (ERS).

Understanding of predisposing factors for venous thromboembolism (VTE) is essential for identifying the at-risk patient profiles. VTE arises as a result of patient related and setting related factors, and these risks can be classified into high, moderate and low risk factors.

Initial risk assessment is recommended to allow clinicians to identify PE in suspected high-risk cases and guide immediate treatment. High-risk PE is often associated with the presence of right ventricular dysfunction. The presence of hemodynamic instability is associated with poor outcomes. CTPA remains the gold standard for diagnosis of acute pulmonary embolism, however, in patients who cannot be transported due to significant hemodynamic instability, bedside echocardiography demonstrating echo signs of RV dysfunction or the rare finding of clot in transit can be used to initiate emergent reperfusion therapy.

In other cases, the use of clinical judgement or standardized prediction rules for pre-test probability (Revised Geneva and Wells Rule) should continue to be used to assist the clinician in their diagnostic algorithm. The Pulmonary Embolism Rule-out Criteria (PERC) can also be used in decision-making for further work-up.


According to the prediction probability, investigations outlined below can be employed to finalize the diagnosis of PE.

  • Low to Intermediate probability (PE-unlikely)
    • D-Dimer testing is recommended with age-adjusted cut-offs (age x 10 ug/L in > 50 years old) and correlations to clinical probability (YEARS model).
      • Negative D-Dimer: Exclusion
      • Positive D-Dimer: Require further testing
    • High probability (PE-likely)
      • D-Dimer testing not recommended.
      • Computed tomographic pulmonary angiography (CTPA) is the gold standard for visualization of pulmonary vasculature.
        • Concordance
          • Unlikely PE with negative CTPA: Exclusion
          • Likely PE with positive CTPA: Diagnosis of PE
        • Discordance
          • Unlikely PE with positive CTPA: Further testing required
          • Likely PE with negative CTPA: Further testing required
        • Additional diagnosis of chronic thromboembolic pulmonary hypertension (CTPEH) must not be missed (supplementary data table 2)
      • Alternative testing that may be contextually effective.
        • Lung scintigraphy (Planar V/Q scan) preferred in patients with low pre-test probability and contraindications to contrast and radiation (table 6 provides updates information on radiation dosage). The recruitment of single-photon emission CT (SPECT) imaging may be useful in reducing inconclusive results.
          • Normal scan: Exclusion
          • Nondiagnostic scan combined with negative proximal CUS in unlikely PE: Exclusion
          • High probability scan: Diagnosis of PE
        • Lower-limb compression ultrasonography (CUS) is also preferred in patients with CT contraindications in the diagnosis of deep vein thrombosis and indirect confirmation of PE.
          • Positive proximal result: Diagnosis of VTE (and PE) requiring PE severity assessment
          • Positive distal result: Further testing required
        • Other testing not recommended currently due to major limitations.
          • Pulmonary angiography
          • Magnetic resonance angiography (MRA)
          • CT venography

Advanced risk stratification is applied to patients with confirmed PE that were not identified as high-risk in the earlier stages to further guide respective management. It adopts 2 main prognostic themes for consideration:

  1. Indicators relating to presence of RV dysfunction
  • Clinical parameters (i.e. tachycardia, low systolic BP, respiratory insufficiency and syncope)
  • Imaging findings (echocardiography and CTPA findings featured in supplementary data table 3)
  • Laboratory biomarkers (i.e. elevated concentrations of cardiac troponin I or T, H-FABP, BNP, NT-proBNP, lactate and copeptin including acute kidney injury signs such as raised serum creatinine and lower GFR)
  • Combination of factors using validated scores (Bova and FAST score)
  1. Baseline comorbidity and other aggravating conditions
  • Pulmonary Embolism Severity Index

Overall prognostic classification of PE severity and risk of early mortality with the integration of the two themes are summarized below. This is contiguous with the revised management algorithm according to severity.



In the resuscitation of a PE patient, the first step in management focuses on hemodynamic and respiratory support.


Oxygen supplementation is necessitated where saturations are reduced (less than 90% SaO2). Escalating to higher oxygen flow and even mechanical ventilation in refractory cases may be required. Non-invasive ventilation is preferred due to the adverse hypotensive effect from invasive techniques. Caution should be taken to reduce positive end-expiratory pressure (ideally <30 cm H2O) with low tidal volumes (6 mL/kg lean body weight).

A treatment strategy for RV failure should be kept in mind and rapidly executed when such cases are encountered.

Advanced life support guidelines should be followed in cases of cardiac arrest with attention to the early diagnosis and decision to treat PE via thrombolysis. The temporary use of mechanical cardiopulmonary support such as ECMO is increasingly being observed, but more studies to prove benefit are required.

Initial anticoagulation is given as a rapid temporizing measure pending diagnostic test results especially in PE-likely patients. A summary of the drugs used is given below:




Subcutaneous low-molecular weight heparin (LMWH) or fondaparinux


*Supplementary table 5 for dosage

– Preferred for most patients due to lower risks and need for monitoring i.e. bleeding, heparin-induced thrombocytopenia

Intravenous unfractionated heparin (UFH)


*Supplementary table 7 for dosage

– High risk cases with hemodynamic instability requiring primary reperfusion treatment

– Indicated for severe renal impairment (CrCl ≤30 mL/min*) and severe obesity


Non-vitamin K antagonist oral anticoagulant (NOAC)


*Characteristics of agents in supplementary table 6

– Preferred for most patients due to similar efficacy with less risks compared to VKA

Vitamin K antagonist (VKA)


*requires overlap with parenteral anticoagulation until INR-adjusted to 2.0-3.0

– Gold standard of oral anticoagulation

– Indicated for severe renal impairment, pregnancy and lactation, and antiphospholipid syndrome


Reperfusion treatment enhances recovery and reversal of effects of PE especially in high-risk patients but is not recommended in low to intermediate risks.



Systemic thrombolysis


*Regimens and contraindications to fibrinolysis summarized in table 10

– IV alteplase (rTPA) preferred to prolonged infusions of streptokinase and urokinase

Percutaneous catheter-directed treatment


– Alternative option if systemic thrombolysis fails

– Some evidence of support for combined treatment with ECMO in refractory cases of hemodynamic collapse

Surgical embolectomy

Other recommendations include the setting up of a multidisciplinary response team for management of severe cases of PE to enhance clinical decision making as well as the use of IVC filters as mechanical interruption considered in patients with recent proximal DVT or prophylaxis, failed or contraindications to anticoagulation.

There are further guidelines on management provided for specific situations and resultants from pregnancy, cancer and non-thrombotic forms of pulmonary embolism. More information on chronic treatment and prevention can also be found in the main article.

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