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CMAJ : Canadian Medical Association Journal logoLink to CMAJ : Canadian Medical Association Journal
. 2026 Jul 13;198(26):E1002–E1010. doi: 10.1503/cmaj.250944

Initial management of intermediate- and high-risk pulmonary embolism

Asher A Mendelson 1,✉, Lana A Castellucci 1, Sebastian Mafeld 1, Kerstin de Wit 1; for Pulmonary Embolism Canada1
PMCID: PMC13374698  PMID: 42442786

Key points

  • Pulmonary embolism (PE) occurs when a venous thrombus becomes lodged in lung arteries, causing impairment in oxygenation, circulation, and heart function, potentially with fatal consequences.

  • Risk stratification is important to guide optimal treatment, particularly for intermediate-risk and high-risk PE, in which patients show cardiac dysfunction progressing to hemodynamic instability or cardiac arrest.

  • Patients with intermediate–high-risk and high-risk PE should receive parenteral anticoagulation; low-molecular-weight heparin is preferred over intravenous unfractionated heparin.

  • Patients with high-risk PE require further treatment with advanced therapies, including systemic thrombolysis or catheter-based therapy, which are currently underused, and a subset of patients with intermediate–high-risk PE may benefit from advanced therapies.

  • Equitable access to optimal treatment for PE across Canada should be a priority for improving population-level outcomes and mitigating disparities.

Pulmonary embolism (PE) is the third leading cause of cardiovascular death in Canada, with an annual incidence of 1 in 1000; it affects more than 46 000 people in Canada and leads to about 1 death every 8 hours.1,2 Between 9% and 11% of patients diagnosed with PE die within 30 days, with PE-related death occurring in 2% and bleeding-related death occurring in 0.5%.3–5 Pulmonary embolism occurs when a venous thrombus becomes lodged in lung arteries, usually causing impairment in oxygenation, circulation, and heart function.6,7 As many as 1% of patients who survive PE subsequently develop chronic thromboembolic pulmonary hypertension,8 and almost 50% experience chronic exertional breathlessness secondary to chronic thromboembolic disease or post-PE syndrome.9 As many as half of patients report reduced quality of life,10 with depression, anxiety, and posttraumatic stress disorder all prevalent among PE survivors.11,12

Because patients with PE present with a wide range of disease severity, risk stratification at the time of diagnosis is essential to establish a prognosis and guide therapy.13,14 The requirement for time-sensitive adjuvant interventions once anticoagulation has been initiated increases with disease severity. Selection of appropriate patients for advanced therapy (systemic thrombolysis or catheter-based therapy) is often complex, with competing risks and benefits, and lack of high-level randomized evidence to guide decision-making.

We discuss the treatment of PE following initial diagnosis confirmed with contrast-enhanced computed tomography (CT). Following a confirmed diagnosis of PE, immediate anticoagulation therapy is indicated, in concert with risk stratification to guide further management options (Figure 1, Table 1). Herein, we focus on the acute management of intermediate–high-risk (American Heart Association [AHA] categories C3, D1, and D2) and high-risk PE (AHA categories E1 and E2). We outline an approach to risk stratification based on clinical features and guidelines, and discuss the latest evidence for advanced therapies, including systemic thrombolysis and catheter-based interventions in select patients (Box 1).

Figure 1:

Figure 1:

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Approach to initial management of acute pulmonary embolism. Note: LMWH = low-molecular-weight heparin, PERT = pulmonary embolism response team. See Related Content tab for accessible version.

Table 1:

Emergency medication dosing for intermediate–high-risk and high-risk pulmonary embolism

Drug Dosing Important details
Anticoagulation *
Low-molecular-weight heparin

  • There is no preference for any type of low-molecular-weight heparin over another.

  • If high concern for bleeding, consider giving a dose every 12 h.

  • If administering systemic or catheter-directed thrombolysis, continue low-molecular-weight heparin at usual 12-h or 24-h intervals.
 Dalteparin 200 U/kg subcutaneously every 24 h or 100 U/kg subcutaneously every 12 h
 Tinzaparin 175 U/kg subcutaneously every 24 h or 88 U/kg subcutaneously every 12 h
 Enoxaparin 1 mg/kg subcutaneously every 12 h
Unfractionated heparin 80 U/kg IV bolus (maximum 5000 U), followed by IV infusion rate of 18 U/kg/h

  • Anticoagulant of preference in patients with creatinine clearance < 30 mL/min.

  • Systemic thrombolysis causes derangement in PTT and anti-Xa levels for up to 12 h, making therapeutic monitoring unfeasible.
Systemic thrombolysis
Alteplase 100 mg IV over 2 h13
0.6 mg/kg, maximum 50 mg IV over 15 min13

  • Consider for patients with low body weight or patients with an elevated risk of bleeding.

  • In setting of cardiac arrest, dosing may vary as per local institutional practice.
Tenecteplase By patient weight

  • < 60 kg: 30 mg

  • 60–70 kg: 35 mg

  • 70–80 kg: 40 mg

  • 80–90 kg: 45 mg

  • > 90 kg: 50 mg

IV push over 5–10 s

  • No study has compared alteplase versus tenecteplase.

  • May be preferred in cardiac arrest because it can be given as an IV push dose.
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Note: IV = intravenous, PTT = partial thromboplastin time.

*

Administer promptly upon confirmation of diagnosis of pulmonary embolism.

Box 1: Evidence used in this review .

We searched PubMed from 1980 to 2025 using the terms “pulmonary embolism,” “intermediate-risk,” “high-risk,” “submassive,” and “massive” with additional keywords “diagnosis,” “management,” and “treatment.” We manually searched the reference lists of relevant original articles, review articles, and practice guidelines. Emphasis was placed on evidence published within the last 15 years.

Why is risk stratification important for PE?

Intermediate–high-risk and high-risk PE are life-threatening emergencies. The main determinant of morbidity and death from acute PE is right ventricular (RV) dysfunction,15 whereby obstruction of the pulmonary arteries leads to abrupt increases in RV afterload, causing a vicious cycle of elevated RV pressure, progressive RV dilation, RV ischemia, RV systolic dysfunction, impaired left ventricular (LV) filling, and low cardiac output.16 Right ventricular dysfunction confers an elevated risk of hemodynamic deterioration, adverse events and, in its most severe form, culminates in cardiovascular collapse and death.17–19

How are intermediate–high-risk and high-risk PE defined and classified?

According to the 2019 European Society of Cardiology (ESC) guideline13 and category E in the AHA 2026 guideline,20 high-risk PE, previously referred to as “massive,” is defined by the presence of hemodynamic instability, characterized by a systolic blood pressure less than 90 mm Hg, the use of vasopressors, a persistent drop in systolic blood pressure of more than 40 mm Hg from baseline, or cardiac arrest. Intermediate-risk PE, previously referred to as “submassive” (AHA categories C2 to D2), is defined by normal blood pressure (i.e., systolic blood pressure > 90 mm Hg) with the presence of RV dysfunction at the time of diagnosis. Patients with intermediate-risk PE are categorized as intermediate–low risk (AHA category C2), based on the presence of either RV dysfunction or elevated biomarkers of cardiac injury, or intermediate–high risk if both RV dysfunction and elevated cardiac biomarkers are present (AHA categories C3, D1, and D2). In large database registries, the high-risk group comprises 5% to 10% of patients and is associated with an in-hospital mortality of 15% to 50%;21–25 when PE presents with cardiac arrest, mortality ranges from 65% to 90%.23,26,27 Short-term mortality with intermediate–high-risk PE is between 5% and 15%, and this risk group comprises approximately 35% to 55% of patients with PE.28–31

Right ventricular dysfunction is assessed with CT or echocardiography (e.g., RV-to-LV ratio ≥ 1.0 s) and general biomarkers of cardiac injury such as elevated troponin, brain natriuretic peptide (BNP), or N-terminal pro BNP (NT-proBNP) levels (Box 2).32,33 Although binary cut-off values are used to determine increased risk of death in PE, RV dysfunction and troponin levels should be viewed as continuous risk factors with graded severity of risk, rather than being normal or abnormal.34 The Pulmonary Embolism Severity Index,35 Simplified Pulmonary Embolism Severity Index,36 and Bova score37 are variably validated to predict adverse outcomes, and elevated scores are reflected in the intermediate-risk PE categories. However, in a comparative study, these models showed only moderate discrimination in identifying patients who will deteriorate into high-risk status.38

Box 2: Diagnostic criteria for intermediate-risk pulmonary embolism13 .

Imaging signs of RV dysfunction

  • CT scan

    • RV-to-LV ratio ≥ 1.0

    • Bowing or flattening of the intraventricular septum toward the LV

    • IV contrast reflux into the inferior vena cava and hepatic veins

  • Echocardiography

    • RV-to-LV ratio ≥ 1.0

    • Bowing or flattening of the intraventricular septum toward the LV

    • RV dilation (mid-cavitary diameter ≥ 35 mm)

    • Decreased TAPSE ≤ 16 mm

    • McConnel sign (hypokinesis of RV free wall with apical sparing)

    • Decreased peak systolic velocity of tricuspid annulus equal to or lesser than 9.5 cm/s

Biomarkers of cardiac injury

  • Elevated serum troponin level

  • Elevated BNP or NT-proBNP level

Intermediate–high-risk PE: both imaging and biochemical signs of RV strain

Intermediate–low-risk PE: either imaging or biochemical signs of RV strain

Note: BNP = brain natriuretic peptide, CT = computed tomography, ESC = European Society of Cardiology, IV = intravenous, LV = left ventricle, NT = N-terminal, RV = right ventricle, TAPSE = tricuspid annular plane systolic excursion.

Beyond risk stratification, what clinical features are important to guide management?

It is imperative to identify anticoagulated patients with PE of intermediate–high risk who are likely to deteriorate to determine whether they would benefit from advanced therapies. No specific tests or diagnostic criteria are currently available to identify which patients are likely to respond to anticoagulation alone. Many clinical features are not reflected in the 2019 ESC classification for intermediate–high-risk PE but have been used in clinical practice and research, and now appear in the 2026 AHA guideline for category D PE (incipient cardiopulmonary failure) (Box 3).17

Box 3: Clinical and laboratory features associated with elevated risk of deterioration and death in intermediate–high-risk pulmonary embolism .

  • Persistent tachycardia > 110 beats/min35–37

  • Borderline hypotension with SBP 90–100 mm Hg39

  • Shock index (HR divided by SBP) > 140

  • Large central clot burden (common pulmonary artery, main right or left pulmonary artery)41,42

  • Hypoxemia or rapidly escalating oxygen requirements (FiO2 > 4L NP)43

  • Presentation with syncope or pre-syncope

  • Symptoms of low cardiac output, including prolonged capillary refill, cool extremities, reduced urine output, and altered mental status44

  • Elevated lactate > 2.0 mmol/L45

Note: FiO2 = fraction of inspired oxygen, HR = heart rate, NP = nasal prongs, SBP = systolic blood pressure.

Intermediate-risk patients with signs of impaired end-organ perfusion despite normal blood pressure are at risk for deterioration. In an observational study, 34% of such patients demonstrated an invasive cardiac output measurement of 2.2 L/min/m2 or less, meeting criteria for normotensive cardiogenic shock.44 This reinforces the limitations of using systolic blood pressure as a cut-off for assessment of end-organ perfusion; even pressures of 90 to 110 mm Hg are associated with increased risk of death.39 In another study of patients with intermediate–high-risk PE, those with elevated serum lactate of 2 mmol/L or higher had a markedly higher 30-day mortality than patients with intermediate-risk PE who had normal lactate levels (16.4% v. 1.6%).45 Hypoxemia and elevated respiratory rate have also been identified as high-risk features of acute PE;43 the AHA guideline includes a “respiratory modifier” as an additional risk.

The Composite PE Shock score helps to identify normotensive shock in intermediate-risk PE. It consists of 6 features: moderate or severely reduced RV function on echocardiography, an elevated troponin level, an elevated BNP level, tachycardia greater than 100 beats/min, central clot burden (in at least 1 main pulmonary artery), and concomitant deep vein thrombosis.41,42 In a validation study,42 no patients with 1 or 2 features had normotensive shock, but having 3 or more features was associated with normotensive cardiogenic shock, with the risk increasing with each additional feature. Point-of-care ultrasonography can identify patients with PE with normotensive cardiogenic shock using a cut-off for RV outflow tract velocity time integral of 9.5 cm/s or less,46 or a cut-off for LV outflow tract velocity time integral of 15 cm/s or less.47

Other tools using vital signs, such as the National Early Warning Score, have been applied to identify patients with intermediate–high-risk PE who may be deteriorating.48,49 Clinical features are dynamic, changing over hours and days. Clinicians may find it helpful to follow these clinical and laboratory parameters (e.g., lactate and oxygen requirements) to identify patients who are deteriorating despite therapeutic anticoagulation.

How are intermediate–high-risk and high-risk PE managed?

Initial management

All patients with intermediate–high-risk and high-risk PE should receive immediate parenteral anticoagulation to reduce the risk of PE death, unless contraindicated in the case of severe active bleeding (Figure 1, Table 1).50 Parenteral anticoagulation is preferred over oral anticoagulation during the first 48 hours of admission to hospital. In the case of clinical deterioration, systemic thrombolysis can be administered in addition to therapeutic dose anticoagulation, even when low-molecular-weight heparin was used as the initial parenteral therapy.

The ESC and AHA guidelines recommend low-molecular-weight heparin as first-line therapy over unfractionated heparin for parenteral anticoagulation in intermediate-risk and high-risk PE (AHA categories C to E).13,20 An observational study of 505 patients with a PE receiving unfractionated heparin found that fewer than 50% of patients achieved therapeutic anticoagulation within the initial 48 hours of heparin infusion, with both supra- and subtherapeutic activated partial thromboplastin time (aPTT) values occurring in all patients for at least 1 time point.51 Another retrospective study found that enoxaparin use was associated with reduced mortality for intermediate-risk and high-risk PE compared with unfractionated heparin.52 A 2017 Cochrane review of 29 randomized controlled trials (RCTs) for acute venous thromboembolism (VTE) (n = 10 390, including PE and deep vein thrombosis) found that fixed-dose low-molecular-weight heparin resulted in lower rates of VTE recurrence at 3 months, reduced thrombus size, and lower rates of major hemorrhage when compared with adjusted-dose unfractionated heparin.53 Despite the ESC recommendations, an audit of 1045 hospitals and 299 016 PE cases in the United States showed that unfractionated heparin use increased from 40% to 60% of cases over the period of 2011 to 2020, signifying an important gap in care for patients.54

Given the risk of death, all patients with high-risk PE should receive care in an intensive care unit (ICU). Patients with intermediate–high-risk PE should be considered for admission to an inpatient unit (e.g., medical ward or step-up unit) for a period of observation to ensure they do not deteriorate into the high-risk category, particularly if additional clinical features for elevated risk of deterioration are present (Table 1). When evaluating a patient with high-risk PE at a hospital without ICU services, clinicians should consider interfacility transfer55 and the risks and benefits of initiation of reperfusion therapies (i.e., systemic thrombolysis) before patient transport.

Approximately 65% of hospital beds in Canada are in community hospitals, where treatment disparities may arise compared with academic centres.56,57 These treatment gaps can be addressed by multidisciplinary pulmonary embolism response teams (PERTs), who can provide real-time evaluation and management recommendations for patients with intermediate–high-risk and high-risk PE.58 The AHA guideline now recommends PERT referral for all patients with PE in categories C to E.20 These teams can offer regional support to smaller centres and facilitate transfer of care when required.

Advanced reperfusion therapies

Advanced reperfusion therapies (i.e., systemic thrombolysis or catheter-based therapies) are available as adjunctive treatment for patients with high-risk PE and intermediate–high-risk PE. All patients with high-risk PE should be considered for advanced reperfusion therapy, in addition to anticoagulation. However, retrospective data from Europe and the US consistently show that fewer than half of those with high-risk PE are treated with reperfusion modalities.21,23,25,30,59 Understanding and addressing this gap in care is an important priority for PE researchers and clinicians to improve PE outcomes.

In contrast to those with high-risk PE, the vast majority of patients with intermediate–high-risk PE require no additional treatments beyond high-quality anticoagulation, enjoying very low rates of mortality and morbidity.17,60 A subset of patients with intermediate–high-risk PE (AHA category D2) should be considered for advanced reperfusion therapy if they demonstrate additional high-risk clinical features for deterioration or death (Box 3). Advanced therapies can be considered after failure of an initial trial of anticoagulation, or at the time of presentation, if there is a sufficient index of concern.

Advanced therapies include systemic thrombolysis, where fibrinolytic medication is given intravenously; catheter-directed thrombolysis, where fibrinolytics are administered within the pulmonary arteries; and mechanical thrombectomy, where the thrombus is aspirated and removed from the pulmonary arteries. Surgical embolectomy via sternotomy and cardiopulmonary bypass is now used only in exceptional circumstances.61 Advanced therapies should always be used with ongoing anticoagulation. The goal of advanced therapies is to rapidly reduce pulmonary artery obstruction, relieve RV pressure, and treat obstructive shock.

Systemic thrombolysis

The ESC and AHA guidelines recommend systemic thrombolysis as first-line advanced therapy for the treatment of high-risk (category E) PE (Table 1).13,20 Systemic thrombolysis is a potent fibrinolytic treatment administered intravenously to dissolve a thrombus in the pulmonary arteries. Tenecteplase and alteplase are the tissue plasminogen activators currently available in Canada. Bleeding (e.g., intracranial, gastrointestinal, retroperitoneal, intra-articular, intramuscular, hematuria) is the major risk of treatment, with contraindications outlined in Box 4. Patients with high-risk PE who receive systemic thrombolysis in addition to anticoagulation have significantly reduced mortality than patients who receive anticoagulation alone.21,62,63 Because of the high mortality rate in this patient population, the benefit of systemic thrombolysis in high-risk PE persists despite the increased risk of severe bleeding, including intracranial hemorrhage. The number of patients with high-risk PE studied in RCTs is small (approximately 224 patients) and no RCTs comparing thrombolysis with placebo have been performed since 1995.62 Although tenecteplase appears to have an increased risk of bleeding compared with alteplase in PE, no studies have directly compared different dosing or drug regimens for thrombolysis.62 Thus, the ideal agent and dosing regimen for thrombolysis in high-risk PE is still an area for ongoing research.

Box 4: Contraindications to systemic thrombolysis for acute pulmonary embolism 13 .

Absolute:

  • History of previous intracranial hemorrhage

  • Ischemic stroke in previous 6 mo

  • Brain or spine surgery in previous 3 mo

  • Head trauma with fracture or serious intracranial injury in previous 3 mo

  • Severe active bleeding (e.g., intracranial, trauma, gastrointestinal hemorrhage)

  • CNS neoplasm

Relative:

  • Major trauma or surgery in previous 3 wk

  • Coagulopathy (INR ≥ 1.6, platelets ≤ 50 × 109/L)

  • Therapeutic oral anticoagulation or dual antiplatelet usage at presentation (antiplatelet monotherapy is not a contraindication)

  • Blood pressure ≥ 180 mm Hg systolic or ≥ 110 mm Hg diastolic

  • Transient ischemic attack in previous 6 mo

  • Age ≥ 75 yr

  • Structural CNS abnormality (e.g., arteriovenous malformation) or GI tract neoplasm

  • Pregnancy (third trimester or first postpartum week)

  • Traumatic cardiopulmonary resuscitation (multiple rib fractures, sternal fracture, or hematoma)

  • Bleeding from a noncompressible site

  • Advanced liver disease

Note: CNS = central nervous system, ESC = European Society of Cardiology, GI = gastrointestinal, INR = international normalized ratio.

The role of systemic thrombolysis for the treatment of intermediate–high-risk PE is less clear. Although observational studies show an association with reduced mortality, RCTs have not consistently yielded positive results. The Pulmonary Embolism Thrombolysis (PEITHO) trial randomized 1005 patients with intermediate–high-risk PE to receive intravenous tenecteplase or placebo, in addition to standard anticoagulation.64 Despite the primary composite outcome of hemodynamic decompensation or death being significantly lower in the systemic thrombolysis group, the frequency of both extracranial bleeding and intracranial hemorrhage in this group was significantly higher. The finding of the composite outcome was driven mostly by hemodynamic decompensation, without a significant impact on mortality. Markers of RV dysfunction were not different between the thrombolysis and placebo groups at 6-month follow-up.65 Thus, routine use of full-dose systemic thrombolysis is not recommended in the ESC guideline for intermediate-risk PE.13 The AHA guideline has indicated that systemic thrombolysis can be considered as a treatment option for patients with incipient cardiopulmonary failure (category D).20 An RCT is currently investigating the role of reduced-dose systemic thrombolysis in improving reperfusion while minimizing the risk of bleeding for a subset of patients with intermediate–high-risk PE.66

Catheter-based interventions

Use of both catheter-directed thrombolysis and mechanical thrombectomy for the treatment of high-risk and intermediate–high-risk PE has been increasing over the past decade. The ESC guideline recommends use of catheter-based interventions for patients with high-risk PE and contraindications to systemic thrombolysis;13 high-risk patients who fail to improve with systemic thrombolysis should also be considered for catheter-based therapies. The AHA guideline recommends catheter-based therapy as a treatment option for intermediate–high-risk patients with PE with incipient cardiopulmonary failure (category D) and those with cardiogenic shock (category E1).20 A recent network meta-analysis suggested that catheter-directed thrombolysis may be associated with reduced mortality and reduced bleeding compared with systemic thrombolysis,67 although comparisons within the high-risk PE category were less common, and only 1 small randomized study comparing systemic with local thrombolysis in high-risk PE was reported.68 A recent observational registry using mechanical thrombectomy for the initial first-line treatment of high-risk PE demonstrated favourable in-hospital mortality and low bleeding rates.69 Because the mortality rates reported in this study (1.9%) were dramatically less than historical rates reported in large database registries, the results should be interpreted cautiously until randomized evidence is available.70

Within the intermediate-risk PE category, the timing and patient selection for catheter-based therapies are areas of ongoing research and have not been fully elucidated within guideline documents. When catheter-based interventions are used, earlier treatment may be associated with improved survival,56,71,72 although these observations may reflect inherent differences in natural clinical trajectory. Meta-analyses have shown reduced mortality with catheter-directed thrombolysis compared with anticoagulation alone, with no increased rates of bleeding.67,73 This was further clarified in an international RCT comparing ultrasonography-assisted catheter-directed thrombolysis plus anticoagulation with anticoagulation alone.74 Notably, eligibility required at least 2 additional high-risk clinical features including blood pressure of 90 to 110 mm Hg, respiratory rate greater than 20 breaths/min, and heart rate greater than 100 beats/min. Catheter-directed therapy was associated with a lower 7-day composite rate of cardiorespiratory decompensation, death, or PE recurrence, compared with anticoagulation alone, in intermediate–high-risk patients with PE (4.0% v. 10.3%). This composite outcome was driven primarily by reduced rate of hemodynamic decompensation, although rates of mortality, PE recurrence, or major bleeding were not significantly different between groups.

A recent RCT compared the effectiveness of mechanical thrombectomy and catheter-directed thrombolysis for the treatment of intermediate-risk PE, with 95% of patients being of intermediate–high risk.75 Rates of mortality, clinical deterioration, and bleeding were low in both groups, but clinical deterioration was less frequent in the mechanical thrombectomy group (1.5% v. 3.6%). Another RCT of 100 patients comparing mechanical thrombectomy plus anticoagulation with anticoagulation alone for the treatment of intermediate–high-risk PE demonstrated greater reduction in the RV-to-LV ratio and more frequent normalization of vital signs in the thrombectomy group; rates of major adverse events were not significantly different between groups.76 Other high-quality RCTs comparing catheter-based therapies plus anticoagulation with anticoagulation alone in intermediate–high-risk PE are anticipated to substantially clarify the potential role of advanced interventions in the treatment of intermediate–high-risk PE.77,78

Extracorporeal membrane oxygenation

As a form of mechanical circulatory support, extracorporeal membrane oxygenation (ECMO) is used to provide hemodynamic stabilization for extreme cases of high-risk PE with impending or existing cardiovascular collapse.61,79 This intervention may be effectively deployed during cardiac arrest,80 but is limited by feasibility and the low number of centres in Canada that offer it. The selection of appropriate patients and timing of initiation of ECMO are areas of open investigation. Although certain cohorts in retrospective studies have demonstrated improvement in favourable outcomes and likelihood of survival to hospital discharge,81,82 other studies have shown no benefit or increased risk of death.80,83,84 Bleeding, ischemic, and infectious complications are common.85,86 The use of systemic thrombolysis before or during ECMO improves the odds of survival to hospital discharge without substantial increases in rates of bleeding compared with ECMO alone.83,87,88 If ECMO is being considered for high-risk patients with PE, early discussion and logistical planning with quaternary referral centres are strongly advised.

How should a clot-in-transit be managed?

A clot-in-transit is an image-detected embolization of a thrombus before it has reached the pulmonary arteries, most often visualized on echocardiography or CT in the right heart chambers. The incidence of clot-in-transit may be as high as 8% to 9% in patients with PE,89,90 and its occurrence is associated with higher mortality.23,90,91 Consensus on management strategies is lacking; these include anticoagulation alone, systemic thrombolysis, catheter-based therapies, and surgical embolectomy. The use of systemic thrombolysis or catheter-based therapies may be associated with reduced mortality.89,92 In cases where a thrombus is straddling a patent foramen ovale, posing a risk of embolization into the systemic circulation, surgical embolectomy with closure of the patent foramen ovale may be considered.89

Conclusion

Management of intermediate–high-risk and high-risk PE starts with prompt administration of anticoagulation and risk stratification. In patients for whom PE is causing hemodynamic instability, shock, or cardiac arrest, immediate advanced therapy may be life-saving. Patients with intermediate–high-risk PE should be carefully and repeatedly evaluated over time for worsening clinical features of impaired perfusion. Catheter-based interventions are increasingly used for select patients with intermediate–high-risk PE. Equitable access to advanced PE therapies in Canada should be a priority for improving population-level outcomes and mitigating disparities across geographic regions and within health care systems. Few hospitals in Canada have established emergency systems of care to ensure a standardized and rigorous approach to diagnosis and management of PE, regardless of the patient’s hospital of origin. The implementation of access to consultations with PERTs may help establish such an approach. Despite advances in the treatment of PE, several questions remain unanswered to ensure optimal care is available for all patients in Canada (Box 5).

Box 5: Unanswered questions .

  • What are the barriers to appropriate use of anticoagulation and advanced therapies for intermediate–high-risk and high-risk pulmonary embolism in Canada?

  • Which subgroup of patients with intermediate–high-risk pulmonary embolism should receive advanced therapies, and what modality should be selected?

  • Can catheter-based therapies be used effectively as first-line treatment of high-risk pulmonary embolism?

Acknowledgements

The authors would like to recognize the following people who have contributed significantly to Pulmonary Embolism Canada: Fayad Al-Haimus, David Christiansen, Dennis Christopher, Christine D’Arsigny, Surinder Dhaliwal, Stuart Douglas, Suzanne Dubois, Stephanie Dyck, Federico Germini, John Granton, Keerat Grewal, Eric Herget, Susan Kahn, Maral Koolian, Gregoire Le Gal, Owen Mooney, Sameer Parpia, Reza Nasirzadeh, Bram Rochwerg, Juan Ronco, Barret Rush, Japandeep Sethi, Siuchan Sookhoo, Vicky Tagalakis, Jonathan Taylor, Carol West, and Ryan Zarychanski.

Footnotes

Competing interests: Lana Castellucci’s research institution has received honoraria from Bayer, BMS-Pfizer Alliance, The Academy for Continued Advancement in Healthcare Education, AMAG Pharmaceuticals, LEO Pharma, Sanofi, Valeo Pharma, and Servier, outside the submitted work. Dr. Castelluci holds volunteer positions with Thrombosis Canada, the International Society on Thrombosis and Haemostasis Scientific and Standardization Committee, and the Thrombosis and Hemostasis Summit of North America. No other competing interests were declared.

This article has been peer reviewed.

Contributors: All of the authors contributed to the conception and design of the work. Asher Mendelson drafted the manuscript. All of the authors revised it critically for important intellectual content, gave final approval of the version to be published, and agreed to be accountable for all aspects of the work.

Funding: Asher Mendelson is supported by the Manitoba Medical Services Foundation’s Dr. F.W. Du Val and John Henson Clinical Research Professorship. Lana Castellucci is supported by a University of Ottawa Tier 2 Research Chair in Thrombosis and Anticoagulation Safety. Kerstin de Wit is supported by a Tier 1 Canada Research Chair in Emergency Venous Thromboembolism (FRN CRC-2023-00154).

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