# Pulmonary Embolism: The Vascular Surgeon's Role

## Overview

Pulmonary embolism (PE) ranks as the third most common cardiovascular cause of death, following myocardial infarction and stroke. Its annual incidence ranges from 60 to 70 cases per 100,000 individuals, with an overall mortality rate between 2% and 10%. However, in cases of massive PE, mortality can escalate dramatically to between 30% and 65%. Vascular surgeons have become increasingly involved in the management of PE through catheter-directed interventions and the placement of inferior vena cava (IVC) filters. The emergence of Pulmonary Embolism Response Teams (PERTs) has facilitated rapid, multidisciplinary assessment and management of these patients.

## Classification and Risk Stratification

### Hemodynamic Classification

Pulmonary embolism is classified hemodynamically into massive, submassive, and low-risk categories based on clinical presentation and right ventricular (RV) function. Massive PE is characterized by sustained hypotension, defined as a systolic blood pressure (SBP) below 90 mmHg lasting at least 15 minutes, pulselessness, or the need for vasopressors or mechanical circulatory support. This category carries a high mortality rate of 25% to 65% and necessitates immediate reperfusion therapy.

Submassive PE refers to patients who are hemodynamically stable but exhibit RV dysfunction and/or myocardial injury. RV dysfunction can be identified by an RV to left ventricular (LV) ratio greater than 0.9 on computed tomography (CT), RV dilation on echocardiography, or elevated levels of brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP). Myocardial injury is indicated by elevated troponin levels. Mortality in this group ranges from 3% to 15%.

Low-risk PE patients are hemodynamically stable without evidence of RV dysfunction or biomarker elevation. Their mortality is less than 1%, making them suitable candidates for outpatient management.

| PE Category | Hemodynamics | RV Dysfunction | Biomarkers | Mortality | Primary Treatment |
|-------------|-------------|----------------|------------|-----------|-------------------|
| Massive | SBP <90 mmHg or vasopressors required | Present | Elevated | 25–65% | Systemic thrombolysis or CDT/embolectomy |
| Submassive | Stable (SBP ≥90) | Present (RV/LV >0.9) | Troponin/BNP elevated | 3–15% | Anticoagulation ± CDT (selective) |
| Low-risk | Stable | Absent | Normal | <1% | Anticoagulation; consider outpatient |

### Risk Scoring Systems

Risk stratification is further refined using scoring systems such as the Pulmonary Embolism Severity Index (PESI) and its simplified version (sPESI). The PESI incorporates variables including age, sex, presence of cancer, heart failure, lung disease, heart rate, systolic blood pressure, temperature, mental status, and oxygen saturation. The sPESI simplifies this to six factors: age over 80, cancer, cardiopulmonary disease, heart rate of 110 beats per minute or greater, systolic blood pressure below 100 mmHg, and oxygen saturation under 90%. A score of zero on the sPESI indicates low risk with a 30-day mortality around 1%, suggesting that outpatient treatment may be appropriate. Scores of one or higher indicate increased risk and warrant hospital admission.

<image>Risk stratification algorithm for acute pulmonary embolism showing classification into massive, submassive, and low-risk categories with corresponding management pathways</image>

## Diagnosis

### Clinical Presentation

The most common symptom of PE is dyspnea, often accompanied by pleuritic chest pain, cough, hemoptysis, and occasionally syncope. Physical examination may reveal tachycardia, tachypnea, and hypoxemia. In massive PE, hypotension, syncope, and cardiac arrest presenting as pulseless electrical activity (PEA) are common. The classic triad of dyspnea, pleuritic chest pain, and hemoptysis is present in fewer than 20% of cases.

### Diagnostic Workup

The Wells score is a clinical prediction tool used to estimate the pretest probability of PE. A score of 4 points or less suggests that PE is unlikely, prompting a D-dimer test; a negative D-dimer effectively excludes PE. Scores above 4 indicate that PE is likely, and CT pulmonary angiography (CTPA) is the next diagnostic step.

D-dimer testing is highly sensitive; a negative result combined with low clinical probability reliably excludes PE. CTPA remains the gold standard imaging modality, allowing visualization of clot location and burden as well as assessment of the RV/LV ratio. Echocardiography provides bedside evaluation of RV function, with findings such as the McConnell sign—hypokinesis of the RV free wall with apical sparing—being suggestive of PE. Echocardiography is especially useful in hemodynamically unstable patients.

Ventilation-perfusion (V/Q) scanning serves as an alternative when CTPA is contraindicated, such as in cases of contrast allergy, renal insufficiency, or pregnancy. Lower extremity duplex ultrasound can identify deep vein thrombosis (DVT), and in the presence of clinical suspicion for PE, a positive DVT may guide treatment without the need for CTPA.

### Biomarkers

Troponin elevation indicates myocardial injury resulting from RV strain, while elevated BNP or NT-proBNP reflects RV dysfunction and pressure overload. These biomarkers assist in classifying submassive PE and predicting adverse outcomes.

## Treatment

### Anticoagulation (All PE Categories)

Anticoagulation forms the cornerstone of PE treatment regardless of severity. Unfractionated heparin (UFH) is preferred in massive PE due to its titratability and short half-life, which is advantageous if surgery or intervention is anticipated. Low molecular weight heparin (LMWH) or direct oral anticoagulants (DOACs) are typically used for submassive and low-risk PE. DOAC regimens mirror those for deep vein thrombosis, with rivaroxaban or apixaban used as monotherapy, and edoxaban or dabigatran administered following a parenteral lead-in. The duration of anticoagulation follows the same principles as for DVT: three months for provoked events and extended therapy for unprovoked or recurrent cases.

### Systemic Thrombolysis

Systemic thrombolysis is indicated primarily for massive PE with hemodynamic compromise. Alteplase (tPA) is administered as 100 mg intravenously over two hours in the standard regimen or as a 0.6 mg/kg dose over 15 minutes in accelerated protocols, such as during cardiac arrest. Tenecteplase, given as a weight-based single bolus, has been studied in the PEITHO trial for submassive PE. Contraindications to thrombolysis include active bleeding, recent surgery within three weeks, hemorrhagic stroke, and intracranial neoplasm. The risk of major bleeding ranges from 9% to 20%, with intracranial hemorrhage occurring in 2% to 3% of cases. Despite these risks, systemic thrombolysis reduces mortality in massive PE by approximately 50%.

### Catheter-Directed Therapy (CDT)

Catheter-directed therapy has an expanding role in managing massive and high-risk submassive PE. Catheter-directed thrombolysis involves the infusion of low-dose tPA directly into the pulmonary arteries, typically at 1 mg per hour per catheter for 12 to 24 hours, resulting in a total dose of 12 to 24 mg—significantly lower than systemic doses. The EKOS system combines ultrasound with catheter-directed thrombolysis to enhance drug delivery. The SEATTLE II trial demonstrated improvements in RV/LV ratio and pulmonary artery pressures at 48 hours, while the ULTIMA trial showed that CDT was superior to heparin alone in improving RV function in submassive PE.

Aspiration thrombectomy devices such as FlowTriever (evaluated in the FLARE trial) and Inari mechanically remove clots without the use of thrombolytics. These devices offer the advantage of lower bleeding risk and can be performed in a single session. Fragmentation combined with aspiration can be achieved by rotating a pigtail catheter to break up central clots.

### Surgical Pulmonary Embolectomy

Surgical pulmonary embolectomy involves open removal of clots from the main and lobar pulmonary arteries through a sternotomy with cardiopulmonary bypass. Indications include massive PE with contraindications to thrombolysis, failed thrombolysis accompanied by ongoing hemodynamic collapse, right heart thrombus or clot-in-transit, and chronic thromboembolic disease (the latter addressed by pulmonary thromboendarterectomy, a distinct procedure). Mortality rates range from 6% to 30%, depending on preoperative hemodynamic status. Outcomes are best in high-volume centers with established PERT programs.

<image>CT pulmonary angiography showing saddle pulmonary embolism with clot straddling the main pulmonary artery bifurcation, with accompanying echocardiographic image of right ventricular dilation</image>

## IVC Filters (See Also Topic 37)

In the context of PE, IVC filters are indicated when there is an absolute contraindication to anticoagulation in patients with acute venous thromboembolism (VTE), recurrent PE despite therapeutic anticoagulation, or massive PE in patients with marginal hemodynamic reserve where another embolic event would be fatal. Retrievable filters are preferred, with plans for removal once anticoagulation can be safely resumed. It is important to note that IVC filters do not treat PE but serve to prevent recurrent embolization from lower extremity DVT.

## Pulmonary Embolism Response Team (PERT)

PERTs are multidisciplinary teams comprising vascular surgery, interventional radiology, pulmonology, cardiology, cardiac surgery, hematology, and critical care specialists. They are activated for massive and high-risk submassive PE to facilitate rapid risk stratification and treatment decisions. Evidence suggests that PERTs improve time to treatment and patient outcomes. An increasing number of centers are establishing formal PERT programs.

## Chronic Thromboembolic Pulmonary Hypertension (CTEPH)

CTEPH develops in approximately 2% to 4% of PE survivors and results from organized thrombus causing chronic obstruction of the pulmonary arteries and subsequent pulmonary hypertension. Patients typically present with progressive dyspnea, exercise intolerance, and signs of right heart failure. Diagnosis involves ventilation-perfusion scanning, which reveals mismatched perfusion defects, right heart catheterization, and CTPA. The definitive treatment is pulmonary thromboendarterectomy (PTE), a potentially curative surgery performed at specialized centers. For inoperable cases, balloon pulmonary angioplasty is an option, and medical therapy with riociguat, a soluble guanylate cyclase stimulator, may be used.

<image>Diagram showing catheter-directed thrombolysis for pulmonary embolism with bilateral pulmonary artery catheter placement and infusion of low-dose tPA directly into the clot burden</image>

## Outpatient Management of Low-Risk PE

Outpatient management is appropriate for patients with an sPESI score of zero, no significant comorbidities, and adequate home support. Direct oral anticoagulants, particularly rivaroxaban or apixaban, are preferred for outpatient initiation. The Hestia criteria provide an additional safety checklist to determine outpatient eligibility. Close follow-up within 48 to 72 hours is essential. Properly selected patients have a 30-day mortality rate below 2%.

## Clinical Pearls

In hemodynamically unstable patients with suspected PE, bedside echocardiography demonstrating RV dilation is sufficient to initiate systemic thrombolysis without delay for confirmatory CTPA. Catheter-directed therapy administers approximately 10% to 25% of the systemic thrombolytic dose, potentially reducing major bleeding risk; however, definitive randomized controlled trials comparing catheter-directed therapy to systemic thrombolysis are lacking. The PEITHO trial showed that systemic tenecteplase for submassive PE reduced hemodynamic decompensation but increased major bleeding and stroke, so routine systemic thrombolysis for submassive PE is not recommended. After PE, all patients with persistent dyspnea at three to six months should be screened for CTEPH, as early diagnosis significantly improves prognosis with pulmonary thromboendarterectomy. Mechanical thrombectomy devices such as FlowTriever and Inari are increasingly used for intermediate-high risk PE as lytic-free options, though long-term outcome data are still evolving. The presence of free-floating IVC thrombus or right atrial clot-in-transit carries a high risk of PE and warrants consideration of surgical embolectomy or catheter intervention.

## References
- Konstantinides SV, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. *Eur Heart J*. 2020;41(4):543-603.
- Piazza G, et al. (SEATTLE II) A prospective, single-arm, multicenter trial of ultrasound-facilitated, catheter-directed, low-dose fibrinolysis for acute massive and submassive PE. *JACC Cardiovasc Interv*. 2015;8(10):1382-1392.
- Meyer G, et al. (PEITHO trial) Fibrinolysis for patients with intermediate-risk pulmonary embolism. *N Engl J Med*. 2014;370(15):1402-1411.
- Tu T, et al. (FLARE trial) FlowTriever for acute massive and submassive pulmonary embolism. *Circ Cardiovasc Interv*. 2019;12(6):e007809.
- Jaff MR, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the AHA. *Circulation*. 2011;123(16):1788-1830.