Pulmonary embolism definition,causes, evaluation and management
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"pulmonary embolism"[MeSH Terms]
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2026 pulmonary embolism diagnosis management guideline ESC ASH
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https://www.escardio.org/guidelines/clinical-practice-guidel…
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site:hematology.org venous thromboembolism treatment guideline direct oral anticoagulant pulmonary embolism
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Pulmonary embolism (PE)
Definition
Pulmonary embolism is obstruction of one or more pulmonary arteries by material traveling through the venous circulation, most commonly a blood clot that has detached from a deep vein thrombosis (DVT), usually in the leg or pelvis. DVT and PE together are called venous thromboembolism (VTE). - Sabiston Textbook of Surgery, p. 1834
The embolus raises pulmonary vascular resistance and can cause impaired oxygenation, right-ventricular strain or failure, shock, and death when severe.
Causes and risk factors
Common cause
- Thromboembolism from DVT, especially proximal lower-limb or pelvic DVT.
Less common embolic material
- Fat embolism after major long-bone trauma
- Air embolism
- Amniotic-fluid embolism
- Tumor emboli
- Septic emboli
Predisposing factors: Virchow triad
- Venous stasis
- Immobility, hospitalization, paralysis
- Long travel
- Heart failure
- Endothelial injury
- Major surgery, especially pelvic, abdominal, hip, or knee surgery
- Trauma, fractures, central venous catheters
- Hypercoagulability
- Active cancer
- Pregnancy and puerperium
- Estrogen-containing contraceptives or hormone therapy
- Previous VTE
- Inherited thrombophilia, for example factor V Leiden
- Antiphospholipid syndrome
Other clinically important factors include older age, obesity, acute medical illness, and inflammatory disease. - Bailey & Love's Short Practice of Surgery, p. 10128-10144
Clinical presentation
PE can be silent, but common features are:
- Sudden unexplained dyspnea
- Pleuritic chest pain
- Tachypnea and tachycardia
- Hypoxemia
- Cough or hemoptysis, especially with pulmonary infarction
- Syncope, hypotension, shock, or cardiac arrest in massive PE
- Unilateral leg pain, swelling, or tenderness suggesting DVT
- Raised JVP or other signs of acute right-heart failure in severe cases
Neither normal oxygen saturation nor a normal arterial blood gas rules out PE. - Murray & Nadel's Textbook of Respiratory Medicine, p. 960
Evaluation
1. Immediate assessment
Assess:
- Airway, breathing, circulation
- Blood pressure and oxygen saturation
- Signs of shock or right-ventricular failure
- Bleeding risk before anticoagulation or thrombolysis
A patient with hypotension, shock, or cardiac arrest is treated as high-risk PE until proved otherwise.
2. Estimate pretest probability
Use clinical judgment plus a validated score such as:
- Wells score
- Revised Geneva score
This determines whether D-dimer testing is appropriate and how urgently imaging is needed. - Fuster and Hurst's The Heart, p. 1743
3. D-dimer
- Use in patients with low or intermediate clinical probability.
- A negative high-sensitivity D-dimer can exclude PE in an appropriate low/intermediate-risk patient.
- A positive result is not diagnostic, because D-dimer may be elevated in older age, cancer, infection, inflammation, pregnancy, recent surgery, trauma, myocardial infarction, and hospitalization.
- Consider an age-adjusted threshold in older adults when locally recommended.
Do not delay definitive imaging for D-dimer testing when clinical probability is high or the patient is unstable. - Fuster and Hurst's The Heart, p. 1743
4. Imaging
| Test | Main role |
|---|---|
| CT pulmonary angiography (CTPA) | First-line confirmatory test in most stable patients |
| V/Q scan | Alternative if iodinated contrast is unsuitable, renal impairment is significant, or radiation considerations favor it, such as selected pregnant patients |
| Compression ultrasonography of legs | Finds proximal DVT; a positive result may establish VTE when chest imaging is unsuitable |
| Echocardiography | Not a routine rule-out test in stable PE; useful in shock to identify RV strain and support urgent decisions |
| Chest X-ray, ECG, ABG | Supportive and help identify differentials, but do not diagnose or exclude PE |
The diagnostic work-up combines probability assessment, D-dimer where appropriate, and pulmonary vascular imaging. - Murray & Nadel's Textbook of Respiratory Medicine, p. 1831
5. Risk stratification after diagnosis
Classify PE according to early mortality risk:
- High risk: shock, persistent hypotension, or cardiac arrest.
- Intermediate-high risk: normotensive but both RV dysfunction and positive cardiac biomarkers, for example troponin.
- Intermediate-low risk: some adverse prognostic features but not both RV dysfunction and biomarker elevation.
- Low risk: hemodynamically stable without significant RV dysfunction or biomarker elevation.
Risk classification helps decide monitoring location, suitability for outpatient care, and need for reperfusion treatment.
Management
General measures
- Give oxygen if hypoxemic.
- Establish IV access, monitor ECG, blood pressure, oxygen saturation, and urine output in severe cases.
- Treat hypotension/shock with cautious fluid administration and vasopressors when needed. Excess fluid can worsen right-ventricular distension and ischemia.
- Analgesia for pleuritic pain.
- Avoid unnecessary delays in anticoagulation when PE is strongly suspected and bleeding risk is acceptable.
1. Anticoagulation: main treatment
Anticoagulation prevents clot extension and recurrent PE. It does not immediately dissolve the existing clot.
For most stable patients:
- A direct oral anticoagulant (DOAC) is often preferred, if suitable.
- Low-molecular-weight heparin (LMWH), fondaparinux, or unfractionated heparin (UFH) are alternatives.
- UFH is often preferred in severe renal impairment, anticipated thrombolysis/procedure, or high-risk unstable PE because it can be stopped and reversed more readily.
- Warfarin remains appropriate in selected situations, including some patients with antiphospholipid syndrome or where DOACs are unsuitable.
ASH guidance prefers DOAC therapy for many patients with primary VTE treatment and supports outpatient care for selected uncomplicated, low-risk PE cases. ASH VTE guidance
2. Duration of anticoagulation
- Provoked PE due to a transient risk factor such as surgery, trauma, or temporary immobility: usually at least 3 months.
- Unprovoked PE, recurrent VTE, or persistent risk factor: consider extended or indefinite anticoagulation if bleeding risk is acceptable.
- Active cancer-associated PE: anticoagulation is commonly continued longer while cancer remains active or treatment continues, reassessing bleeding risk regularly.
Duration must balance recurrence risk against bleeding risk.
3. Reperfusion treatment
For high-risk PE with shock or persistent hypotension:
- Give immediate cardiopulmonary support.
- Systemic thrombolysis is generally first-line reperfusion therapy unless contraindicated.
- If thrombolysis is contraindicated or unsuccessful, consider:
- Catheter-directed therapy, including catheter thrombectomy or catheter-directed thrombolysis
- Surgical embolectomy
In unstable patients, bedside echocardiography and venous ultrasound can support the diagnosis while resuscitation proceeds. - Murray & Nadel's Textbook of Respiratory Medicine, p. 1877
Intermediate-risk PE: routine thrombolysis is generally avoided because major bleeding risk may exceed benefit. It may be considered as rescue treatment if hemodynamic deterioration develops.
4. Inferior vena cava filter
An IVC filter is not routine. Consider it when:
- Anticoagulation is absolutely contraindicated, or
- Recurrent PE occurs despite adequate anticoagulation.
Filters can reduce recurrent PE but have complications and do not replace anticoagulation when anticoagulation becomes possible. - Goldman-Cecil Medicine, p. 2833-2835
Emergency warning
Seek emergency care immediately for sudden unexplained breathlessness, chest pain, coughing blood, fainting, persistent rapid heart rate, or low blood pressure, especially after surgery, prolonged immobility, pregnancy, or with cancer. PE can deteriorate rapidly and needs urgent clinician-led assessment.
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