Pulmonary Embolism
Summary
Pulmonary embolism (PE) is the obstruction of pulmonary arteries by thrombus, most commonly arising from deep vein thrombosis (DVT) of the lower limbs. PE is the third most common cardiovascular cause of death after myocardial infarction and stroke. Clinical presentation varies from asymptomatic to haemodynamic collapse. Diagnosis relies on clinical pre-test probability assessment (Wells score), D-dimer, and CT pulmonary angiography (CTPA). Risk stratification using clinical, imaging, and biomarker criteria determines treatment intensity — from outpatient anticoagulation for low-risk PE to systemic thrombolysis or embolectomy for massive PE. DOACs are now the preferred anticoagulant for most patients.
Key Facts
- Definition: Obstruction of pulmonary arteries by thrombus
- Source: 90%+ from lower limb DVT
- Mortality: 5% overall; 30% if untreated; 65% if massive/cardiac arrest
- Diagnosis: Wells score → D-dimer → CTPA
- Risk Stratification: ESC (2019) — High/Intermediate-high/Intermediate-low/Low
- Treatment: Anticoagulation (DOAC preferred); thrombolysis if haemodynamically unstable
- Duration: 3 months minimum; indefinite if unprovoked
Clinical Pearls
"Think PE — It's a Great Imitator": PE can present with dyspnoea, chest pain, syncope, or even just tachycardia. Maintain a high index of suspicion.
"Wells Score Drives the Pathway": If Wells score is PE unlikely (<4), D-dimer can rule out PE. If PE likely (≥4), proceed directly to CTPA.
"Risk Stratification is Key": Not all PEs are the same. Massive PE needs urgent thrombolysis; low-risk PE can be treated at home.
Why This Matters Clinically
PE is common, potentially fatal, and often missed. Timely diagnosis and appropriate treatment save lives. Missed PE has a 30% mortality, while treated PE has ~5% mortality. Risk stratification guides the intensity of therapy and setting of care.
Incidence & Prevalence
- Annual Incidence: 1-2 per 1,000 population
- Hospital-related VTE: 10% of hospital deaths are VTE-related
- Mortality: 30-day mortality 5-15% (depends on risk category)
Demographics
| Factor | Details |
|---|---|
| Age | Incidence increases with age |
| Sex | Equal (slight male predominance) |
| Recurrence | 30% at 10 years if unprovoked |
Risk Factors (Virchow's Triad)
| Factor | Examples |
|---|---|
| Stasis | Immobility, long travel, paralysis |
| Endothelial Injury | Surgery, trauma, central lines |
| Hypercoagulability | Cancer, pregnancy, OCP/HRT, thrombophilia |
Common Provoking Factors
| Major (High Risk) | Minor (Lower Risk) |
|---|---|
| Major surgery | Minor surgery |
| Major trauma, fractures | Long-haul travel (>6h) |
| Hospitalisation | OCP, HRT |
| Spinal cord injury | Pregnancy, postpartum |
| Active cancer | Minor injury, immobility |
Mechanism
Step 1: Thrombus Formation
- DVT forms in deep veins (usually leg, pelvis)
- Follows Virchow's triad
Step 2: Embolisation
- Thrombus (or fragment) dislodges
- Travels via IVC → Right heart → Pulmonary arteries
Step 3: Pulmonary Artery Obstruction
- Partial or complete occlusion
- Increased pulmonary vascular resistance
Step 4: Haemodynamic Consequences
- RV pressure overload → RV dilatation → RV failure
- Reduced LV filling → Reduced cardiac output
- Hypotension, shock
Step 5: Gas Exchange Impairment
- V/Q mismatch → Hypoxia
- Dead space ventilation
- Reflex bronchoconstriction
Severity Spectrum
| Severity | Haemodynamics | Mortality |
|---|---|---|
| Subsegmental | Usually asymptomatic | Low |
| Segmental | Dyspnoea, chest pain | Low |
| Lobar | Moderate symptoms | Intermediate |
| Saddle | RV strain, possible shock | High |
| Massive | Hypotension, cardiac arrest | Very high (30-65%) |
Symptoms
Signs
Red Flags
[!CAUTION] High-Risk/Massive PE Features:
- SBP <90 mmHg for >15 minutes
- Need for vasopressors
- Cardiac arrest
- Syncope
- Severe hypoxia
- RV dysfunction on echo + elevated troponin
Structured Approach
General:
- Distress, diaphoresis
- Conscious level
Cardiovascular:
- HR, BP, JVP
- RV heave, loud P2
- Signs of right heart failure
Respiratory:
- RR, SpO2
- Pleural rub
- Reduced breath sounds
Legs:
- Unilateral swelling
- Calf tenderness
- Warmth, erythema (DVT)
First-Line
| Test | Purpose | Notes |
|---|---|---|
| Wells Score | Pre-test probability | Drives diagnostic pathway |
| D-Dimer | Rule-out if low probability | Age-adjusted (Age × 10 if >50) |
| CTPA | Confirm PE | Gold standard imaging |
Additional Investigations
| Test | Purpose |
|---|---|
| ECG | S1Q3T3, sinus tachycardia, RBBB, T-wave inversion V1-V4 |
| CXR | Exclude other causes; may show Hampton's hump, Westermark sign |
| ABG | Hypoxia, hypocapnia, raised A-a gradient |
| Troponin | Risk stratification (RV strain) |
| BNP/NT-proBNP | Risk stratification |
| Echocardiography | RV dysfunction, McConnell's sign |
| Leg Doppler USS | Confirm DVT |
| V/Q Scan | Alternative to CTPA if contrast contraindicated |
Risk Stratification Scores
sPESI (Simplified Pulmonary Embolism Severity Index):
| Criteria | Points |
|---|---|
| Age >80 | 1 |
| Cancer | 1 |
| Chronic cardiopulmonary disease | 1 |
| HR ≥110 | 1 |
| SBP <100 | 1 |
| SpO2 <90% | 1 |
- sPESI = 0: Low risk (suitable for outpatient)
- sPESI ≥1: Higher risk (consider admission)
Haemodynamically Unstable (Massive PE)
- Resuscitation, oxygen, IV access
- Anticoagulation: UFH bolus (80 units/kg) + infusion
- Systemic Thrombolysis: Alteplase 100mg IV over 2 hours
- Alternative: Catheter-directed thrombolysis or Surgical embolectomy
- VA-ECMO if cardiac arrest refractory to thrombolysis
Haemodynamically Stable
Anticoagulation (First-Line: DOAC):
- Rivaroxaban 15mg BD for 21 days, then 20mg OD
- Apixaban 10mg BD for 7 days, then 5mg BD
- Edoxaban/Dabigatran: Need 5-10 days LMWH lead-in
Duration:
- Provoked (major): 3 months
- Unprovoked: ≥3 months; consider indefinite
- Recurrent/cancer: Indefinite
Low-Risk PE (sPESI 0):
- Consider outpatient management
- Hestia criteria to assess suitability
- Early follow-up
Special Situations
| Situation | Approach |
|---|---|
| Pregnancy | LMWH (DOACs contraindicated) |
| Cancer | LMWH or DOAC (edoxaban, rivaroxaban) |
| Renal Impairment | Dose adjustment or UFH |
| HIT | Fondaparinux or argatroban |
IVC Filter
Indications:
- Absolute contraindication to anticoagulation with acute PE
- Recurrent VTE despite adequate anticoagulation
Note: Retrievable filters should be removed when anticoagulation possible
Acute
| Complication | Notes |
|---|---|
| Right Heart Failure | Major cause of death |
| Cardiogenic Shock | Massive PE |
| Cardiac Arrest | PEA common mechanism |
| Death | 30-65% in massive PE |
Chronic
| Complication | Notes |
|---|---|
| CTEPH | Chronic thromboembolic pulmonary hypertension (2-4%) |
| Post-PE Syndrome | Persistent dyspnoea, exercise intolerance |
| Recurrent VTE | 30% at 10 years if unprovoked |
| Bleeding | Anticoagulation-related |
Mortality
| Risk Category | 30-Day Mortality |
|---|---|
| Low Risk | <1% |
| Intermediate-Low | 1-3% |
| Intermediate-High | 3-15% |
| High Risk (Massive) | 20-65% |
Prognostic Factors
- Haemodynamic status
- RV dysfunction
- Elevated troponin/BNP
- Cancer
- Age
- Comorbidities
Key Guidelines
-
ESC Guidelines on Acute Pulmonary Embolism (2019) — Gold standard.
-
NICE NG158: Venous thromboembolic diseases (2020)
Landmark Trials
EINSTEIN-PE (2012) — Rivaroxaban for PE
- Key finding: Rivaroxaban non-inferior to standard therapy
- Clinical Impact: Established DOACs for PE
AMPLIFY (2013) — Apixaban for VTE
- Key finding: Apixaban non-inferior with less bleeding
- Clinical Impact: DOAC as safer alternative
PEITHO (2014) — Thrombolysis in intermediate-risk PE
- Key finding: Tenecteplase reduced haemodynamic decompensation but increased bleeding
- Clinical Impact: Thrombolysis reserved for high-risk or deteriorating patients
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| DOAC for PE | 1a | EINSTEIN-PE, AMPLIFY |
| Thrombolysis for massive PE | 1b | Case series, PEITHO |
| D-dimer rule-out | 1a | CHRISTOPHER study |
What is a Pulmonary Embolism?
A pulmonary embolism (PE) is a blood clot that has travelled to your lungs. It usually starts in the leg (deep vein thrombosis) and breaks off, travelling through your bloodstream to block blood flow in your lungs. This can be serious and even life-threatening.
What are the symptoms?
- Sudden shortness of breath
- Sharp chest pain, especially when breathing
- Coughing (sometimes with blood)
- Fast heartbeat
- Feeling faint or passing out
- Leg swelling or pain
How is it treated?
- Blood thinners: Tablets or injections to prevent more clots forming and allow your body to break down the clot
- Clot-busting drugs: For severe cases where your blood pressure is very low
- Supportive care: Oxygen, fluids, monitoring
What to expect
- Most people recover well with treatment
- You'll need blood thinners for at least 3 months
- Some people need them for longer or indefinitely
- Follow-up appointments will check your progress
When to seek urgent help
Call 999 or go to A&E immediately if:
- You're very short of breath
- You have severe chest pain
- You cough up blood
- You feel faint or pass out
- Your heart is racing
Primary Guidelines
- Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603. PMID: 31504429
Key Trials
-
The EINSTEIN-PE Investigators. Oral Rivaroxaban for the Treatment of Pulmonary Embolism. N Engl J Med. 2012;366(14):1287-1297. PMID: 22449293
-
Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for Patients with Intermediate-Risk Pulmonary Embolism (PEITHO). N Engl J Med. 2014;370(15):1402-1411. PMID: 24716681
Further Resources
- Thrombosis UK: thrombosisuk.org
- ESC: escardio.org
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate guidelines and specialists for patient care.