Pulmonary embolism (PE) is a potentially life-threatening manifestation of venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and PE. The majority (≈90%) of clinically significant PE originates from thrombi in the proximal deep veins of the lower extremities (popliteal, femoral, or iliac veins).

PE results from obstruction of pulmonary arterial flow by thrombotic material, leading to ventilation–perfusion mismatch, hypoxemia, increased pulmonary vascular resistance, right ventricular (RV) strain, and potentially cardiogenic shock.

PE severity ranges from asymptomatic incidental findings to massive PE with hemodynamic collapse.

Risk Factors

Risk factors are classically categorized according to Virchow’s triad:

A. Venous Stasis

• Prolonged immobilization (bed rest, long-haul travel)

• Recent surgery (especially orthopedic)

• Stroke with paralysis

• Heart failure

B. Endothelial Injury

• Major trauma

• Surgery

• Central venous catheters

C. Hypercoagulability

• Malignancy

• Pregnancy and postpartum

• Oral contraceptives / hormone therapy

• Inherited thrombophilia (Factor V Leiden, Protein C/S deficiency)

• Antiphospholipid syndrome

• Obesity

• Smoking

Previous VTE is the strongest predictor of recurrence.

Clinical Presentation (Signs and Symptoms)

Presentation varies depending on clot size and cardiopulmonary reserve.

Common Symptoms

• Sudden onset dyspnea

• Tachypnea

• Pleuritic chest pain

• Cough ± hemoptysis

• Syncope (massive PE)

Physical Findings

• Tachycardia

• Hypoxia

• Hypotension (massive PE)

• Signs of DVT (unilateral leg swelling, tenderness)

Transient dyspnea and tachypnea in the absence of other clear causes should raise suspicion.

4. Diagnostic Criteria

Diagnosis is based on:

1. Clinical probability assessment (e.g., Wells score)

2. D-dimer testing (low/moderate risk)

3. Imaging confirmation (CT pulmonary angiography)

PE is classified according to severity:

• Massive PE: sustained hypotension or shock

• Submassive PE: RV dysfunction without hypotension

• Low-risk PE: hemodynamically stable without RV strain

5. Investigations

Laboratory

• D-dimer (elevated in acute PE)

• Arterial blood gases (hypoxemia, respiratory alkalosis)

• Cardiac biomarkers (troponin, BNP in RV strain)

Imaging

• CT Pulmonary Angiography (CTPA) – gold standard

• Ventilation–perfusion (V/Q) scan (if CTPA contraindicated)

• Compression ultrasonography of lower limbs

• Echocardiography (RV dysfunction in massive PE)

ECG Findings

• Sinus tachycardia (most common)

• S1Q3T3 pattern (classic but uncommon)

• Right heart strain pattern

6. Management

A. Non-Pharmacological

• Oxygen therapy for hypoxia

• Hemodynamic support (IV fluids cautiously)

• Vasopressors if hypotensive

• Intensive care monitoring in massive PE

• Inferior vena cava (IVC) filter if anticoagulation contraindicated

B. Pharmacological

Long-term anticoagulation is required to prevent recurrence and extension.

1. Initial Anticoagulation

Option 1: Warfarin-based regimen

• Warfarin 5 mg PO daily

• Overlap with heparin/LMWH for 4–5 days

• Continue overlap until INR 2.0–3.0 for ≥24 hours

Option 2: Low Molecular Weight Heparin (LMWH)

• Enoxaparin (Clexane) 1 mg/kg SC every 12 hours

Option 3: Unfractionated Heparin (UFH)

• 75 units/kg IV bolus

• Continuous infusion 18 units/kg/hour

• Adjust to target aPTT 1.5–2.5 × control

Monitoring

• Warfarin: Monitor INR after 5–7 days

  • Target INR: 2.0–3.0

• UFH: Monitor aPTT every 6 hours until therapeutic

• LMWH in pregnancy: Monitor anti-Xa levels

Special Populations

Adolescents / Children

• Lower loading dose

• 15–25 units/kg/hour IV infusionOR

• 250 units/kg SC every 12 hours

Pregnancy

• LMWH preferred (1 mg/kg SC twice daily)

• Warfarin contraindicated

• Monitor anti-Xa levels

Thrombolysis

Indicated in:

• Massive PE with shock

• Persistent hypotension

Example:

• Alteplase 100 mg IV over 2 hours

Duration of Therapy

• Provoked PE: 3–6 months

• Unprovoked PE: ≥6 months or extended therapy

• Recurrent VTE: long-term anticoagulation

Prevention

Primary Prevention

• Early mobilization after surgery

• Mechanical prophylaxis (compression stockings)

• Prophylactic LMWH in high-risk hospitalized patients

Secondary Prevention

• Long-term anticoagulation

• Risk factor modification (weight reduction, smoking cessation)

Complications

• Chronic thromboembolic pulmonary hypertension (CTEPH)

• Recurrent PE

• Right heart failure

• Sudden cardiac death