Introduction
Pulmonary embolism (PE) is a life-threatening condition caused by the obstruction of the pulmonary artery or its branches by a thrombus (blood clot). It is a part of venous thromboembolism (VTE) and is often associated with deep vein thrombosis (DVT). PE can lead to significant morbidity and mortality if not diagnosed and treated promptly.
Etiology and Risk Factors
1. Virchow’s Triad (Predisposing Factors for PE)
Hypercoagulability: Malignancy, pregnancy, oral contraceptive pills, thrombophilia (e.g., Factor V Leiden mutation).
Venous Stasis: Prolonged immobilization, surgery, long-haul travel, heart failure.
Endothelial Injury: Trauma, surgery, central venous catheters, smoking.
2. Additional Risk Factors
Previous history of VTE
Obesity
COVID-19 infection
Hormonal therapy
Pathophysiology
A thrombus, typically from deep veins of the legs (DVT), dislodges and travels to the pulmonary arteries.
This results in ventilation-perfusion (V/Q) mismatch, hypoxia, and increased pulmonary vascular resistance.
Large emboli can cause right ventricular strain, leading to acute cor pulmonale and hemodynamic collapse.
Clinical Presentation
1. Symptoms
Dyspnea (Most common symptom)
Pleuritic chest pain
Hemoptysis (uncommon, suggests pulmonary infarction)
Syncope or pre-syncope (suggestive of massive PE)
Leg pain/swelling (signs of DVT)
2. Signs
Tachypnea (Most common sign)
Tachycardia
Hypoxia
Jugular venous distension (JVD) in massive PE
Hypotension and shock in severe cases
Diagnosis of Pulmonary Embolism
1. Clinical Scoring Systems
Wells Score for PE
Low risk: <2 points → Consider D-dimer
Moderate risk: 2–6 points → Consider imaging
High risk: >6 points → Direct imaging
Modified Geneva Score
PERC (Pulmonary Embolism Rule-Out Criteria) – Used to rule out PE in low-risk patients
2. Laboratory Tests
D-dimer: Elevated in PE but non-specific (high negative predictive value).
ABG (Arterial Blood Gas): Hypoxia, respiratory alkalosis (due to hyperventilation).
Troponins: Elevated in right heart strain.
BNP (Brain Natriuretic Peptide): May be elevated in massive PE due to right ventricular dysfunction.
3. Imaging
CT Pulmonary Angiography (CTPA): Gold standard for PE diagnosis.
V/Q Scan: Used in patients with contrast allergy or renal impairment.
Lower Limb Doppler Ultrasound: To detect DVT in suspected cases.
Echocardiography: Signs of right ventricular dysfunction in massive PE.
Management of Pulmonary Embolism
1. Risk Stratification
Massive PE (High-risk PE): Hypotension or shock → Requires thrombolysis.
Submassive PE (Intermediate-risk PE): Right ventricular strain but hemodynamically stable → Consider anticoagulation ± advanced therapies.
Low-risk PE: Stable patients with no RV dysfunction → Anticoagulation alone.
2. Anticoagulation Therapy
First-line:
Direct Oral Anticoagulants (DOACs) – Apixaban, Rivaroxaban.
Low Molecular Weight Heparin (LMWH) – Preferred in cancer-associated PE.
Alternative: Unfractionated heparin (UFH) in critically ill patients or those requiring rapid reversal (e.g., surgery).
Warfarin: Used with initial LMWH bridging in some cases.
3. Thrombolysis (Fibrinolysis)
Indications: Massive PE with hypotension or cardiac arrest.
Agents: Alteplase (tPA) IV bolus followed by infusion.
4. Mechanical and Surgical Interventions
Embolectomy: Surgical removal of clot in massive PE.
Catheter-directed thrombolysis: Used in selected submassive PE cases.
Inferior Vena Cava (IVC) Filter: Indicated if anticoagulation is contraindicated or recurrent PE despite anticoagulation.
Prognosis and Complications
Chronic Thromboembolic Pulmonary Hypertension (CTEPH): Long-term consequence of unresolved PE.
Right Ventricular Failure: Can occur in severe cases.
Recurrent PE: High risk without anticoagulation.
Prevention of PE
Early mobilization in hospitalized patients
Prophylactic anticoagulation in high-risk patients
Compression stockings for immobilized patients
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