Pulmonary Embolism (PE) – Overview 

Definition: 
A pulmonary embolism is the obstruction of the pulmonary arteries (or their branches) by a thrombus, fat, air, or tumour. Most commonly, it is due to a thrombus originating from a deep vein thrombosis (DVT) in the lower extremities. 

Clinical Relevance: 

PE is a potentially life-threatening condition. Rapid recognition and treatment are crucial.

Aetiology / Risk Factors 

Virchow’s Triad helps explain the risk factors: 

Stasis of blood flow 
Prolonged immobility (bed rest, long flights, hospitalization) 
Obesity 
Heart failure 

Endothelial injury 
Surgery (especially orthopaedic, pelvic, or hip) 
Trauma 
Central venous catheters 

Hypercoagulability 
Genetic: Factor V Leiden, Prothrombin G20210A mutation, Protein C/S deficiency 
Acquired: Malignancy, pregnancy, oral contraceptives, hormone replacement therapy 
Other notable causes: 
Fat embolism (long bone fractures) 
Air embolism (central line procedures) 
Septic emboli (infective endocarditis)
 
Pathophysiology 

Obstruction of pulmonary arteries → increased pulmonary vascular resistance. 
Right ventricular (RV) strain → RV dilation and dysfunction. 
Impaired gas exchange → hypoxemia. 
Hemodynamic compromise → hypotension, shock, and possibly death (in massive PE). 
 
 
Clinical Presentation
 
Symptoms: 
Dyspnoea (most common) 
Pleuritic chest pain 
Cough, sometimes haemoptysis 
Syncope or pre-syncope (massive PE) 
Anxiety or ‘sense of impending doom’

Signs: 
Tachypnoea (most sensitive sign) 
Tachycardia 
Hypotension (if massive PE) 
Jugular venous distention 
Signs of DVT: unilateral leg swelling, erythema, tenderness
 
Classic Triad: 
Dyspnoea + Haemoptysis + Pleuritic chest pain 
(Not always present together) 

Diagnosis 

1. Clinical Assessment 

Wells Score for PE Risk Stratification: 
Clinical signs of DVT (+3) 
PE more likely than alternative diagnosis (+3) 
Heart rate >100 (+1.5) 
Immobilization or surgery within 4 weeks (+1.5) 
Previous DVT/PE (+1.5) 
Haemoptysis (+1) 
Malignancy (+1) 

Interpretation: 
Low risk: ≤4 
High risk: >4 

Pulmonary Embolism Rule-out Criteria (PERC) can help rule out PE in very low-risk patients. 
 
2. Laboratory Tests
 
D-dimer: Highly sensitive, not specific. Useful in low-risk patients. 
Arterial blood gas: May show hypoxemia, hypercapnia, or respiratory alkalosis.
 
3. Imaging
 
CT Pulmonary Angiography (CTPA): Gold standard. 
Ventilation-Perfusion (V/Q) scan: If CTPA contraindicated (e.g., contrast allergy, renal failure). 
Doppler ultrasound of lower extremities: Detects DVT; can support PE diagnosis. 
ECG: Non-specific; may show sinus tachycardia, S1Q3T3 pattern, right heart strain. 
Chest X-ray: Often normal; may show atelectasis or wedge-shaped infarct (Hampton’s hump).
 
Management 

1. Acute Treatment 
Hemodynamically unstable (massive PE): 
Thrombolysis (e.g., alteplase) 
Consider embolectomy if thrombolysis contraindicated 
Hemodynamically stable: 
Anticoagulation: 
Direct oral anticoagulants (DOACs): Apixaban, Rivaroxaban 
Heparin (LMWH or UFH) followed by warfarin in certain cases
 
2. Supportive Measures 
Oxygen supplementation 
Fluids cautiously (avoid RV overload) 
Vasopressors if hypotensive 

3. Secondary Prevention 
Extended anticoagulation (3–6 months or lifelong if high risk) 
Address risk factors: mobility, thromboprophylaxis in surgery/hospitalization 

Complications 
Pulmonary infarction 
Pulmonary hypertension 
Right heart failure (cor pulmonale) 
Recurrent PE or chronic thromboembolic pulmonary hypertension (CTEPH) 
Death (especially if untreated) 

Key Points: 

Most common origin: proximal lower limb DVT 
Most sensitive symptom: dyspnoea 
Most sensitive sign: tachypnoea 
Massive PE = hypotension + shock 
D-dimer: high sensitivity, low specificity 
CTPA: diagnostic gold standard 
Anticoagulation is mainstay of treatment; thrombolysis for massive PE