Pulmonary Thromboembolism (Pulmonary Embolism)

Source and risk factors

• More than 95% arise from deep venous thrombosis (DVT) of the lower limbs, particularly thrombi that extend into the popliteal, femoral, or iliac veins.
• Major predisposing factors reflect Virchow triad:
  • Prolonged immobilization or bed rest
  • Major surgery, especially hip or knee orthopedic surgery
  • Trauma, burns, and multiple fractures
  • Malignancy
  • Congestive cardiac failure
  • Pregnancy, puerperium, oral contraceptive use
  • Hypercoagulable states, for example factor V Leiden mutation

Pathogenesis and consequences

1. Size of embolus
2. Site and extent of pulmonary arterial obstruction
3. Previous cardiopulmonary status

1. Massive pulmonary embolism

• A large embolus may lodge at the bifurcation of the main pulmonary artery as a saddle embolus, or obstruct major pulmonary arterial branches.
• It causes abrupt obstruction of pulmonary blood flow, pulmonary vasoconstriction, and acute rise in pulmonary arterial pressure.
• Consequences:
  • Acute right ventricular dilatation and failure, termed acute cor pulmonale
  • Reduced left ventricular filling and cardiac output
  • Hypotension, shock, syncope, and sudden death

2. Embolism of medium-sized arteries

• May cause pulmonary hemorrhage due to rupture of capillaries in the ischemic area.
• Often produces a peripheral, pleural-based, wedge-shaped lesion.
• If infarction occurs, it is typically a hemorrhagic (red) infarct.

3. Small emboli

• May be clinically silent.
• Repeated small emboli can lead to pulmonary hypertension and chronic right-sided heart strain or failure.

Pulmonary infarction

• Pulmonary arteries
• Bronchial arteries

• Left-sided cardiac failure or pulmonary venous congestion
• Impaired bronchial circulation
• Severe underlying lung disease or hypoventilation

• Usually peripheral and subpleural
• Wedge-shaped, with base toward pleura and apex toward hilum
• Initially hemorrhagic and red-blue
• Later becomes pale as hemosiderin-laden macrophages remove erythrocytes
• Heals by organization and fibrosis, leaving a pleural-based scar

Mechanism of hypoxemia in PE

• Ventilation-perfusion mismatch due to perfusion defects
• Atelectasis in ischemic areas, partly from reduced surfactant
• Reduced cardiac output, causing widened arterial-venous oxygen difference
• Occasionally right-to-left shunting through a patent foramen ovale

Clinical features

• Sudden dyspnea
• Pleuritic chest pain
• Tachypnea and tachycardia
• Hemoptysis, especially with pulmonary infarction
• Syncope, hypotension, or sudden death in massive embolism

Fate

• Undergo lysis
• Organize and become incorporated into the vessel wall
• Recanalize
• Recur, leading to chronic thromboembolic pulmonary hypertension