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Pulmonary Embolism for ABIM

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Pulmonary Embolism for the American Board of Internal Medicine Exam
Etiology and Risk Factors
  • Pulmonary Embolism (PE):
    • A pulmonary embolism (PE) is caused by the obstruction of a pulmonary artery by a thrombus, typically originating from the deep veins of the legs or pelvis (deep vein thrombosis, DVT). This results in impaired blood flow to the lung parenchyma.
  • Virchow's Triad:
    • PE is associated with Virchow’s triad, which includes:
    • Endothelial injury: Trauma, surgery, or inflammation of the vessel wall.
    • Venous stasis: Prolonged immobility (e.g., bed rest, long flights, surgery).
    • Hypercoagulability: Conditions such as malignancy, pregnancy, oral contraceptive use, and genetic thrombophilias (e.g., factor V Leiden, prothrombin gene mutation, antiphospholipid syndrome).
  • Other Risk Factors:
    • Major surgery (especially orthopedic surgery of the hip or knee)
    • Cancer: Especially lung, pancreatic, or gastrointestinal malignancies.
    • Immobilization: Hospitalization, bed rest, or long-distance travel.
    • Obesity, smoking, heart failure, and advanced age.
    • Pregnancy and postpartum period.
Pathophysiology
Deep vein thrombosis to pulmonary embolism
  • Clot Formation and Migration:
    • PE typically originates from a thrombus in the deep veins of the lower extremities or pelvis (DVT). The thrombus dislodges and travels through the venous system into the pulmonary arteries, causing obstruction.
  • Hemodynamic Effects:
    • PE leads to increased pulmonary vascular resistance, resulting in right ventricular strain. In massive PE, the right ventricle can dilate and fail, leading to cardiogenic shock or sudden death.
    • Ventilation-perfusion mismatch (V/Q mismatch) occurs as blood flow is diverted from the blocked pulmonary arteries, leading to hypoxemia.
  • Consequences:
    • In small, subsegmental emboli, the effects may be minimal. In large or multiple emboli, impaired oxygenation and circulatory collapse may occur. Tissue infarction can lead to pulmonary infarction.
Clinical Features
  • Symptoms:
    • Dyspnea: The most common presenting symptom, typically sudden in onset.
    • Pleuritic chest pain: Sharp pain that worsens with deep inspiration.
    • Cough: Often non-productive, but hemoptysis may occur if pulmonary infarction develops.
    • Tachypnea and tachycardia: Common findings in PE.
    • Leg swelling or pain: Suggestive of a DVT.
  • Massive PE:
    • If the embolus is large, patients may present with syncope, hypotension, or signs of shock (e.g., cold, clammy skin). Right heart failure can lead to jugular venous distension (JVD) and cardiogenic shock.
Diagnosis
Clinical Probability Assessment
  • Wells Score:
    • A validated scoring system used to estimate the probability of PE:
    • Clinical signs of DVT: 3 points
    • PE is the most likely diagnosis: 3 points
    • Heart rate >100 bpm: 1.5 points
    • Immobilization or recent surgery: 1.5 points
    • Previous DVT/PE: 1.5 points
    • Hemoptysis: 1 point
    • Malignancy: 1 point
    • Interpretation:
    • >6: High probability
    • 2-6: Moderate probability
    • <2: Low probability
  • Modified Geneva Score:
    • Another scoring system that stratifies PE risk based on clinical features and risk factors, similar to the Wells score.
Diagnostic Testing
  • D-dimer:
    • Elevated in patients with PE but is nonspecific. Useful in ruling out PE in low-risk patients if negative. High D-dimer requires further imaging.
  • Imaging:
    • CT Pulmonary Angiography (CTPA): The gold standard diagnostic test for PE. It provides direct visualization of the thrombus within the pulmonary arteries.
    • Ventilation-perfusion (V/Q) scan: Used when CTPA is contraindicated (e.g., in patients with renal failure or contrast allergy). A mismatch between ventilation and perfusion indicates PE.
    • Compression ultrasonography: Used to diagnose DVT, especially in patients who cannot undergo CTPA.
  • Electrocardiogram (ECG):
    • May show sinus tachycardia, the most common finding. Other findings include S1Q3T3 pattern, right ventricular strain, and right bundle branch block in massive PE.
  • Echocardiography:
    • May demonstrate right ventricular dysfunction or dilatation in massive PE.
Management
Initial Stabilization
  • Oxygen:
    • Supplemental oxygen is provided for hypoxemia.
  • Hemodynamic Support:
    • IV fluids or vasopressors (e.g., norepinephrine) are used in patients with hypotension or shock.
  • Anticoagulation:
    • Immediate initiation of anticoagulation is critical unless contraindicated. Options include:
    • Low-molecular-weight heparin (LMWH): Preferred in most cases, especially in cancer-related PE.
    • Unfractionated heparin: Used in unstable patients or those requiring thrombolysis.
    • Direct oral anticoagulants (DOACs): Include rivaroxaban and apixaban, increasingly used as first-line agents.
    • Warfarin: Used less frequently, with an initial overlap with heparin until the therapeutic INR (2-3) is achieved.
Thrombolysis and Thrombectomy
  • Thrombolysis:
    • Considered in massive PE with hemodynamic instability or shock. Alteplase (tPA) is the most common thrombolytic agent used.
    • Thrombolysis is contraindicated in patients with a high risk of bleeding.
  • Surgical or Catheter-Based Thrombectomy:
    • Considered in patients with massive PE who fail thrombolysis or have contraindications to thrombolytics.
Long-Term Anticoagulation
  • Duration:
    • Anticoagulation is typically continued for 3-6 months in provoked PE (e.g., after surgery). In unprovoked PE or patients with ongoing risk factors (e.g., cancer), longer duration is considered.
  • Inferior Vena Cava (IVC) Filter:
    • Used in patients who have contraindications to anticoagulation or recurrent PE despite adequate anticoagulation. The filter prevents emboli from traveling to the lungs.
Complications
  • Chronic Thromboembolic Pulmonary Hypertension (CTEPH):
    • A long-term complication of unresolved PE, leading to persistent pulmonary hypertension, right ventricular dysfunction, and progressive dyspnea.
  • Right Heart Failure:
    • Due to chronic increased pulmonary vascular resistance.
Prevention
  • Prophylaxis in High-Risk Patients:
    • Low-dose LMWH, unfractionated heparin, or pneumatic compression devices are used postoperatively or during hospital stays for immobilized patients to reduce the risk of DVT and PE.
  • Lifestyle Modifications:
    • Smoking cessation, weight management, and physical activity reduce the risk of venous thromboembolism.
Key Points
  • Pulmonary embolism is primarily caused by thrombi originating from the deep veins of the legs or pelvis (DVT), leading to obstruction of the pulmonary arteries.
  • Risk factors include recent surgery, immobilization, malignancy, pregnancy, and inherited thrombophilias.
  • Common symptoms are dyspnea, pleuritic chest pain, tachypnea, and tachycardia. Massive PE may present with hypotension, syncope, or shock.
  • Diagnosis is confirmed with CT pulmonary angiography (CTPA) or ventilation-perfusion (V/Q) scan in selected patients.
  • Management includes anticoagulation (LMWH, DOACs), and in cases of massive PE with hemodynamic instability, thrombolysis or surgical thrombectomy may be required.
  • Long-term anticoagulation duration depends on whether the PE is provoked or unprovoked.

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