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Classically, patients with PE experience the sudden onset of shortness of breath and severe chest pain that increases with inspiration. Patients may complain of hemoptysis and associated unilateral leg swelling.


  1. Pathophysiology

    1. Most commonly occurs when a lower extremity venous thrombus embolizes to the lung

    2. Thrombi in the upper extremity, often associated with vascular catheters, and pelvic veins may also cause PE.

    3. 80% of patients with PE have deep venous thrombosis (DVT).

    4. 48% of patients with DVT have PE (often asymptomatic).

  2. Symptoms vary markedly.

    1. Massive obstruction may result in RV failure and death

    2. However, lesser obstruction may be asymptomatic.

  3. Mortality

    1. 3-month mortality is 17.5%

    2. When left untreated, mortality rate approaches 30%

    3. With appropriate treatment, mortality rates drop to as low as 2%

  4. Risk factors

    1. A variety of risk factors increase the likelihood for VTE, including a personal history of VTE, estrogen use, surgery within the last 4 weeks, personal history of thrombophilia, active malignancy, immobilization, and age over 50.

    2. Thrombophilia (presence of more than 1 thrombophilia may greatly increase risk)

      1. Antiphospholipid antibodies: Present in 2–8.5% of patients with VTE

      2. Factor V Leiden

        1. Mutation in factor V causes resistance to cleavage by activated protein C

        2. Most common thrombophilia, but < 5% lifetime risk of VTE in heterozygotes

        3. Present in 11% of patients with DVT

        4. Heterozygote OR for VTE 4.2, homozygote OR 11.5

        5. Combined with oral birth control pill, mutation increases risk 35 times

      3. Prothrombin gene mutation

        1. Heterozygote OR for VTE 2.8

        2. Homozygote OR for VTE 6.7

      4. Protein C or S deficiency (rare)

        1. Protein C and S are naturally occurring anticoagulants whose synthesis by the liver requires vitamin K

        2. Deficiency is associated with hypercoagulability.

        3. Warfarin decreases synthesis of both factors.

        4. Assays for protein C and S must be performed while patients are not taking warfarin and when acute thrombosis is not present.

      5. Antithrombin III deficiency (also rare): Assay must be done while patient is not taking heparin.

      6. Hyperhomocysteinemia: 3 × increased risk of VTE

      7. Increased factor VIII: 6 × increased risk

  5. PE may be an overlooked cause of “COPD exacerbation”

    1. One interesting study reported that 16% of patients with a COPD exacerbation have PE.

    2. The rate was 25% among patients with an unexplained exacerbation of COPD, compared with 8% in those with an exacerbation of known etiology.

    3. Unexplained exacerbation was defined as patients without parenchymal consolidation on chest radiograph without fever or chills (ie, not obviously due to pneumonia) and patients who lacked the common factors precipitating COPD exacerbations:

      1. Lower respiratory tract infection (increased sputum, purulence, fever, cold, or sore throat)

      2. Exposure to noxious irritants

      3. Objective signs of HF

      4. Medication nonadherence

  6. image Consider PE in patients with a COPD exacerbation that is unexplained.


  1. Clinical presentation: The diagnosis of PE is complicated because patients present in a variety of ways and signs and symptoms are neither sensitive nor specific.

    1. Although dyspnea and chest ...

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