l6 pulmonary embolism

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  • DR.Bilal Natiq Nuaman,MD C.A.B.M.,F.I.B.M.S.,D.I.M.2016-2017


  • Definition Sudden occlusion of the pulmonary vasculature, which results

    in obstruction of the blood flow to the lung parenchyma . Commonly blood clot (80%) Fat Air Amniotic fluid Placenta Parasites Septic emboli (from right sided endocarditis) Clumped tumor cells (especially choriocarcinoma)


  • EpidemiologyPE is the third most common cause of deathEtiology Pulmonary embolism is most commonly due to a

    thrombus (blood clot) originating from Deep Veins of the lower extremities and pelvis. pelvis (10 15%) leg (70-80%)


  • Pathophysiology Thrombus-blood clot along the wall of a normal or

    slightly damaged blood vessel Virchow s triad gives the 3 primary influences of a

    thrombus formation Endothelial Injury Stasis or turbulent flow Blood hypercoagulability


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  • Criteria of diagnosis Presence of risk factors for PE. Clinical presentation consistent with PE. Exclusion of alternative diagnoses .


  • Most important clinically identifiable risk factors for DVT and PE: Prior history of DVT or PERecent surgery or pregnancyProlonged immobilizationUnderlying malignancy.


  • Classic Triad of pulmonary embolism

    Sudden onset of unexplained dyspnea is the most common, and often the only symptom of pulmonary embolism. Pleuritic chest pain and Hemoptysis are present only when infarction has occurred.

    1.Dyspnea, 2.Hemoptysis3.Pleuritic chest pain

    In reality the triad occurs in

  • Classification Based on clinical presentation and investigations Treatment of Pulmonary Embolism (PE) are best

    understood when classified Acute Massive PE Acute Small/Medium PE


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  • D-dimer Dimerized plasmin fragment D Fibrin degradation product A negative D-dimer result (< 500 U/mL) excluded

    PE with a sensitivity of 83.0% Sensitive but not specific indicator of

    thromboembolic disorders Raised in inflammatory conditions e.g. Pneumonia


  • Arterial Blood Gas Hypoxemia occurs in about 90% of patients with PE The degree of hypoxemia doesnt accurately predict

    the size of the PE

    PaO2 of

  • Chest X-Ray Use to Rule out other causes Initial CXR normal in 1/3rd of patients


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  • Electrocardiograph

    The most common ECG abnormalities are: Sinus tachycardia Right axis deviation Nonspecific ST segment abnormalities (40% of pts) RBBB

    These findings are not sensitive or specific enough to aid in the diagnosis of PE

    S1Q3T3 pattern is observed in only 20% of patients ECG pattern is normal in 1/3rd of patients Exclude: Myocardial Infarction and Pericarditis


  • Spiral CT Contrast material infused Spiral chest CT scans are excellent for detecting

    pulmonary emboli in the central pulmonary arteries Does not detect emboli in beyond segmental vessels


  • CT Scan

    Fig 1. Spiral CT of patient showing large thrombus (arrowed) within the left pulmonary artery


  • Doppler Ultra sound Detection of thrombosis in femoral & popliteal veins

    vessels Primarily or secondarily involved in the majority of

    patients with PE Doppler Ultra sound has a sensitivity and specificity of



  • Pulmonary Arteriography Gold Standard Called upon when clinical suspicion of PE is high

    and other studies are inconclusive.


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  • Ventilation/Perfusion Scan It is based on identifying areas of ventilation without

    perfusion (mismatched defects) Technetium isotope is given IV to detect areas of non-

    perfusion Labeled xenon is inhaled to demonstrate non-aerated



  • Management General Measures


    O2 in all PE (if hypoxemia restore to >90%)


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    Treatment of acute PE includes immediate anticoagulation with unfractionated heparin (UFH), low molecular weight heparin (LMWH), fondaparinux, or oral rivaroxaban

    1-normal renal function:LMWH or fondaparinux are preferred agents because of the ease of subcutaneous administration and their lower rates of thrombocytopenia. 2-renal impairment :intravenous UFH After (5days) of initiation of heparin or fondaparinux, warfarin should be administered. Infusion of heparin or fondaparinux needs to be continued for at least the first 5 days of warfarin therapy until a therapeutic INR of 2 to 3 is reached. 3-advanced renal failureOral rivaroxaban without initial treatment with heparin or fondaparinux.

  • Medical Heparin should be stopped when the INR>2 Warfarin therapy should be continued

    3- 6 weeks for patients with identifiable risk factor 3-6 months for patients with no identifiable risk factor life for patients with recurrent embolism.


  • Thrombolytic therapyIndication- Massive PE manifested by:(1)hypotension or shock or

    (2)right ventricular enlargement or dysfunction from massive PE .

    types Streptokinase- Urokinase- Recombinant Tissue Plasminogen activator (r-tPA)-

    100mg over 2hr fastest


  • Surgical Vena caval filter Percutaneous thrombectomy Pulmonary embolectomy


  • Caval filter Filter inserted in IVC below

    origin of renal vessels Indications

    Pts with recurrent PE despite adequate anticoagulation

    (prophylacticaly)Pts for whom anticoagulation is contraindications (eg. immediately after surgery)

    Patients with massive PE who survived but in whom recurrent embolism will be invariably fatal 32

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