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Pulmonary Emboli

Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities; however, they rarely also originate in the pelvic, renal, upper extremity veins, or the right heart chambers (see the image below). After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.

The pathophysiology of pulmonary embolism. Althoug The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.

Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system.

Essential update: FDA extends indication for apixaban to PE and DVT treatment

The US Food and Drug Administration (FDA) has extended the indications for the oral anticoagulant apixaban, a selective factor Xa inhibitor, to include the treatment of pulmonary embolism (PE) and deep venous thrombosis (DVT), as well as the reduction of PE and DVT recurrence risk. The drug was previously approved for stroke and systemic embolism risk reduction in nonvalvular atrial fibrillation and for PE and DVT prophylaxis following hip- or knee-replacement surgery.[1]

The FDA based its approval for the extended indication primarily on the outcome of the Apixaban for the Initial Management of Pulmonary Embolism and Deep-Vein Thrombosis as First-Line Therapy (AMPLIFY) and AMPLIFY-EXT studies, in which apixaban therapy was compared with enoxaparin and warfarin treatment. The AMPLIFY study showed that, in comparison with the standard anticoagulant regimen, apixaban therapy resulted in a 16% reduction in the risk of a composite endpoint that included recurrent symptomatic venous thromboembolism (VTE) or VTE-associated death.[2, 3]

Signs and symptoms

The classic presentation of pulmonary embolism is the abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia. However, most patients with pulmonary embolism have no obvious symptoms at presentation. Rather, symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea. The diagnosis of pulmonary embolism should be suspected in patients with respiratory symptoms unexplained by an alternative diagnosis.

Patients with pulmonary embolism may present with atypical symptoms, such as the following:

  • Seizures
  • Syncope
  • Abdominal pain
  • Fever
  • Productive cough
  • Wheezing
  • Decreasing level of consciousness
  • New onset of atrial fibrillation
  • Hemoptysis
  • Flank pain [4]
  • Delirium (in elderly patients) [5]

See Clinical Presentation for more detail.


Evidence-based literature supports the practice of using clinical scoring systems to determine the clinical probability of pulmonary embolism before proceeding with testing.[6] Validated clinical prediction rules should be used to estimate pretest probability of pulmonary embolism and to interpret test results.[7, 8]

Physical signs of pulmonary embolism include the following:

  • Tachypnea (respiratory rate >16/min): 96%
  • Rales: 58%
  • Accentuated second heart sound: 53%
  • Tachycardia (heart rate >100/min): 44%
  • Fever (temperature >37.8°C): 43%
  • Diaphoresis: 36%
  • S 3 or S 4 gallop: 34%
  • Clinical signs and symptoms suggesting thrombophlebitis: 32%
  • Lower extremity edema: 24%
  • Cardiac murmur: 23%
  • Cyanosis: 19%


Perform diagnostic testing on symptomatic patients with suspected pulmonary embolism to confirm or exclude the diagnosis or until an alternative diagnosis is found. Routine laboratory findings are nonspecific and are not helpful in pulmonary embolism, although they may suggest another diagnosis.

A hypercoagulation workup should be performed if no obvious cause for embolic disease is apparent, including screening for conditions such as the following:

  • Antithrombin III deficiency
  • Protein C or protein S deficiency
  • Lupus anticoagulant
  • Homocystinuria
  • Occult neoplasm
  • Connective tissue disorders

Potentially useful laboratory tests in patients with suspected pulmonary embolism include the following:

  • D-dimer testing
  • Ischemia-modified albumin level
  • White blood cell count
  • Arterial blood gases:
  • Serum troponin levels
  • Brain natriuretic peptide

Imaging studies

Imaging studies that aid in the diagnosis of pulmonary embolism include the following:

  • Computed tomography angiography (CTA): Multidetector-row CTA (MDCTA) is the criterion standard for diagnosing pulmonary embolism
  • Pulmonary angiography: Criterion standard for diagnosing pulmonary embolism when MDCTA is not available
  • Chest radiography: Abnormal in most cases of pulmonary embolism, but nonspecific
  • V/Q scanning: When CT scanning is not available or is contraindicated
  • ECG: Most common abnormalities are tachycardia and nonspecific ST-T wave abnormalities
  • MRI: Using standard or gated spin-echo techniques, pulmonary emboli demonstrate increased signal intensity within the pulmonary artery
  • Echocardiography: Transesophageal echocardiography may identify central pulmonary embolism
  • Venography: Criterion standard for diagnosing DVT
  • Duplex ultrasonography: Noninvasive diagnosis of pulmonary embolism by demonstrating the presence of a DVT at any site

See Workup for more detail.


Anticoagulation and thrombolysis

Immediate full anticoagulation is mandatory for all patients suspected of having DVT or pulmonary embolism.[9] Diagnostic investigations should not delay empirical anticoagulant therapy.

Thrombolytic therapy should be used in patients with acute pulmonary embolism who have hypotension (systolic blood pressure< 90 mm Hg) who do not have a high bleeding risk and in selected patients with acute pulmonary embolism not associated with hypotension who have a low bleeding risk and whose initial clinical presentation or clinical course suggests a high risk of developing hypotension.[9]

Long-term anticoagulation is critical to the prevention of recurrence of DVT or pulmonary embolism, because even in patients who are fully anticoagulated, DVT and pulmonary embolism can and often do recur.

Anticoagulation medications include the following:

  • Unfractionated heparin
  • Low-molecular-weight heparin
  • Factor Xa Inhibitors
  • Fondaparinux
  • Warfarin

Thrombolytic agents used in managing pulmonary embolism include the following:

  • Alteplase
  • Reteplase
  • Urokinase
  • Streptokinase

Surgical options

Surgical management options include the following:

  • Catheter embolectomy and fragmentation or surgical embolectomy
  • Placement of vena cava filters
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