Pulmonary embolism overview

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Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Pulmonary embolism (PE) is an acute obstruction of the pulmonary artery (or one of its branches).

The obstruction in the pulmonary artery that causes a PE can be due to thrombus, air, tumor, or fat. Most often, this is due to a venous thrombosis (blood clot from a vein), which has been dislodged from its site of formation in the lower extremities. It has then embolized to the arterial blood supply of one of the lungs. This process is termed thromboembolism. In other rare forms of pulmonary embolism, material other than a blood clot may be responsible; this may include:

PE is a potentially lethal condition. The patient can present with a range of signs and symptoms, including dyspnea, chest pain while breathing, and in more severe cases collapse, shock, and cardiac arrest.

PE treatment requires rapid and accurate risk stratification before the development of hemodynamic collapse and cardiogenic shock. Treatment consists of an anticoagulant medication, such as heparin or warfarin, and in severe cases, thrombolysis or surgery.

Pulmonary embolism can be classified based on the time course of symptom presentation (acute and chronic) and the overall severity of disease (stratified based upon three levels of risk: massive, submassive, and low-risk).

Classification Based on Acuity and Size

Acute Pulmonary Embolism

A pulmonary embolism is classified as acute if it meets any of the following criteria:

  • Time Criterion: Symptom onset and physical sign presentation occur immediately after obstruction of pulmonary vessels.
  • Embolus Size Criteria:
    • Embolus is located centrally within the vascular lumen.
    • Embolus occludes a vessel.
    • Embolus causes distention of the involved vessel.

Chronic Pulmonary Embolism

A pulmonary embolism is classified as chronic if it meets any of the following criteria:

  • Time Criterion: A markedly progressive development of dyspnea over time, generally as a result of pulmonary hypertension.
  • Embolus Size Criteria:[1]
    • Embolus is eccentric and contiguous with the vessel wall.
    • Embolus reduces the arterial diameter by ≥ 50%.
    • Evidence of recanalization within the thrombus.
    • Presence of an arterial web.

Classification Based on Disease Severity

In addition to the time of presentation and the size of the embolus, a pulmonary embolism can also be classified based on the severity of disease. Three major classifications exist: massive (5% of cases), submassive ( 40% of cases), and low-risk ( 55% of cases).

Massive Pulmonary Embolism

Submassive Pulmonary Embolism

  • Submassive pulmonary embolism patients share the following characteristics:[4][5]
    • A significantly higher rate of in-hospital complications.
    • A higher potential for long-term pulmonary hypertension and cardiopulmonary disease.
  • Though patients with submassive pulmonary emboli may initially appear hemodynamically and clinically stable, there is potential to undergo a cycle of progressive right ventricular failure. A submassive pulmonary embolism requires continuous monitoring to prevent irreversible damage and death.[6]

Saddle Pulmonary Embolism

  • A saddle pulmonary embolism is classified as an embolus that lodges at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries.
  • Saddle pulmonary embolisms are typically classified as submassive.

Low-Risk Pulmonary Embolism

  • 55% of pulmonary emboli
  • The American Heart Association defines a low-risk pulmonary embolism as an acute pulmonary embolism without the life threatening clinical markers that define massive or submassive pulmonary emboli. [3]


References

  1. Castañer E, Gallardo X, Ballesteros E, Andreu M, Pallardó Y, Mata JM; et al. (2009). "CT diagnosis of chronic pulmonary thromboembolism". Radiographics. 29 (1): 31–50, discussion 50-3. PMID doi=10.1148/rg.291085061 19168835 doi=10.1148/rg.291085061 Check |pmid= value (help).
  2. Miller GA, Sutton GC, Kerr IH, Gibson RV, Honey M (1971). "Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism". Br Heart J. 33 (4): 616. PMID 5557502.
  3. 3.0 3.1 3.2 Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ; et al. (2011). "Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association". Circulation. 123 (16): 1788–830. doi:10.1161/CIR.0b013e318214914f. PMID 21422387.
  4. Ribeiro A, Lindmarker P, Johnsson H, Juhlin-Dannfelt A, Jorfeldt L (1999). "Pulmonary embolism: one-year follow-up with echocardiography doppler and five-year survival analysis". Circulation. 99 (10): 1325–30. PMID 10077516. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)
  5. Fengler BT, Brady WJ (2009). "Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm". Am J Emerg Med. 27 (1): 84–95. doi:10.1016/j.ajem.2007.10.021. PMID 19041539. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)
  6. Cannon CP, Goldhaber SZ (1996). "Cardiovascular risk stratification of pulmonary embolism". Am. J. Cardiol. 78 (10): 1149–51. PMID 8914880. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)

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