Pulmonary embolism classification

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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 is classified based on the nature of symptom presentation and the overall severity of disease. Symptom presentation is largely influenced by the time of appearance of symptoms and size of the embolus. Disease severity can be further stratified into three levels of risk: massive, submassive, and low-risk.

Classification Based on Temporality & Size

The classification of a pulmonary embolism is considerably influenced by the temporal manifestation and the overall physical size at presentation. Classification on this criteria is not mutually exclusive from disease severity. Thus, an acute or chronic embolus can be further classified into any of the categories of disease severity discussed further below.

Acute Pulmonary Embolism

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

  • Time Criterion: Symptoms 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:

  • Embolus is eccentric and contiguous with the vessel wall.
  • Embolus reducing the arterial diameter by ≥50%.
  • Evidence of recanalization within the thrombus.
  • Presence of an arterial web.

Classification Based on Disease Severity

In addition to time of presentation and size of embolus, a pulmonary embolism can be additionally classified based on the severity of disease. Three major classifications exist: massive, submassive, and low-risk. The incidence of these severity levels are 5%, 40%, and 55%, respectively.

Massive Pulmonary Embolism

  • Historical classification: A massive pulmonary embolism was defined using the Miller Index of angiographic burden.[2] This is a retrospective diagnosis based upon the pulmonary angiogram that does not inform prospective decisions.
  • Contemporaneous classification: Recently, the American Heart Association has proposed that an acute pulmonary embolism can be a massive pulmonary embolism if it includes any of the following:
  • Sustained hypotension, defined as systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction
  • Pulselessness
  • Persistent profound bradycardia, defined as heart rate <40 bpm with signs or symptoms of shock)[3]

Submassive Pulmonary Embolism

The American Heart Association has proposed the following definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis. [3]

Submassive PE patient population has the following characteristics:[4][5]

  • Significantly higher rate of in-hospital complications.
  • Have potential for long-term pulmonary hypertension and cardiopulmonary disease.

These patient, though hemodynamic stable and may initially appear to be clinically stable, but patient can undergo a cycle of progressive RV failure. Thus watchful waiting of such patients could lead to irreversible damage and death.[6]

Saddle PE

A saddle PE is one that lodges at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries. Most of the saddle PE are submassive.

Low-risk Pulmonary Embolism

The American Heart Association has proposed the following definition for Low-risk PE: Acute PE and the absence of the clinical markers of adverse prognosis that define massive or submassive PE.[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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