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 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:
- Silent
- Symptomatic
- Fatal
Acute PE are also classified as Massive pulmonary embolism or Submassive pulmonary embolism or Low-risk pulmonary embolism.
- 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
- 5% of pulmonary emboli
- 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.
- Contemporary classification: Recently, the American Heart Association has proposed the following definition for a massive PE:
- An acute pulmonary embolism with:
- Sustained hypotension (systolic blood pressure <90 mm Hg) for at least 15 minutes or requiring inotropic support. This is not due to other possible causes of hypotension such as arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction.
- Pulselessness.
- Persistent profound bradycardia (heart rate < 40 bpm with signs or symptoms of shock).[3]
- An acute pulmonary embolism with:
Submassive Pulmonary Embolism
- 40% of pulmonary emboli
- The American Heart Association has proposed the following definition for submassive PE: An acute PE without systemic hypotension but with either right ventricular dysfunction or myocardial necrosis.[3]. Myocardial necrosis is defined as either elevation of troponin I (>0.4 ng/mL) or elevation of troponin T (>0.1 ng/mL).
- 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
- ↑ 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). - ↑ 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.
- ↑ 3.0 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.
- ↑ 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) - ↑ 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) - ↑ 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)