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
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 19168835 doi=10.1148/rg.291085061.
- ↑ 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 (March 1999). "Pulmonary embolism: one-year follow-up with echocardiography doppler and five-year survival analysis". Circulation 99 (10): 1325–30. PMID 10077516. Retrieved on 2011-12-21.
- ↑ Fengler BT, Brady WJ (January 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 on 2011-12-21.
- ↑ Cannon CP, Goldhaber SZ (November 1996). "Cardiovascular risk stratification of pulmonary embolism". Am. J. Cardiol. 78 (10): 1149–51. PMID 8914880. Retrieved on 2011-12-21.
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