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: Rim Halaby, M.D. [2]
Overview
Pulmonary embolism (PE) 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). Massive PE is characterised by the presence of either sustained hypotension, or pulselessness, or bradycardia. Submassive PE is characterized by the presence of either right ventricular dysfunction or myocardial necrosis in the absence of hypotension. In low risk PE, there is absence of hypotension, shock, right ventricular dysfunction and myocardial necrosis.[1]
Classification Based on Acuity
Acute Pulmonary Embolism
Acute PE is the sudden obstruction of the pulmonary arteries by an embolism, which may result in the immediate occurrence of symptoms. Acute PE can be either silent, symptomatic, or fatal. Acute PE can also classified by its severity (as discussed below) as massive PE, submassive PE, or low-risk PE.
Chronic Pulmonary Embolism
Chronic PE, referred to as chronic thromboembolic pulmonary hypertension, is the presence of persistent pulmonary hypertension for at least 6 months following acute PE.[2] The episode of acute PE preceding the chronic thromboembolic pulmonary hypertension can be either symptomatic or asymptomatic.[3]
Classification Based on Disease Severity
In addition to the time of presentation and the size of the embolus, a PE can also be classified based on the severity of disease. PE can be classified into three types based on the severity: massive (5-10% of cases), submassive (20-25% of cases), and low-risk (70% of cases).
| Classification of PE by Severity | Criteria[1] |
| Massive PE (also known as high risk PE) |
- Sustained hypotension (systolic blood pressure <90 mm Hg), not due to arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction, and either lasting for at least 15 minutes or necessitating the administration of inotropes OR |
| Submassive PE (also known as intermediate risk PE) |
- Right ventricular dysfunction OR myocardial necrosis AND |
| Low risk PE | - Absence of hypotension, shock, right ventricular dysfunction and myocardial necrosis |
Massive Pulmonary Embolism
- Massive PE accounts for 5-10% of pulmonary emboli.
- Massive PE falls under the category "high risk patients" in the European guidelines. High risk PE patients have a risk of PE-related early mortality of > 15%.[4]
- According to the American Heart Association, massive PE is characterized by the presence of:
Sustained hypotension (systolic blood pressure <90 mm Hg), not due to arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction, and either lasting for at least 15 minutes or necessitating the administration of inotropes
OR
Pulselessness
OR
Persistent profound bradycardia (heart rate < 40 bpm) plus findings of shock[1]
Submassive Pulmonary Embolism
- Submassive PE accounts for 20-25% of pulmonary emboli.
- Submassive PE falls under the category "intermediate risk patients" in the European guidelines. Intermediate risk PE patients have a risk of PE-related early mortality ranging between 3 and 15%.[4]
- According to the American Heart Association, submassive PE is characterized by:
Right ventricular dysfunction OR myocardial necrosis
AND
Absence of systemic hypotension (systolic blood pressure >90 mm Hg)[1][5]
- Submassive PE patients share the following characteristics:[6][7]
- 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 PE requires continuous monitoring to prevent irreversible damage and death.[5]
Right Ventricular Dysfunction
Right ventricular (RV) dysfunction is characterized by the presence of AT LEAST ONE of the following:[1][5]
- Echocardiography findings:
- RV dilation (ratio of apical 4-chamber RV diameter to left ventricle (LV) diameter > 0.9)
- RV systolic dysfunction
- CT findings: RV dilation (ratio of 4-chamber RV diameter to LV diameter > 0.9)
- BNP > 90 pg/mL
- N-terminal pro-BNP >500 pg/mL
- EKG findings:
- New complete or incomplete right bundle-branch block
- Anteroseptal ST elevation or ST depression
- Anteroseptal T-wave inversion
Myocardial Necrosis
Myocardial necrosisis defined as the presence of:[1][5]
- Elevation of troponin I (>0.4 ng/mL)
OR
- Elevation of troponin T (>0.1 ng/mL)
Low-Risk Pulmonary Embolism
- Low risk PE accounts for 70% of pulmonary emboli.
- Low risk PE patients have a risk of PE-related early mortality of <1%.[4] According to the American Heart Association, low risk PE is characterized by the absence of hypotension, shock, right ventricular dysfunction and myocardial necrosis.[1]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 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.
- ↑ Piazza G, Goldhaber SZ (2011). "Chronic thromboembolic pulmonary hypertension". N Engl J Med. 364 (4): 351–60. doi:10.1056/NEJMra0910203. PMID 21268727.
- ↑ Hoeper MM, Madani MM, Nakanishi N, Meyer B, Cebotari S, Rubin LJ (2014). "Chronic thromboembolic pulmonary hypertension". Lancet Respir Med. doi:10.1016/S2213-2600(14)70089-X. PMID 24898750.
- ↑ 4.0 4.1 4.2 Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). "Guidelines on the diagnosis and management of acute : the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)". Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.
- ↑ 5.0 5.1 5.2 5.3 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) - ↑ 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)