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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. | 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. | ||
The | 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 Temporality and 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:''' 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:'''<ref name="pmid19168835">{{cite journal| author=Castañer E, Gallardo X, Ballesteros E, Andreu M, Pallardó Y, Mata JM et al.| title=CT diagnosis of chronic pulmonary thromboembolism. | journal=Radiographics | year= 2009 | volume= 29 | issue= 1 | pages= 31-50; discussion 50-3 | pmid=19168835 doi=10.1148/rg.291085061 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19168835 }} </ref> | |||
**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.<ref name="pmid5557502">{{cite journal| author=Miller GA, Sutton GC, Kerr IH, Gibson RV, Honey M| title=Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism. | journal=Br Heart J | year= 1971 | volume= 33 | issue= 4 | pages= 616 | pmid=5557502 | doi= | pmc= | url= }} </ref> 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]]).<ref name="pmid21422387">{{cite journal| author=Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ et al.| title=Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. |journal=Circulation | year= 2011 | volume= 123 | issue= 16 | pages= 1788-830 | pmid=21422387 | doi=10.1161/CIR.0b013e318214914f |pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21422387 }} </ref> | |||
===Submassive Pulmonary Embolism=== | |||
* 40% of pulmonary emboli | |||
* The [[American Heart Association]] has proposed the following definition for submassive PE: An acute PE without [[hypotension|systemic hypotension]] but with either [[right ventricular dysfunction]] or [[myocardial necrosis]].<ref name="pmid21422387">{{cite journal| author=Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ et al.| title=Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. | journal=Circulation| year= 2011 | volume= 123 | issue= 16 | pages= 1788-830 | pmid=21422387 | doi=10.1161/CIR.0b013e318214914f | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21422387 }} </ref>. 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:<ref name="pmid10077516">{{cite journal |author=Ribeiro A, Lindmarker P, Johnsson H, Juhlin-Dannfelt A, Jorfeldt L |title=Pulmonary embolism: one-year follow-up with echocardiography doppler and five-year survival analysis |journal=Circulation |volume=99 |issue=10 |pages=1325–30 |year=1999 |month=March |pmid=10077516 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10077516 |accessdate=2011-12-21}}</ref><ref name="pmid19041539">{{cite journal |author=Fengler BT, Brady WJ |title=Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm |journal=Am J Emerg Med |volume=27 |issue=1 |pages=84–95 |year=2009 |month=January |pmid=19041539 |doi=10.1016/j.ajem.2007.10.021 |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-6757(07)00699-7 |accessdate=2011-12-21}}</ref> | |||
** 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.<ref name="pmid8914880">{{cite journal |author=Cannon CP, Goldhaber SZ |title=Cardiovascular risk stratification of pulmonary embolism |journal=Am. J. Cardiol. |volume=78 |issue=10 |pages=1149–51 |year=1996 |month=November |pmid=8914880 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914996005802 |accessdate=2011-12-21}}</ref> | |||
====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. <ref name="pmid21422387">{{cite journal| author=Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ et al.| title=Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. | journal=Circulation| year= 2011 | volume= 123 | issue= 16 | pages= 1788-830 | pmid=21422387 | doi=10.1161/CIR.0b013e318214914f | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21422387 }} </ref> | |||
==References== | ==References== | ||
Revision as of 19:01, 30 October 2012
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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:
- Fat
- Bone (usually in association with significant trauma)
- Air (often when diving)
- Clumped tumor cells
- Amniotic fluid (affecting mothers during childbirth).
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 Temporality and 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: 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)