Pulmonary embolism resident survival guide: Difference between revisions
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{{CMG}}; '''Associate Editor-In-Chief:''' [[User:Rim Halaby|Rim Halaby]] | {{CMG}}; '''Associate Editor-In-Chief:''' [[User:Rim Halaby|Rim Halaby]]; {{PB}} | ||
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! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align=center| {{fontcolor|#2B3B44|Pulmonary embolism Resident Survival Guide Microchapters}} | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Pulmonary embolism resident survival guide#Overview|Overview]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Pulmonary embolism resident survival guide#Causes|Causes]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Pulmonary embolism resident survival guide#FIRE: Focused Initial Rapid Evaluation|FIRE]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Pulmonary embolism resident survival guide#Complete Diagnostic Approach|Diagnosis]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Pulmonary embolism resident survival guide#Treatment|Treatment]] | |||
: [[Pulmonary embolism resident survival guide#General Approach|General Approach]] | |||
: [[Pulmonary embolism resident survival guide#Choice of Intervention|Choice of Intervention]] | |||
: [[Pulmonary embolism resident survival guide#Type of Valve and Discharge Anticoagulation Therapy|Type of Valve and Discharge Anticoagulation Therapy]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Aortic stenosis resident survival guide#Do's|Do's]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Aortic stenosis resident survival guide#Don'ts|Don'ts]] | |||
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== Overview== | == 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 [[embolism|embolized]] to the [[pulmonary artery|arterial]] blood supply of one of the lungs. This process is termed [[thromboembolism]]. 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 (medical)|collapse]], [[shock]], and [[cardiac arrest]]. 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). 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. | |||
==Causes== | ==Causes== | ||
Line 27: | Line 49: | ||
* [[Protein S deficiency]] | * [[Protein S deficiency]] | ||
* [[Prothrombin|Prothrombin mutation]] | * [[Prothrombin|Prothrombin mutation]] | ||
==Classification== | |||
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). | |||
====Massive Pulmonary Embolism==== | |||
*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==== | |||
*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> | |||
==FIRE: Focused Initial Rapid Evaluation== | |||
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention. The algorithm below is based on the 2011 AHA Guideline for the Management of Patients With Pulmonary Embolism. | |||
== Management== | == Management== |
Revision as of 02:56, 12 April 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Rim Halaby; Pratik Bahekar, MBBS [2]
Pulmonary embolism Resident Survival Guide Microchapters |
---|
Overview |
Causes |
FIRE |
Diagnosis |
Treatment |
Do's |
Don'ts |
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. 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. 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). 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.
Causes
Life Threatening Causes
Life-threatening causes include conditions which result in death or permanent disability within 24 hours if left untreated.
Common Causes
- Antiphospholipid syndrome
- Antithrombin deficiency
- Factor V Leiden
- Hyperhomocysteinemia
- Long-distance air travel
- Malignancy
- Nephrotic syndrome
- Obesity
- Post surgery
- Pregnancy
- Protein C deficiency
- Protein S deficiency
- Prothrombin mutation
Classification
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).
Massive Pulmonary Embolism
- 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).[1]
Submassive Pulmonary Embolism
- An acute PE without:
- Systemic hypotension but with either right ventricular dysfunction or myocardial necrosis.[1]. 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:[2][3]
- 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.[4]
FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention. The algorithm below is based on the 2011 AHA Guideline for the Management of Patients With Pulmonary Embolism.
Management
Step 1: Establish The Diagnosis Of Pulmonary Embolism
In hospitals that have experience in performing and interpreting CT pulmonary angiography, the following flowchart approach can be adopted.
Determine chances of PE | |||||||||||||||||||||||||||||||||
Low chance | High chance | ||||||||||||||||||||||||||||||||
D-dimer | |||||||||||||||||||||||||||||||||
<500 ng/ml | >500 ng/ml | CT Pulmonary angiography | |||||||||||||||||||||||||||||||
PE excluded | Negative | Positive | |||||||||||||||||||||||||||||||
PE excluded | PE confirmed | ||||||||||||||||||||||||||||||||
Note: If there is a high clinical suspicion of pulmonary embolism, then anticoagulation can begin with a parenteral agent such as unfractionated heparin during the process of performing the diagnostic studies.
Step 2: Use A Risk-Stratified Approach to Treat the Patient with Pulmonary Embolism
Confirmed PE | |||||||||||||||||||||||||||||||||||||||||||||||
Assess Clinical Stability | |||||||||||||||||||||||||||||||||||||||||||||||
Unstable | Stable | ||||||||||||||||||||||||||||||||||||||||||||||
Blood pressure ≦ 90mm Drop in BP ≧ 40mm for > 15 min | Assess RV function Biomarkers of injury | ||||||||||||||||||||||||||||||||||||||||||||||
Thrombolysis Catheter embolectomy Surgery | No Dysfunction + No injury | Dysfunction + No injury | Dysfunction + Injury | ||||||||||||||||||||||||||||||||||||||||||||
Anticoagulation Early discharge | Anticoagulation Ward admission | Thrombolytics ICU admission | |||||||||||||||||||||||||||||||||||||||||||||
Step 3: Assess Treatment Response and Need for Device Based Therapy
Acute PE confirmed | |||||||||||||||||||||||||||||||||||||||||||||||
Anticoagulation contraindicated ? | |||||||||||||||||||||||||||||||||||||||||||||||
Yes | No | ||||||||||||||||||||||||||||||||||||||||||||||
IVC filter | Risk stratification | ||||||||||||||||||||||||||||||||||||||||||||||
Low-risk PE | Submassive PE | Massive PE | |||||||||||||||||||||||||||||||||||||||||||||
Anticoagulation | Anticoagulation | ||||||||||||||||||||||||||||||||||||||||||||||
Assess clinically for evidence of increased severity | |||||||||||||||||||||||||||||||||||||||||||||||
Evidence of shock (SBP <90 mmHg) or respiratory failure | Is thrombolytic contraindicated? | ||||||||||||||||||||||||||||||||||||||||||||||
Yes | No | ||||||||||||||||||||||||||||||||||||||||||||||
Surgical emblectomy or catheter based interventions | Hold anticoagulation, give thrombolytics then resume anticoagulations | ||||||||||||||||||||||||||||||||||||||||||||||
Patient shows clinical improvement | |||||||||||||||||||||||||||||||||||||||||||||||
No | Yes | ||||||||||||||||||||||||||||||||||||||||||||||
Surgical emblectomy or catheter based interventions | Continue anticoagulation | ||||||||||||||||||||||||||||||||||||||||||||||
References
- ↑ 1.0 1.1 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)