Pulmonary embolism overview

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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.

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 Acuity and Size

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

Submassive Pulmonary Embolism

  • Submassive pulmonary embolism is associated with:[3][4]
  • 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.[5]

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
  • An acute pulmonary embolism without the life threatening clinical markers that define massive or submassive pulmonary emboli. [2]

Pathophysiology

The diagram below summarizes the sequence of pathophysiologic events in pulmonary embolism:[4]

Differentiation of Pulmonary Embolism from other Disorders

Pulmonary embolism must be distinguished from other life-threatening causes of chest pain including acute myocardial infarction, aortic dissection, and pericardial tamponade, as well as a large list of non-life-threatening causes of chest discomfort and Shortness of breath.

Epidemiology and Demographics

Overview

Each year in United States, there are between 300,000-600,000 cases of pulmonary embolism (PE). The prevalence of the disease increases as age increases.

Risk Factors

The most common sources of pulmonary emboli are proximal leg deep venous thromboses (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk of pulmonary embolism, and therefore DVT and PE are considered to be a continuum termed venous thromboembolism (VTE). Approximately 15% of patients with a DVT will develop a pulmonary embolus. Smoking, estrogen-containing hormonal contraceptives, and immobilization (including long distance travel) are common risk factors.

The development of thrombosis is classically due to a group of causes referred to as Virchow's triad. Virchow's triad includes alterations in blood flow, factors in the vessel wall, and factors affecting the properties of the blood. It is common for more than one risk factor to be present.

Figure: Virchow's triad encompasses three broad categories of factors that are thought to contribute to venous thrombosis.

Medical conditions included in the triad are:

Complications

Pulmonary embolism can be acutely complicated by the development of cardiogenic shock, pulseless electrical activity and sudden cardiac death and chronically by the development of pulmonary hypertension. The medical management of pulmonary embolism often requires the administration of potent parenteral anticoagulants and fibrinolytics and massive bleeding can be a complication of their administration. If left untreated almost one-third of patients with pulmonary embolism die, typically from recurrent pulmonary embolism. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. The true mortality associated with pulmonary embolism may be underestimated as two-thirds of all pulmonary embolism cases are diagnosed by autopsy.

Acute Complications

Chronic Complications

Complications of Firbrinolytic Therapy for Pulmonary Embolism[7]

  • Severe bleeding can occur as a complication of fibrinolytic treatment:

Prognosis

If left untreated, almost one-third of the patients die, typically from recurrent PE. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. Unfortunately, two-thirds of all PE cases are diagnosed by autopsy. [8] Pulmonary embolism causes death in approximately 16% of hospitalized patients.

A 26% mortality rate associated with untreated pulmonary embolism is often cited based upon a trial published in 1960 by Barrit and Jordan[9] which compared anti-coagulation against placebo for the management of pulmonary embolism. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the efficacy of anticoagulants in the treatment of pulmonary embolism. The results of this were so convincing that the trial has not been repeated. On the other hand, the reported mortality rate of 26% in the placebo group may underestimate the true mortality insofar as the sensitivity and specificity of diagnostic technology in 1957 may have only allowed the detection of massive pulmonary emboli.

Risk Stratification in Assessing Prognosis

The prognosis in a patient with pulmonary embolism depends upon:

  • The extent of the pulmonary vasculature that is occluded
  • Co-existence of other medical conditions (i.e. the patient's comorbidities)

Clinical correlates of mortality among patients with pulmonary embolism are listed below.

Hemodynamic status

Observational studies such as the International COoperative Pulmonary Embolism Registry (ICOPER) and the Management and Prognosis in Pulmonary Embolism Trial (MAPPET) have shown that shock and hypotension are principal high risk markers of early death in acute PE.[10] The MAPPET study demonstrated that systemic shock was associated with mortality of 24.5% where as hypotension (but not shock) was associated with the mortality of 15.2%.

A post-hoc analysis of the ICOPER study demonstrated that the 90-day all-cause mortality rate was 52.4% (95% CI,43.3–62.1%) among patients with a systolic blood pressure less than 90 mm Hg compared to 14.7% (95% CI, 13.3–16.2%) among patients with a normal blood pressure.[11]

The PESI (Pulmonary Embolism Severity Index) study demonstrated that hypotension (blood pressure <100 mm Hg) is associated with a mortality of nearly 50%. [12]

Markers of Right Ventricular Dysfunction (RVD) [13]

The presence of right ventricular dysfunction (RVD) on echocardiography has been associated with a higher mortality in the setting of pulmonary embolism.

Association of RV Dysfunction (RVD) on Echocardiography With Mortality in Pulmonary Embolism
Study Year Patients (n) Blood pressure Echocardiographic criteria RVD(present) vs. RVD(absent): Mortality percentage(%)
Goldhaber et al.[14] 1993 101 Normotensive RV hypokinesis and dilatation 4.3% vs. 0%
Ribeiro et al. [15] 1997 126 Normotensive and hypotensive RVD 12.8% vs. 0%
Kasper et al.[16] 1997 317 Normotensive and hypotensive RV >30 mm or TI >2.8 m/s 13% vs. 0.9%
Grifoni et al.[17] 2000 162 BP ≥ 100 mmHg Atleast one of the following
  • RV >30 mm or RV/LV >1
  • Paradox septal systolic motion
  • AcT <90 ms or TIPG >30 mmHg
 4.6% vs. 0%
Kucher et al.[18] 2005 1035 BP ≤ 90 mmHg RVD 16.3% vs. 9.4%

Abbreviations Used: RV , right ventricle; TI, tricuspid insufficiency; LV, left ventricle; AcT, ACceleration Time of right ventricular ejection; TIPG, tricuspid insufficiency peak gradient.

Brain Natriuretic Peptide

In patients with a pulmonary embolism, elevated plasma levels of natriuretic peptides (brain natriuretic peptide and N-terminal pro-brain natriuretic peptide) have been associated with higher mortality.[19] Levels of N-terminal pro-brain natriuretic peptide greater than 500 ng/L serve as an indicator of the burden of PE and are associated with death.[20]

Serum Troponin

Elevated serum troponin levels are associated with an increased risk of death among pulmonary embolism patients. The elevation of troponin in patients with a massive pulmonary embolism does not reflect epicadial coronary artery disease but rather transmural RV infarctions on autopsy.[21] [22]

Hyponatremia

Hyponatremia at the time of presentation is associated with increased mortality and hospital readmission

Electrocardiographic Abnormalities

The electrocardiographic findings in pulmonary embolism can provide prognostic information (click here to read more). EKG findings that are associated with a poor prognosis include:[23]

  1. Atrial arrhythmias
  2. Right bundle branch block
  3. Q-waves in the inferior leads
  4. Precordial T-wave inversion and ST-segment changes.
  5. Development of a QR wave in lead V1 is identified as an independent risk factor for an adverse prognosis.[24]

Pre-Test Probability of Pulmonary Embolism

Wells Score

The Wells score is a simple, commonly used clinical risk prediction tool to evaluate the need for further testing in patients suspected to have pulmonary embolism.[25][26][27][28]

Wells Score Calculator for PE

Variable Wells[27]
Clinically suspected DVT (leg swelling, pain with palpation) 3.0
Alternative diagnosis is less likely than PE 3.0
Immobilization/surgery in previous four weeks 1.5
Previous history of DVT or PE 1.5
Tachycardia (heart rate more than 100 bpm) 1.5
Malignancy (treatment for within 6 months, palliative) 1.0
Hemoptysis 1.0

Wells criteria [27][28]

  • The following scoring system is used to assess the possible risk to a patient.[29] It also shows if there is a need for further testing with D-dimer or CT scan:
  • Score >6.0 - High probability (~59%).
  • Score 2.0 to 6.0 - Moderate probability (~29%).
  • Score <2.0 - Low probability (~15%).
  • The modified extended version of the Wells score has been proposed.[30]
  • Score > 4 - PE likely. Consider diagnostic imaging.
  • Score 4 or less - PE unlikely. Consider D-dimer to rule out PE.
  • A simplified Wells criteria has been proposed[34], according to which all the 7 risk variables (table) are assigned 1 point each. A score ≤ 1 is categorized as unlikely to be PE. This score needs further validation in prospective studies.

Diagnosis

Symptoms

The symptoms of pulmonary embolism (PE) depends on the severity of the disease. A Pulmonary embolism may be an incidental finding in so far as many patients are asymptomatic.[35][36] The common symptoms of PE range from mild dyspnea, chest pain, and tachypnea, to sustained hypotension and shock.[37][36] The absence of these symptoms may be associated with a reduced clinical probability of pulmonary embolism, however it does not exclude the diagnosis of pulmonary embolism. The symptoms of lower extremity deep venous thrombosis may also be present.

References

  1. ↑ 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).
  2. ↑ 2.0 2.1 2.2 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.
  3. ↑ 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)
  4. ↑ 4.0 4.1 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)
  5. ↑ 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)
  6. ↑ "Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER) : The Lancet". Retrieved 2012-10-07.
  7. ↑ "Thrombolysis Compared With Heparin for the Initial Treatment of Pulmonary Embolism". Retrieved 2012-10-06.
  8. ↑ American Heart Association. (2007). Venous Thromboembolism & Pulmonary Embolism - Statistical Fact Sheet: 2007 Update. Retreived from http://stopdvt.org/Documents/AMA%20Fact%20Sheet%20Current%20Research.pdf
  9. ↑ "Anticoagulant drugs in the treatment of pulmonary embolism: a controlled trial". Lancet. 1: 1309&ndash, 1312. 1960. PMID 13797091. Text " Barritt DW, Jorden SC " ignored (help)
  10. ↑ Kasper W, Konstantinides S, Geibel A, Olschewski M, Heinrich F, Grosser KD; et al. (1997). "Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry". J Am Coll Cardiol. 30 (5): 1165–71. PMID 9350909.
  11. ↑ Kucher N, Rossi E, De Rosa M, Goldhaber SZ (2006). "Massive pulmonary embolism". Circulation. 113 (4): 577–82. doi:10.1161/CIRCULATIONAHA.105.592592. PMID 16432055.
  12. ↑ Donzé J, Le Gal G, Fine MJ, Roy PM, Sanchez O, Verschuren F; et al. (2008). "Prospective validation of the Pulmonary Embolism Severity Index. A clinical prognostic model for pulmonary embolism". Thromb Haemost. 100 (5): 943–8. PMID 18989542.
  13. ↑ Konstantinides S (2005). "Pulmonary embolism: impact of right ventricular dysfunction". Curr Opin Cardiol. 20 (6): 496–501. PMID 16234620.
  14. ↑ Goldhaber SZ, Haire WD, Feldstein ML, Miller M, Toltzis R, Smith JL; et al. (1993). "Alteplase versus heparin in acute pulmonary embolism: randomised trial assessing right-ventricular function and pulmonary perfusion". Lancet. 341 (8844): 507–11. PMID 8094768.
  15. ↑ Ribeiro A, Lindmarker P, Juhlin-Dannfelt A, Johnsson H, Jorfeldt L (1997). "Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate". Am Heart J. 134 (3): 479–87. PMID 9327706.
  16. ↑ Kasper W, Konstantinides S, Geibel A, Tiede N, Krause T, Just H (1997). "Prognostic significance of right ventricular afterload stress detected by echocardiography in patients with clinically suspected pulmonary embolism". Heart. 77 (4): 346–9. PMC 484729. PMID 9155614.
  17. ↑ Grifoni S, Olivotto I, Cecchini P, Pieralli F, Camaiti A, Santoro G; et al. (2000). "Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction". Circulation. 101 (24): 2817–22. PMID 10859287.
  18. ↑ Kucher N, Rossi E, De Rosa M, Goldhaber SZ (2005). "Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher". Arch Intern Med. 165 (15): 1777–81. doi:10.1001/archinte.165.15.1777. PMID 16087827.
  19. ↑ Cavallazzi R, Nair A, Vasu T, Marik PE (2008). "Natriuretic peptides in acute pulmonary embolism: a systematic review". Intensive Care Med. 34 (12): 2147–56. doi:10.1007/s00134-008-1214-5. PMID 18626627.
  20. ↑ Alonso-Martínez JL, Urbieta-Echezarreta M, Anniccherico-Sánchez FJ, Abínzano-Guillén ML, Garcia-Sanchotena JL (2009). "N-terminal pro-B-type natriuretic peptide predicts the burden of pulmonary embolism". Am J Med Sci. 337 (2): 88–92. doi:10.1097/MAJ.0b013e318182d33e. PMID 19214022.
  21. ↑ Becattini C, Vedovati MC, Agnelli G (2007). "Prognostic value of troponins in acute pulmonary embolism: a meta-analysis". Circulation. 116 (4): 427–33. doi:10.1161/CIRCULATIONAHA.106.680421. PMID 17606843.
  22. ↑ Jiménez D, Uresandi F, Otero R, Lobo JL, Monreal M, Martí D; et al. (2009). "Troponin-based risk stratification of patients with acute nonmassive pulmonary embolism: systematic review and metaanalysis". Chest. 136 (4): 974–82. doi:10.1378/chest.09-0608. PMID 19465511.
  23. ↑ Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M (1997). "The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports". Chest. 111 (3): 537–43. PMID 9118684.
  24. ↑ Kucher N, Walpoth N, Wustmann K, Noveanu M, Gertsch M (2003). "QR in V1--an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism". European Heart Journal. 24 (12): 1113–9. PMID 12804925. Retrieved 2011-12-05. Unknown parameter |month= ignored (help)
  25. ↑ Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon C, Weitz J, D'Ovidio R, Cogo A, Prandoni P (1995). "Accuracy of clinical assessment of deep-vein thrombosis". Lancet. 345 (8961): 1326–30. PMID 7752753. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  26. ↑ Wells PS, Ginsberg JS, Anderson DR, Kearon C, Gent M, Turpie AG, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (1998). "Use of a clinical model for safe management of patients with suspected pulmonary embolism". Ann Intern Med. 129 (12): 997–1005. PMID 9867786.
  27. ↑ 27.0 27.1 27.2 27.3 Wells P, Anderson D, Rodger M, Ginsberg J, Kearon C, Gent M, Turpie A, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (2000). "Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer". Thromb Haemost. 83 (3): 416–20. PMID 10744147.
  28. ↑ 28.0 28.1 Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D, Forgie M, Kovacs G, Ward J, Kovacs MJ (2001). "Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer". Ann Intern Med. 135 (2): 98–107. PMID 11453709.
  29. ↑ Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, Sos TA, Quinn DA, Leeper KV, Hull RD, Hales CA, Gottschalk A, Goodman LR, Fowler SE, Buckley JD (2007). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II Investigators". Radiology. 242 (1): 15–21. doi:10.1148/radiol.2421060971. PMID 17185658.
  30. ↑ Sanson BJ, Lijmer JG, Mac Gillavry MR, Turkstra F, Prins MH, Büller HR (2000). "Comparison of a clinical probability estimate and two clinical models in patients with suspected pulmonary embolism. ANTELOPE-Study Group". Thromb. Haemost. 83 (2): 199–203. PMID 10739372.
  31. ↑ Geersing, G.-J. (2012-10-04). "Safe exclusion of pulmonary embolism using the Wells rule and qualitative D-dimer testing in primary care: prospective cohort study". BMJ. 345 (oct04 2): e6564–e6564. doi:10.1136/bmj.e6564. ISSN 1756-1833. Retrieved 2012-10-05. Unknown parameter |coauthors= ignored (help)
  32. ↑ van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW; et al. (2006). "Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography". JAMA. 295 (2): 172–9. doi:10.1001/jama.295.2.172. PMID 16403929.
  33. ↑ Anderson DR, Kahn SR, Rodger MA, Kovacs MJ, Morris T, Hirsch A, Lang E, Stiell I, Kovacs G, Dreyer J, Dennie C, Cartier Y, Barnes D, Burton E, Pleasance S, Skedgel C, O'Rouke K, Wells PS (2007). "Computed tomographic pulmonary angiography vs ventilation-perfusion lung scanning in patients with suspected pulmonary embolism: a randomized controlled trial". JAMA. 298 (23): 2743–53. doi:10.1001/jama.298.23.2743. PMID 18165667.
  34. ↑ Gibson NS, Sohne M, Kruip MJ, Tick LW, Gerdes VE, Bossuyt PM; et al. (2008). "Further validation and simplification of the Wells clinical decision rule in pulmonary embolism". Thromb Haemost. 99 (1): 229–34. doi:10.1160/TH07-05-0321. PMID 18217159.
  35. ↑ Stein PD, Matta F, Musani MH, Diaczok B (2010). "Silent pulmonary embolism in patients with deep venous thrombosis: a systematic review". The American Journal of Medicine. 123 (5): 426–31. doi:10.1016/j.amjmed.2009.09.037. PMID 20399319. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
  36. ↑ 36.0 36.1 Agnelli G, Becattini C (2010). "Acute pulmonary embolism". The New England Journal of Medicine. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
  37. ↑ Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK (2007). "Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II". The American Journal of Medicine. 120 (10): 871–9. doi:10.1016/j.amjmed.2007.03.024. PMC 2071924. PMID 17904458. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)

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