Pulmonary embolism overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Pulmonary embolism occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of clot formation and embolization is termed [[thromboembolism]]. | Pulmonary embolism occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of clot formation and embolization is termed [[thromboembolism]]. | ||
==Causes== | |||
[[Pulmonary embolism]] (PE) is the acute obstruction of the [[pulmonary artery]] or one of its branches by a [[thrombus]], [[Air embolism|air]], [[Tumor embolism|tumor]], or [[Fat embolism|fat]]. Most often, PE is due to a [[venous thrombosis|venous thrombus]] which has been dislodged from its site of formation in the deep veins of the lower extremities, a process referred to as [[venous thromboembolism]]. | |||
==Differentiation of Pulmonary Embolism from other Diseases== | ==Differentiation of Pulmonary Embolism from other Diseases== | ||
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==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The precise number of people affected by venous thromboembolism (VTE), that is either [[deep vein thrombosis]], pulmonary embolism (PE), or both, is unknown, but estimates range from 300,000 to 600,000 (1 to 2 per 1,000, and in those over 80 years of age, as high as 1 in 100) each year in the United States. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited [[thrombophilia]]s in which a genetic defect can be identified that increases the risk for [[thrombosis]].<ref name=CDC>[http://www.cdc.gov/ncbddd/dvt/data.html CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein]</ref><ref name="pmid20331949">{{cite journal| author=Beckman MG, Hooper WC, Critchley SE, Ortel TL| title=Venous thromboembolism: a public health concern. | journal=Am J Prev Med | year= 2010 | volume= 38 | issue= 4 Suppl | pages= S495-501 | pmid=20331949 | doi=10.1016/j.amepre.2009.12.017 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20331949 }} </ref> | |||
==Risk Factors== | ==Risk Factors== | ||
The most common sources of pulmonary | The most common sources of pulmonary embolism (PE) are proximal leg [[deep venous thrombosis|deep venous thromboses]] ([[DVT]]s) or pelvic vein thromboses; therefore, any risk factor for [[DVT]] also increases the risk of PE. Approximately 15% of patients with a DVT will develop a PE. In these chapters on [[venous thromboembolism]] (VTE), the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing [[venous thrombosis]]. The word triggers refer to those factors in the patients immediate history or environment that may have lead to the occurrence of the [[venous thrombosis]]. The risk factors for VTE are a constellation of predisposing conditions which stem from the three principles of [[Virchow's triad]]: stasis of the blood flow, damage to the vascular [[endothelial cell]]s, and [[hypercoagulability]]. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited [[thrombophilia]]s in which a genetic defect can be identified that increases the risk for [[thrombosis]].<ref>[http://www.cdc.gov/ncbddd/dvt/data.html CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein]</ref><ref name="pmid20331949">{{cite journal| author=Beckman MG, Hooper WC, Critchley SE, Ortel TL| title=Venous thromboembolism: a public health concern. | journal=Am J Prev Med | year= 2010 | volume= 38 | issue= 4 Suppl | pages= S495-501 | pmid=20331949 | doi=10.1016/j.amepre.2009.12.017 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20331949 }} </ref> The risk factors for VTE can be classified as temporary, modifiable and non-modifiable. It is suggested that [[venous thrombosis]] also shares risk factors with [[arterial thrombosis]], such as [[obesity]], [[hypertension]], [[smoking]], and [[diabetes mellitus]].<ref name="pmid20620709">{{cite journal| author=Goldhaber SZ| title=Risk factors for venous thromboembolism. | journal=J Am Coll Cardiol | year= 2010 | volume= 56 | issue= 1 | pages= 1-7 | pmid=20620709 | doi=10.1016/j.jacc.2010.01.057 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20620709 }} </ref> | ||
==Triggers== | |||
The triggers of VTE include injury to a deep vein from [[surgery]], a fracture, or other [[trauma]], especially a paralytic spinal cord injury.<ref name="pmid12814980">{{cite journal |author=Anderson FA, Spencer FA |title=Risk factors for venous thromboembolism |journal=Circulation |volume=107 |issue=23 Suppl 1 |pages=I9–16 |year=2003 |month=June |pmid=12814980 |doi=10.1161/01.CIR.0000078469.07362.E6 |url=}}</ref> Another trigger for VTE is prolonged immobilization that causes [[stasis]] in the deep veins which may occur after [[surgery]], prolonged bed-rest, or prolonged seating during travel. | |||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
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]]. | Pulmonary embolism (PE) 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 PE 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 PE die, typically from recurrent PE. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. The true mortality associated with PE may be underestimated as two-thirds of all PE cases are diagnosed by autopsy. Estimates suggest that 60,000-100,000 Americans die of VTE, 10 to 30% of which will die within one month of diagnosis. Sudden death is the first symptom in about one-quarter (25%) of people who have a PE. One-third (about 33%) of people with VTE will have a recurrence within 10 years.<ref>[http://www.cdc.gov/ncbddd/dvt/data.html CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein]</ref><ref name="pmid20331949">{{cite journal| author=Beckman MG, Hooper WC, Critchley SE, Ortel TL| title=Venous thromboembolism: a public health concern. | journal=Am J Prev Med | year= 2010 | volume= 38 | issue= 4 Suppl | pages= S495-501 | pmid=20331949 | doi=10.1016/j.amepre.2009.12.017 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20331949 }} </ref> | ||
==Diagnosis== | ==Diagnosis== | ||
Revision as of 02:30, 15 July 2014
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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:
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).
Historical Perspective
Throughout history, many renowned researchers and health care professionals have contributed to the understanding, definition, and treatment of pulmonary embolism. Though the first documented case of pulmonary embolism occurred in 1837, historical record of thrombotic disease dates as far back as the 7th century BCE.[1]
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).
Pathophysiology
Pulmonary embolism occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of clot formation and embolization is termed thromboembolism.
Causes
Pulmonary embolism (PE) is the acute obstruction of the pulmonary artery or one of its branches by a thrombus, air, tumor, or fat. Most often, PE is due to a venous thrombus which has been dislodged from its site of formation in the deep veins of the lower extremities, a process referred to as venous thromboembolism.
Differentiation of Pulmonary Embolism from other Diseases
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
The precise number of people affected by venous thromboembolism (VTE), that is either deep vein thrombosis, pulmonary embolism (PE), or both, is unknown, but estimates range from 300,000 to 600,000 (1 to 2 per 1,000, and in those over 80 years of age, as high as 1 in 100) each year in the United States. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited thrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.[2][3]
Risk Factors
The most common sources of pulmonary embolism (PE) are proximal leg deep venous thromboses (DVTs) or pelvic vein thromboses; therefore, any risk factor for DVT also increases the risk of PE. Approximately 15% of patients with a DVT will develop a PE. In these chapters on venous thromboembolism (VTE), the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have lead to the occurrence of the venous thrombosis. The risk factors for VTE are a constellation of predisposing conditions which stem from the three principles of Virchow's triad: stasis of the blood flow, damage to the vascular endothelial cells, and hypercoagulability. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited thrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.[4][3] The risk factors for VTE can be classified as temporary, modifiable and non-modifiable. It is suggested that venous thrombosis also shares risk factors with arterial thrombosis, such as obesity, hypertension, smoking, and diabetes mellitus.[5]
Triggers
The triggers of VTE include injury to a deep vein from surgery, a fracture, or other trauma, especially a paralytic spinal cord injury.[6] Another trigger for VTE is prolonged immobilization that causes stasis in the deep veins which may occur after surgery, prolonged bed-rest, or prolonged seating during travel.
Natural History, Complications and Prognosis
Pulmonary embolism (PE) 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 PE 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 PE die, typically from recurrent PE. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. The true mortality associated with PE may be underestimated as two-thirds of all PE cases are diagnosed by autopsy. Estimates suggest that 60,000-100,000 Americans die of VTE, 10 to 30% of which will die within one month of diagnosis. Sudden death is the first symptom in about one-quarter (25%) of people who have a PE. One-third (about 33%) of people with VTE will have a recurrence within 10 years.[7][3]
Diagnosis
Assessment of Clinical Probability
The diagnosis of pulmonary embolism is based primarily on the clinical evaluation combined with diagnostic modalities such as spiral CT, V/Q scan, use of the D-dimer and lower extremity ultrasound.
History and 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.[8][9] The common symptoms of PE range from mild dyspnea, chest pain, and tachypnea, to sustained hypotension and shock.[10][9] 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.
Physical Examination
Pulmonary emboli are associated with the presence of tachycardia and tachypnea. Signs of right ventricular failure include jugular venous distension, a right sided S3, and a parasternal lift. These signs are often present in cases of massive pulmonary emboli.[10]
Laboratory Findings
The results of routine laboratory tests including arterial blood gas analysis are non-specific in making the diagnosis of pulmonary embolism. These laboratory studies can be obtained to rule-out other cause of chest discomfort and tachypnea. In patients with acute pulmonary embolism, non-specific lab findings include: leukocytosis, elevated ESR with an elevated serum LDH and serum transaminase (especially AST or SGOT).
Arterial Blood Gas Analysis
Hypoxemia, hypocapnia, increased alveolar-arterial gradient, and respiratory alkalosis are common findings that may be observed in patients with pulmonary embolism. In patients with suspected PE, Rodger et al, demonstrated that ABG analysis did not have sufficient negative predictive value, specificity, or likelihood ratios to be considered useful in the management these patients.[11] Similar findings were observed by the PIOPED II investigators.[12]
D-dimer
D-dimer is a fibrin degradation product. D-dimer levels are elevated in the plasma after the acute formation of a blood clot. The majority of patients with pulmonary embolism have some degree of endogenous fibrinolysis with an elevation in D-dimer levels, therefore there is a high negative predictive value in ruling out a pulmonary embolism when D-dimer levels are low. However a wide range of diseases are associated with mild degree of fibrinolysis which elevate D-dimer levels and contribute towards a reduced specificity and a poor positive predictive value of a high D-dimer level. This means that it is more likely that one can rule out a PE with a low D-dimer level, but cannot necessarily confirm the diagnosis of a PE based on a high D-dimer level. Other disease states that can also have a high d-dimer level include pneumonia, congestive heart failure (CHF), myocardial infarction (MI) and malignancy. False-negative values may occur in patients with prolonged symptoms of venous thromboembolism (≥14 days), patients on therapeutic heparin therapy, and patients with suspected deep venous thrombosis on oral anticoagulation, as these patients have will have low D-dimer levels in the presence of a PE.[13][9]
Biomarkers
Although the success of brain natriuretic peptide levels to diagnose pulmonary embolism is limited due to the reduced sensitivity of the test,[14] elevated BNP and pro-BNP levels accurately predict right ventricular dysfunction and associated mortality, and are therefore useful prognostic markers. [9] The evaluation of troponin levels also serves as a useful prognostic marker to identify right ventricular myocardial injury[15][16] and mortality associated with acute pulmonary embolism.[17]
Electrocardiogram
EKG abnormalities in the setting of pulmonary emolism are non-specific.[18][19] The EKG may also lack sensitivity as the EKG may be normal in the setting of a pulmonary embolus. In a prospective study EKG abnormalities were present in 70% of patients with documented acute pulmonary embolism. The most common EKG abnormality was nonspecific ST-segment and T-wave changes.[20] An electrocardiogram (ECG) is routinely performed in all patients with chest pain to assess for a myocardial infarction, but the diagnosis of a pulmonary embolism should be kept in mind as well.
Chest X Ray
A chest X ray is often obtained in patients with shortness of breath to diagnose pneumonia, congestive heart failure, and rib fracture. Although the chest X ray in the setting of a pulmonary embolism is often abnormal, the findings are non-specific and are not diagnostic of a pulmonary embolus.[21]
Ventilation/Perfusion Scan
A ventilation/perfusion scan (otherwise known as V/Q scan or lung scintigraphy) is a study which shows whether an area of the lung is being ventilated with oxygen and perfused with blood. In the setting of a PE, perfusion can be obstructed due to the formation of a clot. The V/Q scan is less commonly used due to the more widespread availability of CT technology, however it may be useful in patients who have an allergy to iodinated contrast. It may also be useful in pregnant patients in an attempt to minimize radiation exposure.
Echocardiography
Approximately 40% of patients with pulmonary embolism have evidence of right heart strain on echocardiography. When RV dysfunction or RV thrombus are identified on echocardiography, this finding provides further risk stratification. Routine echocardiography in patients with suspected pulmonary embolism is not required. However if elevations in the cardiac troponins or brain natriuretic peptide are present, then acute right ventricular strain may be present and echocardiography may be warranted.[22]
Compression Ultrasonography
Compression Ultrasonography, also known as a Doppler study of the legs, or lower extremity noninvasive studies (LENIS) is used to evaluate a patient for the presence of deep venous thrombosis (DVT) in the lower extremities, which can lead to the development of a pulmonary embolism. The presence of a DVT shown by ultrasonography is enough to warrant anticoagulation without a V/Q or spiral CT scans. The decision to anticoagulant patient with a positive compression ultrasound is due to the strong association between deep vein thrombosis and subsequent pulmonary embolism. Compression ultrasonography is also a preferred method of evaluation during pregnancy, a time during which the other modalities would increase the risk of birth defects due to radiation exposure. A negative compression ultrasound does not rule out a pulmonary embolism, and an additional low-radiation dose scanning may be required in a pregnant patient to further rule out pulmonary embolism.
CT
Contrast pulmonary angiography is the gold standard when diagnosing a PE. The disadvantages of using pulmonary angiography are its invasiveness, high costs, limited availability, and the need of an expert radiologist. This chapter deals with the advantages of multidetector CT over CTPA.
CT Pulmonary Angiography
Computed tomography with radiocontrast is the imaging modality of choice in the diagnosis of pulmonary embolism.
MRI
Magnetic resonance pulmonary angiography should be considered in the setting of a pulmonary embolism only at centers that routinely perform it well and only for patients for whom standard tests are contraindicated. MRA has a sensitivity and specificity of 78% and 99% respectively.[23]
Other Imaging Findings
Pulmonary angiography is the gold standard for diagnosing a pulmonary embolism (PE). The Pulmonary angiogram has a sensitivity and specificity of >95% in diagnosing a PE. The estimated false-negative rate is 0.5% – 1.7%. Pulmonary angiography is presently used less frequently in the diagnosis of pulmonary embolism due to wider acceptance of CT scans, which are non-invasive. CT pulmonary angiography is the recommended first line diagnostic imaging test in most people. A negative CT pulmonary angiogram excludes a clinically important pulmonary embolism.[24] Multi-Detector Computed Tomography (MDCTA) has rapidly replaced the use of pulmonary angiography in the clinical setting because MDCT is less invasive and easier to perform. Therefore, pulmonary angiography should only be performed first if MDCTA is unavailable or contraindicated.
Treatment
Treatment Algorithm
Prompt recognition, diagnosis and treatment of pulmonary embolism is critical. Anticoagulant therapy is the mainstay of treatment for patients who are hemodynamically stable. If hemodynamic compromise is present, then fibrinolytic therapy is recommended.
Surgery
Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients.[25] Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.
References
- ↑ Wood KE (2009). "A history of pulmonary embolism and deep venous thrombosis". Crit Care Clin. 25 (1): 115–31, viii. doi:10.1016/j.ccc.2008.12.014. PMID 19268798.
- ↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
- ↑ 3.0 3.1 3.2 Beckman MG, Hooper WC, Critchley SE, Ortel TL (2010). "Venous thromboembolism: a public health concern". Am J Prev Med. 38 (4 Suppl): S495–501. doi:10.1016/j.amepre.2009.12.017. PMID 20331949.
- ↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
- ↑ Goldhaber SZ (2010). "Risk factors for venous thromboembolism". J Am Coll Cardiol. 56 (1): 1–7. doi:10.1016/j.jacc.2010.01.057. PMID 20620709.
- ↑ Anderson FA, Spencer FA (2003). "Risk factors for venous thromboembolism". Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980. Unknown parameter
|month=ignored (help) - ↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
- ↑ 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) - ↑ 9.0 9.1 9.2 9.3 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) - ↑ 10.0 10.1 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) - ↑ Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS (2000). "Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism". American Journal of Respiratory and Critical Care Medicine. 162 (6): 2105–8. PMID 11112122. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ 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 (2006). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators". The American Journal of Medicine. 119 (12): 1048–55. doi:10.1016/j.amjmed.2006.05.060. PMID 17145249. Retrieved 2012-04-30. Unknown parameter
|month=ignored (help) - ↑ Bruinstroop E, van de Ree MA, Huisman MV (2009). "The use of D-dimer in specific clinical conditions: a narrative review". Eur J Intern Med. 20 (5): 441–6. doi:10.1016/j.ejim.2008.12.004. PMID 19712840.
- ↑ Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR (2006). "Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism". Journal of Thrombosis and Haemostasis : JTH. 4 (3): 552–6. doi:10.1111/j.1538-7836.2005.01752.x. PMID 16405522. Retrieved 2012-05-01. Unknown parameter
|month=ignored (help) - ↑ Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB (2000). "Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction". Journal of the American College of Cardiology. 36 (5): 1632–6. PMID 11079669. Retrieved 2012-05-02. Unknown parameter
|month=ignored (help) - ↑ Horlander KT, Leeper KV (2003). "Troponin levels as a guide to treatment of pulmonary embolism". Current Opinion in Pulmonary Medicine. 9 (5): 374–7. PMID 12904706. Retrieved 2012-05-02. Unknown parameter
|month=ignored (help) - ↑ Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S; et al. (2008). "Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism". Eur Respir J. 31 (4): 847–53. doi:10.1183/09031936.00113307. PMID 18094010.
- ↑ Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV (2005). "Prognostic value of the ECG on admission in patients with acute major pulmonary embolism". Eur Respir J. 25 (5): 843–8. doi:10.1183/09031936.05.00119704. PMID 15863641.
- ↑ Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P; et al. (2000). "Diagnostic value of the electrocardiogram in suspected pulmonary embolism". Am J Cardiol. 86 (7): 807–9, A10. PMID 11018210.
- ↑ Stein PD, Saltzman HA, Weg JG (1991). "Clinical characteristics of patients with acute pulmonary embolism". Am J Cardiol. 68 (17): 1723–4. PMID 1746481.
- ↑ Worsley D, Alavi A, Aronchick J, Chen J, Greenspan R, Ravin C (1993). "Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study". Radiology. 189 (1): 133–6. PMID 8372182.
- ↑ Kucher N, Goldhaber SZ (2003). "Cardiac biomarkers for risk stratification of patients with acute pulmonary embolism". Circulation. 108 (18): 2191–4. doi:10.1161/01.CIR.0000100687.99687.CE. PMID 14597581.
- ↑ Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR (1997). "Diagnosis of pulmonary embolism with magnetic resonance angiography". N. Engl. J. Med. 336 (20): 1422–7. doi:10.1056/NEJM199705153362004. PMID 9145679. Retrieved 2011-12-14. Unknown parameter
|month=ignored (help) - ↑ Stein PD, Henry JW, Gottschalk A (1999). "Reassessment of pulmonary angiography for the diagnosis of pulmonary embolism: relation of interpreter agreement to the order of the involved pulmonary arterial branch". Radiology. 210 (3): 689–91. PMID 10207468.
- ↑ Augustinos P, Ouriel K (2004). "Invasive approaches to treatment of venous thromboembolism". Circulation. 110 (9 Suppl 1): I27–34. PMID 15339878.