Acute Care Advisor
Acute chest pain and pulmonary embolism
By Jennifer Wilbeck, DNP, ACNP-BC, FNP-BC, CEN and Dian Evans, PhD, FNP-BC, ENP-BC
For nurse practitioners (NPs) evaluating patients who present with chest pain, understanding how to diagnose and manage these patients is critical. In fact, chest pain was the second most common reason for seeking emergency care in the United States in 2010.1 Numerous guidelines regarding the assessment and management of patients with cardiac chest pain (for example, acute myocardial infarction or unstable angina) have been disseminated.2-4 With the increased emphasis on identifying chest pain of cardiac origin, the NP must remain equally vigilant to consider pulmonary embolism (PE) as a differential diagnosis. Although pulmonary symptoms such as dyspnea are classical presentations of PE, chest pain is also a frequent complaint.5 Nonspecific symptoms of PE, such as cough and mild shortness of breath, may result in missed diagnoses and increased mortality.6 Although actual prevalence and incidence is difficult to determine, as estimates may combine PE with broader diagnoses, such as venous thromboembolism (VTE) or deep vein thrombosis (DVT), PE is the third leading cause of death in hospitalized patients and is responsible for 230,000 nonfatal cases of PE annually in the United States.7-9 This article will highlight strategies for risk stratification, discuss diagnostic modalities, and review treatment strategies according to recent national guidelines. www.tnpj.com
■ Risk factors and presentation Conditions that predispose patients to hypercoagulable states (such as malignancy, inherited thrombophilias, estrogen therapies, trauma), venous stasis (such as immobility or prolonged travel), or endothelial injury (such as recent surgery, trauma, endovascular procedures, smoking) are risk factors for developing VTE.9 Although there are various types of pulmonary emboli, the most common results when a thrombus forms and travels from the original site (most often in the lower extremities) to a distant site. Once the thrombus dislodges and travels through the venous system and lodges in the pulmonary artery, pulmonary infarction with subsequent alveolar hemorrhage and pleural irritation may occur.10,11 Similar to chest pain of cardiac origin, clinical presentations of PE are varied and depend on the size and location of the emboli. Often referred to as the “classical presentation,” hallmark symptoms include pleuritic chest pain, new or worsening dyspnea, hypoxia, or hypotension. Cough, hemoptysis, and substernal chest pain are seen less often. Syncope may also occur if hemodynamic parameters become significantly altered.10 ■ Objective risk stratification Objective risk stratification is crucial due to the varied manifestations of this high-risk diagnosis. Among outpatients, noncancer-related thrombophilia, pleuritic chest pain, and a family history of VTE were shown to increase the likelihood of the diagnosis of PE.12 PE rates have also been found to be
higher among Blacks, women, patients with malignancies, and those 70 years of age and older.7 Validated risk stratification tools such as the Wells criteria are useful for guiding providers in selection of appropriate testing and management of patients at risk for PE. Wells score. The Wells Criteria considers seven parameters, assigning a point value to each, to determine the risk of PE. These include: clinical suspicion for DVT (3 points); alternative diagnosis less likely than PE (3 points); heart rate greater than 100 (1.5 points); recent immobilization (1.5 points); previous PE or DVT (1.5 points); hemoptysis (1 point); and current malignancy requiring treatment or palliative care (1 point). Numerical scores are calculated based on the presence of those factors and are then used to stratify risk.12,13 Patients with a score of less than 2 are considered low risk, those scoring 2 to 6 are at moderate risk, and those scoring greater than or equal to 7 are considered high risk. While there remains concern surrounding the subjectivity of the scoring, prospective validation studies have supported the Wells Criteria, and it is recommended that clinicians utilize these criteria in risk stratification.10,14,15 ■ Diagnostic testing Based on initial presentation and risk stratification, diagnostic testing must proceed to rule out life-threatening conditions. The ECG, as a diagnostic tool for identifying PE, has limited sensitivity due to diverse, nonspecific findings.5-8,10 Normal ECGs have been found in one-third of patients with PE, while others have nonspecific ST changes. A The Nurse Practitioner • January 2015 43
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
AcuteC are Advisor pattern of right heart strain may also be noted in conjunction with PE but is also nonspecific.10,11 Ultimately, the ECG is important in identifying changes associated with other acute cardiac pathology but is not diagnostic for confirming PE. d-dimer testing. A specific byproduct of fibrin degradation, the d-dimer is typically elevated in patients with thromboembolic disease. Although highly sensitive (nearing 100%), the test has low specificity of only 30% to 40%.16 Conditions such as acute infections, pregnancy, active cancers, trauma, inflammation, peripheral vascular disease, necrosis, recent surgery, liver disease, and kidney dysfunction may cause fibrin elevations.17,18 Current research is exploring the utility of raising the limit for the d-dimer in patients over 75 years of age, as d-dimer levels in this population are falsely elevated.19 For these reasons, the d-dimer is most appropriately used in conjunction with the history and physical exam as a tool to exclude patients with a low pretest probability for diagnosis of PE. It is now generally accepted (based on strong evidence) that a negative highsensitivity quantitative d-dimer can exclude the diagnosis of PE in patients considered at low risk for the diagnosis. However, among patients with intermediate probability of the diagnosis, based on risk stratification, the evidence is not as strong to support the use of negative d-dimers for PE exclusion, and further testing is warranted.14 Radiographic imaging. Anteriorposterior and lateral chest radiographs are recommended as an initial first study to help identify other sources of chest pain and dyspnea.20 Computed tomography pulmonary angiography (CTPA) is the current standard for diagnosis of PE. However, the use of CTPA carries risks of contrastinduced nephropathy and anaphylaxis and malignancy from exposure to high-dose computed tomography chest radiation.16,20 The use of CTPA 44 The Nurse Practitioner • Vol. 40, No. 1
should, therefore, be reserved for those with a high suspicion for PE based on screening criteria and history. A negative CTPA can be used to exclude PE for patients with a low risk for PE in whom further testing is warranted (perhaps a positive d-dimer or quantitative d-dimer not available).14 Ventilation perfusion imaging (V/Q scan), once the preferred test for assessing abnormal lung perfusion diagnostic of PE in the presence of a normal chest radiograph, is another option for assessing PE. Similar to the CTPA, the V/Q scan is associated with radiation exposure and offers no benefit over CTPA testing except in the case of pregnancy where the contrast media may be reduced, allowing for less radiation absorption.20 ■ Treatment and management Treatment strategies are determined based on the patient’s hemodynamic stability once the diagnosis of PE is made. A rapid-onset anticoagulant is the cornerstone of initial therapy for patients who are hemodynamically stable. Typically, unfractionated heparin or low-molecular-weight heparin is given for 5 to 7 days followed by a vitamin K antagonist, such as warfarin, for 3 months. Long-term therapy is required for patients at risk for repeated emboli, such as those with active malignancies or recurrent thrombolic events. Among patients with pregnancy or cancers, lowmolecular-weight heparin is preferred for both immediate and extended therapies. Vena cava filters may be utilized in patients with contraindications to anticoagulant therapy.10,21,22 Fibrinolytic therapy. Similar to the patient with a cardiac occlusion, fibrinolytic therapy must be viewed in terms of risks and benefits. The benefits of fibrinolytics are often supported in hemodynamically unstable patients with confirmed PE. Fibrinolytics may
also be considered for hemodynamically unstable patients when the clinical suspicion for PE is high but the diagnosis cannot be definitely confirmed or excluded in a timely manner.14 Alternately, surgical or mechanical thrombectomy may be performed for those whom fibrinolytics are considered too risky (for example, those with known intracranial disease, uncontrolled hypertension, or status-post recent trauma or surgery) or for those who remain hemodynamically unstable despite fibrinolytics.10,14,21 Current studies do not support use of fibrinolytics for hemodynamically stable patients; however, antiplatelet medications for VTE are recommended.14 ■ Implications for advanced practice nursing PE is a serious and often elusive diagnosis. Maintaining awareness of the possibility of PE in patients presenting with chest pain and shortness of breath is vital to avoiding a missed diagnosis because PE may be lethal if undiagnosed and/or not treated. Significant sequela, such as cardiac dysfunction, hemodynamic decompensation, or death may result from PE, and the NP is uniquely poised to prevent these complications. Recognition of risk factors and utilization of risk stratification to ensure the correct use of diagnostic modalities can reduce unnecessary diagnostic testing and improve patient outcomes. REFERENCES 1. Centers for Disease Control and Prevention. National hospital ambulatory medical survey: factsheet emergency department. http://www. cdc.gov/nchs/data/ahcd/NHAMCS_2010_ed_ factsheet.pdf. 2. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):485-510. 3. AHRQ. Guideline Summary NGC-7890. Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. 2012.
www.tnpj.com
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Acute Care Advisor 4. AHRQ. Guideline Summary NGC-9521. Diagnosis and treatment of chest pain and acute coronary syndrome (ACS). 2012. 5. McConaghy JR, Oza RS. Outpatient diagnosis of acute chest pain in adults. Am Fam Physician. 2013;87(3):177-182. 6. Duriseti RS, Brandeau ML. Cost-effectiveness of strategies for diagnosing pulmonary embolism among emergency department patients presenting with undifferentiated symptoms. Ann Emerg Med. 2010;56(4):321-332. 7. DeMonaco NA, Dang Q, Kapoor WN, Ragni MV. Pulmonary embolism incidence is increasing with use of spiral computed tomography. Am J Med. 2008;121(7):611-617. 8. Heit JA, Cohen AT, Anderson FA, Jr., on Behalf of the VTE Impact Assessment Group. Estimated Annual Number of Incident and Recurrent, Non-Fatal and Fatal Venous Thromboembolism (VTE) Events in the US. ASH Annual Meeting Abstracts. 2005;106:910. 9. Ouellette DR. Pulmonary embolism. Medscape. emedicine.medscape.com/article/300901overview#a0156. 10. Cohen AT, Dobromirski M, Gurwith MM. Managing pulmonary embolism from presentation to extended treatment. Thromb Res. 2014;133(2):139-148. 11. Strange JA, Pilcher D. Management of pulmonary embolism. Anaesthesia and Intensive Care Medicine. 2014;15:72–77.
www.tnpj.com
12. Courtney DM, Kline JA, Kabrhel C, et al. Clinical features from the history and physical examination that predict the presence or absence of pulmonary embolism in symptomatic emergency department patients: results of a prospective, multicenter study. Ann Emerg Med. 2010;55(4):307-315. 13. Kline JA, Wells PS. Methodology for a rapid protocol to rule out pulmonary embolism in the emergency department. Ann Emerg Med. 2003;42(2):266-275. 14. Fesmire FM, Brown MD, Espinosa JA, et al. Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism. Ann Emerg Med. 2011;57(6):628-652. 15. Huisman MV, Klok FA. Diagnostic management of acute deep vein thrombosis and pulmonary embolism. J Thromb Haemost. 2013;11(3): 412-422. 16. van Es J, Beenen LF, Gerdes VE, Middeldorp S, Douma RA, Bossuyt PM. The accuracy of D-dimer testing in suspected pulmonary embolism varies with the Wells score. J Thromb Haemost. 2012;10(12):2630-2632. 17. Kabrhel C, Mark Courtney D, Camargo CA Jr, et al. Factors associated with positive d-dimer results in patients evaluated for pulmonary embolism. Acad Emerg Med. 2010;17(6):589-597. 18. Yin F, Wilson T, Della Fave A, et al. Inappropriate use of D-dimer assay and pulmonary CT angiog-
raphy in the evaluation of suspected acute pulmonary embolism. Am J Med Qual. 2012;27(1):74-79. 19. Righini M, Van Es J, Den Exter PL, et al. Ageadjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014;311(11):1117-1124. 20. American College of Radiology Appropriateness Criteria. Acute chest pain-suspected pulmonary embolism. 2013. http://www.acr.org/~/media/ ACR/Documents/AppCriteria/Diagnostic/Acute ChestPainSuspectedPulmonaryEmbolism.pdf. 21. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med. 2010;363(3):266-274. 22. American College of Chest Physicians Evidence-Based Clinical Practice Guidelines: Antithrombotic Therapy and Prevention of Thrombosis. 9th ed. Chest. 2012;141(2 Suppl):7S-47S. Jennifer Wilbeck is an associate professor and FNP/ ACNP-ED program coordinator at Vanderbilt University, Nashville, Tenn. Dian Evans is an emergency nurse practitioner and specialty coordinator associate professor at Emory University, Nell Hodgson Woodruff School of Nursing, Atlanta, Ga. The authors have disclosed that they have no financial relationships related to this article. DOI: 10.1097/01.NPR.0000457439.35283.05
The Nurse Practitioner • January 2015 45
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Acute chest pain and pulmonary embolism
By Jennifer Wilbeck, DNP, ACNP-BC, FNP-BC, CEN and Dian Evans, PhD, FNP-BC, ENP-BC
For nurse practitioners (NPs) evaluating patients who present with chest pain, understanding how to diagnose and manage these patients is critical. In fact, chest pain was the second most common reason for seeking emergency care in the United States in 2010.1 Numerous guidelines regarding the assessment and management of patients with cardiac chest pain (for example, acute myocardial infarction or unstable angina) have been disseminated.2-4 With the increased emphasis on identifying chest pain of cardiac origin, the NP must remain equally vigilant to consider pulmonary embolism (PE) as a differential diagnosis. Although pulmonary symptoms such as dyspnea are classical presentations of PE, chest pain is also a frequent complaint.5 Nonspecific symptoms of PE, such as cough and mild shortness of breath, may result in missed diagnoses and increased mortality.6 Although actual prevalence and incidence is difficult to determine, as estimates may combine PE with broader diagnoses, such as venous thromboembolism (VTE) or deep vein thrombosis (DVT), PE is the third leading cause of death in hospitalized patients and is responsible for 230,000 nonfatal cases of PE annually in the United States.7-9 This article will highlight strategies for risk stratification, discuss diagnostic modalities, and review treatment strategies according to recent national guidelines. www.tnpj.com
■ Risk factors and presentation Conditions that predispose patients to hypercoagulable states (such as malignancy, inherited thrombophilias, estrogen therapies, trauma), venous stasis (such as immobility or prolonged travel), or endothelial injury (such as recent surgery, trauma, endovascular procedures, smoking) are risk factors for developing VTE.9 Although there are various types of pulmonary emboli, the most common results when a thrombus forms and travels from the original site (most often in the lower extremities) to a distant site. Once the thrombus dislodges and travels through the venous system and lodges in the pulmonary artery, pulmonary infarction with subsequent alveolar hemorrhage and pleural irritation may occur.10,11 Similar to chest pain of cardiac origin, clinical presentations of PE are varied and depend on the size and location of the emboli. Often referred to as the “classical presentation,” hallmark symptoms include pleuritic chest pain, new or worsening dyspnea, hypoxia, or hypotension. Cough, hemoptysis, and substernal chest pain are seen less often. Syncope may also occur if hemodynamic parameters become significantly altered.10 ■ Objective risk stratification Objective risk stratification is crucial due to the varied manifestations of this high-risk diagnosis. Among outpatients, noncancer-related thrombophilia, pleuritic chest pain, and a family history of VTE were shown to increase the likelihood of the diagnosis of PE.12 PE rates have also been found to be
higher among Blacks, women, patients with malignancies, and those 70 years of age and older.7 Validated risk stratification tools such as the Wells criteria are useful for guiding providers in selection of appropriate testing and management of patients at risk for PE. Wells score. The Wells Criteria considers seven parameters, assigning a point value to each, to determine the risk of PE. These include: clinical suspicion for DVT (3 points); alternative diagnosis less likely than PE (3 points); heart rate greater than 100 (1.5 points); recent immobilization (1.5 points); previous PE or DVT (1.5 points); hemoptysis (1 point); and current malignancy requiring treatment or palliative care (1 point). Numerical scores are calculated based on the presence of those factors and are then used to stratify risk.12,13 Patients with a score of less than 2 are considered low risk, those scoring 2 to 6 are at moderate risk, and those scoring greater than or equal to 7 are considered high risk. While there remains concern surrounding the subjectivity of the scoring, prospective validation studies have supported the Wells Criteria, and it is recommended that clinicians utilize these criteria in risk stratification.10,14,15 ■ Diagnostic testing Based on initial presentation and risk stratification, diagnostic testing must proceed to rule out life-threatening conditions. The ECG, as a diagnostic tool for identifying PE, has limited sensitivity due to diverse, nonspecific findings.5-8,10 Normal ECGs have been found in one-third of patients with PE, while others have nonspecific ST changes. A The Nurse Practitioner • January 2015 43
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
AcuteC are Advisor pattern of right heart strain may also be noted in conjunction with PE but is also nonspecific.10,11 Ultimately, the ECG is important in identifying changes associated with other acute cardiac pathology but is not diagnostic for confirming PE. d-dimer testing. A specific byproduct of fibrin degradation, the d-dimer is typically elevated in patients with thromboembolic disease. Although highly sensitive (nearing 100%), the test has low specificity of only 30% to 40%.16 Conditions such as acute infections, pregnancy, active cancers, trauma, inflammation, peripheral vascular disease, necrosis, recent surgery, liver disease, and kidney dysfunction may cause fibrin elevations.17,18 Current research is exploring the utility of raising the limit for the d-dimer in patients over 75 years of age, as d-dimer levels in this population are falsely elevated.19 For these reasons, the d-dimer is most appropriately used in conjunction with the history and physical exam as a tool to exclude patients with a low pretest probability for diagnosis of PE. It is now generally accepted (based on strong evidence) that a negative highsensitivity quantitative d-dimer can exclude the diagnosis of PE in patients considered at low risk for the diagnosis. However, among patients with intermediate probability of the diagnosis, based on risk stratification, the evidence is not as strong to support the use of negative d-dimers for PE exclusion, and further testing is warranted.14 Radiographic imaging. Anteriorposterior and lateral chest radiographs are recommended as an initial first study to help identify other sources of chest pain and dyspnea.20 Computed tomography pulmonary angiography (CTPA) is the current standard for diagnosis of PE. However, the use of CTPA carries risks of contrastinduced nephropathy and anaphylaxis and malignancy from exposure to high-dose computed tomography chest radiation.16,20 The use of CTPA 44 The Nurse Practitioner • Vol. 40, No. 1
should, therefore, be reserved for those with a high suspicion for PE based on screening criteria and history. A negative CTPA can be used to exclude PE for patients with a low risk for PE in whom further testing is warranted (perhaps a positive d-dimer or quantitative d-dimer not available).14 Ventilation perfusion imaging (V/Q scan), once the preferred test for assessing abnormal lung perfusion diagnostic of PE in the presence of a normal chest radiograph, is another option for assessing PE. Similar to the CTPA, the V/Q scan is associated with radiation exposure and offers no benefit over CTPA testing except in the case of pregnancy where the contrast media may be reduced, allowing for less radiation absorption.20 ■ Treatment and management Treatment strategies are determined based on the patient’s hemodynamic stability once the diagnosis of PE is made. A rapid-onset anticoagulant is the cornerstone of initial therapy for patients who are hemodynamically stable. Typically, unfractionated heparin or low-molecular-weight heparin is given for 5 to 7 days followed by a vitamin K antagonist, such as warfarin, for 3 months. Long-term therapy is required for patients at risk for repeated emboli, such as those with active malignancies or recurrent thrombolic events. Among patients with pregnancy or cancers, lowmolecular-weight heparin is preferred for both immediate and extended therapies. Vena cava filters may be utilized in patients with contraindications to anticoagulant therapy.10,21,22 Fibrinolytic therapy. Similar to the patient with a cardiac occlusion, fibrinolytic therapy must be viewed in terms of risks and benefits. The benefits of fibrinolytics are often supported in hemodynamically unstable patients with confirmed PE. Fibrinolytics may
also be considered for hemodynamically unstable patients when the clinical suspicion for PE is high but the diagnosis cannot be definitely confirmed or excluded in a timely manner.14 Alternately, surgical or mechanical thrombectomy may be performed for those whom fibrinolytics are considered too risky (for example, those with known intracranial disease, uncontrolled hypertension, or status-post recent trauma or surgery) or for those who remain hemodynamically unstable despite fibrinolytics.10,14,21 Current studies do not support use of fibrinolytics for hemodynamically stable patients; however, antiplatelet medications for VTE are recommended.14 ■ Implications for advanced practice nursing PE is a serious and often elusive diagnosis. Maintaining awareness of the possibility of PE in patients presenting with chest pain and shortness of breath is vital to avoiding a missed diagnosis because PE may be lethal if undiagnosed and/or not treated. Significant sequela, such as cardiac dysfunction, hemodynamic decompensation, or death may result from PE, and the NP is uniquely poised to prevent these complications. Recognition of risk factors and utilization of risk stratification to ensure the correct use of diagnostic modalities can reduce unnecessary diagnostic testing and improve patient outcomes. REFERENCES 1. Centers for Disease Control and Prevention. National hospital ambulatory medical survey: factsheet emergency department. http://www. cdc.gov/nchs/data/ahcd/NHAMCS_2010_ed_ factsheet.pdf. 2. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):485-510. 3. AHRQ. Guideline Summary NGC-7890. Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. 2012.
www.tnpj.com
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Acute Care Advisor 4. AHRQ. Guideline Summary NGC-9521. Diagnosis and treatment of chest pain and acute coronary syndrome (ACS). 2012. 5. McConaghy JR, Oza RS. Outpatient diagnosis of acute chest pain in adults. Am Fam Physician. 2013;87(3):177-182. 6. Duriseti RS, Brandeau ML. Cost-effectiveness of strategies for diagnosing pulmonary embolism among emergency department patients presenting with undifferentiated symptoms. Ann Emerg Med. 2010;56(4):321-332. 7. DeMonaco NA, Dang Q, Kapoor WN, Ragni MV. Pulmonary embolism incidence is increasing with use of spiral computed tomography. Am J Med. 2008;121(7):611-617. 8. Heit JA, Cohen AT, Anderson FA, Jr., on Behalf of the VTE Impact Assessment Group. Estimated Annual Number of Incident and Recurrent, Non-Fatal and Fatal Venous Thromboembolism (VTE) Events in the US. ASH Annual Meeting Abstracts. 2005;106:910. 9. Ouellette DR. Pulmonary embolism. Medscape. emedicine.medscape.com/article/300901overview#a0156. 10. Cohen AT, Dobromirski M, Gurwith MM. Managing pulmonary embolism from presentation to extended treatment. Thromb Res. 2014;133(2):139-148. 11. Strange JA, Pilcher D. Management of pulmonary embolism. Anaesthesia and Intensive Care Medicine. 2014;15:72–77.
www.tnpj.com
12. Courtney DM, Kline JA, Kabrhel C, et al. Clinical features from the history and physical examination that predict the presence or absence of pulmonary embolism in symptomatic emergency department patients: results of a prospective, multicenter study. Ann Emerg Med. 2010;55(4):307-315. 13. Kline JA, Wells PS. Methodology for a rapid protocol to rule out pulmonary embolism in the emergency department. Ann Emerg Med. 2003;42(2):266-275. 14. Fesmire FM, Brown MD, Espinosa JA, et al. Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism. Ann Emerg Med. 2011;57(6):628-652. 15. Huisman MV, Klok FA. Diagnostic management of acute deep vein thrombosis and pulmonary embolism. J Thromb Haemost. 2013;11(3): 412-422. 16. van Es J, Beenen LF, Gerdes VE, Middeldorp S, Douma RA, Bossuyt PM. The accuracy of D-dimer testing in suspected pulmonary embolism varies with the Wells score. J Thromb Haemost. 2012;10(12):2630-2632. 17. Kabrhel C, Mark Courtney D, Camargo CA Jr, et al. Factors associated with positive d-dimer results in patients evaluated for pulmonary embolism. Acad Emerg Med. 2010;17(6):589-597. 18. Yin F, Wilson T, Della Fave A, et al. Inappropriate use of D-dimer assay and pulmonary CT angiog-
raphy in the evaluation of suspected acute pulmonary embolism. Am J Med Qual. 2012;27(1):74-79. 19. Righini M, Van Es J, Den Exter PL, et al. Ageadjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014;311(11):1117-1124. 20. American College of Radiology Appropriateness Criteria. Acute chest pain-suspected pulmonary embolism. 2013. http://www.acr.org/~/media/ ACR/Documents/AppCriteria/Diagnostic/Acute ChestPainSuspectedPulmonaryEmbolism.pdf. 21. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med. 2010;363(3):266-274. 22. American College of Chest Physicians Evidence-Based Clinical Practice Guidelines: Antithrombotic Therapy and Prevention of Thrombosis. 9th ed. Chest. 2012;141(2 Suppl):7S-47S. Jennifer Wilbeck is an associate professor and FNP/ ACNP-ED program coordinator at Vanderbilt University, Nashville, Tenn. Dian Evans is an emergency nurse practitioner and specialty coordinator associate professor at Emory University, Nell Hodgson Woodruff School of Nursing, Atlanta, Ga. The authors have disclosed that they have no financial relationships related to this article. DOI: 10.1097/01.NPR.0000457439.35283.05
The Nurse Practitioner • January 2015 45
Copyright © 2015 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
