1. Goals Understand the historical context of pulmonary emboli Comprehend the pathophysiology and know some common risk factors Be aware of the clinical features of PE and have a basic understanding of various diagnostic test Gain a therapeutic approach to the treatment of PE and discuss a simplified method in the work-up of PE Attempt to dispel a few “myths”about pulmonary emboli 1

2. Perspective A common disorder and potentially deadly 650000 cases occuring annually Highest incidence in hospitalized patients Autopsy reports suggest it is commonly “missed” diagnosis

3. Perspective Presentation is often “atypical” Signs and symptoms are frequently vague and nonspecific and rarely “classic” Untreated mortality rate of 20% - 30%, plummets to 5% with timely intervention 3

4. Historical Context Pre-1930’s Heparin 4

5. Historical Context PIOPED (Prospective Investigation of Pulmonary Embolism Diagnosis) The Electronic Era, 2000 and Beyond… 5

6. So What Do We Do ??? Confusing for Emergency Physician Do we under diagnose/over diagnose? Why don’t we have a standardized method of work up after all these years? 6

7. Etiology Rudolph Virchow, 1858 Triad: Hypercoagulability Stasis to flow Vessel injury 7

8. Pathophysiology.incresed deadspace.hyperventilation.hypoxemia due to :.V/Q mismatch.pulmonary shunt Reduced cardiac output

9. Risk Factors Hypercoagulability Malignancy Nonmalignant thrombophilia Pregnancy Postpartum status (<4wk) Estrogen/ OCP’s Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor VIII, Prothrombin mutations, anti-thrombin III deficiency) Venous Statis Bedrest > 24 hr Recent cast or external fixator Long-distance travel or prolong automobile travel Obesity Vessel Injury Recent surgery requiring endotracheal intubation Recent trauma (especially the lower extremities and pelvis) 9

10. Clinical Presentation The Classic Triad: ( Hemoptysis, Dyspnea, Pleuritic Pain) Not very common! Occurs in less than 20% of patients with documented PE Three Clinical Presentations – Pulmonary Infarction – Submassive Embolism – Massive Embolism : sys pressure 40 10

11. Mythology of PE Myth – “Patients with pulmonary embolism are short of breath and have chest pain!” Reality: You can forget about making the diagnosis on clinical grounds, but wait…don’t plan on completely ruling it out either! 11

12. Clinical Features Symptoms in Patients with Angio Proven PTE SymptomPercent Dyspnea84 Chest Pain, pleuritic74 Anxiety59 Cough53 Hemoptysis30 Sweating27 Chest Pain, nonpleuritic14 Syncope13 12

13. Clinical Features Signs with Angiographically Proven PE SignPercent Tachypnea > 20/min92 Rales58 Accentuated S253 Tachycardia >100/min44 Fever > 37.843 Diaphoresis36 S3 or S4 gallop34 Thrombophebitis32 Lower extremity edema24 13

14. Who do we work up? - Pretest Probability Definition: “The probability of the target disorder (PE) before a diagnostic test result is known”. Used to decide how to proceed with diagnostic testing and final disposition 14

15. Well’s Scoring Sign & symptoms of dvt Alternative diag. Less likely Heart rate> 100 Immobilization>3days surgery within 4 weeks Prior PE or DVT Hemoptysis Cancer 3 1.5 1

16. Prognostic factors Dysfunction of right ventricle Rise of brain natriuretic peptide>90pg/ml Or N-terminal pro-BNP Simultaneous DVT Thrombus in right ventricle Rise of troponin Hyponatremia

17. Diagnostic Test Imaging Studies – CXR – V/Q Scans – Spiral Chest CT – Pulmonary Angiography – Echocardiograpy Laboratory Analysis – CBC, ESR, Hgb/Hc t, – D-Dimer – ABG’s Ancillary Testing – EKG – Pulse Oximetry 17

18. Diagnostic Testing - CXR’s Chest X-Ray Myth: “You have to do a chest x-ray so you can find Hampton’s hump or a Westermark sign.” Reality: Most chest x-rays in patients with PE are nonspecific and insensitive 18

19. Diagnostic Testing - CXR’s Chest radiograph findings in patient with pulmonary embolism ResultPercent Cardiomegaly27% Normal study24% Atelectasis23% Elevated Hemidiaphragm20% Pulmonary Artery Enlargement19% Pleural Effusion18% Parenchymal Pulmonary Infiltrate17% 19

20. Chest X-ray Eponyms of PE Westermark's sign – A dilation of the pulmonary vessels proximal to the embolism along with collapse of distal vessels, sometimes with a sharp cutoff. Hampton’s Hump – A triangular or rounded pleural-based infiltrate with the apex toward the hilum, usually located adjacent to the hilum. 20

21. Radiographic Eponyms - Hampton’s Hump, Westermark’s Sign 21 Westermark’s Sign Hampton’s Hump

22. Diagnostic Testing – EKG’s EKG – Most Common Findings: Tachycardia or nonspecific ST/T-wave changes – Acute cor pulmonale or right strain patterns Tall peaked P-waves in lead II (P pulmonale) Right axis deviation RBBB S1-Q3-T3 (occurs in only 20% of PE patients) 22

23. Diagnostic Testing - Pulse Oximetry The Pulse Oximetry Myth: – “ You must do a pulse oximetry reading, since patients with pulmonary embolism are hypoxemic!” Reality: – Most patients with a PE have a normal pulse oximetry, and most patients with an abnormal pulse oximetry will not have a PE. 23

24. Diagnostic Testing - ABG’s The ABG/ A-a Gradient myth: – “You must do an arterial blood gas and calculate the alveolar-arterial gradient. Normal A-a gradient virtually rules out PE”. Reality: – The A-a gradient is a better measure of gas exchange than the pO2, but it is nonspecific and insensitive in ruling out PE. 24

25. Diagnostic Testing Echocardiography – Consider in every patient with a documented pulmonary embolism EKG maybe helpful in demonstrating right heart strain – Early fibrinolysis can reduce mortality 50%! 25

26. Ancillary Test WBC – Poor sensitivity and nonspecific Can be as high as 20,000 in some patients Hgb/Hct – PTE does not alter count but if extreme, consider polycythemia, a known risk factor ESR – Don’t get one, terrible test in regard to any predictive value 26

27. D-dimer Test Fibrin split product Circulating half-life of 4-6 hours Quantitative test have 80-85% sensitivity, and 93-100% negative predictive value False Positives: Pregnant PatientsPost-partum < 1 week MalignancySurgery within 1 week Advanced age > 80 yearsSepsis HemmorrhageCVA AMICollagen Vascular Diseases Hepatic Impairment 27

28. Diagnostic Testing D-dimer – Qualitative Bed side RBC agglutination test – “SimpliRED D-dimer” – Quantitative Enzyme linked immunosorbent asssay “Dimertest” Positive assay is > 500ng/ml VIDAS D-dimer, 2 nd generation ELISA test 28

29. Ventilation/Perfusion Scan - “V/Q Scan” A common modality to image the lung and its use still stems from the PIOPED study. Relatively noninvasive and sadly most often nondiagnostic In many centers remains the initial test of choice Preferred test in pregnant patients 50mrad vs 800mrad (with spiral CT) 29

31. V/Q Scan Technique Interpretation – Normal – Low probability/”nondiagnostic” (most common) – High Probability Simplified approached to the interpretation of results: High probability  Treat for PE Normal Scan  If low pre-test, your done Everything else  Purse another study (CT, Angio) 31

32. Spiral (Helical) Chest CT Advantages – Noninvasive and Rapid – Alternative Diagnosis Disadvantages – Costly ($600 - 900/scan) – Risk to patients with borderline renal function – Hard to detect subsegmental pulmonary emboli 32

37. Pulmonary Angiography “Gold Standard” – Performed in an Interventional Cath Lab Positive result is a “cutoff” of flow or intraluminal filling defect “Court of Last Resort” 37

39. Treatment: Goals: Prevent death from a current embolic event Reduce the likelihood of recurrent embolic events Minimize the long-term morbidity of the event 39

40. Treatment Anticoagulants – Heparin Provides immediate thrombin inhibition, which prevents thrombus extension Does not dissolve existing clot Will not work in patients with antithrombin III def. – In this case use hirudins Few absolute contraindications 40

41. Treatment Anticoagulants – Heparin Available as Unfractionated or LMW Heparin – FDA approved dosing: » Unfractionated: 80 units/kg bolus, 18 units/kg/hr » LMWH: 1 mg/kg Q 12 or 1.5mg/kg Q D LMWH (Lovenox) prefered in pregnant patients 41

42. Treatment Anticoagulants – Warfarin (Coumadin) Interferes with the action of Vit-K dependent factors: II, VII, IX, and X, as well as protein C & S Causes temporary hypercoagulable state in first 5 days of treatment – Important a patient is anticoagulated with heparin before initiating warfarin therapy Target INR is 2.5 – 3.0 42

43. Treatment Fibrinolytic Therapy (Alteplase) – Indications: Documented PE with: – Persistent hypotension – Syncope with persistent hemodynamic compromise – Significant hypoxemia – +/- patient with acute right heart strain Approved alteplase regimen is 100mg as a continuous IV infusion. 43

44. Contraindication to fibrinolytic therapy Absolute: History of hemorrhagic stroke Active intracranial neoplasm Recent <2 month intracranial surgery Active or recent internal bleeding in prior 6 month Relative: Bleeding diathesis Uncontrolled severe hypertension> 200/110 Nonhemorrhagic stroke Surgery whithin previous 10 days Thrombocytopenia< 100000

45. Treatment Embolectomy – Prefininolytic therapy this was only therapy for massive PE – Carries a 40% operative mortality – Alternative is Transvenous Catheter Embolectomy 45

46. A Simplified Algorithm Pre-test probability D-dimer (VIDAS-DD) CT angiography 46 Low Pre-test, D-dimer (-), patient had < 1.7% 90 day PE occurrence in a Mayo Clinic Study

47. Special Circumstances Morbid Obesity Pregnancy V/Q has considerable less radiation – 50mrad vs. 800 mrad Almost all will have positive D-Dimer Heparin safe in pregnancy Witnessed Cardiac Arrest Standard ACLS, if known PE, the lytics. 47

48. Conclusion Summary Points Pulmonary Emboli remain a potentially deadly and common event which may present in various ways Don't’ be fooled if your patient lacks the “classic” signs and symptoms! Consider PE in any patient with an unexplainable cause of dyspnea, pleuritic chest pain, or findings of tachycardia, tachpnea, or hypoxemia 2 nd Generation Qualitative D-Dimers have NPV of 93-99% Heparin remains the mainstay of therapy with the initiation of Warfarin to follow Simplified Algorithm: ( Pretest probability, D-Dimer, +/- CT angio), then disposition) 48

49. The End! 49 Questions????

50. 1. Which of the following is not a part of virchows triad? a)Hypercoagulability b)Stasis to flow c)Vessel injury d)History of previous DVT 50

51. 2.Which of the following is the propper treatment of fat emboli? a)Platelets b)High dose steroids c)Heparin d)cryoprecipitate 51

52. 3.The Classic Triad of patients presenting to the ED with PE includes all of the following except: a)Hemoptysis b)Dyspnea c)+ Homans’ sign d)Pleuritic Pain 52

53. 4.What is the most common symptom in a patient with Angio Proven PTE? a)Dyspnea b)Chest Pain, pleuritic c)Anxiety d)Cough 53

54. 5.What is the most common ecg finding in patients with PE? a)Right axis deviation b)RBBB c)S1-Q3-T3 d)Tall peaked T-waves in lead II (P pulmonale) e)Sinus tachycardia 54

55. Answers 1.D 2.B 3.C 4.A 5.E 55