Pulmonary Embolism

1. Pulmonary Embolism David Putnam, MD Albany Medical College March, 2000

3. Clinical spectrum varies from small, incidental PE to massive PE associated with sudden death due to cardiogenic shock

4. PE: Presentation Agenda Epidemiology Diagnosis Therapy Prevention

5. Epidemiology

6. PE: Epidemiology Pulmonary embolism and deep venous thrombosis should be considered part of the same pathological process Up to 40% of patients with DVT have PE Up to 29% of patients with PE have DVT

7. PE: Epidemiology More than 250,000 patients hospitalized annually in the US with PE or DVT 33% of patients suffer recurrent events

8. PE: Epidemiology Mortality rates remain high 20% for treated patients with concomitant diseases 6 to 8% for treated patients entered into clinical trials

9. PE: Epidemiology PIOPED Trial A. One year mortality 24% B. Only 2.5% of deaths due directly to PE C. Cardiac disease, pulmonary disease, cancer, and sepsis accounted for 2/3 of deaths

10. PE: Mortality

11. PE: Role of DVT 80 to 100% of patients with PE at autopsy have lower extremity thrombi Clinical manifestations of DVT are absent in about 50% of patients with DVT

12. PE: Risk Factors Virchow Triad A. Local trauma to the vessel wall B. Hypercoagulability C. Stasis

13. PE: Risk Factors Pregnancy Oral contraceptives Postmenopausal hormone replacement therapy Cancer Surgery Factor V Leiden (protein C inhibitor) Hyperhomocysteinemia Lupus anticoagulant

14. Diagnosis

15. PE: Acute Events Pulmonary arterial obstruction and platelet secretion of vasoactive agents elevate pulmonary vascular resistance Increased alveolar dead space impairs gas exchange Stimulation of irritant receptors causes alveolar hyperventilation

16. PE: Acute Events Reflex bronchoconstriction augments airway resistance Lung edema decreases pulmonary compliance Elevation in right ventricular pressure can cause RV dysfunction

17. PE: Diagnosis Known as �the great masquerader� Extensive differential diagnosis Over diagnosed in normal people and under diagnosed in chronically ill and post surgical patients

18. PE: Differential Diagnosis Pneumonia, asthma, COPD exacerbation, bronchitis, lung cancer Myocardial infarction Costochondritis, �viral syndrome�, anxiety Aortic dissection Pericardial tamponade Lung cancer Primary pulmonary hypertension Rib fracture or pneumothorax Musculoskeletal pain

19. PE: Diagnosis Symptoms Signs Electrocardiogram Chest X-ray Arterial Blood Gas Plasma D-dimer Ventilation/Perfusion Lung Scan Echocardiogram Spiral Chest CT Scan Angiography

20. PE: Symptoms Symptom Dyspnea Pleuritic chest pain Apprehension Cough Hemoptysis Diaphoresis Syncopy Incidence 84% 74% 59% 53% 30% 36% 13%

21. PE: Signs Sign Tachypnea Rales Accentuated P2 Tachycardia Fever Phlebitis Cyanosis Incidence 92% 58% 53% 44% 43% 32% 19%

22. PE: Electrocardiogram Usually normal T-wave inversion V1 to V4 New onset right bundle branch block New onset atrial fibrillation S in lead I, Q in lead III, and T-wave inversion in lead III (rarely seen)

24. PE: Chest X-ray Often normal Focal oligemia (Westermark�s sign) Peripheral wedge-shaped density above the diaphragm (Hampton�s hump) Enlarged right descending pulmonary artery (Palla�s sign) Pleural effusion Small infiltrates

25. PE: Arterial Blood Gas Unreliable Hypoxemia may not always be present May demonstrate hypocapnea respiratory alkalosis

26. PE: Arterial Blood Gas

27. PE: Arterial Blood Gas

28. PE: Plasma D-dimer Fibrin-specific degradation product of thrombus Increased in most PE patients Low specificity

29. PE: Plasma D-dimer Test D-dimer ELISA>500 ng/ml is abnormal and present in >90% of patients with PE Normal D-dimer ELISA provides reassurance in >90% of patients that PE is not present Most helpful to screen patients in ED without other systemic illness

30. PE: V/Q Lung Scan Best data to date provided by PIOPED Trial (JAMA 1990;263:2753-2759) High-probability scans have 88% positive predictive value High-probability scans in conjunction with high clinical suspicion have 96% positive predictive value Majority of PE associated with non-high-probability scans

31. PE: V/Q Scan Totally normal scan excludes the diagnosis May have PE in presence of low-probability scan Consider angiography for definitive diagnosis in non-high-probability scans

32. PE: Echocardiogram Can help identify conditions that mimic PE (MI, aortic dissection, pericardial tamponade) Thrombus itself is rarely visualized Signs of right ventricular pressure overload About 40% of patients have abnormalities of the right ventricle

34. PE: Spiral Chest CT Scan New diagnostic approach Best suited for identifying PE in the proximal pulmonary vascular tree

35. PE: Angiography Remains the gold standard Generally can be performed safely Likelihood of visualization of emboli increases when angiography is performed soon after the acute event Might resolve dilemma of high clinical suspicion with nondiagnostic scanning

36. PE: Diagnostic Algorhythm

38. Therapy

39. PE: Heparin Accelerates the action of antithrombin III Prevents additional thrombi from forming Permits endogenous fibrinolysis to dissolve some of the PE clot Promotes endothelialization of thrombus Decreases likelihood of embolization of thrombus from venous wall

40. PE: Heparin Constitutes the cornerstone of management

41. PE: Heparin

42. PE: Heparin

43. PE: Heparin Anticoagulation should be started as soon as the diagnosis is suspected unless contraindications exist Loading dose: 5,000 to 10,000 U Maintenance dose: 18U/kg/hr (not to exceed 1600 U/hr) Monitoring: adjust for aPTT between 60 and 80 seconds Heparin nomograms facilitate proper dosing

44. PE: Heparin

45. PE: Heparin Inpatient administration of low-molecular-weight heparin has been shown to be as safe and effective as unfractionated heparin when treating hemodynamically stable PE NEJM 1997;337:663-669

47. PE: Heparin Patients at risk for bleeding A. Age greater than 75 years B. Uremia C. Severe hypertension D. Recent surgery or trauma E. Recent GI bleed F. Massive pulmonary embolism G. Documented hemostatic defect H. Platelet suppressive drugs

48. PE: Heparin

49. PE: Heparin

50. PE: Heparin

51. PE: Inferior Venal Caval Filters Indicated for PE patients with active hemorrhage or recurrent PE despite intensive and prolonged anticoagulation Appears to offer no advantage in patients with free-floating proximal DVT Does not reduce mortality compared with anticoagulation alone

53. PE: Coumadin Loading warfarin does not shorten the usual five days needed to achieve adequate oral anticoagulation Initial average dose of 5 mg/d in most Initial 2 mg/d dose in small, debilitated, or elderly patients Target INR 2 to 3

54. PE: Coumadin Six months of anticoagulation prevents far more recurrences than does six weeks Indefinite anticoagulation should be considered in patients with recurrent PE

55. PE: Coumadin

56. PE: Thrombolytic Therapy Rationales A. Resolves recent clots promptly B. Improves pulmonary hemodynamics C. Does not reduce mortality

57. PE: Thrombolytic Therapy Can be lifesaving in patients with massive PE, cardiogenic shock, or overt hemodynamic instability Controversy persists regarding its use in PE patients with stable systemic arterial pressure and right ventricular dysfunction

58. PE: Thrombolytic Therapy

59. Prevention

60. PE: Prevention

61. PE: Prevention

62. PE: Prevention

63. Conclusion

64. PE: Conclusion Knowledge is rapidly advancing Increased understanding of risk factors Array of diagnostic tools has expanded Keen appreciation of importance of risk stratification Availabiliy of LMWH broadens our treatment options

65. PE: Conclusion Diagnostic suspicion and vigilance in prophylaxis remain our first line of defence

66. PE: Reading List Goldhaber SZ. Pulmonary embolism. NEJM 1998(JUL);339:93-104. Brieger DB, et al. Heparin-induced thrombocytopenia. JACC 1998(JUN);31:1449-59. Ginsberg JS. Management of venous thromboembolism. NEJM 1996(DEC);335:1816-1828.