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Dept.Pulmonology, University of Szeged, Deszk, Hungary

Attila Somfay. Dept.Pulmonology, University of Szeged, Deszk, Hungary. Pulmonary embolism , pulmon ary h y pert ension , cor pulmonale chronicum. KEY POINTS. 1/1000/year early treatment is highly effective, but is under- diagnosed, therefore, remains a major health problem

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Dept.Pulmonology, University of Szeged, Deszk, Hungary

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  1. Attila Somfay Dept.Pulmonology, University of Szeged, Deszk, Hungary Pulmonary embolism, pulmonary hypertension, cor pulmonale chronicum

  2. KEY POINTS • 1/1000/year • early treatment is highly effective, but is under- diagnosed, therefore, remains a major health problem • diagnostic strategy should be based on clinical evaluation (probability assessment) • value of PPV and NPV are high when concordant with clinical assessment • additional tetsting is neccessery when test result is inconsistent with clinical probability

  3. Epidemiology • USA: 117 %000VTE- 48 %000 DVT - 69 %000 PE (Arch Intern Med 1998; 158:585-593) • Europe: 183 %000 VTE- 124 %000 DVT - 60 %000 PE (Thromb Haemost 2000; 83:657-660)

  4. Trends in ED visits with PE diagnosis

  5. PE and DVT mortality Goldhaber SZ, NEJM, 1998

  6. Pathogenesis of VTE • Venous stasis – immobility (hospitalization-DVT), CHF, gravidity, obesity, elderly patients • Intima injury– surgery(orthopedic, obstetrical), trauma • venous lines, venography • Abnormalities ofcoagulation – fibrinolysis • - malignancy • - lupus anticoagulant • - thrombophilias: AT III, protein S-, protein C deficiency • - mutation (Factor VLeiden) • - myeloproliferativ disorders, policythaemia • - nephrosis sy • - gravidity, contraceptive pills • - colitis ulcerosa

  7. Fedullo PF, Tapson VF NEJM2003

  8. Symptomes of PE Dyspnoe with sudden onset 84% Pleural chest pain 74% Cough 53% Hemoptoe 30% Sweat 27% Non-pleural chest pain 14% Syncope 13%

  9. Physical findings Tachypnoe (>16/min) 92% Crackles, local wheeze 58% PII ! 53% Tachycardia (>100/min) 44% Fever 43% Sweating 36% Phlebitis 32% Anasarca 24% Cyanosis 19% Pleuralfriction rub, fluid11%

  10. Fedullo PF, Tapson VF NEJM2003

  11. Geneva score Low <=4 Medium 5-8 High >=9

  12. Goldhaber SZ, NEJM, 1998

  13. Hemodynamics (mmHg): RARVPA Clinical classification Acute, massive 12 45/0-12 45/20 Acute, minor 5 30/0-5 30/15 Chronic, reccurant 6 90/0-6 90/50 (CTEPH)

  14. Acute, massiv PE • >50% obstruction (mechanic + humoral + neurogenic) • Heavy, retrosternalpain, panic • Pallor, cyanosis, sweating, strongs dyspnoe, tachycardia • Right heart failure, distended jugular veins Diff dg: AMI, dissecant aortic aneurysm, cardiac tamponade, pulmonary edema, ptx, shock

  15. Acute, minor PE • Haemoptysis • Pleural chest pain • Mild dyspnoe • PaO2 normal • Fever, tachycardia • Diff dg: pleurisy, pneumonia, bronchial cc

  16. Chronic, reccurant PE (CTEPH) • Reccurant episodes for months - years • Progression of effort dyspnea • Cyanosis • Angina-likechest pain (decreased myocardial perfusionpressure) • Tachycardia, PII !, systolic ejection click • Death: progression of right heart failure • Diff dg: COPD, CHF, hyperventilation sy

  17. Chest X-ray and ECG

  18. Acute, massive PE rsR’

  19. CTEPH

  20. ABG • PaO2 • PaCO2 • pH  ! • P(A-a)O2 Alveolar gas equation: PA (mmHg)=(PB-47) x FIO2 – 1.2 x PaCO2 102 = 150 - 48

  21. West JB, 1998

  22. D-dimer Goldhaber SZ, NEJM, 1998

  23. Blood chemistry D-dimer (ELISA): sensitive, but notspecific(AMI, pneumonia, CHF, cc, surgery) > 500 ng/ml, in 90%of PE, (latex test 50%) negative test: exclude PE LDH-3  Bi 

  24. ECHO After therapy Acute, massive PE

  25. Pulmonary hypertension by Doppler 62 mmHg 21mmHg

  26. RA thrombus

  27. Massiva PE, TTE Goldhaber SZ, NEJM, 1998

  28. Other diagnostic tests • Vascular Doppler of the leg • Inhalation-perfusion scintigraphy: V/Q mismatch • CT angio: central- segmental – subsegmental • Angiography (gold standard)

  29. Ventilation-perfusion scintigraphy

  30. Multiplex PE Right upper lobe: „match”, Both lower lobes: „mismatch”

  31. Massive PE

  32. Perfusion defect in emphysema Alfa-1 AT deficiency Homogenous Smoker

  33. PIOPED - uncertainity JAMA, 1990

  34. PIOPED II. – no need for V scan Sostman,J Nucl Med, 2008

  35. Angio CT

  36. Angio CT

  37. Angio CT

  38. Angiography

  39. Angiography: massive PE Acute: 45/20 mmHg Subacute: 85/50 mmHg

  40. CTPH mPAP = 75 mmHg

  41. Low clinical probability D-dimer (ELISA v. aggl.) >500g/L VUS < 500g/L: - DVT:Ther. DVT neg. Normál: - Nem dg-cus: - V/Q or CT angio Magas val.:Ther. (?)

  42. Intermedier clinical probability D-dimer (ELISA) >500g/L VUS < 500g/L: - Normál: - DVT:Ther. DVT neg. Non dg: Angio or CT angio: V/Q orCT angio High porbab.:Ther.

  43. High clinical probability VUS DVT neg. DVT:Ther. Normal: - Non dg: Angio or CT angio: V/Q or CT angio High probab..:Ther.

  44. Hemodynamic “ vitious circle”

  45. Therapy • Streptokinase • Urokinase • Alteplase

  46. Treatment • Sodium-heparin iv. bolus (5-10 000 U) followed by either - continouos infusion (control with aPTI) or - low molecular weight (ultrafractionated) heparin (LMWH) s.c. • Coumarin for 6-12 months (if irreversible or unknown etiology: lifeterm anticoagulation) therapeutic level: INR: 2-3

  47. New therapy (NOAC) Oralthrombin inhibitor - dabigatran (Pradaxa) Xa inhibitor - rivaroxaban (Xarelto), apixaban (Eliquis) edoxaban (Lixiana) No needtocontrolcoagulability Sideeffect: bleeding Disadvantage: no antidotum, expansive

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