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Dept.Pulmonology, University of Szeged, Deszk, Hungary

Learn about the epidemiology, pathogenesis, symptoms, and diagnostic strategies for pulmonary embolism. Understand key points in early and effective treatment to combat this major health issue. Discover insights into hemodynamics, diagnostic tests, and treatment options, including novel therapies like NOACs. Stay informed to better recognize, manage, and address this condition.

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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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