Pulmonary Thromboembolic Disease

1. Pulmonary Thromboembolic Disease By Ahmed Mansour, MSc, PhD

2. Definition • PE is a clinically significant obstruction of part or all of the pulmonary vascular tree (usually caused by migrating thrombus from a distant site;DVT). • VTE = PE + DVT

3. Natural History • Death within 1 h 11%. • Survival > 1 h 89% • Diagnosis made & ttt started 29% • Survive 92% • Death 8% • Diagnosis not made 71% • Survive 70% • Death 30%

4. Source of Emboli • Lower extremit (80-95%) especially if popliteal or above. • Pelvic veins in cases of... • Upper extremity... • Right ventricle, more hemodynamic instability and increased mortality. • Other materials...

5. Presisposing Factors • Wirchow’s triad. • Acquired risk factors • Inherited thrombophilias 1- Factor V Leiden mutation (APC resistance) 2- Prothrombin gene mutation 3- Deficienecy of antithrombin III, protein C, protein S.

6. Pathophysiology • Factors determining the outcome: 1- Size and location of emboli 2- Coexisiting cardiopulmonary diseases 3- Secondary humoral mediator release and vascular hypoxic responses 4- Resolution rate of emboli

7. Haemodynamic consequences of acute PE 1- PAP rises. 2- RV after-load increases. 3- RV failure if > 50% of pulmonary vascular bed is obstructed 4- LV filling is reduced…hypotension. 5- Increased RA pressure may lead to intraccardiac shunt through a patent foramen ovale.

8. Gas-Exchange Abnormalities • Hypoxemia: 1- Re-direction of blood flow to other parts of pulmonary vascular bed (V/Q mismatch) 2- Increased alveolar dead space due to atelectasis and bronchiolar constriction. • Hypocapnea due to hyperventilation

9. Clinical features of acute PE 1- Pulmonary infarction and hemoptysis ± pleuritic pain (60%): • Acute pleuretic chest pain and hemoptysis • O/E: local signs e.g. pleura;l rub • ABGs and ECG are usually normal 2- Isolated dyspnea (25%): • Acute SOB in presence of a risk facto for VTE • O/E: patient is hemodynamically stable • ABGs show hypoxemia, CTPA: central thrombus 3- Circulatory collapse, poor reserve (10%): • Usually in elderly patients with cardiopulmonary diseases • Rapid decompensation even with small PE • O/E: features of the underlying diseases. 4- Circulatory collapse in a previously well patient (1%): • Acute chest pain (RV angina), hemodynamic instability due to massive PE • O/E: RV failure... • ECG changes, echocardiography shows RV failure

10. Clinical features of chronic PE • Insidious onset over weeks to months due to recurrent showers of small emboli. • Dyspnea and tachypnea are the commonest features (90%). • Should be considered in the DD of: • Unexplained SOB • RVF • New AF • Pleural effusion • Collapse

11. Examination 1- May be normal 2- Vital signs: tachypnea, tachycardia (may be AF), low grade fever. 3- Heart: Signs of pulmonary hypertension (loud splitted S2) Signs of RV failure (raised JVP, low COP with systemic hypotension, tricuspid gallop) 4- Chest; the affected side may show: Inspection: reduced movement Palpation: diminished expansion Percussion: dullness in case of pleural effusion Auscultation: pleural rub (Pulmonary infarction ) or diminished intensity of breath sounds (pleural effusion) 5- Lower limbs: Signs of DVT.

12. Diagnosis of Acute PE • Pre-test clinical probability scoring: • e.g. BTS scoring system: a- Clinical features consistent with PE 1- Absence of other reasonable clinical explanation 2- Presence of a major risk factor High probability: a+1+2 Intermediate probability: a+ either 1 or 2 Low probability: a only

13. Diagnosis of Acute PE • D-dimer: • A fibrinolysis product generated in many clinical situations e.g... • Indicated in: 1- Low/intermediate clinical probability 2- Acute cases only 3- Outpatient cases only • Sensitive (small no. Of false negatives) but not specific (large no. Of false positives). • Interpretation of the results: * Normal level = negative test, elevated level = positive test * A negative test is valid to exclude PE in cases with low/intermediate clinical probability. A positive test does not cofirm PE but rather further imaging is required

14. Investigations 1- ECG 2- CXR 3- ABGs 4- D-dimer 5- Troponin and natriuretic peptides 5- CTPA 6- Ventilation/perfusion lung scan 7- Others

15. ECG • Sinus tachycardia • AF • RBBB • RV starin • Less commonly; S1Q3T3

16. CXR • Small pleural effusion • Raised hemi-diaphragm • Collapse • Infiltrate

17. ABGs • May be normal • Hypoxemia and hypocapnea • Increased A-a oxygen gradient

18. Troponin and natriuretic peptides • Indicate RVD • Raised troponin predicts poor prognosis

19. CTPA • The gold standard investigation • Highly sensitive (multi-detector scanners) • More sensitive for central emboli • More helpful for patients with abnormal CXR • Negative CTPA: • In those with low/intermediate clinical probability: PE is unlikely. • In those with high clinical probablity: further investigations are required.

20. V/Q scan • Mostly replaced by CTPA • Still helpful in: • Patients with normal CXR • Patients in whom CTPA is not safe e.g... • Results:

21. Other imaging techniques • Echocardiography • Leg U/S • CT venography • Transthoracic U/S • Conventional pulmonary angiography

22. Management of acute massive PE 1- 100% O2 2- IV access, baseline clotting screen, ECG 3- Analgesia 4- Management of cardiogenic shock 5- IV heparin: • Unfractionated vs LMWH • Loading, maintenance • APTT 6- Investigations to confirm PE? 7- Thrombolysis for massive PE causing hemodynamic instablity 8- Embolectomy in patients with a contraindication for anticoagulants or thrombolytics 9- Oral anticoagulants • Outpatient • INR • For how long? 10- IVC filter for patients with: • A contraindication for anticoagulants • Massive PE after survival • Reccurrent VTE despite adequate anticoagulation

23. Thank you