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). 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 VTE = PE + DVT

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

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

5. Presisposing Factors Wirchow ’ s triad. Wirchow ’ s triad. Acquired risk factors Acquired risk factors Inherited thrombophilias Inherited thrombophilias 1- Factor V Leiden mutation (APC resistance) 2- Prothrombin gene mutation 3- Deficienecy of antithrombin III, protein C, protein S. Minor: 1- Cardiovascular 2- HRT, contraceptives 3- Others: obesity, nephrotic syndrome, … Major: 1- Surgery 2- Obstetrics 3- Malignancy 4- LL problems 5- Immobility 6- Previous VTE

6. Pathophysiology Factors determining the outcome: 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: 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 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. Insidious onset over weeks to months due to recurrent showers of small emboli. Dyspnea and tachypnea are the commonest features (90%). Dyspnea and tachypnea are the commonest features (90%). Should be considered in the DD of: 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: 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: 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 Sinus tachycardia AF AF RBBB RBBB RV starin RV starin Less commonly; S1Q3T3 Less commonly; S1Q3T3

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

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

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

19. CTPA The gold standard investigation The gold standard investigation Highly sensitive (multi-detector scanners) Highly sensitive (multi-detector scanners) More sensitive for central emboli More sensitive for central emboli More helpful for patients with abnormal CXR More helpful for patients with abnormal CXR Negative CTPA: 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 Mostly replaced by CTPA Still helpful in: Still helpful in: -Patients with normal CXR -Patients in whom CTPA is not safe e.g... Results: Results: Clinical significance Scan probability Clinical probability No PE Normal??? PE excluded LowLow/intermediate PE diagnosed HighHigh

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

22. Management of acute massive PE 1- 100% O 2 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