Pulmonary thromboembolic disease

Pulmonary Thromboembolic
Ahmed Mansour, MSc, PhD
• 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
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%
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...
Presisposing Factors
• Wirchow’s triad.
• Acquired risk factors
1- Surgery
2- Obstetrics
3- Malignancy
4- LL problems
5- Immobility
6- Previous VTE
1- Cardiovascular
2- HRT, contraceptives
3- Others: obesity, nephrotic
• Inherited thrombophilias
1- Factor V Leiden mutation (APC resistance)
2- Prothrombin gene mutation
3- Deficienecy of antithrombin III, protein C, protein S.
• 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
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.
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
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
Acute SOB in presence of a risk facto for VTE
O/E: patient is hemodynamically stable
ABGs show hypoxemia, CTPA: central thrombus
Usually in elderly patients with cardiopulmonary diseases
Rapid decompensation even with small PE
O/E: features of the underlying diseases.
Acute chest pain (RV angina), hemodynamic instability due to massive PE
O/E: RV failure...
ECG changes, echocardiography shows RV failure
2- Isolated dyspnea (25%):
3- Circulatory collapse, poor reserve (10%):
4- Circulatory collapse in a previously well patient (1%):
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
New AF
Pleural effusion
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.
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
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
Troponin and natriuretic peptides
Ventilation/perfusion lung scan
• Sinus tachycardia
• AF
• RV starin
• Less commonly; S1Q3T3
• Small pleural effusion
• Raised hemi-diaphragm
• Collapse
• Infiltrate
• May be normal
• Hypoxemia and hypocapnea
• Increased A-a oxygen gradient
Troponin and natriuretic peptides
• Indicate RVD
• Raised troponin predicts poor prognosis
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.
V/Q scan
• Mostly replaced by CTPA
• Still helpful in:
- Patients with normal CXR
- Patients in whom CTPA is not safe e.g...
• Results:
Clinical probability
Scan probability
Clinical significance
PE excluded
PE diagnosed
Other imaging techniques
• Echocardiography
• Leg U/S
• CT venography
• Transthoracic U/S
• Conventional pulmonary angiography
Management of acute massive PE
100% O2
IV access, baseline clotting screen, ECG
Management of cardiogenic shock
IV heparin:
– Unfractionated vs LMWH
– Loading, maintenance
Investigations to confirm PE?
Thrombolysis for massive PE causing hemodynamic instablity
Embolectomy in patients with a contraindication for anticoagulants or thrombolytics
Oral anticoagulants
For how long?
A contraindication for anticoagulants
Massive PE after survival
Reccurrent VTE despite adequate anticoagulation
10- IVC filter for patients with:
Thank you
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