Pulmonary Embolism Flashcards
What is the definition of a PE?
Obstruction of one or more of the pulmonary arteries by solid, liquid or gaseous masses (usually a DVT from the leg)
What age group are most likely to get a PE?
> 65
What are the risk factors for PE?
- Increasing age
- DVT
- Surgery in last 2mo
- Bed rest >5 days
- Previous VTE
- FamHx
- Recent trauma or fracture
- Active malignancy
- Pregnancy/post-natal period, high oestrogen states (obesity, OCP, HRT)
- Hypercoagulable states
What are some inherited risk factors for PE/DVT?
Hypercoagulable states!
- Factor V leiden mutation
- Prothrombin G20210A mutation
- Antithrombin deficiency
- Protein S deficiency
- Protein C deficiency
- Anti-phospholipid syndrome
Where do most emboli causing PE come from?
Lower limb proximal veins (iliac, femoral, popliteal) –> through the right ventricle –> pulmonary arteries: lodges
What are the aetiological sources of PE?
Thrombus (from deep veins)= most
Gas emboli
Fat from a fracture
What is the aetiology of a thrombus?
Virchow’s Triad!!
- Vessel wall damage
- Venous stasis
- Hypercoagulability
How does vessel wall damage contribute to virchow’s triad and what causes it?
Endothelial cell damage promotes thrombus formation, usually at venous valves
- Trauma
- Previous DVT
- Surgery
- Venous harvest
- Central venous catheterisation
How does venous stasis contribute to virchow’s triad and what causes it?
Poor blood flow and stasis promote formation of a thrombi + congestion causes valvular damage –> further promotes thrombus formation
- Age >40
- Varicose veins
- Immobility
- GA
- Paralysis
- Spinal cord injury
- Myocardial infarction
- Prior stroke
- Adv CHF
- Adv COPD
How does hypercoagulability contribute to virchow’s triad and what causes it?
Promotes thrombus formation. Inherited and acquired causes
- Cancer
- High oestrogen states
- IBD
- Nephrotic syndrome
- Sepsis
- Blood transfusion
- Inherited thrombophilia
What is the pathophysiology of a PE?
Once the embolus has lodged it results in:
- Decreased gas exchange: due to mechanical obstruction of the vascular bed –> V/Q mismatch –> hypoxia
- Infarction where the clot lodges in smaller pulmonary arteries –> pleuritic chest pain
- Cardiovascular compromise: depends where the clot is but you can have compromised CO –> hypotension
What is a saddle PE?
If the embolus is large enough it can lodge in the main pulmonary artery and obstruct flow from the right ventricle to the lung
Life threatening!
What is the clinical presentation of a PE?
Symptoms:
- Dyspnoea
- Cough
- Pleuritic chest pain
- Haemoptysis
- Calf pain or swelling (DVT symptoms)
Ex:
- Tachypnoea
- Tachycardia
- Hypoxia
- Signs of DVT
- If saddle PE or massive PE: low BP, signs of RHF (raised JVP, leg swelling)
What is the diagnostic algorithm for suspected PE?
What is the Well’s Score for PE?
Brief Summary of what Ix you do for a PE?
Bedside:
- ECG
Labs:
- FBC
- D-dimer
- Baseline coags
- UEC
- Trop
- BNP
- LFTs
- Do a thrombophilia screen
Imaging:
- CXR
- CTPA
- V/Q scan
- Lower limb compression venous USS if concerned for DVT
What bedsides Ix do you do for PE?
ECG
- Mostly sinus tachy
- Can have S1Q3T3
- New RBBB
What laboratory Ix do you do for PE?
- FBC
- D-dimer (elevated)
- Baseline coags (need this to be able to start anti-coags)
- UEC (need baseline when prescribing anti-coags + may need contrast)
- Trop (rule out ACS)
- BNP (rule out CHF)
- LFTs (can influence anti-coag choice)
- Thrombophilia screen if PE is unexplained, FamHx, or cough change the Mx
What imaging do you do for PE?
CXR:
- Mostly to rule out other causes
- Can see a Hampton’s hump (increased dome-shaped opacity in the lower lobe) from haemorrhage
CTPA:
- Most sensitive and specific
- Often see wedge shaped infarctions with pleural effusion
V/Q Scan:
- Pulmonary artery occlusion leads to ventilated areas without perfusion (dead space)
Lower limb compression venous USS if suspect a DVT
WHat’s included in the thrombophilia screen?
- Factor V Leiden mutation
- Prothrombin G20210A mutation
- Antithrombin deficiency
- Protein S deficiency
- Protein C deficiency
- Anti-phospholipid syndrome
What is the DDx of PE?
CHF
MI
Pneumonia
Exacerbation of chronic lung disease
Pericarditis
MSK pain
Valvular insufficiency
What is the overall Mx of PE?
- 45 degrees sitting position
- Oxygen supplementation
- IV fluid resuscitation
- DVT prophylaxis required in future (some people need IVD filter if anti-coags are contra-indicated)
Other Mx depends on whether hemodynamically stable or unstable
What is the management of someone who is hemodynamically stable with a PE?
1st Line: Use a NOAC/DOAC (apixaban or rivaroxaban) as they don’t need parenteral anticoagulation for initiation
- Also don’t need routine anticoagulation monitoring
- If using Dabigatran, lead in with LMWH for 5 days then stop before starting
2nd line: if you can’t use a NOAC/DOAC (pregnancy, cancer, severe kidney impairment), use warfarin + parenteral or LMWH
How do you manage a subsegmental PE?
Management is controversial and varies but surveillance rather than anticoagulation is considered teh best option for most patients
How do you manage a haemodynamically unstable patient with a PE?
- Start UFH
- Thrombolysis: alteplase, streptokinase, urokinase
- After UFH, switch to apixaban or rivaroxaban (LMWH if those unsuitable)
- CONSIDER a vasopressor (noradrenaline) or inotrope (dobutamine) if systolic BP remains <90 after thrombolysis
CONSIDER: surgical embolectomy/percutaneous treatment
What are complications of PE?
- Pulmonary infarction (localised necrosis of lung tissue –> frequent when distal vessels are occluded)
- Acute bleeding during treatment
- Recurrent venous thromboembolic event
- Cardiac arrest from right ventricular collapse due to massive embolism
- Chronic thromboembolic pulmonary hypertension
