Pulmonary Embolism¶
Anna Berry
Background¶
A thrombus originating in a deep vein (LE > UE) embolizing to the pulmonary arterial circulation.
- Risk Factors = Virchow’s Triad
- Stasis: immobilization, hospitalization, spinal cord injury, or long travel
- Hypercoagulable state: cancer, prothrombotic genetic conditions such as Factor V Leiden, OCPs, antiphospholipid syndrome, nephrotic syndrome, pregnancy, infection, etc.
- Endothelial Injury: surgery, trauma
Most originate from a DVT in the iliac, femoral, and popliteal veins
Presentation¶
- Dyspnea and tachypnea
- Respiratory alkalosis on blood gas from hyperventilation
- Hypoxemia
- Sinus Tachycardia or atrial arrhythmias
- Hemoptysis
- Lower extremity pain, swelling, and redness – occurs in 50% of pts with DVT
- RV Failure (large PE) – elevated JVP, hypotension, syncope, R parasternal heave, accentuated P2, hepatomegaly
Evaluation¶
- If hemodynamically unstable and PE suspected, provide hemodynamic support (ie. O2, pressors, etc.) and perform emergent bedside TTE
-
If no RV strain evident on TTE, low likelihood of hemodynamically significant PE. Consider other causes of shock.
-
Hemodynamically stable
- EKG
- Most commonly sinus tachycardia
- Less commonly and indicative of large PE: RAD, RVH, RBBB, RA enlargement, S1Q3T3 (deep S in lead I, deep Q and inverted T in lead III), TWI in V1-V3
- CXR: Typically normal. May see linear atelectasis, pleural effusion, PA cutoff sign
- Labs: ABG, troponin, BNP
- May consider lower extremity dopplers
- Imaging vs d-dimer based on pre-test probability:
- Low pre-test probability (use Wells Criteria) d-dimer
- For moderate to high pre-test probability CTA Chest PE protocol
- If high pre-test probability or moderate pre-test probability with >4 hour delay in work-up, start empiric anticoagulation if bleeding risk is acceptable while work-up is ongoing
- TTE
- EKG
Management¶
PE Class: | Low risk | Submassive | Massive |
---|---|---|---|
Definition | Hemodynamically stable No evidence of right heart strain or myocardial necrosis on labs or TTE |
Hemodynamically stable Evidence of right heart strain or myocardial necrosis: RV strain on TTE (ex: D-sign), BNP >150, trop >0.05 |
Hemodynamically unstable (ex: SBP<90) Evidence of RV strain |
Management | Start anticoagulation LWH or heparin gtt (if renal impairment) Can also use NOAC. Rivaroxaban & apixaban can be used as initial management. Edoxaban & dabigatran can be used after 5-10 days of parenteral therapy |
Provide hemodynamic support, monitor for decompensation Start anticoagulation with unfractionated heparin gtt STAT consult cardiology for consideration of catheter directed thrombolysis (EKOS) or embolectomy |
Provide hemodynamic support. Start anticoagulation with unfractionated heparin gtt Page CCU fellow STAT. Consider systemic tPA (this is a fellow/attending level decision). Discuss with cardiology catheter directed thrombolysis (EKOS) or embolectomy |
tPA Considerations¶
- Dose is 100mg tPA over 2hrs
- Most effective within 24 hours but effective up to 14d
- Contraindications:
- Absolute:
- CNS Pathology: hemorrhagic or ischemic CVA within 3 mo, AVM, CNS neoplasm, recent surgery
- Trauma: Recent head trauma w/ fx or injury
- Relative
- Surgery: surgery w/in 3 wks
- Heme: active bleeding, bleeding diathesis, plt \< 100, oral AC
- Age: >75 yo, dementia
- Absolute:
Long-term management¶
- Anticoagulation: see “Venous Thromboembolism” in Hematology/Oncology