PE

Pulmonary Embolism – Nick Pietrini

Background

  • A thrombus or “clot” originating in a deep vein (LE > UE) embolizing to the pulmonary arterial circulation
  • Virchow’s triad: stasis (immobilization, travel), hypercoagulable state (cancer), injury to endothelium (surgery, trauma). Idiopathic possible but 12% of idiopathic will be diagnosed with cancer within a year.
  • Genetic: Factor V Leiden, prothrombin gene mutation, protein C/S deficiency, antithrombin III deficiency
    • Acquired: antiphospholipid syndrome, cancer, myeloproliferative disorders, nephrotic syndrome, OCPs
  • Classification (requires TTE):
    • Low risk: Hemodynamically Stable without RV strain or myocardial necrosis
    • Submassive: Hemodynamically stable with RV strain and/or myocardial necrosis
        • RV strain seen on TTE (“D-sign”), BNP >150
        • Myocardial necrosis with troponin >0.05
    • Massive: Sustained hypotension and/or concerns for shock

Presentation

  • Dyspnea / Tachypnea – most common, can be only exertional
  • Tachycardia – common, sometimes the only finding
  • Chest pain – usually pleuritic
  • Hemoptysis
  • Lower extremity pain / swelling – occurs in 50% of pts with DVT
  • RV Failure (large PE) – elevated JVP, hypotension, syncope

Evaluation

  • EKG: most commonly sinus tachycardia
    • Less commonly and indicative of large PE: Right axis deviation, RVH, RBBB, RA enlargement, S1Q3T3 (deep S in lead I, deep Q and inverted T in lead III), TWI in V1-V3 (most common finding reflecting severity)
  • CXR (typically normal)
  • Subtle abnormalities: linear atelectasis, pleural effusion, PA cutoff sign
  • ABG: usually with hypoxia, hypocapnia, high A-a gradient
  • Troponin: increases in 30-50% of pts with moderate to large PE associated with RV strain
  • BNP: often increases with large PE (but less so than in HF patients)
  • D-Dimer*: If low pre-test probability (based on Wells criteria)
  • CTA Chest PE protocol; NPV 95-99%
    • Helps identify potential alternative diagnoses as well as determine severity of PE 
  • V/Q scan: Useful when CXR is normal, no severe cardiopulmonary abnormalities, and contraindication to contrast (ie AKI)
  • Lower extremity dopplers
  • TTE: differentiate submassive vs low risk, chronic right sided failure (PAP>50 chronic)

Management

Acute:

  • ABCs: Provide necessary respiratory and hemodynamic support
  • Initial AC:  If PE is highly probable (Wells score > 6) or moderately probable (Wells between 2-6, but workup will take > 4 hours) and bleeding risk is low, empirically start IV heparin drip, then establish a definitive diagnosis as per above (CTA PE).
    • IV heparin drip (EPIC order set): bolus (80 un/kg), then drip starting 18 unit/kg
    • Enoxaparin (Lovenox): 1 mg/kg subQ q12h (*avoid in ESRD)
  • Thrombolytics (tPA): Most effective within 24 hours, but effective up to 14 days. Use 100 mg of tPA over 2 hours, then resume heparin gtt. Attending/fellow level decision.
  • Indications:
      • Massive PE: PE causing hypotension (shock)
      • Refractory hypoxia or respiratory failure requiring mechanical ventilation.
      • RV failure clinically or on echo (relative indication if not shock)
  • IVC filter (very uncommon): AC is contraindicated, bleeding risk unacceptably high, recurrent PE despite optimal AC
  • Embolectomy: Catheter-directed or surgical
    • Indicated for pt with submassive PE, pts with massive PE in whom thrombolytic therapy is contraindicated, or when thrombolytic therapy has failed

Chronic:

  • Long-term AC (DOAC is the mainstay of management)
    • Apixaban (Eliquis): 10 mg BID x7 days à 5 mg BID
        • Can use in renal failure (do not dose reduce like for atrial fibrillation)
    • Rivaroxaban (Xarelto): 15 mg BID x 21 days à 20 mg daily
      • Needs to be taken with food, avoid with CrCl<30
    • Dabigatran (Pradaxa): 150 mg BID AFTER 5 days of parental therapy
    • Warfarin (Coumadin): Goal INR 2-3, requires frequent monitoring
      • Need to be bridged with enoxaparin or heparin gtt
  • Duration of Anticoagulation:
    • Major reversible/transient risk factors (surgery, trauma): 3-6 months
    • Idiopathic, unprovoked, or with less compelling risk factors: 12 months
    • Major permanent risk factors (cancer, homozygote F5L or prothrombin gene mutation, APLS, protein C/S deficiencies, AT III deficiency): At least 1 year, preferably lifelong. 
    • Recurrent DVT/PE: lifelong