March 17th, Treating PE

We spent a separate morning report on treating PE.

We know that ~50% of PE can be treated as an outpatient, refer to the OTPE trial, they classified patients with pulmonary embolism severity index (low and high risk), had patients randomized to outpatient vs inpatient treatment and demonstrated noninferiority.

In the index we specifically look for things like vital sign stability and patients not requiring oxygen.

So what do we use to treat them? First we consider idiopathic vs a cause of PE. With a suspected cause, we generally treat for 3 months (then reassess) and often stop. If idiopathic, we often repeat a D-dimer, if elevated treatment is prolonged. If low, we know there is significantly lower chance of recurrance (refer to PROLONG trial).

The one concerning feature of "idiopathic" PE is that they can be associated with malignancies, especially in the elderly. Basic screening should be assessed (mammogram in woman, colonoscopy, prostate cancer and a good physical exam and history of B symptoms).

Individuals with malignancy related PE have less recurrence when treated with LMWH compared to warfarin (refer to CLOT trial), in this study most patients had solid tumors, dose is 200 Units/kg. We have no available evidence for the New Oral Anticoagulants (NOACs).

When can you use a NOAC, in many patients dabigatran and rivaroxaban are ideal. Apixaban has been studied but is not approved in Canada yet.

Apixaban is ok in individuals with a GFR <25, they will take 15 mg BID x 3 weeks then 20 mg po daily (the afib dose also). The thing to watch out for... there is no clear reversible agent.

If someone has fluctuating creatinine one may consider IV heparin it is not effective much by kidney function. It's short half life also makes it ideal in patients who may bleed, in addition, there is a reversible agent (protamine sulfate).

Finally, what about submassive PE.

Massive is right heart strain (by echo, CT, RBBB or trop increase) and bp <90
Submassive: right heart strain with ok bp ?90

although the PEITHO trial found a decrease in primary ends points (mortality and hemodynamic instability), these aren't quite the same... dying vs hemodynamic stability are NOT the same things.

The MOPETT trial in 2012 showed that low dose TPA (50 mg instead of 100, the same dose in pEITHO) reduced pulmonary artery pressures (RVSP) that was maintained at 28 months. So maybe we have a risk of bleed now... for a decrease chance of pulmonary HTN in the future.

So what do we do now? For patients with submassive, acute onset, age less than 60... one may consider it, but important to rule out contraindications for PE (hemorrhagic stroke, recent surgery, brain tumor, etc. go through the checklist).