Mythbusting

syncopal PE’s, gestalt, & sensationalism.

Want to know how to poke the EM FOAM bear? Make a sweeping generalization that we are “doing it wrong” that goes against the “first do no harm” mentality, while paradoxically potentially putting some patients in harms way…

Shortly after ACEP16 ended and many FOAMites was scrolling through their Twitter timelines, this paper popped up.

11 hospitals looked at 2,584 patients >18 years of age with a first time syncopal event lasting <1 minute, with obvious causes (seizure, trauma, stroke) excluded, as well as patients already on anticoagulation or with Afib. After all said and done, 560 were analyzed.

 

-330 had a low pretest probability via Wells scoring & negative d-dimer; thus PE ruled out.

-230 had high pretest probability, positive dimer, or both.

-180 under went CTPA, 49 underwent VQ (one died and had an autopsy)

-97 of these patients had a pulmonary embolism.

So, 97 of 2,584 total syncopal patients had a PE. (3.7%)

 

PE’s diagnosed by CT:

main artery: 30/72

lobar: 18/72

segmental: 19/72

subsegmental 5/72

 

so, we’ll say 42% (30/72) are “clinically relevant” PE’s . Thats 1.1% of all-comers.

 

Let’s dig in a bit more:

-80% of confirmed PE were 70 years of age or greater (46% over 80)

-11% had prior PE

-45% with PE had a respiratory rate >20breaths / min vs 7% without PE

-33% with PE had a heart rate >100 bpm vs 16.2% without PE

-36% with PE were hypotensive <110mm Hg systolic vs 22.9% without PE

-40% with PE had signs of DVT (leg swelling, redness, etc) vs 4.5% without PE

-20% with PE had active cancer vs 10% without PE

one patient died.

 

So while there are some pretty sensational headlines regarding this paper, it reminds me of a case & a podcast. I remember about 4 years ago, I had an elderly patient who syncopized after standing out of bed. But in the ED, she was tachycardic and I couldnt quite explain why. Something just felt off. She was in good healthy, and didnt seem particularly dry, so I sent a dimer. I then proceeded to get my behind chewed out because I sent a dimer on an elderly patient with clear orthostasis, and it was going to be positive since she was elderly, and we’re busy so it’ll ruin our throughput, yada yada yada. Turns out, she had a dimer in the thousands, and had a main artery PE.

About two years later, I heard this podcast on PE & gestalt.

Before bringing this full circle, a few concerns. I’m fairly certain that this will, at least short term, increase the use of dimers as a part of a syncopal work up, and probably for the “near syncopal” as well.  But what about age-adjusted dimers? A potential role can & should be seen here for those of us with concern enough to send a dimer, particularly if your gestalt dictates.  With 40% of these PE’s not being small, I think something is there, the question is, is it meaningful?  Better yet, is it worth chasing after that 1.1% ?   We do it for chest pain with troponins, we do it with lactics for infectious processes, why not age-adjusted dimers for syncope?  But is any of that actually good care?

 

Sadly, we’re still not exactly sure if we’ve benefitted the patients in this study by treating them since they were not followed for a prolonged period.

So where does this leave us? Well, I’ll leave up for you & your gestalt to decide.  I’m still trying to figure out if I actually helped that poor elderly woman.

Standard

2 thoughts on “syncopal PE’s, gestalt, & sensationalism.

  1. jordanschooler says:

    I appreciate your analysis. This is a paper many of us will struggle to assimilate and I agree we should be critical. However, I do not think it is appropriate to simply change the denominator to the entire patient cohort and conclude that 3.7% of their patients had PEs. There is no evidence of any screening, even PERC in the rest of the patients. We have zero information about them. It is worth commenting that they only worked up a subset of their patients, but your numbers past that point are not valid.

    • Thanks for the comments.

      They do mention a standardized protocol for syncope work up based on European Society of Cardiology & AHA Guidelines for syncope – but references are from 2009 & 2006 respectively, and offer only a passing reference to PE without Wells or PERC mentioned in them. So, based on the protocols of their references, PE was screened for, but how, we’re not exactly so sure. PERC probably could not be used based on the age >50 of a majority of the admitted patients alone, and its worth noting Wells did not evaluate those >85.

      As for changing the denominator, while it may not be ideal, I think it’s important to try and tease out how many of these are actually clinically relevant, particularly given that not an insignificant portion of smaller PEs are false positives. I toyed with the idea of adding in a false positive rate and/or baseline PE rates for the general population, but decided against it.

      Working in the ED, I think its not terribly unreasonable to be reminded that a small percentage of elderly with risk factors will have a PE that I should screen for. When I’m in the observation unit, I have the tincture of time to risk stratify a bit more in depth and have a better risk / benefit discussion.

      I’m not certain this paper changes much for me except reiterate the use of an age-adjusted dimer and serve as a reminder that occasionally, patients have PEs… whether or not its beneficial to treat them? debatable.

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