Is pulmonary embolism really all that bad?… Again…

10 Jan


Pollack, Charles V, Donald Schreiber, Samuel Z Goldhaber, David Slattery, John Fanikos, Brian J O’Neil, James R Thompson, et al. “Clinical Characteristics, Management, and Outcomes of Patients Diagnosed with Acute Pulmonary Embolism in the Emergency Department: Initial Report of EMPEROR (Multicenter Emergency Medicine Pulmonary Embolism in the Real World Registry)..” Journal of the American College of Cardiology 57, no. 6: 700–706. doi:10.1016/j.jacc.2010.05.071. PMID 21292129


  • this was a large ED based registry study from multiple US EDs to see how PE patients present and what happened to them
  • it included both people who ended up having a confirmed PE and those empirically treated for PE awaiting tests and ultimately ruled out for PE
  • PE diagnosis could be based on lots of different tests (all appropriate I think)


  • 2400 pts, 1800 who had PE
  • vast majority (90%) diagnosed by CT
  • 3% were hypotensive on presentation
  • SOB, pain, and symptoms suggesting DVT were commonest presenting complaints
  • 5% presented with syncope: it happens but it’s not common
  • of those who got echoes (only a quarter) there was RV dyskinesia in half
  • 85% of those with PE got anti-coagulated in the ED – this is lower than I expected, though presumably because they had contra-indications.
  • mortality rate attributable to PE was 1.1% (though all cause mortality was 5.4% meaning that lots of sick people get PEs and die of something else)


I know I’ve ranted on this before but I do find it fascinating.

I grew up with the notion that PE killed roughly 1 in 5 of those with the disease. That’s kind of scary. That’s similar to STEMI mortality. There is no doubt that there was a time when the PEs we diagnosed carried that type of mortality. Big feck-off PEs that is.

As the technology has changed we have created a new disease – let’s call them pulmonary fluff instead of pulmonary emboli. Emboli are terrifying, fluff not so much.

We have presumed that pulmonary fluff is the same disease as the big bad pulmonary emboli.

We are left with, i think, with two possible conclusions

  1. we seem to have discovered a treatment (in heparin) that reduces mortality from 20% to 1%. An absolute risk reduction (ARR) of 19%. Considering that lytics for STEMI probably by you a 2% ARR we should be absolutely stunned.
  2. The alternative is that we are now diagnosing lots of pulmonary fluff and the mortality rate from pulmonary fluff is 1% at a baseline and giving all this people heparin to treat their fluff does nothing; an ARR of 0%.

It may be somewhere in between those 2 answers but we have yet to make up our mind which.


16 thoughts on “Is pulmonary embolism really all that bad?… Again…

  1. @ANDY -- I agree with you completely! Simple history and physical should help to distinguish in MOST instances between “pulmonary fluff” vs true hemodynamically significant PE that is the CAUSE of the patient’s acute symptoms of pain/dyspnea/hemodynamic instability. Our diagnostic tests for finding PE have become better and better -- so we are able to pick up smaller and smaller PEs than ever before. Many of these smaller PEs (“pulmonary fluff” as you call them) are small, subsegmental incidental bystanders that are only picked up because of ever increasing tendency in the ED “not to miss anything” -- ergo ordering of chest CT scans at lower threshold indications (ie, for almost anyone with any symptoms of chest discomfort/dyspnea without much regard for realistic likelihood for acute PE as the cause). The reason for “reduced mortality” from PE in recent years is not because of “improved treatment” -- but rather because Heparin (followed by longterm anticoagulation) is being used to treat many patients with incidental unimportant PEs discovered by chest CT scans done for low likelihood indications. Many (most) of these patients probably would have spontaneously cleared their small subsegmental defect without adverse consequence.

    The problem of course is that once someone orders the chest CT and has it come back as “PE” -- you are COMMITTED to a course of treatment (because how can you say for sure that this PE won’t be problematic …). Such treatment is NOT benign. First -- you have made the patient a “longterm patient” by overdiagnosis of “PE” that is probably of no significant danger to them. There is financial cost to longterm anticoagulation (for at least 3 if not 6-12 months) -- as well as potential for adverse effects -- as well as not insignificant radiation exposure -- PLUS -- the “next time” this patient comes back with “not very PE-like-sounding symptoms” -- behavior is “reinforced” because a PE was found on that 1st chest CT when it wasn’t expected -- so “We’d better get another chest CT” -- and the cycle continues. The behavior of doing more and more chest CTs for lesser and lesser valid indications is prophecy-fulfilling -- because it finds more and more insignificant PEs in patients with low-likelihood symptoms -- so more and more chest CTs continue to get ordered …

    MORAL of the STORY: Don’t indiscriminately order chest CT scans. This practice is NOT benign. By all means -- keep a healthy respect for potentially serious PEs that DO have high morbidity/mortality associated with them -- but try to minimize ordering chest CT scans on the very large LOW-RISK population of patients who present with atypical symptoms and relative lack of true predisposing factors to PE … When you REALLY suspect significant acute PE as the cause of your patient’s acute symptoms -- that’s the time to get a CT scan.

  2. I don’t disagree with any of the above -- but what about the ‘fluff’ we miss? At the stage when it is fluff it’s probably not a big deal, but we do know that clots propagate and how do we tell which fluff just gets lysed by the body and which fluff will form a nidus for clot and end up presenting as a scary big clot with the associated mortality?

    • @Chris -- My understanding is that the “fluff we miss” (ie, smaller and for the most part harmless asymptomatic subsegmental incidental bystander PEs) -- by and large is benign -- with this being supported by a number of studies (GO TO: -- with author Stein of the 2nd abstract apparently being one of the “PE gurus” ). So it is true that we cannot absolutely 1,000% guarantee that none of the “fluff we miss” will ever cause a problem …. (medicine just isn’t perfect). That said -- given the RISKS of actively searching for “all the fluff we miss” and acting on it (longterm anticoagulation that a diagnosis of “PE” entails -- probable reanticoagulation of THAT patient any time they present again to the ED with the same soft symptoms -- not to mention radiation exposure -- financial cost -- and making a “non-patient” into a “patient”) -- these real RISKS probably far OUTWEIGH any potential benefit from treating very low risk patients with minimal to no real symptoms who end up with a “fluff-positive” CT.

      It seems the paradigm should change -- but that admittedly AIN’T easy …

      • Thanks for the excellent abstracts!

        Keeping it simple for a simple guy like me sounds like proposed strategy is :

        1. Incidental sub-segmental PE (asymptomatic -- CT done for some other reason?) -- No risk factors for propagation potential = Follow up serial USS of legs
        2. Sub-segmental PE (symptomatic) -- Rx depends on type of symptoms, pulmonary reserve, presence of risk factors = Anti coag vs. serial follow up
        3. All other PEs -- anti-coag

        Where I think some of the controversy may lie is how do we define number 2 above -- questions like:
        A. Pulmonary reserve -- how do we classify? Spirometry? Functional performance? Smoking history?
        B. OCP -- Do we tell patients to cease it (I would ) and if only that risk, can we just follow up w/ serial USS
        C. What symptoms do we consider significant -- SOB? CP? -- they must have had some symptoms to undergo investigations, how do we determine what isn’t significant? Are the symptoms actually due to the fluff or are we missing something else and just hanging a diagnosis on the subsegmental PE?
        D. Where do we class active cancer in the risk factors? I suspect it would be high risk for propagation and such would anti-coag.
        E. What about those with a family hx of DVT/PE? Is this enough to warrant anti-coag over serial USS?

        I guess that’s where the difficulties lie in my mind for me -- repeat CTs, anti-coag is bad, but so are large PEs and I um unsure if we know where we lie with the patients I outlined in 2 (the extremes like 1 and 3 are easy).

        Loving the opportunity to exercise my brain :)


        • Cheers for comments ken and Chris

          At present I think we just don’t have data to answer that question but I think there’s plenty of reason to doubt our current practice of anticoagulanting everything.

          Some of kline’s recent talks suggest he’s working towards getting us out of this mess!

        • I agree with Andy that unfortunately we just don’t have definitive data yet on what to do … That said -- the articles I reference (there are others) suggest that we clearly overtreat many PEs. The bigger we “cast our umbrella” in our search for PE -- the more we are likely to come up with PEs that are not clinically significant (and which most probably would never have caused a problem had we not found them by ordering a CT scan on someone who probably didn’t need a CT …).

          “A physician deserves the results of the laboratory tests that he/she orders”. Once you look (ie, get that chest CT) -- I think you are stuck -- because I would not want to not anticoagulate a patient whose scan comes back “PE”. I think the place to start is to be MORE SELECTIVE in who one orders chest CT scans on. There are “symptoms” -- and there are “symptoms” -- but at least from my former perspective as a primary care attending -- so very often the patients our residents would be called on to admit were patients seen in the ED for whom we never would have gotten the CT scan in the first place (ie, because they were low risk, had a history which no more than remotely sounded like PE, or had some other obvious cause of dyspnea such as COPD, asthma, pneumonia). The Chest CT was already ordered and done by the ED staff who then called us to admit because the scan was “positive”. This is not to say that such patients with low likelihood history for PE can not ever also have PE in addition to their pneumonia or COPD -- but there clearly are times when PE is not at all a likely diagnosis. The articles I reference document that “looking” more often (ie, doing more chest CT scans) has not improved prognosis -- and we definitely know the counter to more chest CT scans is not benign (overdiagnosis in many such patients; overanticoagulation; repetition of the cycle when the patient comes back to the ED; adverse effect from anticoagulation longterm; financial cost; radiation exposure). NOTHING is perfect -- there is no perfect solution -- but more forethought rather than reflex ordering of chest CT scans (as became rampant at the several hospitals I attended at) is the first step in my opinion …

          • Totally agree Ken, could I ask your opinion on the use of rules like PERC and Wills? These are the primary clinical decision rules I see used where I work and their fairly straightforward (although the ‘more likely than alternative diagnosis’ gets debated sometimes, but I wonder if these rules might be behind the more ordering of CT chests?

  3. @Andy…..I really agree and think it would be interesting to do a prospective research about this. That would probably be a treatment changing article. Just look at the next article and you will see that (in the USA) we are over-diagnosing, which (probably) results in more side-effects then benefit from the treatment with anti-coagulation.

    Furthermore the more senstivise CT’s found more PE’s, but there was no decrease in mortality by Carrier, et al, 2010.

    So I agree that are overdiagnosis and overtreating PE’s!

    Gr. Egon

    (I hope the links work! Otherwise the articles are easy to find on pubmed!)

  4. SORRY Chris for my delay in responding to your question -- I was out of town and unable to post …

    EGON -- Thank you for the download of the SUPERB Wiener/Schwartz/Woloshin article in Archives about, “Time Trends in PE in the US: Evidence of Overdiagnosis”. This is the BEST summary of the data I have seen and in my opinion is a reference to be quoted. The Conclusion at the top of the article says it all: “Introduction of Chest CT has been associated with changes (in trends) consistent with OVERDIAGNOSIS = rising PE incidence; minimal change in overall mortality; lower case fatality (ie, most of the PEs that are now picked up by Chest CT which account for the recent “epidemic in PE” are PEs that are NOT significant = Overdiagnosis). AND -- there IS HARM from new increased use of Chest CT (results in many more patients being anticoagulated with all the risks from that -- many more individuals become “patients” -- radiation exposure -- financial cost -- etc.).

    EGON -- I was not “allowed” to access the 2nd link you posted (article by Carrier … ).

    CHRIS -- I assume you mean “Wells” (rather than Wills) together with PERC for the decision rules? That debate (use of Wells & PERC criteria) has already been had in Emergency Medicine circles with “Biggies” in the field. See EXCELLENT posts on Life-In-The-Fast-Lane (GO TO: -- and be sure to scroll all the way down to the insightful Comments! ) -- and be sure to go to Scott Weingart’s EMCrit Blog -- where you can see a great 90-minute video debate between Scott Weingart vs Dave Newman ( ) -- as well as a Weingart/Nickson algorithm for working up PE ( ) -- with many wonderful comments along the way.

    So I don’t have answers beyond this debate other than my ‘gut feeling’ that PE is grossly diagnosed at the current time -- and Chest CT is overused because of fear of “missing “PEs” to the point that potential for harm from using that test often exceeds potential for benefit (which is NOT in best interests of the patient, which should be what counts). Validity of Wells & PERC seems to tremendously depend on prevalence of PE in the population these rules are applied to -- and that prevalence for PE is different in the U.S. vs Europe (due to higher tendency to work up more cases in the U.S.) -- and that prevalence has dramatically decreased over time since Wells first came out with his criteria (initially “low risk of PE” was ~10-15% -- whereas today it is sometimes well under 1-2% … ). And then … -- Do PERC and Wells even begin to look at the issue raised by Wiener/Schwartz/Woloshin about finding a “PE” that isn’t clinically significant … ?

    My Bottom Line is that clinical judgement defies number scale scores. One can begin with whatever assessment scale criteria one wants -- but somehow reason needs to be factored in such that the number of D-Dimers and Chest CT scans ordered starts to decrease. Looking for PE when the likelihood of clinically significant PE (that is likely to benefit from treatment) is low is NOT a good thing …

    I don’t pretend that the decision-making process is easy -- and I’m very happy that at this stage in my life I’m no longer on the front lines having to decide …

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  8. Here is a patients prospective! I had a diagnosis swept under the carpet and ended up with an extensive PE with near occlusion (whatever that all means haha!) Went to the Dr with sore leg, positive d dime came back but no sign of clots in leg. Week and half later went to dr with SOB, was asked if I was anxious about anything? (yes I can’t breath properly!) Had an ECG in rooms, all fine, X-ray the next day, results hadn’t come back by afternoon, went to outpatients after nearly fainting then transferred to larger hospital by ambulance. Spent 4 nights in intensive care then further 5 at our local hospital till INR levels stabilized. So what I am getting at there is sometimes Dr’s can not take some symptoms seriously….well mine anyway!

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