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On "unnecessary" ED visits: background reading

Here are a bunch of very informative pieces on why trying to blame excessive costs or busy-ness on low acuity patients in the ED is, at be...

May 28, 2011

To PE or not PE?

I don't like pulmonary embolism.

My dislike for PE works on many levels. On the one hand, PE can be fatal, and I generally don't like it when my patients die. On the other hand, many or even most PE (or is it PEs? or PE's?*) aren't particularly dangerous.

Further, we don't really know the prevalence of PE, we don't know how to tell dangerous PE from not-particularly-dangerous PE, and we're not even sure about the treatment for PE.

As discussed at length in what I think is still the best episode to date of SMART-EM, the evidence is not only weak but maybe even suggests that perhaps we shouldn't anticoagulate patients with PE at all, despite the clear "standard of care." And while thrombolysis might benefit some very sick patients with PE, nobody really knows.

Further, some very smart people suggest that a main function of the lungs might be to filter clots from making it to the brain.

That's not to say that PE isn't a dangerous entity. A new study by Weiner et al in the Archives of Internal Medicine notes that introduction and widespread adoption of CT pulmonary angiography has increased the diagnosis of PE about 70% but decreased the case fatality rate by only half that much, and overall mortality only modestly decreased. To be honest, I'm not completely clear on whether "case fatality rate" means much; they define it as "the proportion of hospital deaths among patients with a PE."

Not surprisingly, the rate of what appear to be clinically important complications of anticoagulation also increased by about 70%.

This is certainly not a perfect study. The study authors use mortality from death certificates as the primary outcome measure, and as someone put it, cause of death is largely determined by interns.

As the study authors discuss, the increase in PE diagnosis could be a good thing if more diagnosis means better outcomes. However, in the absence of better outcomes, we are likely diagnosing clinically insignificant disease. And there's no way to determine if the PE I just diagnosed is one of the bad ones or not.

So we use a lot more CTPA (not news) to detect a whole lot more PE, with minimal benefit. And I don't think the "ease" of CTPA is the only part of it. The Wells Criteria, d-dimer, and PERC were supposed to help us safely decrease testing, but aren't used properly, have lead to increased testing, and may not even work. Specifically, many physicians seem to use the d-dimer to increase, not decrease, testing. Despite our best intentions, perhaps the overall increase in conversation about PE leads to increased testing on it's own (i.e., availability bias).

Moreover, it's not just about diagnosing more patients with PE or deciding who to anticoagulate. It's not even about the very real radiation risks. As crowding becomes the norm in many EDs, many departments operate at full capacity much of the time. At both of the hospitals where I work, the CT scanners run non-stop. So each extra CT means that other patients have to wait for their own CT scans, each of them requiring nursing care, physician attention, and all of the other trappings of being in the department. In the age of ED crowding, everything has an opportunity costs. Crowding leads to overworked nurses, frustrated physicians, and all sorts of bad outcomes, including worse pain management; delays to antibiotics, thrombolytics and PCI; missing quality measures; increased mortality; and decreased patient satisfaction. If an extra CT means 12 patients wait for an extra half hour (my estimate) that means 6 more patient-in-ED-hours, with a conservative estimate of 2% increased mortality for every 6 extra hours patients spend in the ED. Does that mean every 50 extra CTs could mean that 1 more patient dies from crowding?**

I'm not sure what to do with all of this. Concern about PE seems genuine. (Boehringer Ingelheim developed dabigatran for primary stroke prevention in afib, not to treat PE. Compare about 500 cases per 100,000 vs. 112 cases per 100,000.) PE can be fatal. CTPA can detect PE. Initiating treatment may save a patient's life, but anticoagulation probably has limited benefits and carries very real risks. There don't seem to be easy answers.

But some things are clear:
We irradiate far too many people, and some people are destined to a life of eating rat poison.

*I think it's either PE or PEs, but not PE's.
**This is admittedly a very rough, back-of-the-envelope estimate that I made up. Perhaps in the future it can be quantified more accurately.

UPDATE 7/21/2012:
2 interesting recent articles:

Joe Lex on LITFL's R&R:

Venkatesh AK, Kline JA, Courtney DM, Camargo CA, Plewa MC, Nordenholz KE, Moore CL, Richman PB, Smithline HA, Beam DM, Kabrhel C. Evaluation of pulmonary embolism in the emergency department and consistency with a national quality measure: quantifying the opportunity for improvement. Arch Intern Med. 2012 Jul 9;172(13):1028-32.

Ryan Radecki discusses:

Prasad V, Rho J, Cifu A. The Diagnosis and Treatment of Pulmonary Embolism: A Metaphor for Medicine in the Evidence-Based Medicine Era. Arch Intern Med. 2012 Apr 2. [Epub ahead of print]


  1. The Well blog on the NYTimes had a medical mystery case of a man with recent surgery and persistent hiccups, diagnosed with... PE.

    One of the physicians who solved it explains how he did it:
    “I think everything is a P.E.”

    The other solver:
    “The challenge of course with P.E. is thinking about it, so kudos to the P.A. for figuring it out. He probably saved the patient’s life.”



  2. good discussion of low-risk PE & outpatient treatment by Rob Orman & Ryan Radecki on ERCAST: http://blog.ercast.org/2012/05/pulmonary-embolus-outpatient-treatment/