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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...

September 17, 2012

Chest Pain Gives Me Chest Pain

Low risk chest pain (or any of its analogues) is one of the most common chief complaints in the Emergency Department (I think it's #2?) yet there is a huge amount of practice variability (more on this at the end), discrepant teaching, and huge unanswered questions.

Recently, the European Society of Cardiologists determined that some cardiologists now contend that unstable angina is no longer a thing, much like hypertensive urgency, the American auto worker, travel agents, and rock saxophonistsThe ESC concluded Some cardiologists argue that high-sensitivity troponin (hsTn) is sensitive enough to rule out ALL acute coronary syndrom (ACS).
If hs troponins are completely neutral in a patient with chest pain, it’s impossible that the patient has significant coronary disease. (Freek Verheugt, Dutch cardiologist)
I hope he's right. But I don't think he is. I of course respect cardiologists, the European Society of Cardiologists, and recognize that I am but a junior emergentologist (and resuscitationist). And, I would love for it to be true. If we had an accurate biomarker for ACS, we could admit fewer patients, do fewer unnecessary stress tests and caths, and offload a lot of potentially unnecessary hospital admissions, decompressing some nontrivial level of ED & hospital crowding.

I humbly submit my dissent based primarily on the fact that there are plenty of simple questions left open by the data on hsTn. I am also intentionally not putting robust references in this post precisely because I think there are more questions than answers -- enough that I want readers to have to go to the literature to draw their own conclusions.*

First, some simple background.
The spectrum of acute CAD:
  • none
  • stable angina / baseline CAD: established over time with a PCP or cardiologist.
  • unstable angina: diagnosed based on H&P, ECG, and (arguably) with stress, CTCA, cath, or observation (e.g. autopsy)
  • NSTEMI: diagnosed by cardiac enzymes
  • STEMI: diagnosed by ECG
We care about UA/NSTEMI/STEMI, or what we call ACS, and we include UA in that spectrum of "things we care about" because patients with UA go on to have MI +/- death, which we agree is bad. And all of the money (figuratively & literally) is in UA because MI is "easy" to diagnose, while it is nearly impossible to differentiate stable from unstable angina, or non-cardiac from cardiac causes of chest pain.

If hsTn works, that would be great. But my read of the evidence is that it's not. 

What does that mean?
I think there is a subset of chest pain patients who are hsTn negative, but still have ACS/UA, and are therefore at increased risk for MI or death in the short term.
What to do with them? Stress test may not help; CTCA is probably just another stress test. And PCI during UA probably doesn't help most patients. (except maybe for patients with Wellens syndrome?)

So now what? That means we have patients who have chest pain, aren't having MIs, and might be having UA. Stressing or cathing them probably doesn't add much, but they are still at risk. Is admission the answer? The benefits of admission are essentially monitoring (if your UA progresses to NSTEMI or STEMI it will hopefully be caught in-house), medication optimization (ensured you're put on aspirin, BP managed, etc), scared straight (tobacco cessation?).

Again, I'm not sure what to do with all of this. But back to widely divergent practice patterns:

I recently spoke with a friend who was a year ahead of me in residency. At his hospital group, if you have 2 negative troponins (not high-sensitive) and a normal ECG, you go home. At the same time, a malpractice insurer for a hospital network in the same geographic area told all their ED docs to admit every chest pain because too many cases of ACS were being missed. So the standard of care is somewhere between doing nothing and everything.

UPDATE 9/18/2012

Amal Mattu pointed out yesterday on the twitter that the Third Universal Definition DOES indeed include the concept of UA:

And to the source:

page 5: Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD. Third Universal Definition of Myocardial Infarction. Circulation. Aug 24 2012.
My apologies. I trusted the Cardiology News article cited above and Dr. Verheugt as quoted in the article. The TUD is actually a straightforward and very concise read -- I should have gone there in the first place. I amended the original posting here as the ESC did not discard the diagnosis of UA -- "some cardiologists" have. -- Seth Trueger.

*EMCrit explained this tactic at one point, can't find it now. Obviously it's not good to do all the time and can be abused to cover laziness, but there's such divergent information on chest pain that I think it applies here.

I've been kicking around my thoughts on low risk chest pain for a few years now. Special thanks to Manrique Umana for pushing me over the edge.
Also thanks to Nick Genes, Ryan Radecki, Dave Newman, Luke Hermann, and Richard Body for being the main influences to my gestalt & interpretation of the evidence on this.

September 11, 2012

(Landmark vs US) vs (DL vs VL)

This is adapted from an email I sent to Minh Le Cong.

Haney Mallemat recently hosted a number of us what will hopefully be the first in a long series of international EMCC real-time discussions, with participants including Haney, Scott Weingart, Rob Bryant, Jeremy Faust, Steve Caroll, myselfLaleh Gharahbaghian, and of course, the ubiquitous Minh Le Cong. (video of the discussion should hopefully be up at some point)

Two related topics came up:
  1. Is DL dead? 
  2. Is ultrasound necessary for IJ & femoral lines?
It is not lost on me that these are very similar questions, and I come down on different sides with each.* I want to explain why I see 2 very similar situations and come to 2 different conclusions.

With respect to ultrasound for IJ & femoral lines, I think that it is clear that the landmarks are simply not reliable. I don't have hard references (although people who taught me assure me they exist) but the Sinai US guru Bret Nelson loves to take junior residents, show them the nice "NAVEL" shot and then scan up and down and show how the anatomy changes -- the relationship between the femoral artery and vein is much more complex, variable, and dangerous. I have done this on nearly every femoral line I have done** and it is shocking. Similarly, Scott Weingart has shown data on the IJ similarly just not being reliably related to the carotid.

I think Marik is possibly (probably?) correct and in the era of monitoring CLAB, space-suit CVC placement, and DVT prophylaxis, the infection & DVT rates might be less of a problem.

But the placement issues -- bleeding, neck hematoma, RP hemorrhage, pseudoaneurysm, fistula, or just not being able to place the line -- do still exist.

Plus, IJs and femoral veins both collapse during most cases of hypotension, making blind placement even more difficult. In cardiac arrest, the femoral vein might have the pulse.

Further, once you get over the learning hump (maybe 5 lines in someone who is remotely savvy?) I think that it is easier AND faster to place the lines under US.

And lastly, Scott Weingart puts it very well today: people don't immediately die if I can't get the line in (unlike failed airways).

With central lines, the blind approach works very well most of the time. However, Marty Tobin put it very well:
But here’s the rub. The challenge of clinical medicine is not about taking care of the great majority of patients who do well irrespective of the methods employed by their physicians. Instead, the goal is to take feasible steps that have a high likelihood of circumventing a catastrophe in a small number of instances....Taking simple steps to prevent infrequent occurrences that lead to a clinical catastrophe should dictate the practice of medicine, rather than employing approaches that are convenient to physicians and successful in most patients. (PulmCCM; emphasis mine)
Compare with DL vs VL. As I mentioned during the discussion, the key points are that DL skills are translatable to VL; VL is easily defeated by a speck of blood, vomit, or mucus; equipment issues (ie what happens when your Glidescope blades are all getting strerilized?); and I had one more that I don't recall now. VL will get us the view in a higher percentage of cases (although you may not always be able to deliver the tube) but DL isn't as far behind as landmark lines are behind US lines. The gap is very different.

And I agree that the combo VL/DL devices are very different than the angulated devices, and allow for training of both juniors and skill maintenance over time. During my chief year I think I used the CMAC on nearly every tube but never looked at the screen unless I ran into trouble***

Lastly, Minh made a great but ultimately flawed analogy that I cannot let stand:
Giving someone a Glidescope doesn't make them a great intubator; it's not like how giving someone a lightsaber makes them a Jedi. - MLC (paraphrased
While the lightsaber is the weapon of the Jedi, it is not the source of the Jedi's power. For whatever reason, some people are just force sensitive (to varying degrees) and may be trained to hone those skills. (I do not believe the prequels to be canonical so we can ignore the microbiologic explanation of force sensitivity.)

Giving a monkey a McGRATH MAC doesn't make him an anesthesiologist, just as Luke didn't become a Jedi the moment Obi-Wan handed him his father's lightsaber.

*I do not want to simply explain myself out of some Jungian desire to resolve my cognitive dissonance (in fact, I don't even think Jung had anything to do with cognitive dissonance and simply used him here because he's the psychology giant whose name I know aside from Freud. Wikipedia states that Festinger coined the term) or some sort of unresolved father-issues. 

**both of them

***the jokes pretty much write themselves