Troponin Timing Question

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Disinence2

Emergency Medicine
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Hello,

I've heard some different opinions about "one set" rule outs and the timing of troponins recently...

Here are a few different "rules" different attending's have explained to me. What one do you all tend to use?

1) 6 hours after the onset chest pain (regardless of fluctuations/current pain)
2) 6 hours after the pain stopped
3) 6 hours after the "maximum" intensity of the pain
4) You can't use a one set rule out for someone who still complains of pain (regardless of how long its been going on)
5) You can't use a one set rule out...ever...period

I personally think that 6 hours after the maximum intensity of pain makes the most sense, but not sure that this would hold up in court if something went poorly.

Where I practice a majority of our low to moderate risk chest pain patients get sent home with 72 hour cards F/U for stress testing. We don't have access to the CT calcium scoring system.

Thanks!

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fellow pgy2 also interested in attending's answer to this question. i've heard all the above explanations as well..

at my shop we either stress in the ED or admit our moderate-risk CP, and send the rest home. Mod rx CP is a common point of contention for EM residents here as cards fights everything, including pts w/ cp and elevated troponins..
 
If pain has completely stopped, and is atypical and not concerning for ACS, then 6-8 hours would be reasonable, though some shops do a delta trop (a 2hr difference) to prove no rising in the troponin.
If pain is coming and going, single trops are useless
If pain is constant, unchanging >8 hours, then I single trop, as this doesn't sound like ACS even.

But remember, admissions aren't for r/o MI, they're for r/o ACS. so it's still a case by case basis.
 
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Almost never do I order 1 troponin on patients. The only scenario would be if the have the exact same pain for a long time (i.e. like more than a week)

When it comes to chest pain, I'm super conservative and would CTCA just about everyone if I could because of the med mal system.

The fact is that even with all we do, we still supposedly miss 1-2% of MI, which is fine medically but not in a society that expects a 0% miss rate.

In all honesty, it's just not worth it to me to try and finesse the chest pain angle, so I stick to the AHA guidelines and do a lot of testing. In the event that you have a bad outcome, the patient's attorney will invariably get an expert to say that they would have done an expanded work up.
 
Hello,

I've heard some different opinions about "one set" rule outs and the timing of troponins recently...

Here are a few different "rules" different attending's have explained to me. What one do you all tend to use?

1) 6 hours after the onset chest pain (regardless of fluctuations/current pain)
2) 6 hours after the pain stopped
3) 6 hours after the "maximum" intensity of the pain
4) You can't use a one set rule out for someone who still complains of pain (regardless of how long its been going on)
5) You can't use a one set rule out...ever...period

I personally think that 6 hours after the maximum intensity of pain makes the most sense, but not sure that this would hold up in court if something went poorly.

Where I practice a majority of our low to moderate risk chest pain patients get sent home with 72 hour cards F/U for stress testing. We don't have access to the CT calcium scoring system.

Thanks!

I've seen mostly (5) at my program. I would argue that the population you are comfortable sending just one troponin on is a population you probably shouldn't be sending any on at all. I think (and this is with the reservation that I am only a PGY3, and obvioulsy don't have ton of experience or knowledge yet) the single troponin only has value in testing for myocarditis.

When I am out practicing on my own, I think I will stratify the low risk chest pains that I want to send home (low risk enough, good follow up, etc) as either SO low risk that ACS isn't really even on my differential (age <50, atypical symptoms, few risk factors, no family history, normal ECG) or do 2 troponins 4-6 hours apart.
 
I would argue that the population you are comfortable sending just one troponin on is a population you probably shouldn't be sending any on at all.

Good point. Commit to more than 1 or none at all. Beware of the single troponin.

the single troponin only has value in testing for myocarditis.

Another good point. I've picked up myocarditis in several children with troponins, including a 13 year old that comes to mind. I definitely would have missed it otherwise.

.
When I am out practicing on my own, I think I will stratify the low risk chest pains that I want to send home (low risk enough, good follow up, etc) as either SO low risk that ACS isn't really even on my differential (age <50, atypical symptoms, few risk factors, no family history, normal ECG) or do 2 troponins 4-6 hours apart.

Change your "age < 50" to at least "age < 40." You'll see tons of MIs in people in their 40's and that have had MIs in their 40s. This will worsen with our increasing obese population. In the 30s is uncommon but not rare (especially if a cocaine user, which they may never admit to). Also, you'll see a few in their 20s or even younger from familial early-onset coronary disease, vasospasm and other rare syndromes. (I'm sure you know this). The big risk with those is when you have a perfect story in a super young patient and yourself and everyone else tries to talk you out of the diagnosis. When it's missed the outcome can be bad in a very young person and the lawsuit potential very high. In hindsight, you'll be told the diagnosis was, "obvious." Perfect story, weird EKG: they just happen to be "too young," and "you blew it off."
 
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Change your "age < 50" to at least "age < 40." You'll see tons of MIs in people in their 40's and that have had MIs in their 40s. This will worsen with our increasing obese population. In the 30s is uncommon but not rare (especially if a cocaine user, which they may never admit to). Also, you'll see a few in their 20s or even younger from familial early-onset coronary disease, vasospasm and other rare syndromes. (I'm sure you know this). The big risk with those is when you have a perfect story in a super young patient and yourself and everyone else tries to talk you out of the diagnosis. When it's missed the outcome can be bad in a very young person and the lawsuit potential very high. In hindsight, you'll be told the diagnosis was, "obvious." Perfect story, weird EKG: they just happen to be "too young," and "you blew it off."

Absolutely agree. I guess I should have mentioned that I also have a set of very strict internal criteria for people who can not be classified as low risk at any age (family history of early MI, looks unwell, really good story, unusual PMH but not necessarily classic cardiac risk factors (HIV, lupus, radiation to chest), obese/unhealthy looking. Also I take new or unknown-if-old ECG abnormalities very seriously. If exclusion criteria aren't that strict, would definitely decrease the age cut off. Though of course in reality what I end up doing is mostly dependent on the attending's risk tolerance.
 
It'd be great if we could get some formal guidelines on this from ACEP or whoever.

I use single trops if the story is "chest pain for daaaays" or if the story is more GI-sounding than anything else and I'm trying to prove there's no cardiac element.

Also, MVCs and chest trauma get single trops to check out myocardial contusion.

Edit: Also, singe trop is good for the teenage histrionic female with CP and zero risk factors.
 
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I practice in malpractice heaven, so I don't have to be zero-miss to sleep at night.

ACS and nSTEMI are different &#8211; troponin is basically only useful if your only question is "is this patient having an nSTEMI?" Then you can talk about the sensitivity of a single or 2h troponin based on time of reported symptom onset, pretest probability, and test thresholds. And, I test and discharge patients from the ED with 1 or 2 troponins &#8211; but mostly because our legal climate makes it really easy to do so. I basically only admit chest pain folks with a moderate probability of CAD and a good story, or folks that I've talked to their cardiologist or PCP and they want the patient admitted.

We think so poorly of CTCA that we deleted the protocol out of the software on our scanners so we can't do the test.
 
We are taught that 2h trop is only ok to r/o if the pt is low risk and some moderate risk if they have good f/u (which is appx 0% of the ED population here). Mod/High risk gets a trop in the ED then 23h obs to medicine; NSTEMI/STEMI goes to cards.
 
Good point. Commit to more than 1 or none at all. Beware of the single troponin.

There are other reasons to order troponins (myocarditis, mortality predictive value in PE, etc.). I order troponins frequently and discharge patients with only a single troponin. If the pain is constant, doesn't sound cardiac, and is greater than 6 hours duration, then a negative troponin pretty much rules out a cardiac cause.

However, I will add that I practice in a state that requires gross negligence before you can be sued. Checking one troponin and discharging a patient -- even a cardiac patient -- isn't gross negligence.
 
2h delta is our practice for low risk. Also have a CT calcium scoring protocol. Interesting that your group ditched it, xaelia. We have a different malpractice environment here so we occasionally use CT Ca scoring on the low risk group that would otherwise come in for a stress test. (Perhaps you send those people home?) Does seem to save some admissions/stresses. There are certainly caveats to its use.
 
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So is a pillow to the face, titrated to apnea

I like this better.

One of our docs has noticed that after around 1am at our shop, the only people that come in on most nights are what he calls "FIC" for "Female In Crisis" - that is; no real, objectively verifiable pathology, just a lot of histrionics. I scoffed at him initially until I looked at my tracking board on Sat. night.... 7 patients at 3:15 am.... all... FICs.
 
The troponin out of triage accounts for 90% of the single troponin patients I send home.
 
I definitely don't have a set standard overall. I use patient history to help guide me. Had one today I had to decide what to do after a troponin was ordered by someone else. Ended up sending them home with one trop and follow-up with dr for outpt stress. Constant pain for 7 hrs, then pain was intermittent in the am, gone entire time in ED without any treatment, trop drawn >6hrs past constant pain. Pt also had hives. Odd combo. Also, pt had 0 risk factors.
 
I do all three of the primary rule outs and it all really boils down to the history, clinical picture and my personal intuition which is not an exact science.

1) Singe rule outs on the really low risk, no clinical suspicion and sx +8-12 hrs with no recurrent sx.

2) The 90 min myo/CKMB/Trop for under 8h, again low risk and low suspicion. (I don't do this one as much but then again... I did 2 tonight.)

3) The 2h delta CKMB/Trop for under 8h, and once again...low risk, low suspicion.

If there is any weirdness... I admit to obs for rule out and a.m. stress. The vast majority of ones I send out, I have a stress scheduled for the a.m. The two I sent out tonight have stress test this morning and one I only sent out because he refused obs.

It's really not an exact science but we've got at least a few guidelines to help us out although I'll be the first to admit that there are plenty of problems with the studies supporting these short rule out algorithms.

The majority of my non low-risk ACS rule outs get admitted to obs for serial enzymes and stress.
 
Good discussion -

For you guys with more knowledge than me, where are the studies that say we can use trop 2h r/o for low risk and low pretest patients? And does time of chest pain onset matter to these low risk folks that we are using trop 2h on?

Also - What is the delta rise that is used? <0.01 to 0.01, is this delta enough?

Thanks-
 
Good discussion -

For you guys with more knowledge than me, where are the studies that say we can use trop 2h r/o for low risk and low pretest patients? And does time of chest pain onset matter to these low risk folks that we are using trop 2h on?

Also - What is the delta rise that is used? <0.01 to 0.01, is this delta enough?

Thanks-

Start with the Fesmire paper in Annals regarding the Ehrlanger protocol. PubMed will link the more recent analyses.

Cheers!
-d

Sent from my DROID BIONIC using Tapatalk
 
I had a guy come in yesterday with 2.5 hours of chest pain and some non-specific but concerning EKG stuff (no old one). Our trops are positive at 0.78. First was 0.04. Second, two hours later, was 0.600. Third an hour later was 2.8. Two clots in the LAD pulled out an hour later. I wished I'd gotten cardiology involved a little earlier, but that's the retrospectoscope for you. It would have helped if the guy hadn't just stepped off a 5 hour flight when the pain started and had a markedly (but falsely) positive d-dimer. He also had no (known) cardiac risk factors. I added on lipids and an A1C when the trop turned positive and they were both quite elevated. Be careful with an increasing troponin, even if it is still technically negative.
 
I had a guy come in yesterday with 2.5 hours of chest pain and some non-specific but concerning EKG stuff (no old one). Our trops are positive at 0.78. First was 0.04. Second, two hours later, was 0.600. Third an hour later was 2.8. Two clots in the LAD pulled out an hour later. I wished I'd gotten cardiology involved a little earlier, but that's the retrospectoscope for you. It would have helped if the guy hadn't just stepped off a 5 hour flight when the pain started and had a markedly (but falsely) positive d-dimer. He also had no (known) cardiac risk factors. I added on lipids and an A1C when the trop turned positive and they were both quite elevated. Be careful with an increasing troponin, even if it is still technically negative.

A normal yet "non-zero" troponin to me, is incredibly suspicious and always warrants a repeat, unless you have a chronic chf'er or renal failure patient with documented baseline non-zero "normal" trops. Also, I always considered a doubling of a normal troponin at the 2 hr mark incredibly suspicious, even if still "normal," and a definite need to keep checking troponins, repeating EKGs, and further evaluation. When you get a second normal trop, but it's gone from 0.05 to 0.15 in 2 hr, for example, do you call that "normal" ?

With your labs' trop cutoff of 0.78, for example, a <0.04 is a whole heck of a lot different than a "normal" 0.26.

Non-zero "normal" troponins should always get your attention.

But what do I know? I don't really know anything...
 
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A normal yet "non-zero" troponin to me, is incredibly suspicious and always warrants a repeat, unless you have a chronic chf'er or renal failure patient with documented baseline non-zero "normal" trops. Also, I always considered a doubling of a normal troponin at the 2 hr mark incredibly suspicious, even if still "normal," and a definite need to keep checking troponins, repeating EKGs, and further evaluation. When you get a second normal trop, but it's gone from 0.05 to 0.15 in 2 hr, for example, do you call that "normal" ?

With your labs' trop cutoff of 0.78, for example, a <0.04 is a whole heck of a lot different than a "normal" 0.26.

Non-zero "normal" troponins should always get your attention.

But what do I know? I don't really know anything...

I've caught 2 or 3 of these as well. First trop 0.04, vague story, no (known) risk factors... admit 'cause I should. BOOM. Next trop is .88. Scary thing is: they were in young people, too. They say "I don't have a history of DM/HTN/lipids", but... they've just never had it checked.

Young people aren't healthy anymore.
 
A normal yet "non-zero" troponin to me, is incredibly suspicious and always warrants a repeat, unless you have a chronic chf'er or renal failure patient with documented baseline non-zero "normal" trops. Also, I always considered a doubling of a normal troponin at the 2 hr mark incredibly suspicious, even if still "normal," and a definite need to keep checking troponins, repeating EKGs, and further evaluation. When you get a second normal trop, but it's gone from 0.05 to 0.15 in 2 hr, for example, do you call that "normal" ?

With your labs' trop cutoff of 0.78, for example, a <0.04 is a whole heck of a lot different than a "normal" 0.26.

Non-zero "normal" troponins should always get your attention.

But what do I know? I don't really know anything...

I expect that almost anyone who is advocating for a one troponin approach is going to consider a trop that's 94% below the upper limit of normal "negative". But I wouldn't know, because I'm not a "one troponin" kinda guy. (OK, maybe I'll do one trop for AMS or undifferentiated hypotension or nausea in an elderly diabetic, but not for chest pain.) Because for me, if I'm evaluating your chest pain with a troponin, I'm also evaluating it with provocative testing within 72 hours. (Unless I find something like a PE or pneumothorax along the way.)
 
It would have helped if the guy hadn't just stepped off a 5 hour flight when the pain started and had a markedly (but falsely) positive d-dimer.

I would argue that it wasn't falsely elevated, just that it didn't correlate with the pathology you were looking for.

In my world (where I get a lot more time to think about things than you do, and people rarely die in front of me because of things I do or don't do), I consider a positive D-dimer less of a diagnostic test and more of a confirmation that there is some badness lurking somewhere.

I'm certainly not arguing that that 9 times out of 10, chest pain, a 5 hour plane flight and a positive D-dimer is a PE. But you found the one, and made the diagnosis and got the guy the appropriate therapy so...win.
 
I expect that almost anyone who is advocating for a one troponin approach is going to consider a trop that's 94% below the upper limit of normal "negative". But I wouldn't know, because I'm not a "one troponin" kinda guy. (OK, maybe I'll do one trop for AMS or undifferentiated hypotension or nausea in an elderly diabetic, but not for chest pain.) Because for me, if I'm evaluating your chest pain with a troponin, I'm also evaluating it with provocative testing within 72 hours. (Unless I find something like a PE or pneumothorax along the way.)

completely agree with Wilco's practice
 
A normal yet "non-zero" troponin to me, is incredibly suspicious and always warrants a repeat, unless you have a chronic chf'er or renal failure patient with documented baseline non-zero "normal" trops. Also, I always considered a doubling of a normal troponin at the 2 hr mark incredibly suspicious, even if still "normal," and a definite need to keep checking troponins, repeating EKGs, and further evaluation. When you get a second normal trop, but it's gone from 0.05 to 0.15 in 2 hr, for example, do you call that "normal" ?

With your labs' trop cutoff of 0.78, for example, a <0.04 is a whole heck of a lot different than a "normal" 0.26.

Non-zero "normal" troponins should always get your attention.

But what do I know? I don't really know anything...

very much agree with this. a pt whose only previous trops in the system are <0.02 and such, who presents with a 0.24, techinically normal base don my labs ref range, is alarming to me. whereas the frequent flyer HD pt whose last 40 trops in the system range from 0.39 to 0.45 does not alarm me when they come in severely volume overloaded with CP with a 0.5 trop. They will obviously get a trended set this admission, but I'm not jumping on ACS right away.
 
CTCA isn't appropriate for a low pre-test probability ED population because the relatively low specificity results in poor positive predictive value. The ED-specific literature simply doesn't show any patient-oriented value to the test other than short-term mitigation of all the risk-averse nonsense we otherwise might apply to half the cohort, at the expense of mostly unnecessary additional testing to the other half. The folks profiled who entered the CTCA pathway already had such a low chance of an adverse outcome that they simply didn't demonstrate any incremental value to the test other than reduction in ED LOS &#8211; and only then versus a mega-conservative observation/stress strategy. Quite simply, it's not a test with a net benefit to patients &#8211; only to clinician liability.

I've written a couple articles/posts about all these studies sponsored by GE/Siemens/etc., but Rita Redberg writes an even more eloquent editorial in the NEJM about it:
http://www.emergpa.net/wp/wp-content/uploads/2013/02/Redberg-NEJM-CTCA-Editorial.pdf
 
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