PACU troponins

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waterbottle10

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A lot of my patients have risk factors for cardiac events after non cardiac surgery based on RCRI and I am sure I am not alone since patients in this country are very sick.

DM on insulin is very prevalent, so is CAD. With those 2 factors alone, the estimated risk is already 6.6%, which is 1 in 15 people. 3 Risk factors and it's 10% or 1 in 10.

For those who cover patients in the PACU, do you check troponins on these patients? A lot of cardiac events can present without chest pain so that isn't reliable. EKG changes can be hard to spot especially in the early stages.

For example, a 75 year old man with several medical problems including IDDM, CAD (no stents), HTN gets lipoma excision under sedation. No major problems in surgery and patient goes to PACU. Would you immediately order troponins? What if the patient had a couple episodes of hypotension that responded well to phenylephrine boluses and has since had stable vitals with no support?
 
I am personally not a fan of ordering cardiac biomarkers in the PACU. Why? Because a single data point doesn't necessarily provide the most useful information. If I'm worried, I'll defer to the surgeon/cardiologist because they are the ones that are going to have to decide if they want to draw several sets of them. I mean it's fine and dandy if it's totally negative, but what if it's just a smidge positive? What if you start going down the old "it's not an MI, it's just a troponin leak" conversation. That sort of stuff isn't a PACU problem, it's a floor problem so I let the people that will deal with it on the floor (not me) decide when they want to start that.
 
I think this is going to come up more and more; it even has it's own catchy Acronym now, MINS (myocardial injury after non-cardiac surgery): Link to paper to follow in two posts time . I hear that at the Cleveland Clinic they are aggressively screening for this (getting pre- and post-op troponins in all pt's >65 and in younger patients with any cardiac risk factors) however they have an agreement with their cardiologists that they will come and evaluate (and potentially perform interventions on) patients with MINS who don't meet criteria for MI.
 
We first need to know the clinical and therapeutic value of increased Troponin in asymptomatic post-op patients. I mean we know that increased Troponin after surgery is a risk factor for mortality but we don't really know what to do with that increased Troponin.
Until these studies are done we should not complicate life by ordering tests we don't know how to act on.
 
Ok so let me make sure I’m reading this right: the OP wants to check tropinins on a pt who’s asymptonatic in PACU with no EKG changes who just underwent an uneventful low risk surgical procedure??? WTF?

Should we send out a home health nurse to check troponins after his morning dump just in case he knocked off a few myocytes when straining? Look, if you’re concerned about this guys cardiac status, the time to do the work-up is BEFORE surgery, not in PACU.

Let’s say he’s got a troponin bump - then what? You gonna send him to cath lab where they can heparinize and start anti-platelet agents on a freshly post-op patient? All for what, to stent some otherwise asymptomatic lesion which has been shown to have no effect on mortality?

This along with the CPR in OR thread makes me think the OP has a big “forest for the trees” problem.
 
Ok so let me make sure I’m reading this right: the OP wants to check tropinins on a pt who’s asymptonatic in PACU with no EKG changes who just underwent an uneventful low risk surgical procedure??? WTF?

Should we send out a home health nurse to check troponins after his morning dump just in case he knocked off a few myocytes when straining? Look, if you’re concerned about this guys cardiac status, the time to do the work-up is BEFORE surgery, not in PACU.

Let’s say he’s got a troponin bump - then what? You gonna send him to cath lab where they can heparinize and start anti-platelet agents on a freshly post-op patient? All for what, to stent some otherwise asymptomatic lesion which has been shown to have no effect on mortality?

This along with the CPR in OR thread makes me think the OP has a big “forest for the trees” problem.

Why would you checking for a trop leak pre surgery?

I think the issue is in rcri high risk surgery is only 1 point. Therefore it's saying even after low risk surgery in a patient w 2 risk factors it's still 6 to 7 percent.
 
Why would you checking for a trop leak pre surgery?

I think the issue is in rcri high risk surgery is only 1 point. Therefore it's saying even after low risk surgery in a patient w 2 risk factors it's still 6 to 7 percent.

I’m not saying to check trips pre surgery. I’m saying that’s the time to do any cardiac work-up.

The OP wants to check troponins post-op without an indication - we’ll i guess the indication is “fresh post-op status”. That makes no sense. If the patient has a reason to check trops then check them - chest pain, ekg changes, HD instability. But don’t check them just because the guy just had surgery
 
I agree with everything Salty has said, but I do think in the future trops will be part of a standard postop lab set in all but low risk surgery for risk stratification and early intervention. Postop MI is most common around day 3, you really don’t think there is ANY marker that may allude to that? You don’t think we may be able to tease out who is at much higher risk for that?

But I also agree with Plankton that we just aren’t anywhere close to knowing what it means, how to correlate it, or what to do with it.
 
I agree with everything Salty has said, but I do think in the future trops will be part of a standard postop lab set in all but low risk surgery for risk stratification and early intervention. Postop MI is most common around day 3, you really don’t think there is ANY marker that may allude to that? You don’t think we may be able to tease out who is at much higher risk for that?

But I also agree with Plankton that we just aren’t anywhere close to knowing what it means, how to correlate it, or what to do with it.

"but I do think in the future trops will be part of a standard postop lab set in all but low risk surgery for risk stratification and early intervention"

Why do you think that?
 
"but I do think in the future trops will be part of a standard postop lab set in all but low risk surgery for risk stratification and early intervention"

Why do you think that?

Because people are working on it. Because there’s a difference between preop cardiac clearance and reduction of postop MI after required surgery. Why shouldn’t we care about a pt that required surgery where “cardiac clearance” consisted of no more than hand waving “avoid hypotension, tachycardia, etc” and their possible post op MI? But mostly because I envision a streamlined cookbook future of Medicine.
 
Wait, why would you order it in the PACU unless it was like a 6 hour surgery (or 6 hours after the myocytes died)? Does the timing working out for checking troponins?

Also if we aren't selecting our patients (prevalence is way low) that we test, does that not make our positive predictive value of the test go way down?
 
Wait, why would you order it in the PACU unless it was like a 6 hour surgery (or 6 hours after the myocytes died)? Does the timing working out for checking troponins?

Also if we aren't selecting our patients (prevalence is way low) that we test, does that not make our positive predictive value of the test go way down?
Newer high-sensitivity troponin assays can detect myocardial injury as soon as 3 hours after with a NPV of 99%. The issue becomes that they're too sensitive and detect all sorts of myocardial ischemia that isn't a pure Type 1 (plaque rupture).

I'd definitely suggest everybody read the above linked Canadian guidelines. They advocate against pre-operative stress testing and functional risk assessment and actually propose routine troponin measurement post-operatively in at-risk patients. The only intervention they currently propose is earlier initiation of ASA/statins but there's clearly data suggesting that the old paradigm of perioperative cardiac management being outdated.
 
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From the Canadian recommendations.

“Because most patients who suffer a postoperative myocardial infarction or MINS are asymptomatic, routine troponin monitoring can detect patients who are at markedly increased risk of death within 30 days of surgery. Although the optimal management of patients with MINS remains an area of ongoing investigation, we believe that these individuals can benefit from intensification of medical management and close monitoring during their postoperative recovery.”

They also recommend against preop revascularization of patients with known stable CAD. I agree since the risk of revascularization often exceeds the risk of the non cardiac surgery.

Better postop care and fewer preop interventions make sense to me. We currently front load all our efforts but meticulous pain control, hemodynamic monitoring, stress and inflammation reduction postop might be a more effective approach. Now how to do this?? Checking tropinins postop will allow us to identify patients who are at higher risk of dying within the next few weeks and focus our efforts on them.
 
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We first need to know the clinical and therapeutic value of increased Troponin in asymptomatic post-op patients. I mean we know that increased Troponin after surgery is a risk factor for mortality but we don't really know what to do with that increased Troponin.
Until these studies are done we should not complicate life by ordering tests we don't know how to act on.

I think Plankton's post is the most important point, these post-op troponin elevations are markers of increased post-op mortality. The questions then become 1) can we predict who will have MINS after surgery and intervene before surgery and prevent it (optimization) ? 2) Can early identification of MINs in the post-op period affect the trajectory of these patients (can we reduce 30 day mortality) ? . If you look at the Canadian Guidelines and the MINS paper I posted they both share at least one Author Dan Sessler in Cleveland; he is of the view that the the answer to question 2 is yes. It's not suprizing that the guidelines support the views of the people writing them.
 
We already do too many trops in this country and you want to do even more unindicated testing for which you have no plan. Amazing.

Let me ask you a question. Do you believe that the average American participates in an activity that stresses their heart enough to cause an anginal equivalent? Or, if they do, and they get an anginal equivalent (and would understand the feeling they got was an anginal equivalent) that they would disclose this to their PCP, or a Cardiologist they may be referred to when they desire a surgery? If the answer to that question is No, then I think that shows a need to at least consider the study and development of a risk stratification or MACE reducing intervention in the average American undergoing surgery.

If your answer to that question is Yes, then I’d still argue, that we surely “clear” patients based on their/our subjective assessment of their METS and CV symptomatology (and sometimes even after provocative or invasive testing) that go on to have a post op MI. That most often occurs days after the surgical insult and therefore may be modifiable if we knew the proper test and action to perform with positive result of said test. Why would we not at least look at it?

My point is that we either clear patients based on their asymptomatic status or we perform a cardiac workup preoperatively and yet people still have postoperative MI’s. These occur in delayed fashion which luckily gives us an actionable window. It’s my position, that while we currently don’t know how to accurately assess who is at risk or what to do to reduce the incidence in those that may be at risk, I think smarter people than I will figure this out and we will eventually learn to modify this risk and potentially prevent their postop MI.
 
My point is that we either clear patients based on their asymptomatic status or we perform a cardiac workup preoperatively and yet people still have postoperative MI’s. These occur in delayed fashion which luckily gives us an actionable window. It’s my position, that while we currently don’t know how to accurately assess who is at risk or what to do to reduce the incidence in those that may be at risk, I think smarter people than I will figure this out and we will eventually learn to modify this risk and potentially prevent their postop MI.

Unfortunately the lab tests we have identify MIs that have already happened (or are still evolving). We don't have a lab test that identifies the patient about to have an MI that we can intervene on and prevent.

And while I wish I could share your optimism over future directions of care, the physical mechanics of an MI make me think we probably won't be able to prevent them from happening other than simply modifying identifiable risk factors and treating after the fact when it does happen.
 
And while I wish I could share your optimism over future directions of care, the physical mechanics of an MI make me think we probably won't be able to prevent them from happening other than simply modifying identifiable risk factors and treating after the fact when it does happen.

As far a preventing future MIs I agree that right now we are limited by lack of predictive diagnostics. As far as future directions: On the medical management post MI we have found certain interventions to be protective against secondary morbiditiy and mortality (e.g. ACE/ARB preventing cardiac remodelling). We still have more questions to answer about patients with cardiac risk factors who have an increase in post-op trops that do not meet diagnosis of MI. These patients have increased 30 day mortality, but what is killing them ? It seems unlikely to me that it's primary mortality from the cardiac insult; In which case it might be secondary mortality from something that we can intervene on , I can also think of other things it might be like it might just be a marker of reduced functional reserve and might not be modifiable. We just don't have good answers yet.
 
Not all MI’s are equal in severity. A small tropinin leak representing loss of a few subendocardial myocytes could be an indicator of ongoing ischemia. With that knowledge, the hope is that one can take measures to prevent this from progressing on to a significant transmural infarct.
 
so a 90 yr old with cad, htn, dm, AS, gets lipoma excision and has a positive trop. next step is bring to cath lab?


No, But probably shouldn’t be left to rot overnight with a BP of 80/40, O2 sat of 88%, and nobody checking on him for 8 hours.
 
No, But probably shouldn’t be left to rot overnight with a BP of 80/40, O2 sat of 88%, and nobody checking on him for 8 hours.
Do we really need a lab test to tell us this is poor care? Instead of spending money on shotgun troponins, maybe we should just do what the cardiologists always say and avoid hypotension, tachycardia, and hypoxia in people with proven risk factors.
 
One of the bigger researchers in this area is PJ Devereaux (co-chair of the guidelines) and of POISE and VISION.

Association Between Postoperative Troponin Levels and 30-Day Mortality Among Patients Undergoing Noncardiac Surgery

I don't know enough yet to see how this will all play out, but people are looking at it.


Is anyone else surprised that 11% of patients had troponin leaks? And the consensus here seems to be that it’s better not to look or know.
 
Is anyone else surprised that 11% of patients had troponin leaks? And the consensus here seems to be that it’s better not to look or know.

The question is what are you going to do with the information and on which patients are you sending the test? Patient has chest pain and EKG changes in PACU? By all means he needs a cardiologist evaluation. Pt high risk and has uneventful low risk procedure and is asymptomatic in PACU? Does that warrant checking enzymes because I sure as hell wouldn't know what to do with them if they were slightly positive? And for all those cardiology recommendations we use from ACC/AHA for preop testing? None of them recommend postop troponins.

I defer the troponin ordering to someone that will be following up on it later.
 
I think the question is also when should we check them. Immediately after surgery, or wait a few hours? Troponins take time to rise, unless someone stabbed the heart. Also a lot of people coming into the PACU are still recovering from anesthesia, especially older people who take longer and may not be able to tell you accurately they feel chest pain
 
I think the question is also when should we check them. Immediately after surgery, or wait a few hours? Troponins take time to rise, unless someone stabbed the heart. Also a lot of people coming into the PACU are still recovering from anesthesia, especially older people who take longer and may not be able to tell you accurately they feel chest pain

If I'm worried about post-op MI then I have a low threshold to work-up In the PACU with EKG and Trops with possible repeat trops later for trend and cards involvement, If you diagnose an MI depending on what surgery they just had they might have intervention for them also don't want to miss a post-op MI and have them on the floor or short stay with less monitoring. If the concern is MINS think the best answer is not sure, but I would talk to your local cardiologists and see what they think. My guess is the next time guidelines come out recommendations will say something about MINS.
 
There is also something to be said about establishing a baseline. Quite frequently a positive troponin is shoed away as an intra-operative "leak" that has failed to normalize. Trending an inexpensive test like a troponin does have its benefits.
 
There is also something to be said about establishing a baseline. Quite frequently a positive troponin is shoed away as an intra-operative "leak" that has failed to normalize. Trending an inexpensive test like a troponin does have its benefits.

Such as...
 
There is also something to be said about establishing a baseline. Quite frequently a positive troponin is shoed away as an intra-operative "leak" that has failed to normalize. Trending an inexpensive test like a troponin does have its benefits.

are you arguing to send the troponin in preop holding? Because that's the only way you are getting a baseline that isn't explained as the "intra-op leak". Hell, let's just send troponins from the preop testing clinic.
 
ive never heard of this base line troponin thing. i thought any elevation of troponin is abnormal and should be followed. that's why we trend troponins. if your baseline came back as elevated, i dont count that as a baseline, i think surgery should be postponed, cause i dont think people are just walking around with a baseline troponin of 1 or something
 
Only benefit I see with these random trops is that you may pick up the low to intermediate risk pt with a leak and send them to cards as an outpt for Asa, statin, anti-HTN. Checking trops on someone already on optimal medical mgmt seems like a waste of time unless they have signs/symptoms of an acute MI.
 
ive never heard of this base line troponin thing. i thought any elevation of troponin is abnormal and should be followed. that's why we trend troponins. if your baseline came back as elevated, i dont count that as a baseline, i think surgery should be postponed, cause i dont think people are just walking around with a baseline troponin of 1 or something

I feel like half the reason trops exist is to justify admission from the ED. Troponinemia happens for a variety of reasons and should be interpreted in the global context of the patient (comorbidities, history, physical, ekg abnormalities +/- dynamic chanhes, trop trend, etc). ESRD patients frequently have an elevated trop but it trends flat. They'll represent to the ed with a variety of complaints but a similar trop. I wouldn't say their "baseline troponinemia" is normal per se, and chalking it up to type 2 nstemi without thinking about it dangerous, but more often than not it's not clinically all that meaningful
 
I feel like half the reason trops exist is to justify admission from the ED. Troponinemia happens for a variety of reasons and should be interpreted in the global context of the patient (comorbidities, history, physical, ekg abnormalities +/- dynamic chanhes, trop trend, etc). ESRD patients frequently have an elevated trop but it trends flat. They'll represent to the ed with a variety of complaints but a similar trop. I wouldn't say their "baseline troponinemia" is normal per se, and chalking it up to type 2 nstemi without thinking about it dangerous, but more often than not it's not clinically all that meaningful

I remember having this patient who came in with "chest pain" every time he wanted a place to stay. Problem was he had a cardiomyopathy and always had a low positive trop. Never did anything different for him but was an admission every time.
 
So now we're back to getting baseline preop tests on everyone? CBC, comp, coags, T+S, EKG and now adding baseline trops. May as well throw in echo and CT scan. Wouldn't wanna miss a baseline head bleed. Heck just throw in a head to toe MRI just so I can look back at the scan and say the patient was a fat a$$ at baseline and it wasn't a complication of my anesthetic...
 
We need to do fewer interventions on patients, not more. Drawing any lab, especially one that needs to be followed out with often no real conclusive meaning at the end of that trail just seems like poor care. Please don’t do that to me when I’m old and need your help.
 
I think we have to be careful with the argument about limiting testing. Ordering all the tests for no reason is clearly not beneficial and meaninglessly increases the cost of care. However risk stratification may well be a good reason to order a test. It's even better when the course after the test is modifiable; but we test for all kinds of diseases that we don't have a treatment for so we can appropriately council patients even when it doesn't necessarily alter their clinical course. e.g. Huntington's and Alzheimer's.
 
I think we have to be careful with the argument about limiting testing. Ordering all the tests for no reason is clearly not beneficial and meaninglessly increases the cost of care. However risk stratification may well be a good reason to order a test. It's even better when the course after the test is modifiable; but we test for all kinds of diseases that we don't have a treatment for so we can appropriately council patients even when it doesn't necessarily alter their clinical course. e.g. Huntington's and Alzheimer's.

Do we really need to draw an analogy between Huntington’s and testing asymptomatic patients post surgery for troponin leaks?
 
However risk stratification may well be a good reason to order a test.

We usually think of risk stratification in terms of preop testing, not postop testing.
 
We usually think of risk stratification in terms of preop testing, not postop testing.

Regardless of the cause and effect if MINS is related to an increased post-op mortality then measuring it can be used to separate those at low risk from those at increased risk; whatever discriptor we choose to apply. I don't think we are there yet with MINS, I'm certainly not saying we should screen anyone when we haven't established what it means convincingly.
 
Do we really need to draw an analogy between Huntington’s and testing asymptomatic patients post surgery for troponin leaks?

If the test tells you which of those asymptomatic post surgical patients are at increased risk of dying in the next 30 days, maybe we should consider it ?

Though to be clear, right now I think the majority of troponin testing in asymtomatic pre and post surgical patients if it's being done at all, should be in the context of an IRB approved research study so that we can move towards answering this question which has now be raised.
 
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Regardless of the cause and effect if MINS is related to an increased post-op mortality then measuring it can be used to separate those at low risk from those at increased risk; whatever discriptor we choose to apply. I don't think we are there yet with MINS, I'm certainly not saying we should screen anyone when we haven't established what it means convincingly.

The question is does identifying that postop marker identify the high risk any more than their history already identified them as high risk? And even if it does, is there available interventions that will modify that risk? It's one thing to identify a risk, it's a separate issue to be able to intervene and decrease the risk.
 
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