This blog post is based on the paper published in the EMJ this week – Body R et al. Can emergency physicians rule in or rule out acute coronary syndromes using clinical judgement? EMJ 2014 [Online first].
Anyone who’s worked in Emergency Medicine for any length of time will appreciate that an acute coronary syndrome (ACS) is one of the most difficult diagnoses to rule in or rule out in the Emergency Department. We’ve probably all seen the old stat that 2% of all acute myocardial infractions (AMIs) are missed in the ED. You might also have seen the stat that up to 7% of patients discharged from the ED have prognostically important myocardial damage, which by today’s standards would be considered as acute myocardial infarction. Perhaps that’s why missed ACS is one of the leading causes of medical litigation.
[DDET Why is this such a hard diagnosis to make in the ED?]
Maybe we struggle because, as doctors, we like to use our clinical judgement. We like to think that we can use the clinical information we have to make diagnoses without having to rely on tests. Perhaps we also feel like we lose face if we admit patients for investigation when patients don’t actually have the diagnosis we investigated them for. Don’t you hate it when someone from an admitting team catches you in the corridor and says something like, “Hey, you remember that patient you referred to me yesterday with query ACS? We sent him home – it was just gastritis”? It makes you feel inferior – like you should have been able to know that if your gestalt had been a bit better or if you’d have been just a bit bolder.
However, the literature is quite clear about this. If the patient’s symptoms consist of acute discomfort or pain in the chest, epigastrium, jaw, neck, throat or arms and you haven’t otherwise explained it, you’re right to consider ACS – even if the symptoms may not seem so convincing. This is based on good evidence that patients with ACS often have atypical symptoms. Taking individual symptoms, for example, the character of the pain, the radiation of the pain and the number of risk factors a patient has don’t affect the probability of ACS to any significant extent, as you can see from these slides taken from my talk at SMACC Gold (based on our own research – which you can find here).
Even grouping symptoms together as ‘typical’ or ‘atypical’, the patients with atypical symptoms are no less likely to have ACS than those with typical symptoms – as shown this great study from Louise Cullen’s group, which I was honoured to be involved with.
[DDET So what did we do in this research?]
We ran a cohort study. The main aim of the study was to validate the MACS decision rule but we also ran several substudies using the data collected. In this one, we wanted to know about the diagnostic accuracy of emergency physicians’ clinical judgement for acute coronary syndromes – both alone and in combination with the tests available on arrival – troponin and the ECG. To be honest, we didn’t expect to find a useful ‘rule out’ strategy – we simply wanted to quantify the accuracy to better inform our practice and to find out whether we might be able to refine and improve the MACS rule by incorporating gestalt.
In this study we asked emergency physicians to record their ‘gestalt’ or overall clinical judgement for ACS using a 5 point Likert scale (from ‘definitely ACS’ to ‘definitely not’ ACS. We then cross-tabulated this with the patients’ outcomes – and the outcomes we were interested in were a diagnosis of AMI and the occurrence of major adverse cardiac events (MACE) within 30 days.
[DDET What did we find?]
The bottom line is that, for patients in whom we’ve already considered the possibility of ACS as a diagnosis, our ‘gestalt’ regarding the overall probability of that diagnosis can’t be relied upon by itself to rule out that diagnosis. Nor can gestalt be used to ‘rule in’ the diagnosis – only half of those whom clinicians felt ‘definitely’ had ACS actually had AMI or developed MACE within 30 days. Here’s another slide from my SMACC Gold talk to illustrate that.
[DDET Is that all there is to it?]
No, wait, there’s more. And here’s where the story gets really interesting. Nobody in their right mind would consider the possibility of ACS without doing an ECG, right? So it’s probably unfair to assess clinical judgement alone without at least taking account of the ECG. We’re unlikely to want to discharge these patients if they have ischaemic ECGs, even if we do think that ACS is still unlikely. What’s more, we have another amazing test that we’d always run in these patients – troponin. We run that test on arrival too, and again we wouldn’t send the patients home if they had a positive troponin on admission – even if we did think that ACS was unlikely. So we looked at the overall diagnostic value of gestalt combined with the ECG and initial troponin level.
What we found may seem surprising. If we discharged patients who had a normal ECG, a normal troponin and we felt that the diagnosis was ‘probably not’ ACS, then we wouldn’t have missed a single case in this cohort – the sensitivity was 100%. Almost a quarter of patients could have been discharged using that strategy.
If we used a high sensitivity troponin assay rather than a standard contemporary one, we could also have discharged patients in whom we felt the diagnosis ‘could be’ ACS without missing any cases – 100% sensitivity. Using this strategy, over 40% of patients could potentially have been discharged – without missing a single AMI in this cohort.
And one of the really great things about this strategy is that it didn’t seem to matter if it was an experienced consultant or a junior doctor giving their gestalt – we still achieved 100% sensitivity.
[DDET What does that mean for our practice?]
Before anyone gets carried away by these promising findings, it’s important to recognise that there are some limitations to this work. The 95% confidence intervals for sensitivity extend down to 95.6% and the first reports of new diagnostic technology often overestimate performance (commonly due to reporting and publication bias). Therefore we need to validate these findings – first in observational studies and then, if they still show promise, in interventional trials. Of course, doctors might be slightly less bold when it comes to stating their gestalt if they knew that they’d have to send patients home based on their estimates. We can only find that out by evaluating the strategy in practice.
This means that you shouldn’t use gestalt to rule out ACS right now, even in combination with the ECG and troponin. But you can rest assured that the probability of ACS in patients with normal troponin and ECG on arrival is extremely low if your clinical judgement suggests that the diagnosis is unlikely. This can affect your practice – because we often treat patients with possible ACS on the assumption that they have that diagnosis, before further tests can confirm or refute it. Those treatments have risks (especially bleeding). If the diagnosis of ACS is extremely unlikely, the patients really aren’t going to benefit from early treatment overall. So hang fire with your prescribing pens – and rest assured that your judgement is probably right, even though you do still need to rely on those serial troponins (at least for now!)
[DDET EXCLUSIVE ADDITIONAL #FOAMed ANALYSES, ADDED ON 20TH AUGUST 2014]
We recently had an offline request from Anand Swaminathan (@EMSwami) for some extra data from this study. Swami was keen to know how much high sensitivity troponin really adds once the physician’s gestalt and the ECG findings are taken into account. He asked if we can also report the sensitivity and specificity of the gestalt + ECG – i.e. without high sensitivity troponin. So here we go, in what I believe could be a first in the #FOAMed world – new data being presented as #FOAMed outside of a traditional medical journal. Thanks for the request, Swami!
The table below shows the diagnostic accuracy of the combination of gestalt + the ECG (i.e. the presence or absence of acute ischaemia on the initial ECG in the treating physician’s opinion) for the adjudicated diagnosis of AMI (as described in the paper).
|AMI ‘ruled out’ if no ECG ischaemia and ‘probably not’ or ‘definitely not’ ACS|
(87.8 – 98.6)
(25.4 – 34.9)
(18.3 – 27.4)
(91.5 – 99.1)
|AMI ‘ruled out’ if no ECG ischaemia and ‘could be’, ‘probably not’ or ‘definitely not’ ACS|
(72.7 – 90.2)
(56.7 – 66.7)
(25.5 – 38.5)
(90.7 – 96.9)
|AMI ‘ruled out’ if no ECG ischaemia and anything other than ‘definitely ACS’|
(45.3 – 67.8)
(74.6 – 83.0)
(28.4 – 45.9)
(85.7 – 92.6)
The table shows that this approach isn’t sufficient to rule out AMI. The bottom line is that clinical judgement alone isn’t sufficient to rule out AMI (as reported in the main paper). Even if you combine that with ECG findings, you still can’t rule out AMI (or rule it in). It’s only when you start to incorporate troponins that you potentially get the rule out (pending validation, of course).
So, is troponin a friend or a foe in the Emergency Department? We’ll be posting more on that (from SMACC Gold) imminently, but here’s some good evidence to suggest that it may well be a pretty good friend.
Thanks again for a great request, Swami!