Category Archives: Diagnosis

You Snooze, You Ooze: Anticoagulation and Minor Head Injury

We’re lucky to have NICE guidelines in the UK.  A couple of years ago, on a visit to the US, one of my collaborators from the US mentioned how jealous he was that we have them.  His practice was to get a CT scan for everyone with a head injury.  The NICE guidelines give us a framework for implementing evidence-based decision rules like the Canadian CT head and CHALICE rules on a widespread basis.  One area I think the NICE guideline for head injury can improve, however, is for anticoagulated patients with minor head injury.

The NICE guideline suggests that we scan head injured anticoagulated patients who have lost consciousness or have amnesia.  In the absence of other high risk features, however, the remainder of patients are potentially eligible for immediate discharge without even so much as an INR check.  This makes me worry.

Unfortunately, the Canadian CT head rule can’t really help us out here because that study excluded patients with coagulopathy.  The New Orleans rule didn’t exclude coagulopathic patients but their analysis was, shall we say, somewhat underpowered as they only had 1 patient with coagulopathy in the study!  So what is the evidence behind managing head injury in anticoagulated patients?

Fortunately, we do have some evidence, although it’s relatively limited evidence if we’re honest. A case series of 144 patients demonstrated that the incidence of clinically important intracranial injury in warfarinised patients was 7%.  For me, that’s a sufficient risk to prevent me from ruling out a bleed in this group and to make me want to request a CT brain.  Roughly 7% of patients with chest pain who have a normal ECG are having an acute myocardial infarction.  But I wouldn’t dream of ruling out AMI just because the ECG is normal.  So neither should we consider ruling out intracranial haemorrhage at that level of risk.

What’s more, anticoagulated patients who develop an intracranial haemorrhage may not meet the NICE criteria for CT (which are based on the Canadian CT head rule, incidentally).  This means that they can bleed despite being relatively asymptomatic.  And a subtherapeutic INR doesn’t mean we can relax either, as shown in this great study from John Batchelor and Simon Rendell from my own institution.

OK, so we’re going to get a CT for these patients.  I’ve sold you that, right?  But if the CT’s normal, surely we can relax.  Right?

This great small study from Annals of Emergency Medicine sheds some light on that situation.  The authors implemented a protocol to immediately CT all warfarinised head injured patients, observe them for 24 hours, then re-scan them.  Of 97 patients, 87 agreed to stay in for observation and have a repeat scan.  5 (6%) of those patients had a late bleed, not detected on the initial scan.  OK, it was minimal in 2 patients.  But 1 required craniotomy.  What’s more, only 1 of those 5 patients had showed signs of neurological deterioration in the 24 hour period between scans.  2 further patients developed late bleeds even after a normal scan at 24 hours.   So, this study definitely tells us that there’s an important incidence of late bleeding in anticoagulated patients.  Not only do we need to strongly consider scanning these patients, but we also need to consider repeating the scan 24 hours later, even in the absence of neurological deterioration.  What’s more, the symptoms reported by the patient may not be a great predictor of intracranial bleeding.  Only 1 of the 6 who bled reported a severe headache, and only 1 was vomiting.  If we rely on our patient becoming symptomatic during the period of observation, we may still miss some late bleeds.

Of course, this is just one study.  Other studies do confirm that there’s an incidence of late bleeding in anticoagulated patients, although it may not be quite as high as 6%.  However, what’s clear is that these patients ooze, and they ooze slowly.  Of course, we don’t want to miss a bleed, if present, initially.  Given the prevalence of bleeding at the time of presentation, I suggest that we should still scan these patients at presentation.  But we should also be alert to the possibility of late bleeds.

From discussions on Twitter, I know that people are doing this after 6 hours rather than 24.  There’s no evidence to definitively tell us which strategy is better.  In my practice, I’ll be strongly considering an initial scan, an INR scan, a period of observation and a repeat scan after 24 hours.  It’s not clear whether that’s the optimal strategy.  What is clear is that we must be extremely careful with these patients.  They bleed.  And they bleed late.

So, what about reversal of the anticoagulation?  Well, that’s a whole different debate – you’ll have to watch this space!…

Rick Body

Glasgow Blatchford Score 2 – The case for an RCT!

Thanks for a great post, Gareth.  If you’ve landed here without reading that post, hit the link – this is a follow on, a ‘deep dive’ in the words of Smart EM – to be taken in the context of Gareth’s main post.

This is a landmark study in Emergency Medicine and gives us something useful that could reduce admissions.  With a critical appraisal hat on, however, I do think it’s important to point out a few flaws in the methodology.

Methodology of the Lancet study

The authors have essentially prospectively evaluated the performance of the GBS at several centres by reviewing case notes of patients presenting with upper GI bleed.  They then prospectively implemented the GBS, discharging patients with GBS of 0 and found that it was safe and reduced admissions.  It sounds pretty good, so why is there a problem?

The issue is that there’s no control group in the implementation phase.  When clinicians are told to use a tool that enables discharge of low risk patients, they may decide to use it in particularly low risk patients, who they’re happy to consider early discharge for.  There’s some evidence that this actually happened, as the proportion of low risk patients is greater in the implementation phase (22% vs. 16%) and the overall number of patients is enrolled is greater in the implementation phase (572 vs. 334), despite the overall recruitment period being shorter.  This is the classic problem with simple before and after analyses, and it makes the comparison of admission rates before and after implementation subject to substantial bias.

What’s more, there’s the issue of resource utilisation.  In the derivation phase, 96% of patients were admitted compared to 71% after implementation, which is great.  However, the median length of stay didn’t change (2 days in each group) although the mean length of stay reduced.  This suggests that the patients we’re avoiding admission for after implementation of the GBS would have had a short length of stay anyway (<2 days), so the reductions in length of stay are occurring in that group.  That’s still OK – so far, we’re still on to a cost saving and patients get to go home earlier.

However, you also have to consider that the low risk patients who were discharged were all given outpatient endoscopies and outpatient follow-up.  OK, only 40% actually attended for the endoscopy.  But what we don’t know is how many of them would have undergone endoscopy and out-patient follow-up with standard care – it may well have been less than 40%.  What’s more, using the score might tempt physicians to over-investigate or over-treat those who aren’t in the low risk group.

Overall impact on resource utilisation

It’s therefore possible that implementation of this protocol actually leads to a rebound overuse of resources.  To get a better idea of whether this actually happens, we need a control group.  The most obvious way to do that is to run an RCT.  Patients could be individually randomised to care guided by the GBS or standard care, or we could use cluster randomisation (e.g. randomise each centre to deliver care guided by one intervention or the other).  Alternatively, we could use a stepped wedge design, whereby we enrol a number of centres and all of them sign up to implementation of the GBS-based protocol.  Each centre is given a randomly allocated implementation date.  We then run a before and after analysis to evaluate admission rates and overall resource utilisation.  This is still a before and after analysis, but we have contemporaneous control groups at different centres.

What’s a Service Evaluation?

There’s a final point to make here.  The implementation phase was a service evaluation.  What does this mean?  Essentially, two centres implemented the protocol in practice and audited what happened.  They didn’t get consent from patients.  (They didn’t need it for this type of work).  However, it does mean that they couldn’t actually follow patients up as they would in a research study.  That means that the 60% of low risk patients who failed to show for their endoscopy went out into the ether.  They could have attended other hospitals for further care, perhaps because they were disgusted at being inappropriately discharged!  They may have undergone intervention at those centres – we just don’t know with this design.

The bottom line for clinical practice

Does this stop us from using the Glasgow Blatchford score?  No, excepting a few methodological flaws I think these authors have, on the whole, shown its safety.  I think we can use it.  Even NICE says we can use it!  We shouldn’t be so confident about the overall impact on resource utilisation though, as we just haven’t shown that in this study.

The time bomb of doom: What I think about when I’m tending broad beans


When I have downtime and I’m riding my bike or indeed tending to my Dads “prize winning” broad beans on the allotment; my mind unfortunately often wanders to recent cases in the ED that have gone bad.

I start to reflect on things I could have done better, or wonder if I could have affected patient outcomes for the better….

It’s the curse of the Emergency Physician.

This last week I have been pondering the dissecting thoracic aortic aneurysm (really type A dissections). Perhaps I’m practicing an area of unknown high incidence but I have come across 2 cases in recent months (normal incidence – by the way – 3/100,000) that have ended badly. Now, we all know that it’s a diagnosis that we find scary – the time bomb of doom – 1-2% of patients will die for each hour after onset of symptoms untreated. We know that symptoms aren’t reliable and you’ve gotta have a high index of suspicion (it is the “most undiagnosed serious condition” with up to 30% of diagnosis made at autopsy!).


I don’t claim to be a normal person, but I am always wary of patients (not intentionally, but, their “truths” can vary, they hide things, they’re never classic….) and my index of suspicion is always high….

BUT when you need some diagnostic imaging for your crazy, paranoid  hypotheses – it not always that easy to get a timely solution from our friendly radiologists.

What are the conventional options?

The Chest x-ray whilst much loved is awful as a rule-in or rule-out for dissecting thoracic aneurysm.  It will be completely normal in 20% of your patients and if your looking for mediastinal widening then you’ll only see that in 15%….as for the other myriad of “classic” signs we might as well get our euro millions lottery ticket.

The contrast CT, 79-100% sensitive, 87-99% specific – great, but not as “readily available” at the district hospital (where most EP’s) work as we might hope. The radiologist will argue that there is a high dose of radiation and no-one ever likes to use contrast. Meanwhile as we are debating and waiting for a slot in the scanner the time bomb is ticking.

And, Yes, there are also MR scan, transoesophageal echo and retrograde angiography, but I’m not convinced these diagnostics are available in many centres.

SO… what do I want in an ideal world? I would like bedside diagnostics that I can perform to help me expedite treatment rapidly…..So my big idea has been to use the ED ultrasound to perform Transthoracic echo (TTE) and measure the aortic root and get views of the arch to look for intimal flaps combined with standard descending aorta views. The question is – How confident can I be to use my ultrasound as a rule-out or rule-in for dissecting type A aneurysm?

Allow me to look over the literature:

The European Society of Cardiology have recommendations for aortic disease. They say that “TTE is an excellent modality for imaging aortic root dilatation…..not the ideal tool for visualizing all aortic segments”. In a related article from the Society they quote the “Literature of the past” i.e .1980’s and 1990’s, suggesting that for type A dissection TTE has a sensitivity of 78-100%, but as low as 57% in some series! They do point out that there have been no recent studies…. and certainly they would not use TTE as a rule-out. All very opinion based………

Luckily, to the rescue of evidence based practitioners, comes a diagnostic study published this year by an Italian team headed by Moreno Cecconi. They have asked a question similar to my own – “what is the current diagnostic value and the possible role of TTE in the management of patients with suspected aortic arch syndrome?”

270 patients (retrospectively collected data!?! And selection criteria not explained) all assessed by TTE as first line investigation and subsequently imaged by either CT/MR or transoesophageal echo…..Quoting: Sensitivity 87%, Specificity 91%, PPV 75%, NPV 95%.

In all honesty there are lots of problems with the methodology, and it’s from a dedicated cardiac centre  – not really generalisable for the average EP ultrasound operator – but it’s the only data we have using the latest generation of ultrasound technology. The authors are confident with their results and even go as far to say bedside TTE is “useful in establishing or excluding the differential diagnosis in the acutely unwell patient, particularly in the absence of aortic root dilatation”.

What conclusions can I draw from the limited evidence? Well, as with FAST and FASH etc, bedside TTE is another diagnostic modality in our armoury…. Its highly operator dependent but its quick and safe and can definitely guide your management. Would I rely on it to completely exclude a diagnosis of type A aortic dissection? Probably not… But I would measure the aortic root diameter and think hard about my next move…

Rare conditions with serious outcomes – its like being a goalkeeper facing a penalty in soccer – make a save and you’re a hero, drop the ball and you feel like a villian with the weight of the world on your shoulders… but the odds were always stacked against you. The magic wand of ultrasound – when used wisely – can be a significant arrow in your quiver of imaging diagnostics, but when the incidence is low and the risks are high, think hard before using TTE as a lone rule-out investigation…Its not an ideal world in the world of diagnostics…….

And that is what I think about when I’m tending broad beans.


Deciding Who To Investigate For ACS: The Problem Of ‘Coronary Bridge’

The problem we have with cardiac chest pain

It seems to me that many emergency physicians struggle to understand exactly how we’re supposed to be managing patients with suspected cardiac chest pain.  The first, and arguably most important question, is about who we should investigate in the first place.

The confusion is understandable as there are mixed messages coming out of the literature.  On the one hand, we have to be very cautious as we know that atypical symptoms don’t rule out an acute coronary syndrome (ACS).  We really don’t want to miss ACS as we know that patients who are inadvertently discharged have a worse prognosis than similar patients who are admitted.  What’s more, missed diagnosis of ACS is one of the leading causes of medical litigation.  On the other hand, we get constant negative feedback from inpatient specialties who may feel that we admit too many patients for suspected ACS and others who feel that we may be overusing troponins.  After all, less than 25% of the patients we admit for investigation will actually turn out to have ACS.  So what are we to do?

The value of symptoms and signs

Amal Mattu recently provided some great guidance in a fantastic Medscape article.  He sums up with 3 key pearls of wisdom: (1) Though there are factors that reduce the likelihood of ACS, don’t rely on them – none of them risk stratify the patient to the level of ‘no risk’; (2) If you do discharge a patient with chest pain, make your practice as defensible as possible by documenting as many of the ‘low risk’ factors as possible; (3) Beware of factors known to increase the likelihood of ACS (like pain radiating to both shoulders/arms or to the right shoulder/arm, vomiting, sweating and exertional pain).  I certainly echo these sentiments.  Following a recent conversation on Twitter, I thought it would be useful to expand further on my thoughts.  (Further than you can in a 140 character Tweet!)

Dr. Mattu’s Medscape article referred to my paper in Resuscitation, entitled ‘Symptoms and signs in the emergent diagnosis of acute coronary syndromes’.  In this paper, we reported some interesting findings.  First, there are a number of ‘typical’ symptoms that don’t seem to alter the probability of acute myocardial infarction (AMI) very much at all.  This included pain radiating to the left shoulder or arm, which did not significantly increase the likelihood of AMI or adverse events over the following 6 months. Pain located in the left anterior chest actually made the diagnosis of AMI less likely.  On the other hand, certain atypical symptoms turned out to make the diagnosis of AMI more likely.  This included, notably, pain radiating to the right shoulder or arm!  No features were useful to help rule out an AMI.  For example, 19% of patients who described their pain as sharp or stabbing in nature were either having AMI or developed a major adverse cardiac event within 6 months.  That’s not much of a rule out!  A pleuritic nature to the pain did not significantly alter the probability of AMI or adverse events at all.

There were some more interesting findings in our study.  Patients who were observed to be sweating in the ED were, more often than not, having AMI.  The probability of AMI was, in fact, 59%.  The positive predictive value of sweating observed in the ED is even higher than that of ischaemic ECG changes.  That’s pretty powerful.  AMI was diagnosed in 40% of patients with an initial systolic blood pressure <100 mmHg; 41% of patients who reported vomiting; and 35% of patients whose pain radiated to the right arm or shoulder.  So these are fairly powerful positive predictors, given that we started with a pre-test probability of 18%.  They are things we should be quite concerned about, if present, although of course they should be taken in conjunction with everything else.

So when can we rule out ACS without tests?

It’s time to re-iterate something important: no symptoms or signs can be used alone to rule out ACS.  Let’s be clear about that.  Just because a patient describes the pain as stabbing in nature doesn’t mean you can relax.  Just because it’s worse on inspiration doesn’t mean you can’t relax.  If it’s not worse on exertion, you can’t relax.  Of course, if the patient has sharp, stabbing pain that only appears on inspiration and is located only in a well localised point in the left lateral chest wall, you can relax – you’re clearly not going to suspect ACS.  We do have to retain some common sense.  Document the clinical context carefully and you shouldn’t be criticised.  However, when things aren’t as clear, when you’re relying simply on the fact that the pain is worse on inspiration (alone), stabbing in nature (alone), indigestion-like or whatever else to justify your decision not to investigate the patient for ACS, then to quote Amal Mattu at ICEM 2012, “you should slap yourself before someone else does”.

The golden rule

In practice, therefore, I can suggest 3 things that you ought to remember when considering how to manage patients presenting to the ED with chest pain:

  1. There are patients you can identify as having a high probability of AMI.  Ischaemic ECG changes, sweating observed, vomiting reported, pain radiating to the right arm or both arms, and hypotension all identify high risk groups.  These patients clearly need investigation
  2. There are patients you can rule out immediately who clearly don’t have ACS.  They have other causes for their pain that can be objectively identified, or their history is so clearly non-cardiac that it would be ludicrous to investigate them.
  3. Then there’s the middle group of patients, who aren’t in either of these ‘high probability’ or ‘clearly non-cardiac’ groups.  Investigate these patients.  They could have ACS and you really don’t want to miss it – for the patient’s sake and for your own.

Coronary Bridge

In my first job as a Senior House Officer in Emergency Medicine, one of my seniors told me about a hospital he used to work at.  The main road leading to and from the hospital ran across a bridge.  They apparently named it ‘Coronary Bridge’, after the number of patients who suffered a cardiac arrest there having just been inadvertently discharged from the ED with a missed myocardial infarction.

We do need to reduce unnecessary admissions for cardiac chest pain.  We do, however, need to do this in an evidence based manner, with a validated rule out strategy.  I’m certainly not suggesting that we throw common sense out of the window and investigate everyone.  But next time you consider discharging your patient with ‘vague’ or ‘atypical’ chest pain just because it’s ‘vague’ or ‘atypical’, consider whether you really want to take the chance that your patient won’t make it across ‘Coronary Bridge’.  We want to reduce admissions – but let’s do it safely and scientifically.

Rick Body