Category Archives: Resus & Crit Care

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.


The end for potatoes on the ICU…?


Another Journal club, another fruity (or vegetable-y) discussion today.

The recent large prospective RCT by the Scandinavian 6S trial group on HydroxyEthyl Starch vs Ringer’s acetate in severe sepsis was published in the NEJM this month here. A cracking read which pops the lid off the crystalloid vs. colloid debate once again for old times sake.

So what did we think?

800 patients meeting criteria for severe sepsis within the last 24 hours and randomised on the ICU to receive double blinded HES or Ringers as resuscitation fluid. Reasonably powered. Nice allocation concealment. TSC. DSMB. Most of the boxes ticked.

What happened? Well, the HES group didn’t fare very well at all. An 8% increase in all cause mortality at 90 days. A NNH of 13 – Wow! A Relative Risk (if that is your bag) of 1.17; 95% confidence interval [CI], 1.01 to 1.36; P=0.03.

This was a sick group. Mortality in the control (Ringers) group was 43%, which is fairly high for a developed world ICU treating severe sepsis. Baseline characteristics were pretty evenly distributed, including SOFA and SAPS II scores. Randomisation was stratified, accounting for Acute Kidney Injury (AKI), University hospitals and a few other bits and bobs. Most of the common confounders seemed to have been negated. And with double blinding and an objective endpoint (You are either dead or you’re not) they have also sidestepped the most likely sources of bias in a trial of this nature.

We couldn’t really fault it.

Interesting that the Kaplin Meier curves digress at about day 10, implying that it is a sequential phenomenon that causes problems rather than acute toxicity. Some were postulating within the group whether the increased mortality was all due to the incidence of renal failure and subsequent withdrawal of care. I don’t buy that from the stats presented in the paper, but I would be happily convinced if someone could demonstrate the proof to me.

What I do buy, is that there is now compelling evidence against the use of starch based colloids in acute resuscitation. They are off my shelf until someone can show me some evidence why they should go back on.

However, I do still love the potato. In all it’s many guises. Including chips, crisps, waffles, alphabet shapes, mash, roasties, bubble and squeak, cullen skink, rumbledethumps etc etc………



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

Tranexamic acid needs a make over

I was listening to the EMCRIT podcast today. As usual it was absolutely excellent, but on this occasion it was especially superb as Scott Weingart was joined by the wonderful Prof. Tim Coates from Leicester. Tim is an inspiring EM researcher and speaker who also happens to be largely responsible for one of the largest RCTs in Emergency Medicine history; CRASH-2. Now, this is no time to go over CRASH-2 again. The bottom line is that tranexamic acid is both cheap and fabulous for the treatment of major trauma patients.

We should give it, we should pretty much always give it and neither he nor I know why clinicians have not adopted it as widely as it should. Actually, that’s not entirely true, I have a theory and that is that it’s just not ‘cool’ as a treatment.


What do I mean by ‘cool’? Well it’s just a feeling really based on practicing medicine for many years. When new treatments come into practice we clinicians (and especially EPs with our love of shiny things), love them to be exciting, difficult, even perhaps dangerous. Think of the excitement around stroke thrombolysis in previous posts that seems to based on little evidence. That requires CT scans, expert opinions, senior input, expensive therapies and in our neck of the woods transfer to another facility. It’s difficult, it’s expensive, it’s dangerous….it’s ‘cool’.

Tranexemic acid is not cool. It’s dirt cheap and can be given by any doc in our department.

Just as aspirin used to get missed in the rush for thrombolysis for MI (in the days before PCI) we are now missing TXA in the rush for Whole Body CT, Shock packs and advanced transfusion management. I see history and wonder what we can do to help.

So, how do we make TXA cool? I sometimes think that if I lock it in the controlled drugs cupboard next to the tPA and the Ketamine then tell everyone that it’s potentially fatal and scare them half to death it might get used more often. Perhaps if someone raised the price to £500 a shot we might think of it more often? Obviously that’s ludicrous but we need to do something.

TXA needs a make over, any ideas?

…….but what else? Where do we go next with TXA? If it works in major trauma then what about other bleeding disorders? What will CRASH-3 which will look at TXA in head trauma tell us?  Then what might CRASH-x tell us in the future? Who knows but I was quite surprised to see that there is already evidence out there for it’s potential use in GI Bleeding in this BestBet from the Royal London Hospital. Not convincing but promising enough for consideration in the future?

I think so.

Simon Carley