Tag Archives: emergency medicine

Croup: Riding the Dex Express

Sooooo….this paper turned up at JC last week (thanks to Nicola P) and whilst I’m not sure that it meets all three of our criteria for a top JC paper it is relevant as a week barely seems to go by without someone questioning the dose/route/brand/colour/size/ethnicity of medicine for croup.
Rule of thumb chaps and chapesses ‘The greater the dogma, the greater the ignorance’. Someone cleverer than I said that, but I’m happy to plagiarise ‘cos it’s true.
Anyway, Croup arrives as a question once again in the journal Emergency Medicine Australia, but this time the question relates to speed of onset in mild to moderate croup.

 STOP! If you are in exam mode at this point you should read the paper. See what you think about it and give it a mark out of 10.

We’ve talked about this paper and it’s a tricky one. The first question is why has this paper been done (which we cannot answer, but can surmise privately). The use of steroids in the management of croup is very well established and is something we led on here in Virchester many years ago. It was even one of the very first BETs back in 2004 (amazing to think that we are still talking about this 8 years later).
I’ve also seen the Cochrane review and even examined some CTRs for FCEM on the subject. So, it pretty much seems to me that the question of whether we give steroids for croup is well made. The research that remains is, I suppose, about refining and polishing what is surely a well established fact.

STEROIDS WORK IN CROUP Click the link and read the Cochrane review.

So, what about the paper this week? Is there anything we can draw from it and learn? Well, the authors have done an RCT (good) on mild/moderate croup patients. Interesting this as for the mild ones would you give steroids or just let nature take its course? (Ed – depends on how mild as croup score 1-3 is mild) I’m not sure so there maybe an element of over-treatment in comparison to other practices. Whatever, the authors tell us that there is an effect of giving steroids that they can define and detect at  30 minutes following administration of steroid and that this counteracts the information given through Cochrane about a delayed effect taking up to 6 hours.

I have major concerns with this paper and I just don’t see how this is going to make a significant difference to our practice in PEM.  I don’t think a paper like this would appear in an exam, but if it did I would be pulling holes in it along the following lines.

1. What is the clinically important question here? It seems that we are looking to see the speed of onset of steroid meds in mild/moderate croup. The clinical importance of this is perhaps unclear except in logistical (admission) terms. What defines a significant difference in this low acuity group? Mild croup is not admitted anyway so what is the issue we are addressing?

2. Sample size. OK. An interest of mine, and if you share that interest (you sad person) then hop over to the podcast to hear more about how to understand and interpret sample size calculations. In this paper they appear to be using tests for continuous data for data which is unlikely to be so. Honestly, it seems as though these are the wrong tests for this data, but there is insufficient information in the paper for us to tell. Where is the clue? Well, the Wesley croup score is a categorical score (at best ordinal). It’s not continuous and is unlikely to be normally distributed, so a t-test is rarely going to be the right test. So hmm, not enough information to know but questions are there to be asked. If you want to know more about stats for Critical Appraisal then click here and here. Apart from anything else, a study of just 70 patients would have to show a massive effect if it is be valid and I don’t see that here. Similarly the graph shows average scores only, and I’m not sure that I’m just interested in the change in average score amongst 35 patients. I want to see the distribution as well. This is a common problem in papers as the mean score reporting removes the depth and character of the data.

3. Right, so we are unsure of the validity of the question and also of the sample size what else? Well,  do applaud the authors for defining the numbers of patients that they ‘could’ have recruited and the difference between that number (828) and the number recruited (70) is huge. This suggests a degree of patient selection which may well affect the results. Now, I don’t want to put a massive downer on this as it is an inevitable problem with EM research, but this ratio really asks questions as to whether this is a representative sample, or whether the results will be heavily skewed because it is a sample of convenience.

So, it sounds as though we were pretty down on this paper from a methodological point of view. We gave it a 3/10 to be honest which is clearly not high, but just wait is there ANYTHING we can take away from this piece of work at all. Well, it’s tricky to be honest. It’s likely (but I’m finding it difficult to tell) that oral dex starts working fairly quickly, but that was never a clinical dilemma for me before I read this paper so I’m not going to change practice. However, it’s a useful to use this as a vehicle to discuss Croup (again), to review the relevant BETs and to talk about how to spot flaws in papers.

 bw

Simon C

PS. If you are still in exam mode try answering the following questions…

1. What is meant by the term ‘double-blinded’ and why is it important in a trial like this?

2. Four patients in the placebo group worsened during the initial phase of the trial and were then given steroids. They were analysed in the placebo group despite getting steroids. What is this type of analysis called and is it the right approach?

Journals are dead: Long live the Journal Club

“The report of my death was an exaggeration”

Mark Twain

Just a quicky and a link out to our guide on Emergency Medicine Journal Clubs. Despite the rumours of the imminent demise of all medical journals, we at @stemlyns strongly believe that this will not lead to the death of journal clubs. Even if paper publication wanes (and it probably will) it will be even more important for clinicians to have the skills and abilities to be wary of what ‘evidence’ is out there.

For example anyone can now set up a Blog (Er, not sure that’s the right message here – Ed) and say what they like. How do you know it’s fair comment and good enough to change practice?

You do need, and you will always need to be a sceptic with the skills to critically appraise and critique the evidence and we think that a Journal Club is a great way to learn.

Read more here on our top tips for making your Emergency Medicine Journal Club effective, productive and worthwhile.

Our Journal Club runs on a Friday lunchtime in the ED. We’ll review, debate and then blog on the papers we discuss. Watch the blog for the latest in EM Critical Appraisal.

vb

Simon C

PS: We’ll be keeping a log of papers reviewed in our Journal Club from now on. If it works then we should have a rolling program of the best, most current and most relevant papers for Emergency Medicine. If you’re coming up to an exam….it’s a good place to visit.

Kiddy pills, syrup, compliance and cost.

I was wandering through the Paeds journals looking for something relevant to EM recently (there wasn’t much) when I came across two articles in Archives of diease in childhood. The first by Baguley et al tells me that Kids are more likely to take medicines if they taste nice. Not exactly rocket science I agree, but what I did not know is that there is a scale of drugs which are known/not known to be taste nice, and interestingly Flucloxacillin, a drug widely used in emergency medicine is one of the least pleasant tasting. Augmentin on the other hand, for which the penalty for prescribing off protocol is crucifixion (not really but it feels like it) is apparently very tasty indeed. This may seem fairly benign and obvious but it’s really important for us as EPs as clearly there is no point in prescribing if the compliance is going to be poor.

Here’s a list from the paper ranking some of the more commonly prescribed antibiotics in Paeds ED practice from the paper.

  • ▶ Antibiotics children will normally swallow

    • ▶ Co-amoxiclav (×3/day) or Augmentin Duo (×2/day)

    • ▶ Cefaclor, cefalexin, Amoxil (branded) (all ×3/day)

    • ▶ Co-trimoxazole

  • Antibiotics children might swallow

    • ▶ Penicillin V (×4/day)

    • ▶ Amoxicillin (generic) (×3/day)

    • ▶ Clarythromycin (×2/day), azithromycin (×1/day)

  • Antibiotics children often spit out or grimace when taking

    • ▶ Erythromycin (×4/day)

    • ▶ Trimethoprim (×2/day)

  • ▶ Rarely tolerated with good adherence

    • ▶ Flucloxacillin (×4/day)

    • ▶ Clindamycin (×4/day)

So, is there a way round this rather than just continuing to prescribe and hope for the best? For patients there is some really good generic advice out there on loads of websites and your pharmacy may have advice as well, but what about us as EPs. Is this really a question for us at all or do we just prescribe and say get on with it. There are two suggestions in the journal that I thought were worth a ponder. One we can do right now and one for the future. In the same paper Baguley et al describe the concept of a ‘taste test’ to give the first dose of antibiotics before the child leaves to see if they will tolerate it. This seems perfectly sensible to me. We should probably do this for those drugs down the bottom end of the table, and arguably for all of them. I’m going to suggest and then wait for all the reasons why we can’t, and then I’ll suggest it again, and again…….

The future idea is another paper in Archives which challenges dogma, and I love a bit of dogma baiting! We all know that the only reason we are messing about with antibiotics in syrup form is because kids can’t take tablets. Or can they? Spomer et al have performed a rather nice (admittedly pilot) study looking at whether children aged 0.5-6 years can swallow tablets as compared to syrup….and the result is that they can. Not only that, but they can swallow tablets as well as they can take syrup, and, in children aged 6-12 months they do better with tablets. Ok, it’s a small paper, a pilot and we cannot infer from this that mini-pills are the future, but it does raise some interesting questions that I’d like to see answered over the next few years.

Compliance is a vital component of any successful theraputic intervention but one that we in Paeds EM perhaps do not take account of as much as we should. Better compliance has got to be better for patients, for countering microbiological resistance and ultimately for healthcare costs.

It’s certainly made me think about that next prescription for oral fluclox syrup. I wonder if it will get used in the way that I prescribe it?

Now, at this stage it would be great to tell you the results of my blind tasting of antibiotics in the department. This is of course unethical so I haven’t, but I’d love to hear from anyone who has. It does remind me of my time in Neonates (a long time ago when consultants could make juniors do this sort of thing) when the drug rep came round with all the different types of formula feeds designed from ultraprems right up to full term and beyond. It was possibly the weirdest, most unpleasant and arguably most bizarre taste test I’ve ever undertaken.

Simon C

Through the Looking Glass: Chirocaine vs Bupivicaine


I’ve seen a few paediatric femoral shaft fractures in the last couple of years, and while they always make my spidey-sense tingle for non-accidental injury, most (even the spiral fractures) have been explained away by plausible mechanisms of injury; they are usually late toddling age, have got their feet stuck, twisted and fallen over.

I’ve even seen a few which were pathological – undoubtedly the result of the vitamin d deficiency which stems from the miserable attempt at sunshine we have to put up with here in the North West.

The way I’ve managed these patients has changed with my experience and skill level; as an SHO I looked at them with sympathy while the oramorph, ibuprofen and paracetamol were absorbed slowly from their (no doubt static) GI tracts. As a registrar, they now get a squirt of intranasal diamorphine and an application of ametop over the ipsilateral groin, in anticipation of an ultrasound-guided femoral nerve block when they return from x-ray. I mix up a 50:50 solution of 1% lidocaine with 0.5% bupivacaine and, before ultrasound guidance, used 1mL per year of age. It works out as less than 2mg/kg of lidocaine (usually) and less than 1mg/kg bupivacaine – so relatively small doses. I’ve done it a few times, and it works pretty well, especially in combination with a Thomas splint. The great thing about ultrasound-guidance besides lower failure rates is that you can use even smaller drug volumes – it ends up more like 0.5mL per year of age.

So as I examined the two year old, who was refusing to weight bear, with little deformity to his leg but clear femoral tenderness, I reached for the trusty bupivacaine/lidocaine combination to make splint application less of an auditory assault. But shock! Horror! No bupivacaine!

Instead, there was chirocaine – which completely confused me, as I had no idea what it was (and there was apparently no bupivacaine to be had anywhere). I asked around – and no-one seemed to be entirely sure how the two drugs related to one another. So, after some research, I thought I’d share.

Chirocaine (levobupivacaine), as you may know (I didn’t), is “the pure S-enantiomer” of bupivacaine. The story is that some drugs exist in a 50:50 (racaemic) mixture of two stereo-isomers; molecules which are mirror images of one another. Where the mirror images cannot be superimposed, the molecules are said to be chiral, and the most common cause for this is an asymmetrical carbon atom. There is a right (dex-, or d-) and left (levo-, or l-) version of the molecules which cannot be made symmetrical no matter the orientation in the same way as your left foot just doesn’t fit in your right shoe [NB: an important differential in the non-weight bearing child]. Where drugs bind to receptors, one isomer may be able to bind, while the other cannot – or may generate alternative effects.

You probably knew this already, right? Every time you prescribe levothyroxine, esomeprazole, escitalopram or levofloxacin, you think proudly about how you are selecting out the correct isomer for your patient, yes? And how you are therefore giving half the dose, as they aren’t getting the 50% of isomers which don’t give a clinical effect? Well, it doesn’t quite work as predictably as that. In fact, in some cases the dose is significantly lower for the same clinical effect (notably escitalopram, 30 times more potent than citalopram) and in others confers no therapeutic advantage at equivalent doses (see esomeprazole) or may even be harmful (see thalidomide).

So what’s so special about chirocaine? It’s twice the price of standard bupivacaine per 10mL ampule, so it’s twice as good, isn’t it?

Well, no – it seems to be equivalent at providing analgesia in a variety of blocks (caudal, ilioinguinial, rectus sheath… The list goes on…), but every study is focussed on the reduction in adverse (cardiac) effects with levobupivacaine. It seems the rationale for selecting out this isomer is reducing cardiac toxicity. Where does this come from?

Most data comes from animal studies (in case you didn’t know, children are no more little adults than they are little rats, pigs, rabbits…).

You have to dig quite deep for original studies. All roads seem to lead back to this one paper. 14 healthy, adult, male subjects were injected with bupivacaine or levobupivacaine infusion and asked “do you have any symptoms?”. OK, let’s be fair, they’ve powered the study to detect a 10% difference in their primary outcome (stroke volume), but their bottom line conclusion is “that levobupivacaine may be a safer drug than rac-bupivacaine for procedures requiring high doses of local anaesthetic.” So not really our fractured femur toddlers, then.

Which brings us back to the beginning. Studies in children have suggested that levobupivacaine produces equivalent anaesthetic efficacy, but what they haven’t done is convince me that we should ditch bupivacaine when we are using such tiny doses. It’s cheaper, and with ultrasound guidance we can use a miniscule amount to achieve local anaesthesia long enough to reduce the fracture in a Thomas splint.

So the bottom line is this; use what you’ve got unless there’s specific cardiac risk for your paed patient, and using 50:50 with 0.5% chirocaine provides the same analgesia as bupivacaine (in our hospital the maximum dosing for ilioinguinal block is apparently 1.25mg/kg/side). Whatever you use, do the block; your patients will probably thank you (but we might have to wait to find out).

Natalie May

Ref

  • A comparison of the cardiovascular effects of levobupivicane and rac-bupivicane following intravenous administration to healthy volunteers. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873676/pdf/bcp0046-0245.pdf
  • EPG data sheet on Chirocaine http://www.epgonline.org/drugs/chirocaine/
  • Regional anaesthesia for kids with femoral fractures at BestBets http://www.bestbets.org/bets/bet.php?id=130

Glasgow Scores… Not just for coma any more!

Quick post…

NICE have recently published new guidance on Upper GI bleeding.

It is surprisingly sensible. I was pleased with their position on PPI’s for upper GI bleeding (not before endoscopy…).

The other point that I was happy to see was the inclusion of the Blatchford score for risk assement of these patients.

We all love a good scoring system, especially if really complicated (long hours spent working out APACHE scores on ICU spring to mind)

The Blatchford score however, is simple, and useful. I have been using this to help plan management of these patients for a while, and I was surprised to find that many people have not heard of it.

So what else to do? To the Bat Cave St Emlyn’s!

What is it?

To give it its full name; The Glasgow Blatchford Score was derived in 2000. It is designed to identify patients who require admission for treatment of their UGI bleed, and who can go home for outpatient management.

Previous to this, standard practice was to admit the mass majority of these patients, even the young well ones with minor bleeding or ‘coffee ground’vomits.

Here it is:

It can be easily calcualted using information availble in the ED. You can use the ever useful mdcalc.com

So why use it? 

So we can send people home! This has to be a good thing, as long as it is ‘safe’ to do so.

In 2009 Stanley et al performed a prospective study to establish whether this was the case. Their hypothesis: If the GB score was 0, the patient could go home from the ED, and be followed up as an outpatient.

Sounds great right? Did it work?

The study was split into two parts. First they collected data on all GI bleeds seen in the ED. They recorded the outcomes, and compared the outcomes with the GB score on admission. In the second part they introduced the low risk criteria, and discharged those with a GB score of 0.

So….

In the first part they identified 334 patients with UGI bleed. 319 of them got admitted (96%)

53 of them were low risk (GBS 0). 50 of these were admitted. None of them died or needed any interventions.

So far so good yes? If we could have have sent those patients home, wouldn’t everyone be happier and the world a better place?

So that’s what they did. In the second phase of the study they put their theory in practice. They identified 491 UGI bleed patients. 123 (22%) of them presented with a GBS score of 0, and of this group, 84 got sent home (68%).

They then followed them up to see how they got on. Only 23 (40%) turned up for their outpatient endoscopy, the rest were chased up via GP, case note review and telephone follow up.

So how did they do? Really well as it turns out. Out of the 123 patients with a GBS score of 0 a total of 0 needed an intervention or died from a UGI bleed related cause in the following 6 months. Zero, zilch, nada.

These results are summarised here:

For those concerned with our limited health resources (i.e. all of us), the exciting figure is at the bottom. Before the scoring system was introduced, only 4% of the UGI bleed patients were being discharged from the ED. With the scoring system in place, 29% were sent home.

Considering the numbers of these patients we all see, this is a big deal.

So should we do this? I think so.

Gareth.

The Olympics and the ED physician

It’s a great week to be British. Bradley Wiggins wins the tour and we are just a few short days away from the greatest show on Earth – the Olympics I mean.

(Ed – don’t mention the Cricket, & don’t send this to any South Africans)

So, Virchester is hosting some of the Olympic events and as a result the local EDs have been put on standby to receive athletes and their support teams as patients. We have some experience in this as a few years ago the Commonwealth games were held here and it was interesting to think back to that time and reflect on how it affected us in the ED. Virchester also hosts many elite sporting teams so we are used to famous and/or talented sportsmen and women turning up on our doorstep.

Teams form the large, wealthy countries invariably bring their own team of healthcare staff with them ranging from docs to physios. It’s likely that most problems will be dealt with by these people and therefore they won’t come to you that often. If they do then the athlete/support staff are usually accompanied by one of their physicians. These are usually fairly easy consults as a result.

Athletes and staff from the less well off nations present different problems. They may not have their own supporting staff and as a result it is possible that they may end up in your ED. Now, LOCOG and other major sporting organisations put on fantastic facilities and teams of staff to deal with this issue, but still they may slip through the net. In previous events we have had all sorts of things turning up in the ED, from acute trauma, right through to long term health problems presenting to the ED for treatment (for conditions where treatment might be tricky to get back home).

So, despite the best laid plans, if you are near an Olympic venue you might get Olympic participants through the door. So, what are you going to do about it and where are the dilemmas? These are not the thoughts of a sports physician and I know that many ED docs know more about sports medicine than I do, rather what should we be thinking about as non-sports medicine experts faced with the prospect of high profile, high maintenance, high risk athletes turning up in our EDs over the next few weeks.

  • 1. Who should they see? This is the age old chestnut of how to manage VIPs in the ED. Should anyone be prioritised in terms of time or in the seniority of clinician who sees them? Rightly or wrongly I would suggest ensuring that elite athletes are reviewed by a senior physician. These are high risk (legally and clinically) patients and it makes sense to get the best opinion possible.
  • 2. Costs? All participants in the Olympics are entitled to free health care so there are no concerns here. The NHS committed to “Provide free comprehensive healthcare to Olympic and Paralympic family members throughout their stay for the Games whilst still providing healthcare for our local residents”. Treat them as NHS patients and don’t worry about it.
  • 3. Clinical Vigilance? This is a tricky concept for me to explain, but it’s something along the lines of balancing between delivering normal care (which should be the best you can) with an appreciation that sports medicine is different. It’s different clinically as there are a host of conditions that are sports specific, but also the psychological elements around the relationship between athlete, coach and physician (team and you). Complex factors such as the injury being made public, desire to compete, potential risk etc. may all be at play in the consultation and you may find it difficult to understand everything that’s going on. So close to an Olympics such conflicts are likely to rear their heads. I have found this aspect of treating athletes the most complex and difficult.
  • 4. Expertise? You’re a great emergency physician I know, but don’t step outside your comfort zone. By all means diagnose the undisplaced metacarpal fracture in the water polo player, but think long and hard before you advise them on whether they can play with it strapped up in 5 days time. I have been asked all sorts of stuff about prognosis, therapy etc. Remember that time to healing to sit behind a desk is somewhat different to time to be able to compete at elite level. Similarly, you don’t want to say something is OK to compete on if it then results in more serious injury. If you are going to give advice beyond your competency phone your medical protection organisation soon (see note below).
  • 5. Drugs? This is not about you detecting  the performance enhancing kind, but rather that little stock of drugs in the cupboard that might result in an athlete testing positive. The WADA (World Anti Doping Association) lists can be found here. I guess analgesics and B2 agonists are the areas where the typical ED doc might make an error. That could be rather embarrassing so best avoided.
  • 6. Refer appropriately. LOCOG has a number of health centres specifically for athletes. If in doubt give them a call they probably know more than you (and me). London 2012 Olympic Games Healthcare Guide – December 2011-1

So, hopefully everything will go swimmingly well (the Ozzy swimmers are in Virchester this week), and we won’t see any athletes or staff at all……., but somehow I don’t think so.

vb

Simon Carley
NB. Sports medicine and EM. I actually think they make really great bedfellows as much of what we do is transferable to the sporting arena. I once attended a Cricket match at Old Trafford when a chap collapsed in front of us. Within minutes there were 2 ED consultants, an ICU consultant, a Cardiology consultant and a Rheumatology consultant in attendance. We sorted the chap out and handed him over to the site doctor…..an SHO in pathology who’s domain knowledge was thankfully not required.

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

EM as a career? Yeah, but no……

I have too many jobs!

Amongst other tasks I manage the foundation program for junior docs at my large university teaching hospital. I’m effectively responsible for getting them through the two years of their career with the hope that they will get signed off by the GMC and go on to greater things. I have great trainees, many are high achievers who will go far in whichever career they choose.

I’ve run the program for a few years now and unsurprisingly one of the things I have made everyone do is emergency medicine. All docs do at least 4 months of EM in my hospital. I think it’s good for them, it exposes them to a wide range of clinical problems and tests them to stand by their own decision about diagnosis, treatment and discharge.

So what’s this got to do with recruitment you might ask? Well, at the end of the two years I ask all the trainees which jobs they enjoyed, and as you would expect there are a variety of answers, but it’s perhaps surprising that about a third rate EM as their most interesting and rewarding placement.

So would they consider it is a career I ask?

The responses are consistent and worrying for those of us who are seeking to nurture the next generation of EPs in the UK. Despite their interest in the clinical work, hardly any trainee considers EM as a career choice, and it’s not because of the clinical practice. They love the team working, the unpredictability, the frequent and rapid patient contact. It’s the working conditions, the lifestyle and the career prospects that’s putting them off.

Why they ask should I do EM as opposed to something like medicine or general practice? Fewer weekends, fewer evenings, easier exams……, same pay.

Pay does seem to be a major motivator for todays young medics, but not in the way I originally thought. It’s not so much the amount but the fact that there are no differential pay recognition for those who work the hardest, and at the most socially disruptive times of the week. Why would you do our job for the same pay as your friend who only works every 10th weekend (whilst you do every 2nd). It’s not the absolute amount, rather its the fact that it does not matter which speciality you train in, and indeed practice as a consultant in, the pay and financial reward is the same. So how we find a way of valuing the extra effort and disruption that a trainee embarking on a career in EM takes on? I’m not sure that I can think of many that are not financially orientated. Perhaps time off? More holidays so that we can retain some of our excellent oversees trainees who struggle to find time on busy rotas to travel home to see their families? Ideas please.

But is this not the case with many there specialities? Are there others where personal sacrifice is required as a junior in order to get to the top? Of courses there are. Plastic surgery is a good example where competition is fierce and additional effort is expected with a long and challenging training program…but the rewards at the end are potentially enormous. Not so in EM, there is little or no private practice to rival that of the plastic surgeons nor the prospect of leisurely on calls as a consultant as increasingly EM consultants are moving towards the very same 24-hour rotas that is putting off the juniors.

We are already in a staffing crisis in EM. Consultant posts remain unfilled, Middle grade rotas have been decimated in many departments and trainees in our early training programs are leaving EM for the less onerous and disruptive specialities such as anaesthetics.

What then can we do? A starting point would be to recognise the additional disruption that training in EM causes to the individual and their family. The UK Government is consulting on the idea of differential pay depending on where you work. Perhaps the time is now for us to give additional reward to the hard working trainees in emergency medicine. Perhaps that might convert some of my enthusiastic and brilliant trainees to stay in a speciality where they love to work, and one in which they feel rewarded for doing so.

Simon Carley