Dystonia in the Emergency Department

St Emlyns - Meducation in Virchester #FOAM

Jabba's favourite decoration by Stefan at flickr.com

Jabba’s favourite decoration by Stefan at flickr.com

I’m sure we’ve all seen cases like this. A 25 year old lady walks in to the ED complaining of a swollen tongue. She can’t really talk, seems a bit anxious and is quite tearful. The triage nurse notices that the tongue seems a bit prominent and assumes that this is anaphylaxis. The lady is taken straight to Resus where she’s seen by a junior doc, who promptly gives IM adrenaline, IV hydrocortisone and IV chlorphenamine before calling the anaesthetists in a great hurry. Of course, this makes the lady increasingly anxious. When the anaesthetists arrive they realise that the tongue isn’t actually swollen and everyone calms down, appreciating that the lady must actually be having a panic attack. As she fails to calm down with reassurance and a paper bag the belief that she must be crazy strengthens, which of course makes the situation all the worse.

Eventually, somebody will realise that the lady has been taking metoclopramide for morning sickness in early pregnancy and this is not hysteria – it’s an acute dystonia. Suddenly, with the benefit of hindsight, it’s obvious what’s been happening. Everyone relaxes and we can crack on with getting the lady some treatment.

There are lots of reasons why we miss diagnoses. Sometimes it’s simply because we don’t have the knowledge.  Of course none of us can know everything and this is something that every doctor has to work on constantly to minimise that possibility.  Sometimes we have the knowledge but the problem is how we think: i.e. we put things into the wrong boxes in our minds.  Our perception of the patient in front of us (as with everything else we encounter) is essentially a mental construct. We build up a set of beliefs around that construct about what it actually is and how we expect it to behave.  Once we’ve formed a belief, it’s actually quite hard to change it. We all have a tendency to ignore information that doesn’t support our beliefs and to latch on to information that seems to support them. This is covered really well in Dan Gardner’s fantastic book, Risk: The Science and Politics of Fear.

Because acute dystonia is so rare in comparison to diagnoses like anaphylaxis and panic attack, it’s actually quite likely that the latter diagnoses will be the first ones we consider for a patient with acute dystonia.  We then have to be presented with enough challenges to that belief to make us reconsider, and sometimes that can take a while

Here are some of the presentations of acute dystonia that could easily be misdiagnosed:

  • A ‘swollen tongue’

Patients may present with pseudomacroglossia.   The tongue feels swollen to them and it may protrude but actually it isn’t swollen at all.   When you realise that, you may be tempted to think that the patient is simply anxious.  You need to consider acute dystonia.

  • Hyperventilation and ‘hysterical behaviour’

It’s not uncommon for patients to present prostrate, hyperventilating and behaving strangely.  At the time it may seem that they are incredibly anxious and overwhelmed by panic.  I’ve seen some of our junior docs being tricked into making this diagnosis.  Once you step back from the mental construct that you’ve made about the apparently anxious patient (which as Dan Gardner points out is sometimes difficult), it can be really obvious that the patient is actually having an oculogyric crisis.

Similarly, it’s easy to misdiagnose an oculogyric crisis as a neurological catastrophe.  Here’s a link to a case report of a 14 year old who was misdiagnosed with encephalitis.

  • Torticollis

Acute dystonia can actually present as an isolated torticollis – you can imagine how easy it is to miss this!  Here’s a great video demonstration.  It uses an actress but demonstrates cervical dystonia very nicely.

  • Difficulty swallowing and/or talking

Patients with acute dystonia may present simply with difficulty talking.  I’ve also seen patients present with difficulty swallowing.  This can be really challenging because it may be hard to take the history.    Here’s another nice video, this time of a real patient, which demonstrates the difficulty that a patient with acute dystonia can have talking.  This type of reaction is called a buccolingual crisis.

  • Laryngospasm

Thankfully this is rare and I’ve never seen it.  However, acute dystonia can present with laryngospasm.  You can imagine the difficulties recognising that!  If you do recognise it early, however, you may well be able to prevent an unnecessary escalation of treatment by addressing the dystonia.  It’s important to remember, though, that just because you know the cause doesn’t mean the airway is safe!

  • ‘Writer’s cramp’

This is an unusual focal dystonia and treated in a slightly different way to many of the acute dystonias.  It’s probably unlikely that patients will present to the ED.  Patients complain of spasms or cramps of the hand/arm, often when using the arm such as when writing or playing a musical instrument.  Hand writing may deteriorate.  Naturally, it can be hard to recognise that this is actually a form of dystonia initially.  Here’s a great review article on focal upper limb dystonias.

Actually, with hindsight, in the majority of cases the diagnosis is relatively obvious.  The key is keeping an open mind and not letting your mind latch on to any particular mental construct about the patient and their condition too early.  Take a really good history.  Ask the patient what they’re feeling.  The spasms of acute dystonia are painful and involuntary.  Patients are going to be anxious – but this is secondary.

Remember the cause of an acute dystonia:

  • Primary causes (including genetic causes – family history is important)
  • Secondary causes (notably – and probably most commonly in the ED – including certain medications; but also conditions like Wilson’s disease)

Medications that may cause acute dystonia include: Antipsychotics (dopamine antagonists); Metoclopramide; Antiepileptics (e.g. carbamazepine; phenytoin); Amphetamine (possibly); Cocaine; Antihistamines 

In the UK we tend to use IV procyclidine at a dose of 5-10mg.  I usually find that 5mg works quite quickly but occasionally you need repeat doses.  Procyclidine is an antimuscarinic drug and it won’t work for tardive dyskinesia – but that rarely presents to the ED.  Nobody really knows about safety in pregnancy so you might prefer to give IV diazepam instead.  IV diazepam can also be used in serious refractory cases.  In countries other than the UK, benztropine IV is used more commonly.

There’s one important thing to remember about IV procyclidine.  It can actually cause a feeling of euphoria.  While this may be great for the patient as a one-off, it does come with the potential to cause one or two patients to desire a return visit with a risk of developing  dependency and drug-seeking behaviour – this is worth bearing in mind!

Clearly, if this was a drug induced dystonia, the patient may need to stop that drug!  When that involves stopping something like metoclopramide for nausea, the decision is pretty straight forward and you may be able to offer alternatives.  For other conditions (e.g. schizophrenia) this decision is a bit more complicated and you’ll need the input of the patient’s psychiatrist.  You’ll probably have them feeling in tip top shape within a few minutes so the patient may well be very happy and you will no doubt be feeling very happy too.  If things are back to normal, most patients can be discharged.  Patients with more complex conditions may of course require additional consults.

Some people recommend a 3-day course of oral procyclidine (or benztropine) to prevent recurrences because the half life of procyclidine may be shorter than the offending drug, although the half life of procyclidine is actually as much as 12 hours.   It’s worth giving this some thought for your individual patient.

Wow, sounds dramatic.  And it can be.  Acute dystonia can’t always be treated with 5mg IV procyclidine and the patient immediately discharged.  Sometimes the dystonia is refractory to treatment.  Dystonia can cause respiratory compromise (requiring mechanical ventilation), bulbar compromise (requiring airway protection), exhaustion, rhabdomyolysis and acute kidney injury.  Here’s a great paper describing 12 cases of status dystonicus

By Lauren Manning on Flickr.

By Lauren Manning on Flickr.

Just as acute dystonia isn’t recognised because you want to hang on to your initial mental construct, don’t let yourself hang on to a diagnosis of acute dystonia when the patient may have something else!  Hypocalcaemia, encephalitis and tetanus are other conditions you might need to bear in mind.  

So there we have it.  Acute dystonia is really hard to recognise in the ED but very satisfying to treat!



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JC: Duel of the Rules: Which decision rule for head injury in children?

St Emlyns - Meducation in Virchester #FOAM

Ladies and Gentlemen!

Dual of the Rules

The assessment and investigation of paediatric head injury is a case study in clinical risk management. Similar to chest pain in grown up medicine, it’s a frequent presentation, with a rare but potentially devastating outcome. It’s these kind of patients where we as ED docs come into our own as diagnosticians (or do I mean  probablesticians? ;) ). Head injury in children is also something of an interest of mine; both as a doc, and as the parent of a rambunctious, seemingly fearless, 6 year old boy.

While we all like to feel that our razor sharp clinical acumen is sufficient to pick out the badness, it is  nice to have some evidence based back up for our hunches and ‘gut feelings’. So in order to help guide us through choppy diagnostic waters, a great deal of time and effort has been expended to develop clinical decision rules (CDR’s) (or instruments, if you prefer). For chest pain we have TIMI, PERC, HEART to name just a few. Unsurprisingly, paediatric head injuries also have a selection of decision rules to choose from. Of course, this brings with it yet another question; which rule to use? Which is best? This is the question the authors of this study have tried to answer. They have taken their own cohort, and pitted three decision rules against each other in a Battle Royale!



In the blue corner, all the way from the US of A, weighing in with a super heavy weight derivation cohort of 42000 patients…..It’s PECARN!

In the red corner, it’s our local boy, from right here in Virchester, and basis of the NICE guidance on paediatric head injury….. It’s CHALICE!

And in the um, other corner, last but certainly not least, …. from Pediatric Emergency Research Canada, it’s CATCH!

These rules have been compared to each other before. Pickering et al compared the three rules and concluded that PECARN was the most sensitive with an acceptable specificity. This excellent article by Lyttle et al compared the three decision rules and the methods by which they were derived in great detail, and is well worth a read for a textbook example of how to assess a CDR. It is also worth mentioning that PECARN has been validated in a



separate (but demographically identical cohort) as part of the same study in which it was derived in. CHALICE has not been externally validated, but has been extensively implemented and retrospectively analysed since its inclusion in the NICE guidance.

This is the first paper applying the rules to a new, prospectively collected cohort. Their patients were recruited from the ED at a level 2 paediatric trauma centre in the US. 1009 patients were assessed aged less than 18yrs, who had sustained a head injury within 24 hours of presentation.




Patients with a GCS <13, and those with a coagulopathy, were excluded. There were some eligible patients missed, but they seemed to be demographically similar to those included. While not identical to any of the derivation cohorts from the original studies, this population is probably similar to what we all see as ‘minor’ paediatric head injuries, and therefore the population we would want to apply a CDR to. The outcomes looked at were death from TBI, neurosurgical intervention, ventilation for >24 hours due to TBI, which all seem reasonable and appropriately patient orientated to me – focusing on what happens to the patients rather than findings on CT. By the authors own power calculation, a cohort of 1000 patients would be sufficient, so we’re happy there.

Diagnostic performance of the PECARN, CHALICE and CATCH rules

Diagnostic performance of the PECARN, CHALICE and CATCH rules

As you can see, PECARN comes out fighting with no misses and 100% sensitivity. CHALICE put up a valiant defence with a 85% specificity but falters with a surprisingly low 84% sensitivity. CATCH puts in a solid bout, but is unable to come out on top. So no knock-outs today, so were going to have to ask the judges to make a decision.


Kids and radiation don't mix.

Kids and radiation shouldn’t mix unless they really have to

One hundred percent sensitivity – now that’s the headline figure right there. When we’re dealing with kids and brain injuries and neurosurgery, we want as close to perfect as we can get, and PECARN seems to deliver. This is consistent with the comparison by Pickering et al that also put PECARN on top. Of course, it’s not all about the offence, a CDR needs a good defensive technique too. It’s all well and good to go all out with the sensitivity, but if you haven’t got the specificity, you’re gonna have a problem. Here, CHALICE performs the best, 85% is a impressive specificity for any decision rule, especially if we are concerned about zapping kids brains with CT scans.

The 84% sensitivity of PECARN is a surprise, this is lower than we would have thought. Even more worrying is the fact that the updated NICE guidance has relaxed some of the criteria, so we are not CT’ing all of the children who are ‘CHALICE positive’. This is a concern, and it’s set me off searching for an explanation for this surprising under-performance. The first thing that catches the eye is those confidence intervals, which for the sensitivity results are pretty big. For CHALICE, the sensitivity is 84%, but the 95% CI is 60-97%. The authors themselves point out that as their cohort is far smaller than that of any of the derivation studies, we should be wary about making absolute conclusions. Could it merely be a lack of power that has resulted in CHALICE’s poor performance? That said, even the top end of the confidence interval, a sensitivity of 97%, may not be sufficient for our needs.

CHALICE ‘missed’ three patients, and the authors give us the information to look at. The first is a 17 year old who was hit by a rock. He was picked up by PECARN and CATCH with a severe headache, which CHALICE doesn’t include. Can’t argue with that one. The second was a 16 year old, who scored PECARN and CATCH positive with a GCS <15. He was not picked up by CHALICE, presumably as his GCS was 14 (CHALICE would CT at a GCS of <14). The third was a 15 yr old who fell 2.5 metres. This counts a significant mechanism in PECARN and CATCH, but not in CHALICE. Why not? Because CHALICE would CT after a fall of 3 metres. For me, those last two are pretty subjective, and easy to imagine that they could just have easily have been assessed as being CHALICE positive.

If you take a look at the PECARN decision rule – it has three final outcomes. A low risk, ‘CT not recommended’ group, a high risk ‘CT recommended group’ and also a moderate ‘observation vs CT’ group. The authors of this comparison treated both the moderate and high risk patients as ‘postive’. This gives PECARN an advantage when calculating its sensitivity, and may not reflect how the rule would be used in the real world, where some of those children categorised as moderate risk may have been missed.

I was tempted to cop out and call it a draw, but… Sorry Manchester, but the title has gone overseas. PECARN has taken it. While the specificity is not as good as some, they edge it with an impressive zero miss rate.  The sensitivity of PECARN may have gotten a boost from the way the authors applied the rule. In real life, we may not send every PECARN positive kid to CT, but we would be at least observing them. CHALICE may have had some bad luck with some decisions not going their way, but on the day, its the numbers that count. 


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When Sick Means Sick: Emesemantics and Vomiting in Kids

St Emlyns - Meducation in Virchester #FOAM

When I was preparing for my talk at smaccGOLD I contacted the wonderful Ross Fisher, a Paediatric Surgeon, to ask him for some tips; what did he wish all ED docs and GPs knew about paediatric surgical patients?

He was kind enough to provide me with a list of hints, tips and pearls of wisdom – but in his alter ego as presentation guru I know he will be the least disappointed of all when I admit that most of them didn’t make it into my talk. If you haven’t already grasped this, there is nothing in the world drier than a talk which consists of a list of facts.

BUT – I really wanted to share some of his wisdom and my daily #PaedsTips tweet on Saturday morning was a Paediatric EM truth I sometimes forget that junior doctors don’t appreciate.

Since this started an international twitter conversation, here’s a little bit of wisdom on vomiting in kids.


We have to take good histories; but the quality of the information they provide is at risk because we fail to understand that by the time we leave medical school we spend the majority of our working lives speaking a different language from our patients and carers. Sometimes vomiting in kids is of great significance. Most of the time, it isn’t.


Usually, parents mean yellow vomit – any vomitus that isn’t recognisable food (“It was just bile, doctor”). There’s a lay perception that “bile” means “stomach contents”.

Healthcare professionals mean bile, the cooked-spinach-green substance produced by the gallbladder.

Image courtesy of Spanakopita / Flickr

SPINACH! Image courtesy of Spanakopita / Flickr

Or, at least, that’s what they should mean. Worryingly, they are often confused about what constitutes bilious vomiting as this (free to access) study shows (thanks to Damian Roland and David King for flagging this one up). There’s another great free to access paper here, this time set in a neonatal unit not too far from Virchester and comparing healthcare professionals’ and parents’ interpretations of gastric aspirates, showing that pretty much any vomitus can be (mis)interpreted as bile-stained, depending on who is asked.

If you are in any doubt, here’s a handy colour chart: think “avocado” or “spinach” (via Chris Bidder).

In newborns and infants, bilious vomiting represents intestinal obstruction and is a surgical emergency. There are a variety of causes – duodenal atresia, midgut malrotation and volvulus, jejunoileal atresia, meconium ileus (which has its own subset of causes) and necrotising enterocolitis are a few. Most ED clinicians don’t need to know much detail about this other than that green vomitus in a neonate – with or without abdominal distension – warrants a paediatric (or neonatal) surgical review urgently. These babies are very sick (unwell) and may need access (IV or IO) with fluid replacement and NG placement (free drainage to reduce further vomiting). If you want to read more about bilious vomiting in neonates, there’s a nice open access review here.

Very occasionally a baby with intestinal obstruction will have yellow vomitus, but as they are sick-looking it is usually this combined with other clinical signs which prompts surgical referral, rather than the false reassurance of non-green vomitus.

After the neonatal period, volvulus and malrotation can still occur but bilious vomiting can also happen as part of a viral gastroenteritis. Differentiation can be made clinically; children with volvulus/malrotation are unwell and often in shock, with a taut, tender abdomen, and high pitched or absent bowel sounds.


Parents generally mean “vomit which came out with any sort of force, rather than just dribbling from the baby’s mouth.” Given that human beings have a vomiting reflex which invokes downward contraction of the diaphragm with contraction of the musculature of the abdominal wall and stomach itself, it’s not surprising that vomiting comes out with force at times. In fact, the very definition of the word vomit contains forceful adjectives. Parents often worry if children vomit in their sleep that they will choke on it; the vomiting reflex exists to prevent this from happening.

Projectile vomiting is unusually forceful and the vomitus travels a significant distance. Projectile vomiting of significance usually occurs without retching but there’s not actually a consensus definition of how projectile vomitus should be (or how far it should go) before it is considered pathologically projectile. This is where test feeds in ED come in – there are other signs which might be elicited in a baby with a history of vomiting, but vomitus reaching the end of the cot or more than the length of the child’s body is certainly unusual! 

Projectile vomiting can be a sign of congenital pyloric stenosis, a condition in which hypertrophy and hyperplasia of the pyloric muscle causes a gastric outflow obstruction. Vomiting is not bile stained (but may be yellow as milk curdles in the stomach), because bile cannot pass back into the stomach, just as no feed can pass out. Consequently these babies are hungry – starving – and gulp their feeds, only to vomit it back with plenty of force.

Presentation occurs usually in weeks 4-8 of life and there’s a recognised predominance in first-born male babies. In the early stages the baby may not appear unwell; just hungry and vomiting, often infrequently at first. As the condition progresses, vomiting becomes more predictable (after every meal) and parents often blame the milk and try alternative formula. As time passes the baby can become significantly dehydrated and malnourished, and the neonate with established pyloric stenosis will have a characteristic hypochloraemic hypokalaemic metabolic alkalosis from persistent vomiting of gastric HCl (while potassium is lost through exchange in the kidney as the body attempts to preserve hydrogen ions and correct the alkalosis).

As Casey points out, test feeding in the ED is one of our best diagnostic tools in babies who have not yet become critically unwell. Before the vomit, peristalsis may be visible and the textbook description is of a palpable olive-shaped mass in the right upper quadrant or epigastrium. The video below shows peristaltic waves; a more specific clinical sign than reported projectile vomiting.

There’s a nice clinical case here at Life in the Fast Lane.

And in older children? Well, it’s probably just vomit.

Coffee Grounds

Brown vomit, or sometimes vomit with bits in.

Vomit which looks like the black (or VERY dark brown), granular substance you tip out of your cafetiere in the morning when you’ve had your caffeine fix, you terribly middle class doctor, you! OK, I’m joking (and biased as a tea drinker), but consider the socio-economic balance of our patient population. I have certainly worked in areas where asking patients if the vomit was “avocado” coloured is not helpful; the same is true of coffee grounds.

The best image I could find actually comes from a simulation site, complete with simulated coffee ground vomitus recipe

Image from Healthysimulation.com

Image from Healthysimulation.com

Coffee ground vomitus (emesis) represents blood which has been in the upper GI tract (usually proximal to the duodenojejunal junction) for a little while – long enough to have had contact with gastric secretions.

With contact with gastric acid, the haem molecules in blood are oxidised, giving a dark brown/black appearance.

It’s often taken to represent an upper GI bleed but actually there are plenty of alternative causes of apparent coffee ground vomitus – in adults, this paper from 2012 describes including acute MI, urosepsis and small bowel obstruction presenting as “coffee ground vomiting”.

True upper gastrointestinal bleeding is rare in children. When it does occur it usually represents peptic ulcer disease or an alternative diagnosis (in which case the coffee grounds don’t represent altered blood anyway). Remember to consider button battery ingestion (rare but deadly) in children presenting with haematemesis.

And please – don’t use urine dipsticks in vomit to test for the presence of blood; as far as I can find there are no reliable test characteristics for the performance of urine dipsticks in this setting so interpretation of the result is pretty meaningless. If you’ve got a good paper which demonstrates otherwise, please get in touch!


So, now you’ve got your (hi)story straight…

We need to talk about managing simple vomiting in kids who don’t have any of these features. But that’s probably enough for now – next time…


This blog post was inspired by a twitter conversation and I therefore consider it crowd-sourced (including the title!): credit due to @ffolliett, @broomedocs, @nomadicgp, @rachrwlands, @kangaroobeach, @DrJHurley and, of course, @MDaware (#damnitseth)


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SMACC Gold: All Social Media, No Science?

St Emlyns - Meducation in Virchester #FOAM

It seems the whole medical world has gone all woolly and fluffy since Broadbeach was hit for six by #smaccGOLD. Everyone’s been so nice to each other, you can almost palpate the love. We’ve had stories of staff from the conference venue being perplexed at who we might be because we’re all such wonderful people. Having listened in open mouthed admiration to Vic Brazil we’ve bashed down all our tribal barriers so that the entire profession is now singing from the same hymn sheet. There wasn’t a dry eye in the house as Cliff Reid told 1,200 people how to ‘Resuscitate your neighbour as you would yourself’. Heck, this whole thing even made Simon Carley and me take to publicly singing – and that takes something, I can tell you. At journal club this week Simon and I were smiling at each other from opposite ends of the table – such is the love that #smaccGOLD has spread.

Feeling the love at #smaccGOLD

Feeling the love at #smaccGOLD

So, before everyone who wasn’t actually there dies of nausea, it’s probably about time for some hard facts for hard clinicians from a hard science guy. Well, here goes…

Before we start, let’s get one thing clear. #smaccGOLD was a totally unscientific conference. I mean, I tell my academic friends that I travelled across half the world to go to a conference on ‘social media’ and they look at me like I’m bonkers. It’s not the ACC, it’s not the ESC, it’s not even ICEM. Why did I bother? Look at the publication records of many of the speakers – there’s hardly a New England Journal paper between them and some speakers are completely untraceable in Pubmed. Heck, there were people who aren’t even Professors presenting in plenary sessions. And I met one typical #smaccGOLD chap at coffee who admitted that he doesn’t really go for all that “research stuff”.

By now, of course, you think I’m Emergency Medicine’s answer to Victor Meldrew. You probably think I should calm down. Of course, I don’t really think #smaccGOLD was a bad conference. On the contrary, it was totally flipping awesome. And there were actually lots of people who are international experts in their fields – Karim Brohi, Louise Cullen, Steve Smith, John Myburgh – I could go on and on. But what does a conference on ‘social media’ really have to offer to a serious academic? What scientific value can it possibly have?

Victor Meldrew

The key to this is understanding the essence of #smaccGOLD and, even more importantly, of #FOAMEd. Free, open access medical education is something we should all stand for. If we take Stephen Covey’s lesson and ‘begin with the end in mind’ then those of us who do research should ask ourselves why we are doing it in the first place. Of course, we do it because it’s fulfilling to find better ways of applying science to improve the health and wellbeing of our fellow man or woman. We don’t do it to make profits for large organisations – yet large organisations are clearly the Masters in the world of clinical research right now. That being so, #FOAMEd is a principle we all ought to buy into and we should each play our part in making it work.

That sounds pretty altruistic, right? But there are also some really selfish reasons why an academic should be at #SMACC. Publishing in top journals is, of course, essential. For now, all credible researchers need to do it. Let’s not kid ourselves that #FOAMEd is ready to take over, at least not yet. But journals will only reach a select audience with an interest in research (a minority of doctors). Blogs, micro-blogs, podcasts and forward thinking conferences like SMACC Gold (which celebrate the principle of edutainment, by which we learn while enjoying ourselves – crazy, eh?) are how most of us learn nowadays. And they can make the latest research totally accessible, getting it out there for people to start putting it into practice.

Take, for example, one of my most recent papers, which was on the sources of patient suffering in the ED and how suffering is more than just pain. This paper was published online first and went virtually unnoticed, which isn’t surprising. It’s not exactly the discovery of graphene and I don’t think I’m on the shortlist for any Nobel prizes. In fact it’s a very simple study. But then I blogged on it – and suddenly it attracted loads of attention – more attention than 97% of articles ever published in the EMJ, and it’s still not even out in print yet. That’s the power of social media.

SMACC Gold is all about that. It can take hard research and make it accessible. The beauty is in the branding. Just look at the artistic ability of Oli, Roger and their team. It’s all about presentation and making what’s presented palatable to the audience. Look at the presentations that we saw. There were very few plain slides with bullet points. Most speakers showed enticing pictures or single quotes on their slides. The visual stimulus was enough to draw the audience in and focus their attention on the speaker and the actual message. I’ve never been to a conference where there has been as much emphasis on making the content ‘taste nice’ for the audience.

That’s why SMACC Gold was so awesome. That, and the fact that we all actually enjoyed what we were doing. SMACC Gold reminded us that it’s so important to enjoy life. Take #FOAMaoke, for example. I’d heard about the #FOAMaoke before I got to Australia. In fact Nat never stops banging on about it. So much so that I spent my last night in Broadbeach in just about the seediest karaoke bar in the entire world. And, warm and fluffy as this conference is, they got me singing again. If you can call it singing.

This time it was #smaccCREEP – clearly I had a touch of Impostor Syndrome just like Nat. Have a listen to, and a laugh at, the piano version…


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JC: Paediatric Major Trauma Triage

St Emlyns - Meducation in Virchester #FOAM

There aren’t a lot of things in Emergency Medicine that are more important than managing paediatric major trauma.  St. Emlyn’s in Virchester is a Paediatric Major Trauma Centre, and it’s virtual catchment area is pretty massive.  That means we’re pretty used to the adrenaline surge that you get at 4am when the pager goes off with the words, “Major Trauma, Paediatric Emergency Department”.

Green Beacon

The green flashing light for late night on-call runs

Heart racing and hair all over the place, you throw on your scrubs, chuck the Starsky & Hutch flashing green light on top of the car and away you go into the night, saving a child’s life like a real life superhero.  You can imagine the frustration you feel when you arrive and the child is actually completely uninjured.  Of course, that sense of frustration is nothing compared to the emotional toll and inconvenience this will place on the child and their family, who may have been transported a long distance in the middle of the night for no purpose.

This is over-triage.  Under-triage is also a problem and occurs when the major trauma centre is not activated although the child does actually have major trauma.  In the UK our national PEM research network, PERUKI, set out to try and find out how big a problem this is with each of the triage tools that regional ambulance services are currently using.  This paper is hot off the press (online 1st) at the EMJ:

Screen Shot 2014-04-11 at 17.23.52


 They looked at retrospective data from 4 EDs, two of which were major trauma centres in what is basically a retrospective diagnostic cohort study.  They included children who sustained ‘injury and trauma’ and didn’t present by ambulance over an 18-month period up to June 2012.  They then collected data on 8 pre-hospital triage tools that are being used around the country (which were essentially the ‘diagnostic tests’).  The primary outcome was an ISS > 15.  

  They identified 2,934 patient records that met the inclusion criteria and had an ISS recorded.  4 of these patients had an ISS > 15.  The sensitivity of the triage tools varied from 0% (Paediatric Trauma Score) to 100% (the East Midlands, North West and Northern regional triage tools).  Specificity varied from 79% (for the North West tool) to 99% (Paediatric Trauma Score).  

The authors say that the scores with <95% sensitivity didn’t have acceptable sensitivity.  They thought that all 8 tools had acceptable specificity.  This meant that only the 3 scores with 100% sensitivity were considered acceptable.

 Well, here’s where sample size is so important.  2,934 patients sounds like a really big number, right?  You see that and you instinctively think it’s unlikely to be underpowered.  But they only had 4 patients with the primary outcome.  In a diagnostic study where you want to look at sensitivity, it’s actually the number of cases with the primary outcome that drives the power.  So, to examine sensitivity this study wasn’t actually well powered at all really – they only had 4 cases.  The triage tool that missed all 4 cases might have picked up most of the next 4,000 cases.  The confidence intervals are massive.   You can’t really draw meaningful conclusions about the comparison of sensitivity when there were only. 4 cases.  We need a larger number.

On the other hand, the statistical power for specificity is driven by the number of patients who don’t have the primary outcome.  There were 2,929 of them – so this study is likely to be well powered for that analysis.  So we can take something from the analysis of specificity.  Clearly, the triage tool used in Essex (specificity 93%, with 95% confidence intervals from 91% to 93%) has better specificity than the North West triage tool (79%, with 95% confidence intervals from 78 to 81%).  So we can tell from this that patients in the North West are more likely to be over-triaged than patients in Wessex.  No wonder the emergency physicians in Virchester (which is in north west England, btw) are tired. 

Well, there is one more thing to take from this.  Actually, among children who self-present to the ED, major trauma is very rare.  0.1% of patients who walk in to the ED with an injury will have an ISS > 15.  So major trauma centres need to focus most of their efforts on ambulance arrivals.  I’be not seen the data but I’d imagine that this is different in adults.  

 There’s unfortunately one really limiting factor about this study – and that’s the patient population included.  A diagnostic study should select the patient population in which a test would be applied in practice.  This study wanted to evaluate a pre-hospital triage tool for major trauma.  But they evaluated it in patients who did not present by ambulance?  By definition, that’s the population we wouldn’t apply the triage tool to – because the triage tools are for use in the pre-hospital environment – i.e. in the ambulance.  Are the patients who arrive by ambulance different to those who self present?  Well, yes.  And that’s actually the biggest problem with generalising the findings from this study.

 As with all studies you critically appraise, you tend to be able to pick holes when you look hard enough.  But there may still be things you can take away.  With this study, the key points are:

* Major trauma is vanishingly rare among self-presenting children

* The triage tools being used by paramedics across the country vary in their specificity.  The North West tool isn’t very specific and this may be something to focus on.  We need more work to decide whether it’s sufficiently sensitive.


Most importantly, however, this study has given us a chance to highlight some important critical appraisal issues, and it shows that PERUKI is starting to yield publications.  I think there will be many more to come, and I’m sure that having a national PEM research network will bring some absolutely huge benefits in the long run.  Congrats and keep going, PERUKI!  




The post JC: Paediatric Major Trauma Triage appeared first on St Emlyns.

Who’s That Girl? Impostor Syndrome at #SMACCGold

St Emlyns - Meducation in Virchester #FOAM

Picture courtesy of @mendyourhead - https://twitter.com/mendyourhead/status/328977580013277184/photo/1

Picture courtesy of @mendyourhead

I want to let you into a secret. I’m an impostor.


OK, that’s not quite true. I’m a 34-year-old (shock!) Emergency Medicine trainee with a penchant for karaoke and a passion for education, but I’m really not anybody special. I play the piano (badly) and can struggle through a basic conversation in French or German (even more badly), I have never achieved honours at university or prizes in my post-grad exams and my list of published articles in respected journals is… well, lacking.


So when I found myself sitting onstage, sweaty-palmed and tachycardic, waiting to talk to a packed roomful of people about paediatric EM at SMACC Gold one thought was overriding – “what am I doing here?!”


It wasn’t the first time that fortnight either. I headed to SMACC off the back of an incredible opportunity not only to teach EM trainees in Fiji but also to watch and learn from teaching sessions by my talented and passionate colleagues Nick & Iain – an opportunity which is infrequently afforded in the midst of ED service pressures. There is a lot you can learn from others’ teaching styles and their honest critique of yours. So there I was, having an amazing experience in Fiji and then in Broadbeach. Why on earth did I deserve that?

Breakfast in Fiji - tea and pancakes on the balcony

Breakfast in Fiji – tea and pancakes on the balcony


A potential answer is, I didn’t… But it’s the human tendency to obsessively analyse this perception that can be crippling. I promise you that what follows is not intended to be a self-pity party but my reflection on what makes SMACC so different from other conferences.


The impostor syndrome is well documented and is a little different from the occasional feeling that we are incredibly lucky to find ourselves where we are. This paper, published in 1978, described women who – despite having high achievement or academic excellence – maintain a belief that they are not intelligent and in fact that they have “fooled anyone who thinks otherwise”. The impostor syndrome does occur in men albeit to a lesser frequency and intensity; the great Joe Lex says, in his inspirational talk An Old Dog Learning New Tricks:


There’s been a dreadful mistake. They’re going to find out that I’m not really competent, I’m not really qualified to do this job. I will confess – I still feel this way about once a week.


Joe’s 45 Years on the Frontline talk now also includes the following quote I shared with him at SMACC2013 after I was struck by how his admission resonated with me:



We can feel like impostors regularly in our clinical practice, but as Joe says it tends to be in a low-level, infrequent way. To constantly feel like an impostor would be paralysing and we would struggle to treat our patients effectively.

Pretending not to be totally terrified

Pretending not to be totally terrified


But am I really an impostor? Having been  invited to speak at an International Conference somewhere along the line someone must think I’m good at something. And to be fair if you’ve met me in person you probably realise I don’t come across as lacking confidence – and I don’t have a problem with public speaking; I have an A-Level in Theatre Studies, am very much at home with a karaoke microphone and spoke at the CEM conference in 2013 on the role of social media in medical education with only about an hour’s worth of butterflies-in-the-stomach beforehand. But SMACC was different, and I know I was not alone in feeling an unprecedented weight of expectation. I know that at least four other speakers experienced similar feelings of performance anxiety although I won’t name them without their permission. The Game Face is an important mask we all need to wear at times.


At SMACC, the pressure to deliver an incredible talk was intense and I had felt it continuously for at least two weeks. It was also unspoken, and intrinsic in origin. There was no-one following me around, whispering in my ear that my talk had better be pretty bloody good, but I was unable to escape from that mindset. I’ve spent a lot of time since the conference trying to work out what made this talk – 20 minutes, in a concurrent session (so not even on the main stage) – such a huge deal for me.

SMACC Gold grilled my corn in many ways

SMACC Gold totally grilled my corn


I know that I hold in high esteem the quality of education delivered at SMACC (and I have an investment in preserving its quality). But more importantly, it’s about the people who attend SMACC; these are people who really, genuinely care about delivering the best in Emergency Medicine, Critical Care, Prehospital Care and Rural General Practice – many devote hours every week to generating FOAM blogs, podcasts and teaching resources – and because of this they are people whose opinions I really care about. They simply feel like family and I have a crazy urge to make them proud of me.


Where SMACC2013 was a little male-dominated and (in my opinion, not unfairly) criticised in places for feeling cliquey, SMACCGold was undoubtedly full of love. The unsolicited (and perfectly made to my exacting specification) cup of tea handed to me by Cliff Reid as I left the stage after my talk told me I shouldn’t have worried so much – I could be appreciated for my passion and contribution as much as the clinical and academic content of my talk. And even at the second meeting of the Fabulous Females of FOAM (not just for women – open to anyone feeling like an impostor, regardless of gender) the air was different – the meeting was never about man-hating but this time there was a palpable atmosphere of mutual encouragement, openness and appreciation.

I firmly believe that Impostor Syndrome is the reason the FFF needs to exist, and why women remain under-represented in the FOAM world. SMACC is filled with the great and the good; is the case really that none of us feels great or good enough to be counted among them but we’re too scared/proud/worried that we might be right to admit it openly?


If you saw me at SMACC you might have noticed I spent a lot of time in Amy Cuddy’s famous Power Pose – do watch her incredible TEDtalk on overcoming Impostor Syndrome if you have time. I practiced a great deal of self-talk and it did help. On the final concurrent of the final day of SMACC I stood up and talked for twenty minutes about Paediatric Emergencies. I can barely remember a single thing I said.


The wonderful, visionary, and incredibly hard-working Roger Harris

The wonderful, visionary, and incredibly hard-working Roger Harris

At heart, SMACC is just another conference – but it’s not just another conference. SMACC made me feel like an impostor, but it also made that completely ok. It wasn’t a hostile hotbed of arguments and determination to show speakers up but a meeting of friends and family and an incarnation of our daily struggles against disease, deprivation and death. And when we fight the good fight together we come to value the part we each play and learn that we are much stronger together than we can ever be on our own – and we find ourselves resolving to be the very best that we can be, impostors or not. So bring on SMACC US – I’ll be there, perfecting my power pose.


In heartfelt gratitude, to everyone who attended and tweeted about SMACC Gold; you made it what it was – thank you.


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