All posts by drgdh

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

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? ūüėČ ). 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!

[DDET Contenders…. ready! ]


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!


[DDET We’ve got three fine decision rules here, what kind of form are they in? ]

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.


[DDET So how’s this match shaping up? ]

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.


[DDET Leeeeeeeeeeeet’s get ready to rumble! ]

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.


[DDET Judges’ verdict]


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.


[DDET Let’s see the replay… ¬†What did CHALICE do wrong?]

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.


[DDET Last minute allegations of fight fixing! ]

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.


[DDET And the paediatric head injury CDR champion of the world is…..]

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.¬†


JC: The Trouble With Tonsils. St.Emlyn’s


If we’re preaching to the choir, why are they still singing the wrong tune?

If you are a up to date, #FOAMed positive practioner, I suspect you already have strong opinions on the matter of antibiotics for sore throat. There has been a wealth of research and blog posts and podcasts on this subject already. However this study from the BMJ caught my eye this week and I thought it warranted a look.

Screenshot 2013-11-27 11.27.47

This was a big (n=14610) prospectively collected cohort study.  Adult patients with acute sore throat were recruited from primary care in 6 cities in England and Wales. The aim here was to identify clinical features that could predict the suppurative complications of sore throat, specifically otitis media, sinusitis, quinsy and cellulitis. They also looked at two risk scores РCENTOR and FeverPAIN to see how they fared in predicting complications.


Complications are rare, like, really rare. Otitis media occurred in 0.52% of patients, cellulitis in 0.15%, sinusitis in 0.29%, and quinsy in 0.35%.

These are low numbers, and without going any further you will know that trying to predict such rare outcomes is going to be difficult.

Out of the clinical features assessed for, only two predicted complications with statistical significance:

Very bad earache: OR for bacterial complications: 3.02 (1.91. to 4.76), p <0.01

Severe tonisllar inflammation OR: 1.92 (1.28 to 2.89), p=<0.01

(As one of the complications was otitis media, the fact that severe earache was predictive comes as little surprise, I wonder if it would still have been significant if otitis media was excluded from the calculation….)

However, while the OR’s for complications were enough to reach statistical significance, these earache and severe tonsillitis were of limited use in predicting complications, with PPV’s of only 3.75% and 2.27% respectively.

The two tonsillitis score fared equally poorly at predicting complications. While specificity was reasonable at high cut offs for both FEVERpain and CENTOR, the PPV’s were terrible.

This is the result of applying a test with a reasonably high specificity to a rare condition; even though the specificity is high, the any positive results is likely to be a false positive due to the low prevalence of complications.

This illustrates the advantage of looking at PPV rather than specificity, the PPV takes into account the prevalence of our condition in the population. To use the classic example; this is comparable to using a d-dimer in a very low risk population (like our PERC -ve patients), any positive result is likely to be a false positive simply because the condition is so rare.

All of this sounds very clever, but somewhat of a moot point if predicting complications doesn’t change our practice. The authors looked at the rates of complications in those prescribed antibiotics, given a ‘delayed prescription’ and those who got no antibiotics. They found no difference; no reduction in incidence of quinsy, otitis media, cellulitis, or sinustitis.

This may come as little surprise to you, as accepted practice does seem to be changing to favour no antibiotics for treatment of sore throat. The updated Cochrane review did find a reduction in suppurative complications with antibiotic use, but the incidence of these complications was extremely low, consistent with what we see in this new article.

For a more in depth discussion of this, you should listen to the Smart EM podcast on the subject.

If not for reducing complications, why are we still giving out antibiotics?

62% of patients in this group recieved a prescription. So, if not to prevent these complications, why are we so attached to this practice? Remember that antibiotics have their own burden of adverse effects, from GI symptoms to anaphylaxis.

  • It’s ‘what we’ve always done’
  • Patient expectations? (although, those patients who want antibiotics may simply be after¬†pain and symptom relief)
  • Symptom relief? Having tonsillitis isn’t much fun, and trying to relive symptoms is a valid aim of treatment. Antibiotics may reduce the duration of symptoms (see the Cochrane review), but we do have other options for this (NSAIDs, steroids).
  • The non-suppurative complications, the most feared of which is rheumatic fever. This is an extremely rare complication, and preventing it is probably not a valid reason to treat with antibiotics, at least in developed countries.

The Smart EM podcast linked to above covers all of these points in exhaustive detail.

To sum up

  • This is a very large, observational study looking at adults with sore throats
  • These complications are extremely rare.
  • They found no clinical features that could predict suppurative complications of sore throat
  • The group that got antibiotics were just as likely to develop complications as those who did not.
Is this going to drastically change my practice? No, I’m already a staunch believer in ibuprofen and a single dose of dexamethasone anyway. That said, my practice might be different if I worked with a population where rheumatic fever is more common.
















PCI for OOHCA with NSTEMI post ROSC? An acronym too far?

So you’ve done it. In a dazzling display of medical prowess worthy of a medical TV drama you have restored the dead to life!


With scrupulous airway management, high quality chest compressions (assisted by¬†some waveform capnography, of course), careful administration of adrenaline boluses (I know, I know) and liberal application of Direct Current, your Out Of Hospital Cardiac Arrest (OOHCA) patient now has a pulse. Good job! You’re feeling pretty good about yourself aren’t you?

So what happens now? Your going to cool ’em down right? Get those cold fluids going (if you haven’t already…), pack that patient in ice. Cause you know therapeutic hypothermia is totally great.


You haven’t really fixed the problem have you? You’ve been hard at work managing the cardiac arrest and its aftermath, but this person’s heart didn’t just go and stop for no reason did it?

Unless there’s a really obvious cause here, the chances are your patient has had a heart attack.

¬†So lets get cracking! Pour some aspirin down that NG tube and start some heparin, cause that’s how we treat our ACS patient right?


What about our STEMI patients? In regular patients, the sight of that magic ST-Elevation (STE) in adjacent leads means a rapid trip to the cath lab for the friendly cardiologists to unblock whatever lesion lies beneath. Because we know this works  for our normal, every day, heart still beating kind of STEMI, we have extrapolated this to our OOHCA patients, and we probably all would send patients who had STEMI post ROSC to the lab (with cooling in progress of course!).

Retrospective analysis tends to agree. STEMI predicts lesions on PCI and successful PCI is associated with better outcome.

[learn_more caption=”Before we get too carried away…”] Due to the nature of our study population (patients suddenly who get as poorly as it is a possible to be without warning) randomised trials are hard to do, and the evidence is mostly observational. This means that we have to be very careful when assuming any causative link between the interventions and outcomes. So for the rest of the post, whenever I say “PCI is associated with better outcomes” what I really mean is “being in the group of patients whom were selected to go for PCI is associated with better outcomes”. Further more, the outcomes measured are often what we would consider ‘soft’ outcomes. Many of the papers use ‘acute coronary lesion’ or ‘evidence of recent coronary occlusion’ as an outcome. We then assume that this is a lesion that PCI can treat, and then assume that doing so helps the patient. A lot of assumptions there. Please don’t think I am criticising any of the excellent work I am about to reference, but merely illustrating the limitations of doing research in this population[/learn_more]

So far, so good.

But are we doing enough? It’s fair to say that if your ACS was serious enough to actually stop your heart, then it was a pretty major event. Is is really fair to lump all of the OOHCA NSTEMI patients in with the regular “I’m fine but my 12 hour trop is slightly raised” NSTEMI’s? Could any more of the OOHCA patients benefit from a trip to the cath lab?

The evidence from OOHCA patients suggsts that using STEMI as the sole criteria for post ROSC reperfusion therapy may not be adequate.

Dumas et al published a major paper on this subject in 2010. In a cohort of 435 patients (OOHCA with no obvious non cardiac cause) they found that 58% of patients with no STEMI had an acute coronary artery lesion, with a successful PCI in 26%. They worked out that using STEMI as the test for acute coronary lesions gave a PPV of 0.96 (great!), but a NPV of 0.42 (not so great). A paper by Zannutuni et al this year found similar results, with a PPV of 0.85, but a NPV of 0.67.

A successful PCI may be beneficial to these patients. The Dumas paper also found that a successful PCI was associated with survival, even in those without ST elevation (47% survival with successful PCI versus 31% without, P = 0.001). Hollenbeck et al published this year on this subject, and found that PCI was associated with survival to discharge in OOHCA without STEMI: 65.6% versus 48.6% (p = 0.017).

Remember of course, as we discussed above, that ‘PCI was associated with’ really means ‘being in the group that got PCI is associated with’. The observational nature of these trials means we should not attribute causation to any one intervention, no matter how tempting it might be.

It’s worth noting that both the Dumas and Zannutuni cohorts both had a high rate of VF/VT arrests, 68% and 77% of patients¬†respectively, and the Hollenbeck trial included VF/VT arrests only.

So it seems that by using STEMI as our sole criterion here we may be denying some patients a beneficial treatment, at least in those who present in a shockable rhythm.

What do our guidelines say? The UK Resuscitation Council ALS guidance does suggest that some patients without STEMI may benefit from PCI:

“(PCI) should be considered in all post-cardiac-arrest patients who are suspected of having coronary¬†artery disease as the cause of their arrest”¬†¬†(page 77)

So encouraging, but not very specific. What we need are some pointers, some features that suggest the patient in front of us may benefit from going for PCI. What kind of things should we be looking at?

[learn_more caption=”Rhythm?”] The trials we discussed above including mainly patietns presenting in VF or VT. So it would seem reasable to suggest that in these patients, there may be a culprit lesion that the cardiologists can treat. This idea is further supported by work by Sideris et al, who retrospectively reviewed 165 OOHCA patients (50% VF/VT), who had no obvious non-cardiac cause. They were looking for features that predicted acute MI (as defined on angiography, 36% of patients). They found that presenting in VF predicted MI, with an odds ratio of 7.4 for MI, and presenting in asystole made it much less likely, with an OR or 0.17.[/learn_more]

[learn_more caption=”Symptoms?”] What about the whole ‘taking a history’ thing. Seems a little quaint when we’ve got all this high tech stuff going on right? Often neglected in these patients I think, but can yield some valuble information. I’m thinking about the patient who complained of a crushing chest pain, before keeling over in a VF arrest. Surely he’s having an MI, even if there is no STEMI on the ECG? Can we send him for PCI? Well maybe. Spaulding et al did some of the seminal work in this area. They looked at 84 OOHCA patients, with no obvious non cardiac cause. 83% were VF/VT arrests, and 48% had evidence of coronary occlusion on angiography. In amongst their findings they found that a pre-arrest complaint of chest pain was predictive of acute coronary occlusion – to the tune of an OR of 4.0.[/learn_more]

[learn_more caption=”ECG changes?”] Finally, can the post arrest ECG be used to identify those patietns for PCI? We know about the STEMI patients, but what about the LBBB’s , or the ST depressions or T wave inversions? This is more difficult to tease out, as many patients will have ECG changes as a result of the cardiac arrest that are not due to an underlying MI, and these changes may be temporary. The study by Sideris et al mentioned above attempted to define a set of ECG criteria to predict the need for PCI. In their 165 patient cohort thewy found that using ST elevation alone as a predicotor of MI had a PPV of 76% and a NPV 92%. Not too bad, but still missing some patients. They looked at a few different ECG criteria and came up with this: ST elevation or depression and/or LBBB and/or non specific QRS widening. Using these criteria they found a PPV of 52%, but a NPV of 100%. So no patients missed, but lots of unnesscary angiograms. In real terms, using this criteria meant taking another 7 patients to the lab to find one MI. Worth it? Sounds like it, assuming (there’s that word again…) that finding that lesion is beneficial to the patient.[/learn_more]

[learn_more caption=”Cardiogenic Shock?”] This is a little tricky. We know that a significant number of patients will develop cardiogenic shock after ROSC. The well known SHOCK trial suggests that angiography/angioplasty is beneficial in patients suffering from cardiogenic shock who have not arrested. The confounding factor here is the idea of cardiac ‘stunning’. This is a cardiac dysfunction that occurs quite commonly post ROSC, but often resolves without intervention. Laurent et al found that 49% of post arrest patients developed myocardial dysfunction within hours of ROSC. However, this spontaneously improved over the next 24-72 hours. This suggests to me that cardiovascular instability can’t be used as a predictor of the need for early PCI, at least not without another suggestive feature.[/learn_more]

And breathe….

This has turned into a little bit of an epic….

To sum up:

It appears from what observational evidence we have that there is a group of OOHCA patients who will benefit from emergent angiography/angioplasty/stenting even if they do not have STEMI on their post ROSC ECG.

I think the evidence kind of backs up what we felt already.¬†Personally I’m going to be calling the cardiologist if my patient:

Has had a VF/VT arrest without an obvious non-cardiac cause


Has complained of cardiac chest pain before the arrest


Of course, what the cardiologist decides to do is another matter, but at least now I can back up my arguments.

Would be interested to know if anyone out there works with a PCI protocol that includes post-arrest NSTEMI patients, let me know!

Cheers y’all


A Snake in the Grass at St.Emlyn’s

While not fortunate enough to actually attend SMACC 2013, I was pleased to catch the much anticipated SimWars event, particularly as Team GB was one of the successful finalists. As we kind of expected,¬†they were presented with a patient who had sustained a snake¬†bite, something maybe a little outside of a British team’s experience. None the less, thanks to the sound application of resuscitation principles (and some critical pressure bandaging by¬†Dr May….) the Brits won the day.

*No sign of the SimWars video featuring TeamGB’s victory online yet…. a case of publication bias? ūüėČ Thanks to Dr May for the pic.

 But why a snakebite for the UK team? All of the scenarios were (I think) chosen to be a little out of the comfort zone for each team, but why the assumption that a British team would be confounded by a patient bitten by a venomous reptile?

To be fair, our green and pleasant land lacks the exotic fauna seen in the Australian countryside, such as  this cuddly critter here:

Spiders don’t normally bother me, but I’m very pleased this chap lives 10000 miles away…..

We are however, not completely bereft of poisonous creepy crawlies…..

Meet Vipera berus, more commonly referred to as the common European adder, or just the Adder.

As our only venomous snake, seeing patients bitten by an Adder will probably be a UK docs only exposure to a significant envenomation. We have had two cases recently, which provoked much frantic TOXBASE checking….. ¬†St Emlyns to the rescue!

About 100 patients a year present after being bitten by an Adder. Mortality is rare but not unheard of. It does little for my sense of pride in the Great British public to learn that about half of Adder bites occur after some bright spark decides to try and pick the damn thing up…..

Most Adder bites occur in the summer months, when the snakes are most active. They are timid rather than aggressive and most bites occur when they are disturbed or threatened. The bites are extremely painful, but very rarely life threatening. Many (around 70%) are ‘dry’ bites, where no envenomation occurs. Case reports (1) suggest that patients who are well, and asymptomatic at 4 hours after the bite can be considered for discharge.

If adder venom gets into your wound however, significant morbidity can occur, and recovery can take up to a year.

Local envenomation

Bites are extremely painful, and pain is followed by parasesthesia and swelling that spreads proximally. The spreading swelling and erythema looks like cellulitis, complete with swollen lymph nodes and lymphangitic lines, but the spread occurs much more rapidly. This local inflammation can, rarely, progress to compartment syndrome and/or necrosis.

Treatment involves immobilising the limb in a splint or sling (but, alas, no pressure bandaging this time). Tourniquets, ligatures or cutting into or sucking on the wound are (thankfully) not recommended.

Generous analgesia will of course be needed. The patient will need observation to ensure the swelling is not rapidly progressing or becoming severe. Some cases of local envenomation will need antivenom treatment (see below).

Don’t forget good wound care, thoroughly evaluate and clean the wound, look for foreign bodies (tooth fragments have been reported), and consider your patient’s tetanus status.

The vast majority of bites will involve a local reaction only. Rarely, there is a systemic reaction to the bite which is potentially fatal.

Systemic envenomation

Some patients when bitten, experience a rapid onset of anaphylactoid symptoms within minutes. Shock may be profound, and airway threatening angio-oedema can occur. Multi-organ failure can occur, and the potential for coagulopathy means heparin is contraindicated in these patients.

These patients get all the usual anaphylaxis stuff, airway and cardiovascular support as required, and of course, the antivenom.



If you work in the UK, there should be antivenom for Vipera berus in your hospital somewhere (at least that is what CEM recommends¬†(2)). Antivenom is used to reduce morbidity and mortality after bites from venomous creatures. What evidence we have suggests that this is true for Vipera berus. It seems logical, especially in a sick patient, to make the decision and give the antivenom as soon as possible. There is some animal data to support this¬†(3), so if you’re going to give it, don’t muck about…






The antivenom is given as an IV infusion Рone 10ml vial diluted in 500mls saline (or 5ml/kg  salinefor kids), over 30min. The 10ml dose is the same for adults and kids. This dose can be repeated after 1-2 hours if the patient remains unwell. In severe reactions, such as shock or full blown anaphylaxis, the recommendation is to give two 10ml vials straight away*.

Reactions to antivenom are common, like, really common. About 10% of patients will have an anaphylactoid reaction to the antivenom, so have the adrenaline, steroids and antihistamine ready. There doesn’t seem to be any point in giving a ‘test’ dose to predict who’s going to have the nasty reactions.

This paper from the BMJ (4) suggests that giving a small dose of adrenaline before the antivenom may reduce the incidence of reactions, and comes out with a pretty good NNT of 3. This article (5) also supports the idea, suggesting that pre-treating with adrenaline reduces adverse reactions. The snakes in these studies were of a more tropical nature than our Adder, but it sounds like a pretty good idea none the less.

To sum up…..

Even in the UK, significant envenomations from snake bites can occur and we should be prepared to manage them.

The majority are local reactions, and immobilisation and supportive treatment is all that is necessary.

Rarely, significant anaphylactoid reactions can occur, these need managing as any other anaphylaxis.

Antivenom is indicated in any systemic envenomation, and in severe local relations

Antivenom itself has a high chance of causing an anaphylactoid reaction, so be ready!

Cheers y’all,


Want more slithering, serpentine FOAMed? Try this PK from the Broome Docs gang, essential viewing for those of you are planning to work down under. (Ed – featuring Laura Smith who is a St.Emlyn’s and Virchester alumnus)

This BMJ article (6) covers Adder bites pretty well, and seems to mirror the UK poisons information advice.

*The doses and method of administration for the antivenom given above were taken from the UK National Poisons Information Service Website (TOXBASE) on the 17/08/2013. Obviously, you should check these facts yourself before using the doses given here. Neither I or anyone else associated with St Emlyns can take any responsibility etc…..

[learn_more caption=”References”]

1. Emergency treatment of adder bites: case reports and literature review. Arch Emerg Med. 1993 September; 10(3): 239‚Äď243

2. College of Emergency Medicine Guideline on Antidote Availability for Emergency Departments May 2008. Available on CEM website

3. Karlson-Stiber C, Persson H. Antivenom treatment in Vipera berus envenoming–report of 30 cases. J Intern Med. 1994 Jan;235(1):57-61.

4. Premawardhena AP, de Silva CE, Fonseka MM, Gunatilake SB, de Silva HJ. Low dose subcutaneous adrenaline to prevent acute adverse reactions to antivenom serum in people bitten by snakes: randomised, placebo controlled trial. BMJ. 1999 Apr 17;318(7190):1041-3.

5. Williams DJ, Jensen SD, Nimorakiotakis B, M√ľller R, Winkel KD.¬† Antivenom use, premedication and early adverse reactions in the management of snake bites in rural Papua New Guinea. Toxicon. 2007 May;49(6):780-92. Epub 2006 Dec 2.

6. Warrell DA. Treatment of bites by adders and exotic venomous snakes. BMJ 2005;331:1244


Review: The Essence of Emergency Medicine

It was  a long day. After getting home from a late shift the night before, I was up at 4 to catch my 0530 train, and toddled off down to London. What, you may ask could be worth all that?



I spent the day at the Essence of EM course, run by Cliff Reid, one of the most well known faces of #FOAMed and EM internationally. As if that wasn’t enough, the rest of the faculty were made up of highly experiences EM and ICM doctors, including Dr Louisa Chan (consultant ICM/EM), Phil Hyde (Consultant PICU), and Dr Mike Clancy, until recently president of the College of Emergency Medicine.

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So what was on the agenda for the day? The latest EM literature? Some cutting edge new technique that has twitter all in a flap? No. While clearly a man of many talents, Cliff is best known in the #FOAMed world for speaking on the human factors that affect us every day in EM. These ideas and concepts are as vital as any clinical skills and knowledge, yet are notoriously difficult to teach and assess in today’s world of tick box assessments. Anyone who has heard Cliff speak¬†will know how good he is at getting these ideas across, and will understand why I jumped at the chance to hear him talk ¬†in person.


Story Time

Cliff and his colleagues told us their stories. Some were funny, some were inspiring, some tragic and deeply personal. These weren’t “see how awesome I am” stories. These were stories of the events that had inspired them, or mistakes they have made.



“How could I have done something so dumb?” – Cliff Reid

Hearing such experienced people discuss their mistakes openly and honestly prompted the candidates to open up about the events that have affected them.¬†After all, we learn very little when we get things right. We learn when we screw up, or when a colleague leaves us for dust; that’s when we’re inspired to be better.

The theme of learning from errors and incidents ran through the day. Mike Clancy led a discussion on dealing with a colleague’s error. Presented as an opportunity for improvement, an error is the most valuable learning tool we have – provided we are committed to changing your practice, or the system, to ensure it doesn’t happen again.

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What kind of Emergency Physician do you want to be?

This leads us on to the second theme running through the day. This question was asked of us right at the start. The phrase ‘taking responsibility’ once a constant refrain. Take responsibility for your patients! Do all you can for them, don’t just move them on to become someone else’s problem. If the system you work in is preventing you delivering the best care possible, then take responsibility, change that system. If the patient in front of you needs a lifesaving procedure – ¬†then step up.

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Put your patients first, don’t abdicate responsibility to other specialities if you feel patient care will be compromised. Learn to communicate with your colleagues and advocate for your patient. Don’t abdicate responsibility to the bureaucracy; there may be a four hour wait in minors, but the unwell patient in front of you should be your priority.

To hear Cliff and his colleagues talk like this is music to the ears of UK EP’s currently struggling through a difficult time in the speciality. I think many of us feel that the pressures heaped upon us are compromising our ability to look after our patients, and that the high level, patient focused kind of care that Cliff promotes is not feasible in a world of breaches and under staffed rotas. I found it inspiring to here those eminent in our speciality discussing these concepts, and to see that the majority of attendees on the day were consultants who will take these ideas home to their department.

We all had a great day, and I can only thank Cliff for his time and dedication (plus I think I owe him a pint). Should you get the chance to attend this course in the future, I can not recommend it too highly.


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Well earned drinks afterwards! Left to right: Mike Eddie, Duncan Roche, Louisa Chan, Cliff Reid, Reuben Griscti, Bijou Cherian, Richard Browne