The POP, the chief, his risk assessment and her thrombprophylaxis…

So, we’ve already talked about this. But changing times call for changing posts. And we want to know what you think…

A 30 year old comes in 10 days after being put in an equinus POP for an Achilles rupture. His leg hurts more now than ever. You split the pop – swollen to mid thigh. Whole leg CUS shows a popliteal thrombus. Oh dear. 3 months of warfarin for you, my boy.

The next one out of the box is a 29 year old mother of 2 with a similar injury. She is on the combined oral contraceptive pill but otherwise has no risk factors for VTE. You ask for an equinus cast. She is half way out the door.  But then you stop to think. And you scratch your chin. And you ponder…

Thromoboprophylaxis for ambulatory limb trauma is not a new idea. The French and Germans have been interested in this for ages. There are individual centres in the UK that have tried to tackle the problem head on (and also provide nice slides to say how – good FOAMed even prior to its inception!).  Both NICE and ACCP recognise the issue, but fall short of digging into it based on potential issues with the evidence (see below for the NICE effort). Some people even think it’s not a problem. But we keep seeing harsh lessons in both the media and medical literature. So we need to ask ourselves – how can we manage this issue in an evidence based way?

There is actually a lot of evidence for perusal, including several systematic reviews and a well conducted meta-analysis. As well as this, there are loads of studies from different countries looking at incidence and reiterating the issue: a certain proportion of ambulatory trauma patients discharged in POPs, wherever they are, whoever they are and whatever their injury, will develop VTE. As a global specialty, we should be on top of this.

One of the difficulties with the evidence is trying to segregate the data that applies directly to our patients from the mass of heterogeneous papers looking at post-op patients. I would suggest the evidence is already there to support extended prophylaxis in the majority of patients who have had orthopaedic surgery. What I want to know is: does the plaster on its own warrant prophylaxis?

I think it does. Along with some Virchester colleagues I have recently had the pleasure of reviewing all the evidence and attempting to provide a pragmatic appraisal and translate this into a workable guideline. The result is a 2 page clinical decision support tool (And a lot of additional light reading) recently endorsed  by the UK College of Emergency Medicine – it is front page news at the moment but will be easily found in the guidelines section when the buzz dies down.

Some people have worried about potential morbidity from use of prophylactic anticoagulation. I think the evidence suggests that low molecular weight heparin (LMWH) in prophylactic dose is actually fairly harmless to the majority of these punters, provided you use it properly. And I think any DVT (including distal/calf) is something to be avoided. The risks of untreated thrombi include propagation, embolization, post thrombotic syndrome, symptomatic progression and impaired fracture healing. I’ll take a few weeks of LMWH over that lot any day thank you very much.

Does everyone need it? – probably not. There is good evidence to suggest that low risk punters (those with minor injuries/no fracture/no POP/no additional risks for VTE) will probably have a low chance of subsequent VTE.  But the main thing we wanted to try and change with this guideline is the thought process. Think #/POP?  – think risk assessment for VTE. You’ll be amazed how many 25 year old women say yes to the COCP/Smoking/FH/Long haul travel next week if you take the time to ask them about it properly.

Where next? I know the Dutch are currently in the throes of evaluating Nadroparin in a large sample size for this very indication. I know people demand and expect a higher level of evidence prior to establishing as routine what may involve a significant cost and a degree (likely very small) of morbidity. I personally also think the new oral anticoagulants (NOACs) might have a role to play here. Anyone keen for an international multicentre trial should get in touch – we could knock that out in no time with the right support and funding.

But until this evidence comes, I think there is enough overall to warrant strong consideration on an individual basis. I personally don’t need to see a flawless systematic review to make me think a treatment may benefit my patient. I need to see face validity, a reasonable level of evidence of benefit and a reasonable level of evidence suggesting little harm from the intervention.

Have a read and see what you think. Very very interested to know your opinions and happy to field any queries anyone might have.

And remember – POP in the ED? Think VTE. Don’t let your patient end up RIP. Like the Notorious BIG. Or Eazy E. Or Heavy D. Or ODB.

But not Warren G.

Fo’ real.

Dan

You Snooze, You Ooze: Anticoagulation and Minor Head Injury

Image

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

Image

 

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

 

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

 

Rick Body

You Snooze, You Ooze: Anticoagulation and Minor Head Injury

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

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

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

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

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

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

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

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

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

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

Rick Body

Are they laughing at me?

As the world becomes smaller and our populations more multicultural (Yes I am a “Lefty” Mr Burley)… so communication in our emergency departments becomes even more crucial.

Last week whilst working in the UK, I was involved in the care of a young refugee from Eastern Europe who had not a word of English at her disposal. I’m sure everyone has had a consultation where very little in the way of effective communication has taken place – you try charades, signing, talking loudly and clearly in English and smiles…. But in the end, all that time you put in to learning history taking skills at university  – useless.

Now, in the ED we are used to a lack of information…. (Indeed I think if I have more than 70% of information on which to base a decision I fall into a apoplexy of indecision)…and that is OK; if you know that’s all you’ve got. But it becomes incredibly frustrating when you want to do the best you can for a vulnerable patient and you know your missing vital information because you just can’t get the message through a language barrier.

Back to the patient…There are not many people who can effectively communicate in Baltic state languages in our department so I attempted (for the first time) using “Language Line”. For those that don’t know – this is a telephone service that allows you to contact a translator for any language in the world (except perhaps some dialects in the North-east of the UK!). Once you have you have your translator you then spend an incredibly long time passing the phone between yourself and the patient whilst the person on the other end translates ever more personal information (all in complete confidence – so we are told – and with patient consent).

This is great, a revolution. Instant understanding. Verbatim translation…..Except… those moments when – and you’ve no doubt know it – the patient and translator have an incredibly long conversation and perhaps share a laugh…… and you get a classic one word translation in response.

You wonder… What were they talking about? Were they laughing at me? Have I got some food left around my mouth? And you start to get a bit uncomfortable….

Probably more important you think –  have I missed something?

So, the translator and the patient have a rapport, they share a laugh (perhaps at my expense) but you get a history to write down and everyone’s happy…. Except the real history is often hidden in the nuance of communication – the way something is said, the unspoken words, the carefully selected words, the language.

And we do miss vital information….

A very interesting paper from South Africa by Penn et al. has attempted to characterise the information we miss in translation. But, hold onto your hats it’s Qualitative Research.

From the outset I will say that its not specific to the ED, but the findings are interesting and can be related to translation of all sorts.

What the authors did was record healthcare interviews performed “pas de trois” (their French term not mine), i.e. doctor-patient-translator. Using the interview transcripts they have then decided selected what they term “asides” – times when the translator and patient communicated between themselves and not involved the doctor. They have then taken these asides and classified them as “big talk” (topics like patient beliefs about illness, relationship issues, disclosure issues) or “small talk” (topics such as transport, weather, clarification requests).

Asides were rarely translated for the doctor (even when directly asked)…. And here’s the thing – these nuanced conversation pieces were judged to contained vital health related cues that were never triggered by the doctor in the rest of the consultation. For example, in one consultation a patient discloses information  regarding who has knowledge of her HIV status – and the fact that a partner might not know, which was never relayed to the doctor.

These were issues that gave insight into the patient’s true agenda but weren’t brought out in direct conversation only these non-interpreted “asides”. The treating doctor was left none-the-wiser. Being qualitative there are no hard outcome measures – just developing of these themes…however, this is all interesting stuff because it gives us 2 useful insights:

  1. That we must beware of the translated consultation – we are missing the point!!
  2. History taking (even in your mother tongue) is more than just about asking textbook questions – patients are constantly giving us social cues and clinically important information from each and every aside…. We had better be listen carefully.

So next time you’re in a translated consultation and the patient and translator laugh at you… They probably are laughing at you… But be sure to ask why…

@tombartram

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 Blatchford Score 2 – The case for an RCT!

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

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

Methodology of the Lancet study

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

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

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

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

Overall impact on resource utilisation

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

What’s a Service Evaluation?

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

The bottom line for clinical practice

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

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.