Category Archives: Clinical Guidelines

NICE guidance

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

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

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.


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.


NICE faces the sickle

New guidance out on sickle disease from NICE in the BMJ

I must admit to having a bit of an interest in sickle cell disease and the ED. There are two reasons for this.

Firstly, and most importantly, it is a really important disease to manage well. It’s a proper disease that we have learnt about since the very first weeks of med school, one for which the pathology, pathophysiology and treatment is well described and understood.

Secondly, I am constantly intrigued to see new docs arrive in the ED with preconceptions about the disease and it’s sufferers that I cannot understand or explain.
So, back to basics. Sickle cell anaemia is a ‘proper disease’, it can kill you, and shortens your life expectancy which is bad, very bad indeed. Living with sickle disease can be tough and patients suffer painful vaso-occlusive crises that may require them to come to our EDs for help. If you work in a multi-ethnic practice like Virchester then you will meet many patients with Sickle disease so it’s important that we understand how to help them. In our ED that means that we have a really good working relationship with our haematologists and in particular a specialist nurse in sickle disease who knows our local population really well and who has encouraged the development of personalised treatment plans. These are shared with the ED (the pink file), the patients, and with the haematology team. If not then we have a great pathway for the treatment of ‘unknown’ patients with sickle disease. It’s safe, evidence based and it works. Many of our local patients manage their disease very well at home and only come to see us when home management has failed. With few exceptions they only come to us when they really need help.

So, in Virchester everything is rosy. Except it’s not because I still occasionally come up against ideas which I find difficult to explain and understand, and this is almost always around the use of analgesia in vaso-occlusive crises.

So, let’s think about analgesia. In many ways I think that sickle disease is the poster boy for good analgesia management in the ED. Get this right and you probably have an ED that manages most pain well (there is a poster girl as well – but that’s for another day).

Why is it the poster boy? Well, because the management of sickle disease is one where analgesia is a cornerstone of management, where there are few physical signs, but where I see clinicians manage patients in very different ways. Such variation is not just an issue in my practice, but also in past studies and papers where the experiences of patients attending EDs is far from optimal. Take this quote from a 1999 paper in the BMJ

“The experiences of patients with sickle cell disease of hospital care are characterised by mistrust, stigmatisation, control, and neglect”

Now that was a long time ago (1999) and I like think we have made fantastic progress locally, but I am not convinced that this is the case everywhere because I still see suspicion and concern amongst some junior docs rotating in from St Elsewhere. Why is this I wonder? Where and how did they learn it? Why is it that we have a disease that causes pain, suffering, shortens lives but for which I sometimes see docs and nurses ‘not believe’ that the patient is genuinely in pain and as a result their analgesic management is suboptimal.

Why then? Is it the disease itself? Well perhaps as there are often few physical signs in sickle disease that ‘justify’ the pain to the physician. There is no bleeding, deformity and often few physiological signs. I hear odd comments such as ‘nobody in that much pain has a pulse less than 110’……! Really, do you want me to demonstrate whilst I take your pulse….? Until we have a pain-ometer that can quantify pain then we have to presume that the patient is telling the truth unless we know otherwise. In law we are innocent until proven guilty and the same should apply here. Similarly, on a general approach to pain then we must decide whether analgesia is something that we should freely offer, or should it be something that is earned? What do I mean by this? Well, its that I believe that analgesia is one of the most important things that we can do to improve the patient experience of illness and injury. We should be seeking out pain and treating it, not waiting for our patients to beg for it to be taken away.

This cannot be right and we cannot accept it, but how can we make it better.

I would suggest the following.

  • 1. Speak to your local haematologists and devise a protocol for the management of sickle pain. Why not use something like that advised by NICE and abstracted in this weeks BMJ
  • 2. Use sickle as a teaching tool for analgesia. Ask your colleagues about their attitudes towards sickle disease and the patients. Challenge, argue and question any attitudes that trouble you.
  • 3. Role model the care of sickle patients in the ED. As a senior these are great cases to see with a junior doc. Great for the patient as they get great care. Great for you as it tells you a lot about their attitude towards the disease and analgesia in general. Ask them how they ‘measure pain’, you might be surprised at the results…
  • 4. Talk to your local haematologists. Establish a mechanism for them to tell you about difficult or complex patients.
  • 5. Train the whole team. Analgesia is something often prescribed by docs but prioritised by the nurses. If you only train one of the tribes then you will fail.
  • 6. Listen to Dr Gentile.

When the patient is comfortable ask them what they felt about their experiences in your ED. It’s highly unlikely that this will be their first attendance at the ED. Ask them how you did, ask them about good and bad experiences in the past. In general they will tell you.

Lastly, another plug for the unbelievably fantastic podcast from Dr Gentile on pain management in the ED. Whilst not strictly about sickle disease you just know that if you did have sickle disease (or anything else painful) you would want Dr Gentile to look after you.

I am told that my posts might be too thought provoking where some people just want the answers. I think not. I’d rather write about things that we all find challenging. Where there are answers we can give them, but so much of our practice is dependent not just on the evidence but also on ourselves. We should never stop questioning the evidence, we should never stop questioning ourselves.


Simon C

PS. This is our current management protocol for ‘unknown’ sickle patients. Time for a review I think, but even so this works pretty well at the moment. Advice on changes welcome.



Children bump their heads. A lot. (This article was first posted on the excellent DrGdH blog, make sure you pay it a visit – EMManchester – Ed)               Maybe they’re small, and just getting … Continue reading

Should POPs be mixed with Heparin?

We published an interesting BET in the EMJ earlier (open access version here) this year about the use of low molecular weight heparin for patients placed in below knee POPs in the ED. This is particularly pertinent to me as I have been unlucky enough to deal with several really nasty cases in the last few years.

Standby phone goes…….Young cardiac arrest on the way in…….as the doors to resus open you see the POP on the leg….and you know this is going to end badly.

Some of the conversations with the spouses and children of patients who have died young are memorable for all the wrong reasons.

So, there is no great surprise that the cause of death is inevitably massive PE, and this is where it gets interesting as we assume that this is a preventable death. If only they had been given prophylaxis then surely this would not have happened. Well, perhaps not as the event rate is low and heparin is not without it’s own complications, so what is the evidence?

Well, my colleagues Dan Horner and Cath Roberts found a pretty good systematic review on the subject that came to an interesting conclusion. The NNT for prevention of DVT is 14. Crikey, 14 people treated to prevent one DVT is a shocker to me as that reduction is a result of a big change on a very high event rate (>18% incidence of DVT in the placebo group)….but it’s one that I don’t see coming through the door of the ED. Considering the rate of POP applications in the fracture clinic next door if the rate was that high then why am I not swamped with fracture clinic patients with DVTs? A tricky question and I can only surmise, but arguably this is a different patient group to the spontaneous patients and as the BET states, the incidence of PE and fatality as a result of these rather common DVTs is low.

So, should we routinely treat? Do you routinely treat? Would this change your practice??

I must admit to having changed practice. I am much more likely to prescribe LMWH if there is even a sniff of a risk factor and no contra-indications and up until recently I’ve been using POPs much less frequently.

I’d also say that if I turn up in your ED with a broken leg that requires a POP I will be asking for the LMWH. I don’t think I want to risk a 1:5 – 1:6 chance of getting a DVT.

What about you? Would you, should you, could you, do you??

Simon Carley

The Ondansetron question

In your standard ED practice – do you give anti-emetics (specifically ondansetron) to children with gastroenteritis, hoping to improve the tolerance of oral rehydration?


This has always been a debated topic, but has recently been given extra fuel by the issue of a drug safety warning by the FDA – Ondansetron: risk of abnormal heart rhythms…..

In the resource-rich world use of anti-emetics in gastroenteritis is questioned because we have resources available for NG and IV rehydration strategies and we also rarely see death in this cohort of patients. Still the burden of the attendance to ED’s huge, gastroenteritis in the UK accounts for more than 500,000 consultations and 7% of hospital admissions in children under 5years.

In developing countries, the situation is starkly about mortality: diarrhoeal disease was the third leading cause of death in resource-poor (and middle-income) countries, causing 6.9% of deaths overall. In children under five years old, diarrhoeal disease is the second leading cause of death – 1.5 million deaths (figures from WHO).

Oral rehydration is still the mainstay of treatment of children with gastroenteritis throughout the world. Recently studies have showed that the addition of oral ondansetron can reduce vomiting episodes and facilitate oral rehydration (see Bestbet No.1442 for a succinct overview of the evidence). In the UK, NICE have produced guidance on childhood gastroenteritis (CG84), devoting a large section to a discussion on the evidence for and against ondansetron. In which they fall short of advocating its use (this was produced prior to the drug safety warning).

At the ICEM2012 recently, Hezi Waisman from Israel spoke of the efficacy and advantages of using ondansetron in children with gastroenteritis and was supportive of routine use. However debate was started when Baljit Cheema – a Paediatric Emergency Physician in South Africa – said that ondansetron had been withheld from formularies in ED’s in South Africa since the drug safety warning.

So what is the drug safety warning? Well, the information has come from the FDA who give this advice:

“The anti-nausea drug ondansetron (marketed as Zofran and in generic forms) should not be used in patients with congenital long QT syndrome, as they are at particular risk for developing torsade de pointes while taking the drug. Also at increased risk are patients with congestive heart failure or bradyarrhythmias, those predisposed to low potassium and magnesium levels, and those taking other drugs that can lead to QT prolongation. Accordingly, ECG monitoring is now recommended for such patients using ondansetron.”

The evidence cited by the FDA comes from 3 papers that have been published in anaesthetic journals. These papers have suggested that ondansetron can prolong the cardiac QT interval in some patients and extrapolated that this could be proarrythmic (patients with QTc >500ms are at risk of developing ventricular tachyarrythmia).

Looking closely at the cited evidence:

The first paper (Charbit et al) took a group of 85 patients under going anaesthetic (note that all inhalational anaesthetics and suxamethonium and patient temperature and known to prolong QT interval) then recorded ECG’s after the administration of ondansetron and droperidol (another anti-emetic known to prolong QT intervals). Patients were not randomized and there were no placebo groups. They found that in the ondansetron group showed a significant difference in (prolonged) QT interval after drug administration, however only 13% of these patients showed a QT >500ms and there were no other ECG abnormalities or adverse events during the study. Apart from the metholodical flaws in selection, it is unclear how this study relates to practice outside of the anaesthetic department as the sample had a baseline of 20% prevalence of prolonged QT prior to drug administration compared to the general population prevalence of 0.1% (thought to be due to anaesthetic drugs)….

The second paper (by the same team Charbit et al) is a well-designed, prospective cross-over trial in a healthy population, powered to detect a difference in QT length. This time they found again that ondansetron significantly (statistically) prolonged the QT interval. But no patient reached a QT of >500ms or indeed experience any arrhythmia or adverse event.

The final paper (by Nathan et al) is a retrospective chart based cohort study looking at all adverse events in children with known prolonged QT syndrome undergoing anaesthesia. There were 76 patients with 114 anaesthetic encounters. Only 2 adverse events (i.e. cardiac dysrrythmia requiring treatment) occurred but these were thought to be in close temporal proximity to administration of either reversal agent or ondansetron. Despite the fact that the adverse event rate was only 2.6% in a population known to already have prolonged QT and the fact that the events might or might not have been related to anti-emetic or reversal of anaesthetic or sympathetic drive during emergence from anaesthesia the authors conclude that ondansetron should be avoided…..

This is the evidence that has supported the FDA decision and, whilst I agree patient safety is paramount and all potential drug adverse effects should be flagged, I’m not sure that these 3 papers should induce clinical panic…

Now I want to write an impartial piece to generate discussion around the issue of ondansetron use in the ED, but as I write I am becoming a little distracted and bias – so I will sum up….

Gastroenteritis is a worldwide problem and leading cause of death amongst children under the age of 5years. The mainstay of treatment is oral rehydration, and ondansetron is clinically effective to aid this approach – increasing oral intake and reducing the use of IV therapy. In many countries the use of ondansetron is still debated (and specific to the UK not endorsed by NICE). Based on the evidence presented above the FDA has produced a drug warning that has resulted in some countries – notably a middle income country with a significant disease burden – withholding ondansetron use in children with gastroenteritis.

The question about ondansetron is actually opens a number of clinical, ethical and understanding of risk debates? What conclusions do you draw?

I’d be interested in your opinions.

Tom Bartram