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.

ADAPT my management of low risk chest pain? I’m not sure I will…….

Another Friday another JC in Virchester. Lots of chin stroking and pontification on this one.

We looked at the ADAPT trial by Martin Than and colleagues. Essentially they assessed the diagnostic utility of an accelerated protocol using Timi risk score, 0 & 2 hour troponin I measurements for rapid exclusion of cardiac pathology in patients attending the ED with chest pain. I was rubbing my hands on this one. “think of the bed days we can save on the decision unit. Say goodbye to all the 12 hour boredom of the ‘rule out’ MI admission.”

So what did they actually do? Well, over 2 sites in Oz and NZ they assessed 1975 patients attending with chest pain of suspected cardiac origin. They performed baseline and 2 hour Troponin I measurements that were unavailable to clinicians. They performed usual diagnostic protocols and followed patients up for 3 months. Then an adjudication panel apportioned the diagnosis of Major Adverse Cardiac Events at the end of the study period. They subsequently looked back to ask 2 main questions:

Firstly, what was the sensitivity of their accelerated diagnostic protocol (did it catch all the true positives)?

Secondly, if we assume the ADP is highly sensitive and therefore ‘safe’ how many patients would have been potentially dischargeable directly from the ED within 4 hours?

The methodology was pretty sound. Pretest probability for MACE was a little on the low side (15.3%) compared to our prevalence (20%) or other studies (30%). But their use of MACE is in keeping with much of the literature on the topic. The adjudication committee was not independent but we had a long discussion about this and concluded that actually, if they were blind to the Trop I assay, they couldn’t introduce much bias here even if they wanted to. If they underestimated MACE based on some of the more subjective aspects for example, they could potentially heighten the sensitivity of the diagnostic protocol – but this would worsen specificity and consequent diagnostic utility. Thus they would be shooting themselves in the foot.

And what did they find?

An excellent sensitivity of 99.7% (95% CI 98.1 – 99.9)

A dischargeable proportion of 20% using the ADP, with 1 MACE event in this group only (0.25%).

These are very interesting findings from a large, methodologically robust diagnostic study from 2 countries with a distinguished author list.  So, are we going to start applying the findings in practice?  I’m not so sure.  The findings must be taken in context with other concerns about the paper. We only had a few issues, but here they are:

1. There was no mention of symptom duration at presentation in the cohort. Thus we don’t know how long these patients had had symptoms for prior to presentation. This is important: if most of the 1975 presented at 10 hours then actually, your 2 hour Troponin is predominately a 12 hour Troponin if you use time from symptom onset for your exclusion. We do Troponins 12 hours after symptom onset, but other systems (for example in many American papers) a measure of 12 hours after ED presentation is used.
2. Their findings have not yet been externally validated. The sensitivity especially is likely to be slightly overestimated in a tightly controlled exploratory cohort. Something to be cautious of.
3. They used Trop I rather than one of the new all reaching brand new spanking best in show highly sensitive troponin assays.  This might mean that the findings are more immediately relevant if you’re not using a high sensitivity assay, but for us in Europe this is a concern.  The proportion of patients who could be discharged is likely to be lower with a high sensitivity assay.
4. The proportion of dischargeable patients using this rule was actually not huge at 20%. In the UK, this may be even less (only 7.4% of our patients had a TIMI risk score of 0/7 in previous work).  It follows that the others all end up admitted to some sort of inpatient service. This is a fairly self fulfilling prophecy in terms of investigations and therapeutics, as noted by their figures of 74% ADP negative patients receiving further investigations and 14% recieving therapy of some form.  There are risks with this.  And remember, the actual prevalence is only 15.3% (increased to 18-19% if we discount the ADP positive patients). 60% are still getting a raw deal (full inpatient investigation and treatment with no clear diagnosis at the end) Are we potentially therefore doing more harm by using a strict diagnostic protocol such as this one that will no doubt encourage admission due to the limited specificity?

The accompanying editorial to this paper can be found here and is a really nice summary of how far we have come and how much work still needs to be done on this topic. It also highlights the recent work looking at undetectable HsTnT to exclude MI at the door by a certain Dr Body (who?) and Professor Carley (never heard of him). This kind of work interests me a little more if I am honest.

I want a test which I can use immediately on the young patient with low risk chest pain that will rapidly reassure me about an absence of cardiac pathology. I am happy that Troponin is not this test in the elderly and will often manage them as ACS irrespective of initial trop results.

But if you can find me a way of getting all those 30-40 year olds who wait 12 hours only to be told that they haven’t had a heart attack (no s***) but that we’re not really sure what’s wrong with them,  off my decision ward, then I will applaud you.

Carry on the good work sirs.

dan

Superficial Venous Thrombosis: watch and wait or anticoagulate?

Check out our ICEM poster on this.

So, I see this old chestnut is under discussion again. A couple of us from the EmergINg team brought a poster to ICEM on this very topic. Sure you’ll all degree it’s another thorny VTE question well worthy of discussion.

In keeping with Rick and Simons previous posts, this is a decision very much about risk. I have a young fit man with a clinical thrombophlebitis to the Long Saphenous Vein (LSV). It’s a bit sore, but he is well and has no overt risk factors for VTE. Do I bash out some NSAIDS and tell him that we’ve been ignoring these for ages, it will probably go away? Or do I try and maximise information through USS then go through the risks and benefits of differing treatment strategies?

The initial step to scan is an important one in my opinion. A lot of these will be associated with distally propagating calf DVT. Once you are in the axial deep calf veins then there is an increasing risk that at least warrants serial USS. These calf DVTs can be silent if the Superficial Venous Thrombosis (SVT)  is distractingly sore. Secondly, a scan can delineate the extension of the SVT and help you assess risk further. Is it >5cm for example, in which case the new American guidelines would recommend 45 days prophylactic dose Fonda/LMWH . Is it tiny and chronic? Does it go all the way up to the Sapheno Femoral Junction (SFJ), in which case a vascular surgeon may be interested in acutely tying off the vessel. The scan really helps and reassures the patient that you are taking their symptoms seriously.

Next comes the discussion regarding risk. Both of conservative and aggressive management. In the CALISTO study  1500 patients were treated conservatively for SVT and had a composite endpoint event rate of 5.9%. The Number Needed to Treat (NNT) with Fondaparinux would therefore be 20. Pretty good. But what actually made up the composite outcome?

Only 5 patients out of 1500 in the conservative group developed a PE (0.2%). Only 18 patients developed a DVT (1.2%). The majority of outcome events were made up of propagation within the superficial veins or recurrence. So you may not be doing quite as much good as you think you are with treatment. Also, any anticoagulant treatment of course carries a risk of bleeding. 1% in the Fonda group for any bleeding in this trial, which is likely to be more aggressively monitored than in the real world on more compliant patients (volunteering for research) and therefore reduced as a consequence. There has also been criticism of the study due to the lack of prescribed NSAIDS/monitoring. Many VTE clinicians wanted to see Fonda/LMWH vs naproxen, not Fonda vs placebo.

The Cochrane review on the topic has been updated to reflect the CALISTO trial results and provides a nice overview of the evidence . But we are left in the realms of uncertainty still. And we haven’t even started talking about cost effectiveness yet… though there is a nice article on this in the jounral CHEST here

“If we don’t treat your disease, the risk of serious clot related illness if probably about 1-2%. It will probably be sore for a while also. If we treat it the risks and symptoms are reduced, but about 1% patients may bleed or have a reaction to the drug. Also, you have to stick yourself daily with a needle for 45 days.”

What do you think? What would you want for your relative? What would you want for yourself? Low levels of risk but with emotive consequences like this are clinical situations where we as EPs need to stop and think carefully. We are often in a rush and used to making quick critical decisions. But in a situation like this one we need to understand the evidence and relay that in understandable terms to the person in front of us.

We are good at this overall. It is a particular skill set of Emergency Medicine. We just need to recognise when to use it and to force ourselves to take the time to do so.

Very interested to know what the world is doing about these where you are. Let us know and shout out if you feel strongly one way or the other.

Dan H.

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

Deciding Who To Investigate For ACS: The Problem Of ‘Coronary Bridge’

The problem we have with cardiac chest pain

It seems to me that many emergency physicians struggle to understand exactly how we’re supposed to be managing patients with suspected cardiac chest pain.  The first, and arguably most important question, is about who we should investigate in the first place.

The confusion is understandable as there are mixed messages coming out of the literature.  On the one hand, we have to be very cautious as we know that atypical symptoms don’t rule out an acute coronary syndrome (ACS).  We really don’t want to miss ACS as we know that patients who are inadvertently discharged have a worse prognosis than similar patients who are admitted.  What’s more, missed diagnosis of ACS is one of the leading causes of medical litigation.  On the other hand, we get constant negative feedback from inpatient specialties who may feel that we admit too many patients for suspected ACS and others who feel that we may be overusing troponins.  After all, less than 25% of the patients we admit for investigation will actually turn out to have ACS.  So what are we to do?

The value of symptoms and signs

Amal Mattu recently provided some great guidance in a fantastic Medscape article.  He sums up with 3 key pearls of wisdom: (1) Though there are factors that reduce the likelihood of ACS, don’t rely on them – none of them risk stratify the patient to the level of ‘no risk’; (2) If you do discharge a patient with chest pain, make your practice as defensible as possible by documenting as many of the ‘low risk’ factors as possible; (3) Beware of factors known to increase the likelihood of ACS (like pain radiating to both shoulders/arms or to the right shoulder/arm, vomiting, sweating and exertional pain).  I certainly echo these sentiments.  Following a recent conversation on Twitter, I thought it would be useful to expand further on my thoughts.  (Further than you can in a 140 character Tweet!)

Dr. Mattu’s Medscape article referred to my paper in Resuscitation, entitled ‘Symptoms and signs in the emergent diagnosis of acute coronary syndromes’.  In this paper, we reported some interesting findings.  First, there are a number of ‘typical’ symptoms that don’t seem to alter the probability of acute myocardial infarction (AMI) very much at all.  This included pain radiating to the left shoulder or arm, which did not significantly increase the likelihood of AMI or adverse events over the following 6 months. Pain located in the left anterior chest actually made the diagnosis of AMI less likely.  On the other hand, certain atypical symptoms turned out to make the diagnosis of AMI more likely.  This included, notably, pain radiating to the right shoulder or arm!  No features were useful to help rule out an AMI.  For example, 19% of patients who described their pain as sharp or stabbing in nature were either having AMI or developed a major adverse cardiac event within 6 months.  That’s not much of a rule out!  A pleuritic nature to the pain did not significantly alter the probability of AMI or adverse events at all.

There were some more interesting findings in our study.  Patients who were observed to be sweating in the ED were, more often than not, having AMI.  The probability of AMI was, in fact, 59%.  The positive predictive value of sweating observed in the ED is even higher than that of ischaemic ECG changes.  That’s pretty powerful.  AMI was diagnosed in 40% of patients with an initial systolic blood pressure <100 mmHg; 41% of patients who reported vomiting; and 35% of patients whose pain radiated to the right arm or shoulder.  So these are fairly powerful positive predictors, given that we started with a pre-test probability of 18%.  They are things we should be quite concerned about, if present, although of course they should be taken in conjunction with everything else.

So when can we rule out ACS without tests?

It’s time to re-iterate something important: no symptoms or signs can be used alone to rule out ACS.  Let’s be clear about that.  Just because a patient describes the pain as stabbing in nature doesn’t mean you can relax.  Just because it’s worse on inspiration doesn’t mean you can’t relax.  If it’s not worse on exertion, you can’t relax.  Of course, if the patient has sharp, stabbing pain that only appears on inspiration and is located only in a well localised point in the left lateral chest wall, you can relax – you’re clearly not going to suspect ACS.  We do have to retain some common sense.  Document the clinical context carefully and you shouldn’t be criticised.  However, when things aren’t as clear, when you’re relying simply on the fact that the pain is worse on inspiration (alone), stabbing in nature (alone), indigestion-like or whatever else to justify your decision not to investigate the patient for ACS, then to quote Amal Mattu at ICEM 2012, “you should slap yourself before someone else does”.

The golden rule

In practice, therefore, I can suggest 3 things that you ought to remember when considering how to manage patients presenting to the ED with chest pain:

1. There are patients you can identify as having a high probability of AMI.  Ischaemic ECG changes, sweating observed, vomiting reported, pain radiating to the right arm or both arms, and hypotension all identify high risk groups.  These patients clearly need investigation
2. There are patients you can rule out immediately who clearly don’t have ACS.  They have other causes for their pain that can be objectively identified, or their history is so clearly non-cardiac that it would be ludicrous to investigate them.
3. Then there’s the middle group of patients, who aren’t in either of these ‘high probability’ or ‘clearly non-cardiac’ groups.  Investigate these patients.  They could have ACS and you really don’t want to miss it – for the patient’s sake and for your own.

Coronary Bridge

In my first job as a Senior House Officer in Emergency Medicine, one of my seniors told me about a hospital he used to work at.  The main road leading to and from the hospital ran across a bridge.  They apparently named it ‘Coronary Bridge’, after the number of patients who suffered a cardiac arrest there having just been inadvertently discharged from the ED with a missed myocardial infarction.

We do need to reduce unnecessary admissions for cardiac chest pain.  We do, however, need to do this in an evidence based manner, with a validated rule out strategy.  I’m certainly not suggesting that we throw common sense out of the window and investigate everyone.  But next time you consider discharging your patient with ‘vague’ or ‘atypical’ chest pain just because it’s ‘vague’ or ‘atypical’, consider whether you really want to take the chance that your patient won’t make it across ‘Coronary Bridge’.  We want to reduce admissions – but let’s do it safely and scientifically.

Rick Body

New NICE guidance on Investigation of DVT in the ED

Is Venous Thrombo Embolism the most controversial area of EM practice at the moment? I think it might be as there is rarely a meeting or conference where the subject is not discussed and debated.

So is the National Institute for Clinical Excellent (NICE) here to rescue is from the controversies. Well yes, and of course no…..so basically no.

The new guidance looks to incorporate the Wells score together with d-dimers and USS scanning of the lower limbs to diagnose DVT and there is much to like in their approach. It has an element of pragmatism about it, stating that there are different approaches depending on what is available – I like that – I’ve seen too many guidelines that stipulate processes only available 9-5 Mon-Fri (when the people who wrote them work) and not enough that are similarly useful at 2am on a Saturday night.

So, what’s new. Well the two level Wells score is fine. Previous scores using high, moderate and low scores as originally described seem to confuse lots of people (why?) and in reality the important group to define is the low risk (or DVT unlikely group). The Wells amendment from 2003 seems to make sense and has already been adopted by other centres in the UK.

What else? Well the big difference to me is the early use of proximal scanning for DVT. Fine and dandy as a rule in test if available but above knee DVT scanning misses lots of calf clots. This means that we might get an early diagnosis of a proximal DVT without pursuing d-dimers, waits for blood tests and general delay. I like this if it is available and indeed it is a skill that emergency physicians can own, and it’s unlikely to cause problems.

However, I think it’s fair to say that there is some controversy about what to do about clots below the knee and as the guidance states the evidence out there is not great with just a handful of low quality studies to help us answer the question (see page 50 of the guidance). However,  my feeling is that if they are around then that’s useful to know. In the new NICE guideline scanning below the knee is not recommended in the algorithmn (though it is mentioned as an area for future research in the main text). If a patient is d-dimer positive but above knee DVT scan negative they go home and come back for another scan in 6-8 days to see if it has progressed.

Should we be worried about those 6-8 days without anticoagulation? Or is this a way of avoiding the potential risks associated with unnecessary anticoagulation? What would you do?

So what should we do in a centre such as ours with an excellent service that scans and diagnoses thrombolembolic disease throughout the lower limb venous system? My feeling is that we continue to investigate according to the best technology available. In my centre and several others this means that when we send a patient round for a scan we will be told whether or not they have a below knee DVT. I cannot then not know this information and I need to do something with it, it’s just really hard to ignore information once you have it and arguably very difficult to manage any future complaint or concern when there is an evidence trail back to you. So, I’d be really interested to know what others are doing with their below knee DVTs. Anticoagulate or not? If you do or you don’t who is driving that decision? You, your haematologists or your general physicians? My feeling having spoken to many EPs is that practice is really variable and that cannot be right for patients.

So, whilst the NICE guideline is good it is perhaps based on what is universally achievable rather than what is potentially excellent. Politically it is great when everyone is ‘equally excellent’ (whatever that means), but we all know that to not be the case. So for now I will aspire to be better than NICE and continue to take heed of clots in the calf…until some better evidence comes along at least (and I know a man who is doing just that as we speak @thegreathornero).

Simon Carley

ON POST-EXPOSURE PROPHYLAXIS: a diet PEPSE served on ice

You are on a busy shift in ED when a young man in his twenties presents after having being triaged with a “personal problem” he would not disclose in triage. He has asked to see a senior doctor urgently.
When alone, he discloses unprotected oral intercourse two days ago in a local sauna for gay men. He was the recipient and there was no ejaculation involved. The details of the sexual practice itself baffle you and the patient is requesting PEPSE (post-exposure prophylaxis following sexual exposure).
You scratch your head, as the area you work in is known to have a low HIV prevalence and you are unsure if the described rather unusual sexual intercourse is in itself an indication to start PEPSE.

The British Association for Sexual Health and HIV (BASHH) in the UK have recently revised its guideline on who should receive PEPSE following sexual exposure.
The guideline is based upon a comprehensive review of the literature and the recommendations are based upon a combination of biological plausibility, cohort studies, data from PEP in other settings and expert opinion.

This is clearly a crucial decision for the patient presenting to ED at 2AM and potentially a difficult one for the EP if not aware of the guidelines or the local prevalence of HIV in his/her area of practice.

The risk of an individual acquiring HIV following an exposure is dependent upon the risk that the source is HIV- positive where unknown and the risk of infection following a specific exposure from an HIV-positive individual:
The risk of HIV transmission can therefore be calculated. Risk of transmission = risk that source is HIV-positive X risk of exposure
Knowledge of local HIV prevalence rates will clearly assist in calculating the risk of transmission and cumulative risk should be considered for repeated exposures.

It is worth mentioning that the probability of HIV transmission depends upon the exposure characteristics (anal, oral or other types of sexual practice), the infectivity of the source (viral load) and host susceptibility (immunosuppression). Some factors increase the risk of transmission like the presence of ejaculation, the presence of genital ulceration, the viral load, the absence of circumcision etc.

PEP is not 100% effective and individuals have acquired HIV despite commencing PEP following both occupational and sexual exposures. Delayed initiation of PEP, presence of resistant virus in the source, different penetration of drugs into tissue compartments, poor/non-adherence and further high- risk sexual exposures may explain some transmissions.

Adherence and completion rates to the recommended four weeks of PEP among health-care workers and individuals exposed non- occupationally have been historically poor for several reasons.

There have also been concerns that the availability of PEPSE will reduce commitment to primary prevention strategies (the use of condoms) and consequently result in more frequent high-risk behaviour.

It is essential that emergency physicians perform a risk versus benefit analysis for every individual presenting following an exposure and the decision to initiate PEP is made on a case-by-case basis.
This should consider both the risk of transmission according to exposure and the risk of the source being HIV-positive as well as the viral load in the source if known (this is clearly difficult to ascertain in most of the ED cases).

The writing committee recommends that PEPSE is indicated when the estimated transmission risk is 1 in 1000 or greater.
The same committee also feels that when the exposure is classified as ‘consider’, PEPSE should only be prescribed if there are additional factors that may increase the likelihood of transmission, i.e. following sexual assault, in the presence of an STI (i.e. where the source is known to have an STI or the exposed individual has symptoms or signs suggesting an STI) or where the source is suspected to have acute HIV infection. www.bashh.org/documents/4076

Given that, for optimal efficacy, PEPSE should be commenced as soon as possible after exposure, 24-hour access has now been made be available nationwide in the UK.

Emergency physicians therefore assume significant responsibility for provision of PEPSE, with the need for support and training from areas of local expertise.

It is recommended that individuals presenting for PEPSE should be referred and seen as early as possible by a clinician or team experienced in the management of PEPSE and with expertise in HIV testing and transmission – whether or not PEPSE is offered or accepted.

Take home message:
1. familiarise yourself with your national/local protocol for PEPSE (it is not difficult with 24h internet access)
2. know your local HIV prevalence (get yourself bleeped out of the consult room by your nurse and google it)
3. a systematic and professional approach in the often sensitive details of sexual practice is essential (who knows, you might come across something you could put into practice at home with your partner!)
4. ask for specialist help if in any doubt (pick up that phone and call a friend!)

Janos P Baombe