Prostate Cancer screening: survival vs. mortality

Hi there

In case you missed it – Dr Rob Park has just published an epic review of prostate cancer screening over on the FOAM4GP blog.

If you have any exposure to prostate cancer screening in your practice or just are interested in the way modern medicine works – go over and check it out.  It is a really comprehensive review of where we are at with prostate cancer screening.

I posted a quick interview with Dr Joshua Quaas on the same topic a few years ago (2012).

I have only one thing to add – and it is about how the public perceive prostate cancer screening – their beliefs.  The data is difficult for even the average GP to understand – and it can be distorted by confusing the type of stats used to represent the effects of cancer screening.

So here is a 5 minute Broome Pearl – a rant on one of my pet peeves.  Why Survival data and Mortality data are not the same and should not be used interchangeably.

In fact you could say that the “gap” between Survival and Mortality represents the degree of over diagnosis when it comes to diseases like breast and prostate cancer.

Big thanks to Rob Park for his efforts.


On Sick Kids, Sore Throats, Swabs and Such

Dear Fellow Doctors,

I would like to take a moment of your time to discuss a point of medical practice which seems to remain controversial despite it being really common and a well-researched problem.  I would like to tell you about the modern management of the humble throat infection.  Yes, it is a really common, dare I say dull topic.  However, it would appear that our profession has the wrong end of the proverbial stick when it comes to this quotidian diagnosis.

Firstly, let me introduce myself and tell you why my perspective ought to be relevant and enlightening to you.  I am a small town doctor working in primary care and Emergency Medicine.  I work in a beautiful part of remote northern Australia.  I have an interest in paediatrics and specifically the acute care of Aboriginal kids.  I see a lot of children with common throat infections – don’t we all!  The reason I feel somewhat qualified to discuss this topic is because I work in a population where the complications of acute streptococcal infections still produce massive morbidity.

Our population have a burden of disease rarely seen in the developed world.  Skin infections, STIs, malnutrition, fetal alcohol syndrome… the list goes on.   Last year I saw 3 new cases of Sydenham’s chorea.  I see children with acute rheumatic fever and carditis on a weekly basis.  We are currently in the throes of an epidemic of post-streptococcal glomerulonephritis.  You might say that pus is our bread and butter.  The incidence of those dreaded complications of the common strept throat is astronomical in my neck of the woods.  So that is why I want to chat to you about a few things – namely: throat swabs and antibiotics.

So, how do we decide who has a true “strept throat” and not just a virus?

Let me start on the practice of throat swabbing children with acute tonsillo-pharyngitis.

So, when do I swab a child’s throat?  Easy – never.  I can honestly state that I have not swabbed a child’s throat in order to make the diagnosis of “strept throat” in the last decade.

I have certainly swabbed a number of throats in that time – but only in order to satisfy the diagnostic criteria of the diseases which we worry about i.e. acute rheumatic fever or post-strept GN.  To be clear, I really only swab them after the fact – that is after the diagnosis is clinically apparent and we really just need a microbiological sample to prove the case, satisfy the diagnostic criteria and provide information to the folk in the Public Health office and a few Microbiologists whom might be interested.  This is not a tool for making routine management decisions.

I hear that in much of North America that the rapid throat swab test is used to decide which children require antibiotics.  Well, that opens another whole can of worms – do they really need antibiotics?  But before we get onto that vexed question – lets look briefly at the diagnostic strategy that is “throat swabbing” and why it just doesn’t make much sense.

Before we discuss the “diagnosis” of strept throat – please recall that many children have asymptomatic colonisation with group A streptococci – they are well.  The background rate is between 9 and 14% (Link).  This seems to surprise a lot of doctors when you point this out to them.  We do prefer the binary answers i.e. positive swab equals disease, negative equals no-disease.  But life just does not work that way.

So can we use clinical findings to work out who is likely to have a true strept throat, rather than a viral infection?  This is well studied.  There are a number of ‘clinical decision rules’ that we can utilise.  For example, the modified Centor Criteria or the Fever PAIN score  are easy to use – just a few questions and a cursory exam give you all the data you need to get a score.  Here is how it pans out from the studies:

Kids get +1 point just for being kids[ aged 3 - 14 yrs] .  Then if you have any of the other criteria – tender anterior nodes, exudate or swollen tonsils, fever > 100.4 (38 C) or the absence of a cough you are up to 2 points and you have an 11 – 17% chance of having a positive throat culture.  Or basically – the same as our pretest guess based on what we know about carriage rates.  So having a Centor score of 0, 1 or 2 is pretty good evidence that you are wasting your, and your patient’s time by doing a swab.  If they had a score of 0 or 1 – then you probably wouldn’t be asking the question.  The 3 year old with a runny nose and low-grade fever has a virus 99% of the time.  Don’t apply this rule to those kids!

Incidentally if you have 3 Centor points then your rate of swab positive is about 1/3 and if you have 4 or 5 points – you are up to 50% – even money as they say.  So a kid with a full house of clinical features suggesting strept pharyngitis has a 50:50 chance of having a + swab.  Save your cash – and toss a coin instead.

So do swabs help predict response to antibiotics? Tougher question.  Are they any better than simple clinical exam and history?

There is a very recent large clinical trial out of the UK  – the PRISM trial in the UK.  This looked at the predictive ability of a clinical score (FeverPAIN) and a rapid antigen detection test (RADT) for symptom reduction with targeted antibiotic prescribing.  They found that using the FeverPAIN score was useful to target antibiotic prescription for symptom reduction.  The use of RADT tests also did the same thing.  BUT adding a RADT did NOT add anything to simple clinical scoring when used in tandem.  Therefore it would seem like a waste of resources to use a test where simple clinical exam will do the same job.

So we can use this to identify kids whom are unlikely to benefit from having a swab – i.e. the Centor 0 – 2 group will more likely have commensal strept than actual disease – so do not swab them.  So what about the others…

This is where it gets fun.  Having a high Centor score makes it more likely that you will have a positive swab test.  It DOES NOT predict that you will have a more serious clinical course or be at higher risk of the rare but nasty sequelae [Reference].  However I have had in numerous discussions with folk who genuinely get extra-worried if their patient has a Centor score of 5.  I have even seen a kid get a whack of IM ceftriaxone – purely because he had a high Centor score – not because he looked particularly septic!

Summary of Swabbing:  It is:

– unhelpful,

– can lead to a lot of false positives,

– does not predict “strept throat” any better than a simple clinical scoring tool and

– costs a lot more.

Even in the kid with all the features of Strept throat – there is not much evidence to suggest swabs can help predict who should get antibiotics.  The question of whether or not antibiotics actually help is to be covered next….

So lets assume you have taken a look at a kid and clocked up a full suite of symptoms suggestive of strept (eg. large, kissing exudative tonsils, tender nodes and a fever without a preceding viral prodrome, coryza or cough.)   The Centor scores suggest 50% rate of swab positivity.  It certainly is not 100%!.  Now we come to the big issue – to treat with antibiotics or not….   I am going to break this down into 3 areas for discussion.

(1) patient-oriented benefits i.e. pain and suffering,

(2) preventing suppurative complications : Quinsy, otitis media, sinusitis, cellulitis / impetigo

(3) preventing non-suppurative complications [i.e rheumatic fever, PSGN].

Let’s start with the most likely actual potential benefit of antibiotics.

What do antibiotics do for kids with sore throats in terms of symptoms?

This question should be easy enough to answer – search the Cochrane database.  The reviews there are huge – and they include papers from the last 50 years. So a heterogeneous group of patients, actually there are surprisingly inadequate trials in kids specifically.  There are not many recent trials – so we may be seeing a bias – with antibiotic resistance emerging and improved hygiene etc in the last 50 years.

The simple summary of the data is:

– antibiotics reduce pain after 3 days.  This effect was seen in subjects whom were swab positive.  About half of non-treated patients were improved by day 3, more in the AB groups. The NNT was about 6 for “pain reduction at 3 days”.

– by the 7 day mark the difference was much less with an NNT of 21 for pain resolution by day 7.  That is most of the untreated kids were better, the gap between the treated and untreated cohorts was smaller at one week.

OK, excellent… so what were the downsides?  Unfortunately a lot of these trials do not report harms accurately.  So if you want to know exact rates – it is tricky.  The common adverse effects attributed to penicillin and similar antibiotics commonly used for sore throat are:  diarrhoea, nappy rash, cadidiasis, skin reactions and the big one – anaphylaxis.  Studies looking at the common, minor reactions would put the NNH [number needed to harm] between 6 and 9.  Anaphylaxis is a bit more bothersome – though rarer – maybe 1 in 1,000 to 1 in 10,000 depending on the paper you believe.

To be honest – if you are having a risk vs. benefit chat with the parents about ABs – then anaphylactic reaction does seem a bit over the top.  I just don’t think that it really weighs on a parent’s mind enough to change the way they feel about “fixing” their sick child ASAP.

So here is how I would discuss the risks  and benefits of antibiotics in a kid with a high Centor score / clinical impression of strept:

Jimmy has a nasty throat infection.  Based on how he looks, his age and other symptoms I would estimate that there is a 50:50 chance that he has a “true strept throat” which antibiotics have been shown to help.  When we say ‘help’ – we mean that he is more likely to have less pain etc in 3 days.  For every six kids we treat with antibiotics, one will get this benefit.  The other 5 will not.  However, there are a number of other ways we can reduce Jimmy’s pain without using antibiotics – and they work a lot faster.  On the downside, roughly the same number of kids that we treat with antibiotics will get a side effect – like diarrhoea or a rash from the antibiotics.  So I reckon it is a close balance between risks and harms.  Would you like to hear more about antibiotics or I can give you a plan for managing Jimmy’s pain and fever?”

I would not even delve into the murky waters of the benefits of antibiotics for more serious sequelae – these are so rare and the evidence is so sparse that it would not be a meaningful discussion.  If the family want to discuss problems like quinsy or rheumatic fever then I would imagine they are the type of folk whom are going to insist on at least a “wait and see prescription” – which seems fair enough.  I would however make it clear that the ABs will do very little for their child’s symptoms in the short term – and insist they use a good analgesia plan.  My favourite line in this scenario:  “So are you specifically wanting antibiotics or for your son’s symptoms to get better?”  It really helps parents think about what they want for their kid.  We need to separate the concept of ‘reducing suffering’ from ‘antibiotic prescription’.

There are a few papers out there that suggest the simple NSAIDs give more rapid and significant relief of throat pain. This review of the data from the Brit Journ of GP in 2000 suggests that ibuprofen and paracetamol are both efficacious, quick and well tolerated.  This seems like a reasonable option – paracetamol and ibuprofen are omnipresent in parent’s medicine cupboards – so I am sure most will have already dosed their munchkins – just need advice on how to do this safely and effectively.

I am a fan of a “dose of Dex” for the patient with a nasty sore, swollen throat – as a Paeds Anaesthetic doc – we give a lot of Dexamethasone for prophylaxis of swelling, nausea etc  – it seems to be good.  So is there much data on using steroids for sore throat?  Well – yes… and no.    There have been a series of trials looking at steroids – but they all gave antibiotics concurrently – so tough to say if they are testing steroids, or a combination effect of ABs and steroids.  The Cochrane folk did a review in 2012 – and concluded that the addition of steroids (oral, IM..) roughly tripled your chanced of being symptom-free in 24 hours. So I do use these, but would love to see the trial of Dex vs placebo  vs dex + ABs vs placebo.

Can we prevent local purulent complications of pharyngitis / tonsillitis?

Lets look at the dreaded local suppurative complications of tonsillitis – quinsy, otits media, sinusitis, cellulitis / impetigo.  Do we have any good data on this ?  Yep – the Brits recently published a huge prospective clinical cohort study with over 14,000 patients! Check it out here: Predictors of suppurative complications from acute sore throat in primary care Brit Med Journ  Nov 2013.  And here are some raw numbers for you…. have a guess – how common are these?

Of the 13,288 patients they have data on for complications:  47 developed quinsy (0.35%),   38 got sinusitis (0.29 %),   69 had acute otitis media (0.52 %)   and only 20 (0.15 %)had cellulitis / impetigo at follow up.  So if you take all comers – about 1.3 % will get a suppurative complication – regardless of the antibiotic prescription.  The numbers are tiny!  I am sure most doctors would guess these rates would be closer to 10 or 20 % if asked.

So any benefit is going to be tiny in absolute terms. The NNT for preventing OM or sinusitis was 193 in a Lancet Infectious Dis 2014 paper from the same data set.  Can you sell a reduction in otitis media from 0.6 % down to 0.5 %??  It is just not worth discussing.

Actually if you look at the raw data the rate of quinsy actually went up in the antibiotic groups – from about 0.2 % to roughly 0.4 % [a 100% increase! - see recent blog post on the evils of relative risks.]  I am sure this was biased by the GPs tending to prescribe ABs to folk with really bad looking tonsils that were ‘near quinsy’.  In this older paper from the Brit Journ of GP 2007 – only about a third of patients diagnosed with quinsy actually presented with a sore throat prior to being diagnosed with a quinsy.  So even if antibiotics were effective [maybe they are not?] – you will not see two-thirds of the patients anyway – they will just rock up with a hot, red, angry quinsy de novo – and you should drain it – not so much use antibiotics then! [Oh, use an ultrasound to drain it - very cool.]

So – for suppurative complications the summary discussion ought to be – the risk of another local infection is very low – about 1 in a hundred.  Antibiotics may reduce this a bit, but it is not really clinically significant.  The preferred strategy here should be to safety net and ask patients to come back for review if they develop new symptoms.  Even then – are we going to treat otitis media or sinusitis any more so with antibiotics?

What about rheumatic fever and glomerulonephritis?  Can we prevent these?

OK – now onto the really rare complications – the “non-suppurative” ones.  Namely acute rheumatic fever and post-strept glomerulonephritis.  As I mentioned earlier – we here in tropical Australia are sadly world experts on these diseases.  They remain relatively common despite ours being a very rich country with a decent, socialised health care system.  It just is not too hard to get some antibiotics in most places, and for free!   This is the part where I might get a little controversial as there is a lot of political and medical debate about how we should deal with these diseases.  But to cut a long story short – I am not convinced that antibiotics are going to prevent these problems.

First lets look at a real, first world population – western Scotland .  The incidence of rheumatic fever in the developed world is low, very low, super-super low! In 1985 (30 years ago) this paper in Scotland [Howie, Journ RCGP, 1985] estimated it would take 12 GPs working a lifetime to identify one single new case of acute rheumatic fever.  That is cool: in a medium-sized town – only one single case of ARF would have been diagnosed since that paper was published!

Now in my part of the world acute rheumatic fever is common.  We drill the Jones criteria into our RMOs and medical students.  They need to be able to pick it clinically.  It is common enough.

We throw a lot of antibiotics around – the unofficial policy is to treat any Aboriginal kid with a febrile, sore throat, ears ache or skin infection aggressively.  There is a really proactive immunisation system – with great rates of coverage – over 95% in most communities.  We have been doing this for a few decades now… and yet we are still seeing these complications of streptococcal disease.  Why is this?  Why are these kids still getting sick despite the marvels of modern medicine?

Well – lets take a quick history lesson in streptococcal disease.  These diseases were common in Australia and other first world countries a hundred years ago.  In the early 20th century the rates of rheumatic fever (or scarlet fever) began to decline in urban, developed countries.  Here is a typical graph (this one from the UScarlet fever mortalityK).  Note that the steep part of the decline occurred between 1860 and 1900.

So -this makes it unlikely that antibiotics are the cause of this dramatic decline.  In fact – antibiotics had very little impact of the rates of disease or morbidity when they were introduced towards the middle of the 20th century.

McKinlay & McKinlay out of Harvard wrote this paper: The questionable contribution of medical measures to the decline of mortality in the United States in the twentieth century. – it included streptococcal disease.  I have taken this table from the text and underlined the streptococcal stats for you: as you can see the impact of penicillin between 1946 and 1973 was almost exactly ZERO.

Scarlet fever decline post penicillinOK.  So why did all those nasty diseases go away? Well, the prevailing wisdom would suggest that a change in the “social determinants of health” occurred.  Rheumatic disease is the result of a chronic exposure to strept antigen in a susceptible host.  Streptococci thrive in overcrowded, malnourished people with poor access to basic hygiene (running water, washing facilities, refuse disposal).  This is what we see in the north of Australia – these are diseases of poverty – it is unusual to see rheumatic disease in well nourished, suburban Aboriginal kids.

What happened in that 50 years from 1860 – 1910?  People got running water, toilets and the average size of the household declined.  Folk were able to wash regularly, nutrition generally improved.  So I would say that the decline of these diseases was more the work of plumbers, builders and town planners rather than doctors and microbiologists.

So should we really be worrying about all of those kids with sore throats?

There is a large body of evidence to suggest that rheumatic heart disease are associated with pyoderma (skin infections) rather than pharyngitis. [McDonald, Clinical Infect Diseases 2006]  and as such – treating children with throat infections ay be a wildly misguided strategy in the first instance.  Currie et al also found a strong relationship with impetigo and subsequent post-strept GN disease.  Pharyngitis just does not seem to be particularly common in these kids.  In fact in my time in the tropics – I cannot recall a single case of “non-suppurative” disease in which the doctors were able to identify a clear, antecedent sore throat.  We just do not see this!  Although it is common to do swabs and return a “positive” – but as we know – that is expected in a good number of these kids – based on th known carriage rates.

The majority of the antecedent infections that cause non-suppurative complications fly under our radar – they are not seen by doctors, and hence do not get treated.

For example during the outbreak of ARF in  Salt Lake County, Utah in the mid-80s it was noted that at least  two thirds of the cases reported no clear antecedent sore throat. [NEJM, Veasy et al 1987]  And there was no change in the community rate of acute pharyngitis to suggest an epidemic.  They didn’t mention the rate of antecedent pyoderma!

So – in summary  – for preventing acute rheumatic fever and PSGN…

–  You’ll need to wait a long time to see a case in any first world practice – it is just really rare.

–  Antibiotics seems to reduce the rate of these complications – but we are talking about a near-infinite NNT!

–  There is a good amount of data that the infections that lead to ARF etc are (1) subclinical / not coming to our attention, (2) more likely skin infections than throat infections and (3) the result of chronic host-antigen interactions as a result of chronic exposure.

–  This is a disease of poverty.  If we want to prevent it we need primordial measures – better housing, running water and access to good food.  Doctors and antibiotics (i.e primary prevention) are unlikely to help.

[NB: secondary prevention with long-term antibiotics in children whom have confirmed ARF does benefit that high risk cohort. The Australian Heart Foundation makes it clear: "Secondary prophylaxis with regular benzathine penicillin G (BPG) is the only RHD control strategy shown to be effective and cost-effective at both community and population levels."]

How do I practice?

I live and work amongst some of the sickest kids in the developed world.  I would really love to be able to prevent as much of the morbidity that I see every day.  And yet…  I do not believe that aggressive investigation or antibiotic use will achieve this goal.

Many of my colleagues opt to give antibiotics to Aboriginal kids with a sore throat – and I think this is reasonable.  If you can identify a “high risk” cohort – then the equation tilts in favour of treatment.  I would argue that even within this group – we can further define the “at risk” kids by looking for signs of chronic illness, malnutrition and recurrent skin disease [scabies, impetigo etc].  Asking about the household – how many live there, diet, and the access to hygiene facilities etc.  Then treat this with acute and subsequent follow-up care.

In children with the usual background, “developed world” risk there appears to be no real basis to prescribing antibiotics with the aim of preventing suppurative or non-suppurative complications.

There is clinical equipoise when it comes to using antibiotics for “symptom reduction”.  The NNT was ~6 on day 3.  However, there are more effective and less harmful medications which will achieve this goal faster.  I only prescribe antibiotics after a realistic discussion about the likely risk and benefit has been had, and failed to convince the parents.   I routinely tell them to stop the antibiotics as soon as their child is improved.  Why run the risk of more adverse effects?

I give a written analgesia program – with doses and suggested times.  I see a lot of under-dosing of pain meds in this scenario.

I offer a stat dose of Dexamethasone (0.15 – 0.3 mg/kg) to kids with nasty swelling, bad pain or swallowing difficulty.


Final thoughts…

So that is why I do not swab, treat symptomatically and rarely prescribe antibiotics for an acute sore throat.

If we really want to improve the lot of our patients – and significantly reduce the burden of streptococcal disease – then we need a systematic approach to “primordial prevention”.  We need better houses, schools, nutrition and access to the basic services that we all take for granted in the First world.  We need plumbers, not doctors!

As always – I would be very happy to hear your thoughts.  There is a huge diversity of practice all over the world when it comes to treating kids with sore throats.  I hope that my perspective from the coal-face of post-strept sickness will give you a new perspective in your own practice.


The History of Empathy from SMACC GOLD


About six months ago I was at the SMACC GOLD conference in Queensland having a blast and rubbing shoulders with the great teachers of the FOAM family.  I was lucky enough to be asked to give a talk and really given free reign over the topic.  Which sounds like a good thing, but means that I had to think long and hard about what I really wanted to talk about.

I certainly feel a good measure of the “Imposter Syndrome” when I go to these amazing meetings and give my five cents as a rural generalist.  After all we specialise in knowing just enough to get by – so what can we add to such an amazing group of specialists.  So I chose a topic that I think we GPs know very well and one that I believe can solve many of the dilemmas facing the broader medical community.

Empathy. Yep – sounds like a really dull topic.  Very wishy-washy, touchy feely and far removed from the hardcore airway and resuscitation realm.  But I love a challenge – I wanted to have a crack at making empathy relevant to doctors in the coal face of critical care.  Putting it in terms that we can understand and integrate into our practice.  The challenge – to sell “empathy” to the super smart FOAM docs.

To put this into context – I was sitting in the audience for the opening ceremony where Dr Vic Brazil gave an awesome talk about the Tribes of Medicine – in which she discussed the troubles of intercollegiate empathy.  This was heartening to hear as I was up to speak a few hours later on some similar themes.  And then I saw that I was due to speak at the exact same time as the venerable Dr Cliff Reid – he was talking on Dogmalysis in Resuscitation.  Once again – another theme I wanted to explore – as dogma is an enemy of empathy.

So please have a listen to the podcast.  The audio is here on the ICN website.

NOTE for viewers :-  It is a very visual talk with lots of images.  So it works best if you listen and follow the slides below.

It is a complex and fascinating topic – one that I hope will be the start of a discussion about how we can do better in our moment-by-moment interactions with our patients, friends and colleagues.

I would really love to hear your thoughts and if you have any ideas or practical tips for us all.  How do you enhance your interactions with your patients and colleagues?

Let the conversation begin.


Resus Room Feng Shui

Just had to reblog this one.  My mate and fellow “madman” of rural FOAM has just posted his SMACC talk slides for you all to check out – he was a star of the SMACC stage and did a great job selling the rural scene as the place to do great Medicine .


So Check out his talk here: Resus Room Feng Shui

If you are a rural doc and want to know what all the FOAM noise is about – then this is a good place to start.

If you are just finding your way, and want to be better at the cold face of trauma, critical care or other medical malady – then watch this and you will have a great base to start to shape your practice.

Thanks Tim


Relative Absolute Risk – the discussion

This is a follow up discussion on the recent post on risk – its two flavours being “relative” and “absolute”. This is a quick look at the basics of describing risk and how it can lead one astray!

Lets start by looking at how “relative risk” can be used to sell stuff – newspapers, health messages, whatever.

In February 2014 the Daily Mail in the UK published this report on “Deadly Risk of Pill used by 1 million women

Sounds pretty scary – these 3rd generation OCPs can nearly double the risk of a woman developing a serious thromboembolic problem.  In fact there is in Australia a class-action against the manufacturer of a few brands of these “new Gen pills”. Now lets look at the raw numbers and some data.  There have been a number of trials and all with varying rigidity in terms of how they followed-up who got a DVT or PE.  So the numbers here are ranges given by a Report from the FDA n the US in 2012.  The numbers are the rates of VTE per 10,000 woman-years exposure:

  • Normal women, no OCP, not-pregnant  -  between 1 and 5 clots
  • Women taking “2nd gen, or conventional OCPs” – 3  - 9 clots
  • Women taking drospirenone-based OCPs (3rd / 4th gen) –  10 – 20 clots
  • Pregnant women   – 5 – 20 clots
  • Post-partum period (12 weeks)  -  40 – 65 clots

If you round those numbers off a bit and say that the absolute risk difference between the “old”pill and the “new” pill is at worst 10 clots per 10,000 woman years.  Which is 0.1% per year.  Or…. a really, really small number.  Not the sort of numbers that sells newspapers or makes for a good scare-story on the evening news.  Hardly scary at all!

So what happens when the newspapers run stories like these?  Well bad things happen.  In the UK after a similar story a few years ago – many women stopped taking their OCP and relied on other less-efficacious means of contraception and more became pregnant, more had babies and more had surgical termination of pregnancy.  So as you can see from the higher rates in pregnancy – there were more clots, more morbidity and mortality….  and why?  Because a news editor opted for the drama of “relative risk” over the reality of “absolute risk”.

In the end we recently saw a subsequent prospective, controlled cohort study released in Contraception , April 2014.   more than 200,000 woman-years of exposure was analysed.  This paper showed no significant difference between the various generations of OCP for VTE or other serious adverse effects.  This is unsurprising when you look at the small effects in absolute terms form previous studies – such a small effect can easily evaporate when more data is added.

Relative risk is a poor way to represent data.  In your mind when somebody tells you of a relative risk – your instinct should be to ask: relative to what?!  This is often not done.

In Australia (as in many places) GPs and other doctors are bombarded by drug companies with print, digital and even face-face promotion of their products.  If you actually read the glossy brochures [I don't recommend it] you will notice that the big print numbers heralding the efficacy of the product are invariably the “relative benefit” numbers.  To find the comparator or the raw absolute numbers one must read the infinitely tiny print on the last page of the promo pages.  As the man, Tom Waits sang in Step Right Up (1976):  “The large print giveth, and the small print taketh away!”

Now lets go back to the last post on Relative Absolute Risk – where I gave you 3 cases of long term cardiovascular risk.  The Lancet [August 2014] published an interesting meta-analysis on the effect of BP-reducing therapy on cardiovascular risk.  They looked at individual patient data and divided the patients into 4 risk-strata at baseline.

They then looked at the groups and what the relative and absolute benefits were in terms of cardiovascular events – and here are the basic outcomes:

GROUP    Baseline 5 yr risk    Rel Risk reduction    Abs event reduct

Low                               6                               18%                        14

Medium                       12.1                           15%                        20

High                             17.7                            13%                         24

V. high                         26.8                           15%                          38

The reason I love this paper is that it demonstrates really nicely the uselessness of relative risk in terms of real-world outcomes.  All 4 groups had the same “relative risk reduction” from taking BP-lowering medications…. and yet there was a dramatic difference in the actual numbers of CV events prevented.

Absolute risk reduction is highly dependent on the initial risk conditions.  If you are at low risk of outcome X to start with – then even a massive RRR will still leave you basically where you started.  So when it comes to deciding on treatment for “Cardiovascular Risk” – we really need to look at Absolute risk and then target the patients who have a high starting risk – much more bang for your buck!

The Australian Heart Foundation clearly state that Absolute risk is the primary target of therapy – which should replace the individual BP, cholesterol and other targets as individual risk factors.  But now the problem is communicating this to a patient!  Most people can grasp a high BP reading as being “bad”, i.e. requiring a tablet, but find it tougher to take a pill for a “10% 5-year CV event risk

Hence my bemusement when my 30 year old brother was put on both a BP-lowering agent and a statin – despite being 30, thin and having no other risk factors other than eating too much take-out food!  Clearly the message is not getting through!  According to the calculators his baseline risk is about 2% / 5 years.  And yet taking 2 drugs with all the side-effects will reduce this to…. about 2%.  Really he just needs to be banned from McDonald’s and all is well!

So, should we just simply stop using relative risk?

No.  It does has it uses.  I like relative risk when I am trying to sell  (or scare) a patient into action.  Is this naughty? Or is it a good use of a bad statistic?

For example smoking cessation.  My favourite trick is to use actual data but present it in a scary manner.  For men, there really seems to be a strong fear of rectal carcinoma.  Not sure why – it just seems to be a highly disturbing form of cancer.  The incidence of rectal cancer is around 12 per 100,000 people on average.  Smokers have a higher rate - nearly twice that of “never smokers”.  So instead of saying – “ou should Quit for your lungs”, I say: “you know smoking doubles your chance of rectal cancer”….  Leave that visual image hanging for a bit and then discuss smoking cessation strategies.

OK I  will leave you with that.


- when given “relative risk” ask what the raw numbers are – work out the absolute risk before getting too much further.

-  recall that baseline risk is the best predictor of a benefit from any intervention that works

- beware of any advertising / promotion that uses “relative risk” as a selling point

- feel free to use relative risk when you need to change behaviour – commercial media do this everyday, why can’t we do the same?

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