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

C

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.

Summary

- 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?

The Yellow Stone Ultrasound Course

Are you going to SMACC – flying all that way for 4 days – well why not kill 3 birds with 1 Stone!

(1) Attend SMACC

(2) get some awesome pre-SMACC ultrasound and airway training

(3) help save one of FOAMed’s great teachers from a dark, yellow side

Here is how:
Register for the Yellow Stone Ultrasound Course

Check out the Promo here 


nbsp;

Or hear it from the boys at the Ultrasound Podcast here:

See you there in June 2015

It will be AWESOME!
Casey

Apologies: we are back online

Hi All

Just a quick note to let you know that the blog and comments are now back up and online.

We did have a bit of drama with some seriously heavy spam traffic and had to put a block up to keep it sane. Now back up and functioning.

Apologies if you wrote some really long and insightful comments on the last few posts only to have them blocked by the spam filter…. super annoying I realise!

But now it is up and going – so please share your collective wisdom with us all.

Thanks Casey

Clinical Case 106: The mysterious Pink Lady

Time for another quick clinical case

Your next patient is Joan – a semi-regular attender to your family practice.

Joan is a 67 yo woman who is usually reasonably well.  She works as a book keeper in a small business.

She has been troubled by some gastro-oesophaeal reflux symptoms over the last few years and has been taking some omeprazole “most days” for symptom relief.

Today she presents with a sheaf of discharge letters from the local ED.  7 in total!  She has been seen in the ED 7 times in the last 6 weeks with “chest pain – non-specific”.

She tells you that she has been experiencing dull, spasms of pain in her substernal area that sometimes radiate to her back.   They are not really like her usual ‘heartburn’ symptoms.  She doesn’t feel sick or sweaty.  Just worried.

These are quite unpleasant and stop her from working at her computer.  The last couple of episodes have occurred at night and woken her from sleep – her husband has called the ambulance service twice in the last fortnight!  On each attendance to the ED she has been “fast tracked” into the chest pain protocolised management.  And spent a few uncomfortable nights on a stretcher in the corridor of the ED…..  awaiting a second  troponin.

Amidst the paperwork there are formatted letters from ED interns, Registrars and even one from a consultant ED Physician.

There are a batch of plumb normal ECGs and photocopies of many negative troponin results.  She even stayed in for an exercise stress test one day – which was non-suggestive of ischemia.

She has been diagnosed consistently with:  “Chest pain – non-specific.”  or “Chest pain, not cardiac.” on each occasion.  On the latest visit the senior Doc has ventured a positive diagnosis – “Probable Oesophageal spasm.”

Interestingly there have been a number of therapeutic trials of “Pink Lady” i.e.. the Mylanta & Xylocain viscous cocktail so loved by triage nurses the world over!  Joan says that the pain is usually short-lived – coming in spasms. It seems to go away after a few minutes then return.  She says a lot of the doctors ordered the Pink stuff and when her pain got better…  told her it was from her oesophagus. [ see this post from Dr Seth Trueger on this topic. ]  Maybe best left until after the troponin has settled the question!!

She has received advice to take her omeprazole twice a day and to follow up with her GP.  OK, here she is….

So, it seems clear that she is in the low-risk group for cardiac disease as a cause of her chest pain.  Let us assume that the ED Docs have excluded ACS as a cause.

SO, if you are the GP how do you go about making an actual diagnosis in this scenario?

Is a therapeutic trial of PPIs a reasonable strategy?

Depends…. are you trying to give relief to the patient or make a diagnosis? After searching through the databases I found this decent sized trial from Flook et al, in Amer Journal of Gastroenterology (January 2013)

It looked at 600 patients with reflux symptoms giving chest pain.  A placebo, RCT (esomeprazole 40 mg BD for 4 weeks) They found a significant improvement in symptoms at the end – but this was really only for patients with less frequent reflux sx at the outset.  Not so effective for the pts with more than 2 days a week of symptoms.

There is also a meta-analysis [Wang et al, JAMA, June 2005 ] looking at 6 papers ( only 220 pt in total) which tried to answer the question about the diagnostic characteristics of a “trial of PPI” for reflux-related chest pain in patients with “non-cardiac chest pain” .  The conclusion of the authors was that is was an acceptable “test” with a sensitivity of 80% and specificity of 74% roughly.  So – it might help – but to my mind those are not stellar numbers.  I would want a reasonable high or low pretest probability of “GORD” before hanging my patient’s hat upon those figures.

Should she have endoscopy to look for serious upper GI problems?

Well that is a tricky one.  Not a lot of data.  Just opinion.  The surgeons that I work with would suggest everyone with severe enough , persistent symptoms should probably have a scope to exclude malignancy or other correctable lesions in the oesophagus.  In the good old days we would send them for a Barium swallow.  But nowadays it seems easy to get a scope, and then you have the option of a CLO, biopsy or whatever else they need on the day.

So I think it is reasonable to get a scope if you have persisting symptoms or severe symptoms so that you know what you are dealing with.  It would be disastrous and unfortunate to treat a malignant process for months and months with symptomatic care.

What is the role of manometry or pH monitoring to try and correlate her symptoms with  events in her oesophagus?

This is not something that I really see much of – but I work a long way from any Gastroenterolgists!  Certainly I have seen this done in patients with bad GORD – i.e.. those whom are contemplating a fundoplication procedure.

Found this paper in the BMJ – Barham et al from Gut, 1997. [Diffuse oesophageal spasm: diagnosis ] It is old – but suggests that for intermittent symptoms like our patient is suffering – you really need to get continuous outpatient / 24 hour ambulatory monitoring of pH and pressure in order to make this diagnosis.  Diffuse oesophageal spasm is also known as “nutcracker oesophagus” or “corkscrew oesophagus” as it has characteristic appearances on imaging.  However – you would be lucky to see this phenomenon as it is fleeting!  IN order to correlate symptoms with measured anomalous peristalsis or pH spikes – you would need ambulatory monitoring.  I guess it is like the Holter of the gut?

http://download.figure1.com/broome

Image courtesy of Figure 1

Clinical Case 106: The mysterious Pink Lady

Time for another quick clinical case

Your next patient is Joan – a semi-regular attender to your family practice.

Joan is a 67 yo woman who is usually reasonably well.  She works as a book keeper in a small business.

She has been troubled by some gastro-oesophaeal reflux symptoms over the last few years and has been taking some omeprazole “most days” for symptom relief.

Today she presents with a sheaf of discharge letters from the local ED.  7 in total!  She has been seen in the ED 7 times in the last 6 weeks with “chest pain – non-specific”.

She tells you that she has been experiencing dull, spasms of pain in her substernal area that sometimes radiate to her back.   They are not really like her usual ‘heartburn’ symptoms.  She doesn’t feel sick or sweaty.  Just worried.

These are quite unpleasant and stop her from working at her computer.  The last couple of episodes have occurred at night and woken her from sleep – her husband has called the ambulance service twice in the last fortnight!  On each attendance to the ED she has been “fast tracked” into the chest pain protocolised management.  And spent a few uncomfortable nights on a stretcher in the corridor of the ED…..  awaiting a second  troponin.

Amidst the paperwork there are formatted letters from ED interns, Registrars and even one from a consultant ED Physician.

There are a batch of plumb normal ECGs and photocopies of many negative troponin results.  She even stayed in for an exercise stress test one day – which was non-suggestive of ischemia.

She has been diagnosed consistently with:  “Chest pain – non-specific.”  or “Chest pain, not cardiac.” on each occasion.  On the latest visit the senior Doc has ventured a positive diagnosis – “Probable Oesophageal spasm.”

Interestingly there have been a number of therapeutic trials of “Pink Lady” i.e.. the Mylanta & Xylocain viscous cocktail so loved by triage nurses the world over!  Joan says that the pain is usually short-lived – coming in spasms. It seems to go away after a few minutes then return.  She says a lot of the doctors ordered the Pink stuff and when her pain got better…  told her it was from her oesophagus. [ see this post from Dr Seth Trueger on this topic. ]  Maybe best left until after the troponin has settled the question!!

She has received advice to take her omeprazole twice a day and to follow up with her GP.  OK, here she is….

So, it seems clear that she is in the low-risk group for cardiac disease as a cause of her chest pain.  Let us assume that the ED Docs have excluded ACS as a cause.

SO, if you are the GP how do you go about making an actual diagnosis in this scenario?

Is a therapeutic trial of PPIs a reasonable strategy?

Depends…. are you trying to give relief to the patient or make a diagnosis? After searching through the databases I found this decent sized trial from Flook et al, in Amer Journal of Gastroenterology (January 2013)

It looked at 600 patients with reflux symptoms giving chest pain.  A placebo, RCT (esomeprazole 40 mg BD for 4 weeks) They found a significant improvement in symptoms at the end – but this was really only for patients with less frequent reflux sx at the outset.  Not so effective for the pts with more than 2 days a week of symptoms.

There is also a meta-analysis [Wang et al, JAMA, June 2005 ] looking at 6 papers ( only 220 pt in total) which tried to answer the question about the diagnostic characteristics of a “trial of PPI” for reflux-related chest pain in patients with “non-cardiac chest pain” .  The conclusion of the authors was that is was an acceptable “test” with a sensitivity of 80% and specificity of 74% roughly.  So – it might help – but to my mind those are not stellar numbers.  I would want a reasonable high or low pretest probability of “GORD” before hanging my patient’s hat upon those figures.

Should she have endoscopy to look for serious upper GI problems?

Well that is a tricky one.  Not a lot of data.  Just opinion.  The surgeons that I work with would suggest everyone with severe enough , persistent symptoms should probably have a scope to exclude malignancy or other correctable lesions in the oesophagus.  In the good old days we would send them for a Barium swallow.  But nowadays it seems easy to get a scope, and then you have the option of a CLO, biopsy or whatever else they need on the day.

So I think it is reasonable to get a scope if you have persisting symptoms or severe symptoms so that you know what you are dealing with.  It would be disastrous and unfortunate to treat a malignant process for months and months with symptomatic care.

What is the role of manometry or pH monitoring to try and correlate her symptoms with  events in her oesophagus?

This is not something that I really see much of – but I work a long way from any Gastroenterolgists!  Certainly I have seen this done in patients with bad GORD – i.e.. those whom are contemplating a fundoplication procedure.

Found this paper in the BMJ – Barham et al from Gut, 1997. [Diffuse oesophageal spasm: diagnosis ] It is old – but suggests that for intermittent symptoms like our patient is suffering – you really need to get continuous outpatient / 24 hour ambulatory monitoring of pH and pressure in order to make this diagnosis.  Diffuse oesophageal spasm is also known as “nutcracker oesophagus” or “corkscrew oesophagus” as it has characteristic appearances on imaging.  However – you would be lucky to see this phenomenon as it is fleeting!  IN order to correlate symptoms with measured anomalous peristalsis or pH spikes – you would need ambulatory monitoring.  I guess it is like the Holter of the gut?

http://download.figure1.com/broome

Image courtesy of Figure 1